Collective Consciousness and Its Discontents:: Institutional distributed cognition, racial policy, and public health in the United States

COLLECTIVE CONSCIOUSNESS AND ITS DISCONTENTS: Institutional distributed cognition, racial policy, and public health in the United States

Rodrick Wallace PhD Mindy T. Fullilove MD The New York State Psychiatric Institute

COLLECTIVE CONSCIOUSNESS AND ITS DISCONTENTS: Institutional distributed cognition, racial policy, and public health in the United States

Rodrick Wallace PhD New York State Psychiatric Institute 1051 Riverside Drive New York, NY 10032 Mindy T. Fullilove MD New York State Psychiatric Institute 1051 Riverside Drive New York, NY 10032

COLLECTIVE CONSCIOUSNESS AND ITS DISCONTENTS

Library of Congress Control Number: 2007939054

ISBN-13: 978-0-387-76764-2

e-ISBN-13: 978-0-387-76765-9

Printed on acid-free paper. © 2008 Springer Science+Business Media, LLC. All rights reserved. This work may not be translated or copied in whole or in part without the written permission of the publisher (Springer Science+Business Media, LLC, 233 Spring Street, New York, NY 10013, USA), except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks and similar terms, even if they are not identified as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights. While the advice and information in this book are believed to be true and accurate at the date of going to press, neither the authors nor the editors nor the publisher can accept any legal responsibility for any errors or omissions that may be made. The publisher makes no warranty, express or implied, with respect to the material contained herein.

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Preface

This book appears to be the first comprehensive formal mathematical analysis of distributed cognition. While the main focus is on the relations between policy and public health – particularly surrounding the failure of AIDS and TB control and treatment in the United States – the theory has wider implications and applications. Potential uses include: [1] Better understanding of mechanism and dysfunction in the ‘organizational ecology’ which has become a central focus of business schools, leading toward more effective management strategies for large firms. [2] Exploring error in smaller group settings, such as emergency rooms, aircraft cockpits, medical treatment teams, and similar venues for which moderate-scale technical fixes are sometimes possible. [3] Developing a biologically inspired paradigm for programming the vast parallel arrays of multiple-core chips now relentlessly driving computing technology, and providing a means of understanding and redressing subtle dysfunctions in large networks of intelligent devices. [4] Providing a better picture of individual consciousness, for example of the cooperation and conflict between emotion and ‘higher’ cognitive functions, i.e. the stacking of older and newer brain structures. [5] Giving new, and very general, formal tools for exploring the multifactorial impacts of crossectional socioeconomic conformation and path-dependent historic trajectory on population health and illness. [6] Allowing new approaches in ecosystem resilience theory, particularly the distinction between ‘within’ and ‘between’ transitions in dynamic manifold topology. Furthermore: [7] The discovery of markedly different classes of possible formal models for general broadcast neural structures instantiating consciousness has evolutionary implications: Current conscious animals are the survivors of repeated, highly varied, mutational branching and pruning by chance and selection. Similar considerations apply to the Lamarckian evolution affecting human organizations within and across cultures.

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[8] The mathematical theory provides interesting structures ranging from rate distortion manifolds and groupoid atlases to the geometrization of information theory, and a stochastic differential geometry of cognitive process. Our work may even suggest new asymptotic limit theorems for applied probability. [9] The quantum information theory extension applied to the single workspace problem (Wallace, 2005a) seems extendable to multiple workspaces as well. [10] What we develop is, most fundamentally, a new set of statistical models based on the Rate Distortion and Shannon-McMillan Theorems, in the same sense that conventional statistics follows from the Central Limit Theorem. Their essential scientific purpose is the empirical comparison of similar systems under different conditions, and of different systems under similar circumstances. New science emerges most directly from the dialog between theory and experiment, and the tools constructed here are regression-like procedures whose best use will be in the analysis of empirical data relating to cognitive process, wherever found. The readers of this book will be well equipped to address such themes.

Contents

1

INTRODUCTION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.1 Public policy and public health . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.2 The unfinished business of the American Revolution . . . . . . . . . 1.2.1 African-American serial forced displacement . . . . . . . . . . 1.2.2 Segregation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.2.3 Redlining . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.2.4 Urban renewal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.2.5 Catastrophic disinvestment . . . . . . . . . . . . . . . . . . . . . . . . . 1.2.6 Planned Shrinkage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.2.7 Spreading instability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.2.8 Gentrification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.2.9 HOPE VI . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.2.10 Mass criminalization . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.2.11 Viewing policies in space . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.2.12 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.3 International law on displacement . . . . . . . . . . . . . . . . . . . . . . . . .

1 1 3 3 4 5 5 6 6 8 8 10 11 11 13 13

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CONSCIOUSNESS AND DISTRIBUTED COGNITION . . 2.1 Emergence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.2 Distributed cognition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.3 Baars and Dretske . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

15 15 17 20

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FORMAL THEORY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.1 Cognition as an information source . . . . . . . . . . . . . . . . . . . . . . . . 3.2 The cognitive modular network groupoid . . . . . . . . . . . . . . . . . . . 3.3 Global and local symmetry groupoids . . . . . . . . . . . . . . . . . . . . . . 3.4 Internal symmetry breaking . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.5 External symmetry breaking . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.6 Information system emergence . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.7 Multiple workspaces . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.8 The dynamical groupoid . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

25 25 28 30 32 34 35 36 38

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3.9 3.10 3.11 3.12

The rate distortion manifold . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Institutional resilience . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Variation and selection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Recapitulation of the formal theory . . . . . . . . . . . . . . . . . . . . . . . .

44 51 54 55

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PATHOLOGIES OF COLLECTIVE CONSCIOUSNESS . . . 4.1 Individual consciousness . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.2 Collective consciousness . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.3 Red Queen and Pentagon Ratchet . . . . . . . . . . . . . . . . . . . . . . . . . 4.3.1 Firms and technology interact . . . . . . . . . . . . . . . . . . . . . . . 4.3.2 Punctuated phase transition . . . . . . . . . . . . . . . . . . . . . . . . 4.3.3 Queen and Ratchet . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.4 Failure of therapeutic intervention . . . . . . . . . . . . . . . . . . . . . . . . .

59 59 62 68 71 73 78 81

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DISEASE AND COLLECTIVE CONSCIOUSNESS . . . . . . . 85 5.1 Infectious disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85 5.1.1 Multiple-drug resistant HIV . . . . . . . . . . . . . . . . . . . . . . . . 90 5.1.2 Endemic infection: tuberculosis . . . . . . . . . . . . . . . . . . . . . . 91 5.1.3 Reconsidering infection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 96 5.1.4 The simple epidemic with removal . . . . . . . . . . . . . . . . . . . 97 5.1.5 Endemic infection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 100 5.1.6 Coherence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 107 5.1.7 Resilience of infectious disease ecosystems . . . . . . . . . . . . 111 5.2 Chronic disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 115 5.2.1 Immune function . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 115 5.2.2 Tumor control . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 116 5.2.3 The HPA axis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 117 5.2.4 Blood pressure regulation . . . . . . . . . . . . . . . . . . . . . . . . . . 117 5.2.5 Emotion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 118 5.2.6 Sociocultural network . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 119 5.2.7 Comorbidity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 120 5.2.8 Schizophrenia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 124 5.2.9 Reconsidering Zero mode identification . . . . . . . . . . . . . . . 126 5.2.10 Chronic disease and collective consciousness . . . . . . . . . . 126

6

THE FAILURE OF AIDS CONTROL AND TREATMENT IN THE US . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 129 6.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 129 6.2 CASE STUDY 1: Epidemic Response in Alameda County . . . . 130 6.2.1 Epidemic recognition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 131 6.2.2 Resources for fighting the epidemic . . . . . . . . . . . . . . . . . . 134 6.2.3 Social realignment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135 6.2.4 Overall assessment of epidemic response . . . . . . . . . . . . . . 137 6.3 CASE STUDY 2: Black clergy respond to AIDS . . . . . . . . . . . . . 137 6.3.1 Being right with God . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 139

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6.3.2 Addiction to drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 140 6.3.3 Homosexuality . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 142 6.3.4 Personal transformation . . . . . . . . . . . . . . . . . . . . . . . . . . . . 145 6.3.5 Approaches to AIDS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 147 6.3.6 Overall assessment of epidemic response . . . . . . . . . . . . . . 148 6.4 CASE STUDY 3: Women’s Equity in AIDS Resources . . . . . . . 148 6.4.1 The central antithesis: life vs health . . . . . . . . . . . . . . . . . 149 6.4.2 Care in Combat . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 151 6.4.3 Out of harm’s way . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 153 6.4.4 Can demoralization be overcome? . . . . . . . . . . . . . . . . . . . 154 6.4.5 Overall assessment of epidemic response . . . . . . . . . . . . . . 155 6.5 Epidemic Response and Collective Consciousness . . . . . . . . . . . . 155 7

FINAL REMARKS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 157

8

Mathematical appendix . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 163 8.1 Two basic theorems . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 163 8.1.1 The Shannon-McMillan Theorem . . . . . . . . . . . . . . . . . . . . 163 8.1.2 The Rate Distortion Theorem . . . . . . . . . . . . . . . . . . . . . . . 165 8.2 The mean field approximation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 168 8.2.1 Biological renormalization . . . . . . . . . . . . . . . . . . . . . . . . . . 171 8.2.2 Universality class distribution . . . . . . . . . . . . . . . . . . . . . . . 176 8.2.3 Punctuated universality class tuning . . . . . . . . . . . . . . . . . 177 8.3 Toward a stochastic differential geometry of cognition . . . . . . . . 180

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References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 185

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 203

1 INTRODUCTION

1.1 Public policy and public health The failure of efforts to control and treat acquired immunodefficiency syndrome – AIDS – in the United States, center of the most affluent and powerful empire in history, presents something of an enigma. We are, at this writing, some three decades into the pandemic, and stand at the edge of a Brave New World of widespread and spreading multiple drug resistant human immunodeficiency virus – HIV, the etiological agent of the disorder. Decisions to abandon population level strategies of control and containment in favor of ‘finding the cure’, i.e. focusing on drug treatments for infected individuals, were made in the face of widespread knowledge that HIV has the most relentless evolutionary capacity of any known living thing. The rapid development of evolutionarily transformed HIV’s was clearly inevitable, yet that fact had little if any impact on public policy. Even within the drug treatment paradigm, large segments of the US population have been excluded from reliable access to antiretrovirals and other treatment services. These are the same groups which fill the jails and prisons, and are subjected to policies of serial forced migration, the kind of ‘development displacement’ which the United Nations Commission on Human Rights sees as equivalent to ethnic cleansing in its aftereffects. Prevention efforts have been compromised by relentless Apartheid policies which threaten to create vast centers of multiple-drug resistant HIV having very great force of infection, enmeshing the entire US system in the disease ecology of marginalization. Strategies and patterns of resource allocation determining the ecology of health and illness are outcomes of public policies which are quintessential results of cognitive deliberations by institutions. While one may well take a narrative or descriptive perspective on such matters, we have chosen a less direct route, giving primary focus to an understanding of institutional distributed cognition more akin to studies of emergency rooms or aircraft cockpits than to conventional historical reconstructions. Our approach is, however, both at

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a scale much greater than these canonical examples, and based on a formal extension of recent mathematical treatments of individual consciousness. Using these tools we will, in addition to AIDS, also examine the recent tuberculosis outbreak in and near New York City, and the role of structurallyinduced psychosocial stress across a broad spectrum of comorbid developmental disorders. This is a difficult route, but one which will provide new and important insights regarding public policy and public health in the United States, particularly the critical role of the system of American Apartheid (sensu Massey and Denton, 1993) in creating the ‘cracks in the ice’ down which HIV has propagated, and from which its multiply-drug resistant or other evolutionarily-transformed varieties will emerge. The book is somewhat loosely organized as a series of nearly independent chapters and, in a sense, has something for everyone. The most formal section constructs a ‘necessary conditions’ model of institutional distributed cognition – effectively a collective consciousness – which serves to illuminate the canonical pathologies inherent to it. These systematic dysfunctions will appear repeatedly at different scales, and give an organizing principle to the story we have to tell. One of the more striking outcomes of the analysis is recognition that, just as the varieties of animal consciousness may represent evolutionary polyphyletic parallelism (Wallace and Wallace, 2007), in the same sense that bats and insects both have wings, so too there are many possible paths to, and forms of, distributed institutional cognition – collective consciousness. Although most cultural anthropologists would surely find this statement utterly banal, it emerges from the mathematical development only with difficulty. Such theory is, as always, most useful as a subordinate partner in an ongoing dialog with observational and experimental data. Perhaps now theory will actually have something useful to say regarding distributed cognition. Nonetheless, it seems clear that various, and very different, forms of institutional distributed cognition may coexist and interact to form larger structures. The potential complexities seem to dwarf the difficulties of understanding individual consciousness, which is often cited as the last really big unsolved scientific mystery. Our analysis suggests that collective consciousness is a far more varied and intricate phenomenon, unconstrained by genetic determinism. The evolutionary anthropologist Robert Boyd has asserted that “Culture is as much a part of human biology as the enamel on our teeth”. This may well be true to a degree and in ways we now only dimly comprehend. While much of the book is devoted to theoretical development, we have tried to apply ideas arising from the formalism to case histories of interactions between social structure, historic trajectory, public policy, and public health at different scales. Policy and history have written distorted images of themselve on population patterns of health and illness, accounting in large measure for the ‘mystery’ of health disparities between different ethnic groups. Such disparities are, in the United States, for the most part, a direct and inevitable outcome of practices of serial forced displacement which have reduced large

1.2 The unfinished business of the American Revolution

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African-American populations to permanent internal refugee status. Theories require application, and this is the example we have chosen to test our emerging conception of collective consciousness and its pathologies.

1.2 The unfinished business of the American Revolution Undergraduate European history classes, at least in the US, sometimes focus on the diffusion of ideas from the English civil war of the 1640’s which ended the reign of Charles I, first into the American Revolution, then the French, to the 1848 revolts in Germany and Austria-Hungary, and, finally, the Russian Revolution. Historians sometimes examine the American experience from a similar perspective, seeing the Civil War as the unfinished business of the American Revolution: the early US Constitution treated African-American slaves as equivalent to 3/5 of a ‘man’ for purposes of congressional representation in order to keep the South active in the revolution against England. Subsequent economic trajectory required endless expansion of the slave plantation system outside the South, while the North industrialized. When slavery was threatened with containment, the inevitable secession by the South was met by General U.S. Grant’s new paradigm of industrialized warfare. Most fundamentally, much of the business of the American Revolution remains undone. The Reconstruction period after the Civil War ended with the withdrawal of Federal troops from the South, leading to establishment of the Jim Crow system of segregation and denial of voting and other basic human rights to African Americans. The Civil Rights Movement of the 1950’s and 1960’s – sometimes called the Second Reconstruction – made gains in voting rights and in ending legal segregation based on ‘race’, but recent decades have seen a relentless counterreformation against those gains, often carried out using the tools of development displacement to disperse concentrations of economic, social, and political capital in African-American and other minority communities. At this writing there is not a single intact urban minority neighborhood in the United States. It is of interest to examine serial displacement in some detail, as it is fundamental to the ecology of AIDS in the United States, and accounts for the majority of the variance in the ‘health disparities’ between African Americans and the dominant populations. Forced economic displacement – deindustrialization driven by the diversion of technical resources into the Cold War – appears to account for much of the rest (e.g. Wallace et al., 1999 and the references therein). 1.2.1 African-American serial forced displacement Over the past sixty years development displacement has been implemented under different rubrics, ‘redlining’, ‘urban renewal’, ‘planned shrinkage’ (Wallace and Wallace, 1998), and now ‘Hope VI’ (Fullilove, 2004). To adopt the perspective of the African-American activist Malcom X, “The names have

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changed, but the game’s the same”. These policies created a scenario of incessant spatial and economic displacement, which has fallen most heavily on poor African-Americans, forced to live in segregated neighborhoods and deprived of equal investment opportunity as early as 1937, when the redlining policy of the Federal Homeowners Loan Corporation was instituted. All of these policies have destroyed older buildings in poor neighborhoods, creating a nationwide deficit of low-income housing. For example, the urban renewal program carried out under the Housing Act of 1949 had, by 1967, destroyed many more units than it had created (Weiss, 1985; Schwartz, 1993). Thus, the situation of incessant displacement has been complicated by a situation of ‘musical chairs’ in which some poor people must be homeless at any given time (Sclar, 1990). But the cumulative effects of incessant displacement and insecure housing go far beyond housing to affect community life at every level. To describe these effects we draw on studies of planned shrinkage, urban renewal and spreading urban destruction. The quotes are taken from interviews conducted as part of Fullilove’s study of ‘root shock’, i.e. the long-term consequences of community dismemberment (Fullilove, 2004). The interviews were collected with support from a Robert Wood Johnson Investigator Award which funded a study of five cities – Roanoke, VA, San Francisco, CA, Newark, NJ, Pittsburgh, PA, and St. Louis, MO – in which African American neighborhoods had been destroyed by urban renewal. 1.2.2 Segregation The neighborhoods we have examined in detail were all highly segregated, that is to say, places in which blacks had to settle because of overt formal and/or tacit, hidden, informal policies and practices that blocked their living in other parts of the city. The stories of how these neighborhoods came into being varied to some extent. African Americans had lived in the Hill District in Pittsburgh since the 1800s. By contrast, black settlement in the Fillmore District in San Francisco occurred in the 1940s, spurred by war-time employment and made possible by the internment of the Japanese people who had been earlier settlers in the area. These histories of restricted settlement were entwined with the development of social, economic, political and cultural organizations interior to the segregated area. Frank Bolden, celebrated reporter for the African American newspaper, The Pittsburgh Courier, described in some detail the long struggle by blacks to win political control of their neighborhoods, including the Hill District. This political power allowed them to fight for better services and to improve neighborhood life. At the same time, black residents of the Hill also fought to develop cultural institutions, ranging from symphony orchestras to book clubs, economic institutions, including hotels, beauty shops, pharmacies and jazz clubs, and recreation for children, such as that provided by the Irene Kaufman Settlement House.

1.2 The unfinished business of the American Revolution

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1.2.3 Redlining Redlining was introduced in 1937 by the Homeowners Loan Corporation. It was intended to protect investment by indicating which areas offered the best opportunities. According the HOLC algorithm, new buildings with white inhabitants merited an ‘A’ rating, while old buildings with non-white inhabitants received a ‘D’. Redlining imposed serious hardship on ghetto neighborhoods because it made it difficult to get money for investment. As pointed out by people who lived in the Central Ward of Newark, NJ, redlining made it difficult to get insurance or to borrow for repairs and remodeling. One observer commented that ‘stick built’ housing - i.e., housing built on site – needed regular maintenance and absent regular investment deteriorated more rapidly than it might have otherwise. Because the presence of any number of minority people led an area to be downgraded on redlining maps, all segregated areas were treated as relatively risky sites for investment. 1.2.4 Urban renewal The under-investment in ghetto areas was linked to urban renewal by the increased likelihood that redlined areas would show the greatest wear and tear and be at highest risk for a declaration of ‘blight’. Sala Udin, who grew up in Lower Hill District of Pittsburgh, an area destroyed by urban renewal, emphasized his experience of community while living in a rundown part of the neighborhood: “I think that the sense of community and the buildings are related within an old area. The buildings were old, the streets were cobblestone and old, there many small alleyways and people lived in those alleyways. The houses were very close together. There were small walkways that ran in between the alleyways that was really a playground. So, the physical condition of the buildings helped to create a sense of community. We all lived in similar conditions and had similar complaints about the wind whipping through the gaps between the frame and the window, and the hole in the walls and the leaking fixtures, the toilet fixtures that work sometimes and don’t work sometimes. But that kind of common condition bound us together.” But city officials and power brokers viewed the area as a site for a new use. Pittsburgh’s Lower Hill District, where 8,000 people lived, worked and shopped, was clearcut to make way for a new arena directed at providing entertainment for middle class white people. Urbanist Dennis Gale explained: “Part of the idea behind urban renewal is that the officials in Washington realized that you would never get private capital to invest back in the city, to build new office buildings, build shops, housing, etcetera - you could never encourage them to do that as long as there

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were these significant numbers of minorities and low-income people in the cities... So the idea was, the only way that we can hope to get private capital back into the cities, because we can’t do it alone without federal money, the only way to do it is to get rid of all the slums and deterioration. You label it as bad, you clear it all out. You have a featureless plane, and call it urban renewal. There is no longer any bad, there is nothing. And then you build from scratch.” 1.2.5 Catastrophic disinvestment African Americans displaced by urban renewal were forced to move to other segregated areas. In addition to the continuation of segregation - and in some cases its intensification - redlining practices remained in force in areas of black settlement. While not always achieving the status of stated policy, as did the planned shrinkage policy in New York City (see below), disinvestment did reach catastrophic levels in many U.S. neighborhoods. One such neighborhood was Gainsborough, a section of Roanoke, Virginia, which was marked for urban renewal, but never cleared. The declaration of urban renewal effectively blocked investment in the area. Slowly, the area deteriorated and the housing stock fell apart. Fires destroyed the buildings, and forced the population out. As people left, the businesses and other institutions suffered. As Evelyn Bethel, a resident of the area, pointed out, “The small businesses that we had where people were self-sufficient to a degree, no matter how much or how little they made, they were self-sufficient, and they had a core of ready-made customers. When the people were forced out, your business could no longer survive, so it was a devastating loss to the residents as well as the business owners.” 1.2.6 Planned Shrinkage Within New York City, which, as the peak of the nation’s urban hierarchy, serves as a primary US policy innovator, simplistic operations research models, developed by the Rand Corporation, were used as the central legal justification for a targeted withdrawal of fire extinguishment services from or near African-American and other minority neighborhoods (Wallace and Wallace, 1998a). The policy was described as ‘planned shrinkage’ by Roger Starr, at the time, New York City’s Housing Commissioner (Wallace and Wallace, 1998a), and involved reduction in essential services to ‘declining’ neighborhoods, all of which were, of course, communities of color. Extensive research has shown that these fire service cuts triggered massive loss of housing and community through intensive processes of contagious fire and housing abandonment (Wallace and Wallace, 1990, 1998a; Wallace, 1990). The Rand models themselves were found to be “simplistic and inadequate, failing to consider many

1.2 The unfinished business of the American Revolution

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needed variables, and employ[ing] methodology inappropriate for the intended purposes” by a New York State Senate investigating subcommittee (Duryea, 1978; Mega, 1978; Wallace, 1990). Nonetheless, under US law their invocation acted, and continues to act, as a shield against legal redress. These same, and very similar, models were then spread nationally by the US Dept. of Housing and Urban Development, have been used to justify fire service cuts in many cities across the US: Jersey City, Denver, Tampa, etc. Figure 1.1 shows the percent of occupied housing lost to ‘planned shrinkage’ contagious urban decay in the Bronx section of New York City between 1970 and 1980. The map is of ‘Health Areas’, which are small aggregates of Census Tracts by which mortality and morbidity statistics are reported in New York City.

Fig. 1.1. Loss of housing in the Bronx to contagious urban decay triggered by ‘planned shrinkage’ fire service reductions. Is this really ‘peacetime’ ?

8

1 INTRODUCTION

By itself the Bronx, with 1.4 million inhabitants, would be considered one of the largest urban centers in the industrialized West. Such levels of destruction are unprecedented during peacetime: Large sections of the Bronx lost between 36 and 81 % of their occupied housing in ten years. 1.2.7 Spreading instability Whatever the name of the policy, massive disinvestment triggered instability in areas adjacent those first affected by the withdrawal of services and funds. In order to understand the spread of destruction, we examined the patterns population displacement near Newark, New Jersey. We used census data from 1950-2000 and photographs along an ecological transect from the center of Newark to a wealthy suburb 8 miles away, and were able to discern a propagating front of contagious urban decay, building abandonment, and social disintegration that was moving away from the center of Newark, slowly destroying the neighborhoods - indeed, the cities - in its path. This wave of social and physical disintegration was also pushing the black population from the center of the city towards the west. As the poor population was pushed west, some of the city’s problems spilled over, destabilizing the circumjacent towns of Irvington, Elizabeth and East Orange, New Jersey. An examination of FBI Uniform Crime statistics for 2001, showed that crime rates for Irvington, located in the first ring of cities around Newark, were higher than those in Newark to the east or Union and other suburbs that lay to the west (see figure 1.2). The steady movement of population from east to west over the decades 1950 to 2000 suggested that Newark’s western suburbs lay in the path of a slow-moving glacier of urban troubles. Wallace and Wallace (1998) document a similar spread phenomenon affecting areas adjacent to New York City neighborhoods subjected to planned shrinkage. 1.2.8 Gentrification Investment was evident at the back of the moving front of disinvestment which is to say, near the origins of destabilization by the urban renewal area - in several cities we visited, including Roanoke, Newark, and Pittsburgh. Crawford Square, next to the Civic Arena, was such a site of new investment. Carlos Peterson, a resident of the Lower Hill prior to urban renewal, had watched as disinvestment had caused this next-over neighborhood to sag and disappear. He commented: “I think the city government and urban developers waited twenty years for this area to kind of like, decline on its own, to make it easier for them to come in and redevelop the property. And I think some of the buildings could have been saved. It could have been more of what it was, but upgraded in terms of people, property, and so forth. Right now, I think that what they’ve developed in terms of Crawford

1.2 The unfinished business of the American Revolution

9

Fig. 1.2. The Rates of Crime in Newark and the Surrounding Cities along Springfield Avenue, which runs from downtown Newark deep into the surrounding suburbs. Forced migration from Newark has moved the peak in social disorder into nearby Irvington, and the process continues its relentless propagation.

10

1 INTRODUCTION

Square, they basically razed everything. They just took everything down. And I used to call it the carcass of the Hill. You looked at the Hill and there was this carcass up there. I thought that if they could have saved the structures, because there was so much character. Now it’s like looking at some sort of cul-de-sac from suburbia, you know? People don’t look out their windows, they don’t sit on their porches, they don’t barbecue and work on their cars. You know, it’s just not black folks.” 1.2.9 HOPE VI HOPE VI, a relatively new Federal program designed to demolish ‘troubled’ high-rise public housing, and spatially disperse the tenants, has continued the pattern of forced displacement of African-American population. Federal housing projects linked into the process of serial forced displacement in a number of ways. First, housing projects were an important social reform when first introduced in the 1930s. They offered clean, decent housing for poor and working families. Indeed, housing projects developed in that era were often models of design. However, because housing projects were segregated, they were part of the creation of segregated neighborhoods. Second, many people displaced by urban renewal settled in housing projects, often finding that the housing projects offered great improvements over the housing in urban renewal areas. But in addition to segregation, housing projects created isolation by class, geography and function. This last point is worth comment, because it is clear that people in poor neighborhoods used their housing for shelter and enterprise. Furthermore, houses were situated among businesses of many kinds. Housing projects, by contrast, were strictly residential and were often located on campuses far from commercial or industrial districts. Housing projects in Pittsburgh and San Francisco - located at some distance from the original urban renewal areas and strikingly barren as urban sites - were examples of all four kinds of isolation operating at the same time. Muhandes Salaam Allah in Roanoke, said, with some bitterness: “I don’t know whether the ultimate goal was to impoverish these black communities, but certainly anybody who has any understanding knows that if you spend thirty years in the project and you are not able to build equity, you are not going to be able to pass anything on to your children. And when you destroy a neighborhood where people own their own home, and replace it with a project, where people don’t own nothing, then what is going to be the consequences in a thirty or forty year period? It’s going to be that these people are going to be an impoverished group of people. And they are not participating in the American Dream. They are participating in the Housing Authority nightmare.”

1.2 The unfinished business of the American Revolution

11

In 2001, at the time of our fieldwork in Pittsburgh and Newark, HOPE VI projects were changing the face of public housing. Though HOPE VI was described as an amelioration of distressed housing communities, it had a high cost in terms of social stability. By reconfiguring housing projects, HOPE VI lowered the number of slots of public housing and excluded some people from getting a new apartment because of negative factors in their history. Furthermore, people were displaced before the new housing was built. They often relocated at some distance from the old projects and lost contact with their former homes. By the time it was possible for them to return, it was no longer feasible. For example, in Pittsburgh, people moved to former steel towns along the Monongehela River. 1.2.10 Mass criminalization In response to rising illegal drug use, the US government launched a ‘war on drugs’, which did not reduce drug use, but did greatly accelerate rates of incarceration, especially among African Americans. By 2004, 2.13 million were incarcerated, 41% of them African American (Golembeski and Fullilove, 2005). These high levels of incarceration undermined community life in many ways: destabilizing families; creating the need of women to share men, or be without a man, leading to increasing female disempowerment; increasing levels of infectious diseases; and creating a class of people who have lost their civil rights, including the right to vote. People interviewed in our study described in great detail the ways in which deindustrialization and the collapse of neighborhood social controls shifted social functioning away from the tight control that Sala Udin described. In the small alleyways of the Hill District, or the tight streets of Northeast Roanoke, adults were constantly watching the activities of the children. Furthermore, people had legitimate jobs, which brought money into the neighborhood where it was shared among networks of neighbors and friends. When these factors shifted, the whole culture changed and crime and violence flourished. 1.2.11 Viewing policies in space We have mapped the spatial patterns created by these policies for the five cities in our study. Because these policies are national in scope and substantially similar in their impact, we show only the Pittsburgh map to illustrate the spatial connections between segregation/redlining, urban renewal, catastrophic disinvestment, gentrification, and HOPE VI (see figure 1.3). The Hill District, as we have noted, was a black segregated area by 1930 (Darden, 1973). Urban renewal was implemented in the Lower Hill, clear-cutting the habitat, and severing convenient pedestrian connections to downtown by putting in major roadways. The section of the Hill adjacent to the clearance area - referred to in local parlance as the ‘Middle Hill’ - suffered from catastrophic disinvestment, which

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1 INTRODUCTION

Fig. 1.3. Spatial Reorganization of Pittsburgh’s Hill District. Black segregation of the 1930’s was followed by urban renewal in 1959, disinvestment/contagious urban decay, gentrification, and HOPE VI. These policies have successfully dispersed concentrations of African-American economic, social, and political capital. Map by Richard Brown.

spread north and west from the area of urban renewal. Carlos Peterson, who watched the slow deterioration of the buildings, called this the ‘Carcass of the Hill’. During this process, the population of the Hill fell by half. Gentrification has begun with clearance of the deteriorating homes and stores at the edge of the Civic Arena and the building of Crawford Square. HOPE VI, which is replacing two housing projects, started demolition in 1999. Gentrification at Crawford Square, HOPE VI and elsewhere will increase the population of the Hill, but few of those displaced are expected to return. This is largely attributed to the costs of the new housing. These policies have each contributed to specific trials and tribulations, as noted by the commentators quoted above, but they also have had a cumulative impact of intensifying - relative to the rest of US society - Black impoverishment, political disenfranchisement, and social disconnection.

1.3 International law on displacement

13

1.2.12 Summary The last sixty years of serial forced displacement and resegregation of AfricanAmerican population is consistent with, and follows from, the previous ‘Jim Crow’ era of legal segregation and Apartheid which itself followed the brief window of the Reconstruction period after the Civil War that officially ended slavery. Serial forced displacement has effectively undercut the reforms of the recent Civil Rights movement which ended the legal basis of segregation. This incessant displacement, in synergism with a parallel, cold-war induced, deindustrialization, in our view, accounts for the major part of the ‘health disparities’ now affecting African-Americans. African-American urban and suburban communities have become de-facto refugee camps, subject to relentless forced marches conducted under color of US law, a pattern which, we contend, clearly violates international standards of human rights.

1.3 International law on displacement Policies underlying forced migration in the US have almost always been successfully masked either by ‘development’ rhetoric – ‘This is a slum, and we’re going to make it better’, or else by crying poor – ‘We can’t afford to keep fire companies open and continue collecting garbage in these neighborhoods’. Such assertions, under the US system, provide an absolute shield from legal challenge through present civil rights law, which requires proof of explicit ‘racial’ intent. International law, however, increasingly recognizes ‘Development-induced displacement’ and forced eviction as a serious human rights violations. The Office of the High Commissioner for Human Rights of the United Nations has held many conferences over the past decades examining forced displacement, and has a very sophisticated understanding of development rhetoric (UNHCHR, 1993): “The practice of forced displacement involves the involuntary removal of persons from their homes or land, directly or indirectly attributable to the State... The causes of forced evictions are very diverse. The practice can be carried out in connection with development and infrastructure projects... housing or land reclamation measures, prestigious international events, unrestrained land or housing speculation, housing renovation, urban redevelopment or city beautification initiatives, and mass relocation or resettlement programmes... The practice of forced eviction shares many characteristics with related phenomena such as population transfer, internal displacement of persons, forced removals during or as a result or object of armed conflict, ‘ethnic cleansing’, mass exodus, refugee movements, etc...”

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1 INTRODUCTION

Within the United States policies of development displacement have, over a 60 year period, served to repeatedly disrupt, disperse, and resegregate African Americans and other minorities, creating what amount to permanent internal refugee populations subject to the patterns of disease and disorder common to such groups. These adaptations and responses to displacement and the dispersal of essential capitals include high levels of violence, substance abuse and criminal behavior driven by economic collapse and social disintegration, as well as high rates of sexually transmitted disease. A significant percent of African-American males are in jails or prisons at any given time. These factors interact synergistically to create a context for the disempowerment of women in negotiating the sexual contract, for a variety of obvious and subtle reasons. Jails and prisons in particular become breeding grounds for sexually transmitted disease, and the vast majority of those imprisoned return to their communities of origin: where else are they to go? The unfinished business of the American Revolution represents a determining context for policymaking in the United States. We shall show that public policy, as the outcome of what we shall characterize as a collective consciousness, will inevitably carry within it a distorted image of such a determining context and will, in turn, project that image as patterns of health and illness within the US population. HIV in African American communities, constituting half of all new infections and occurring in only about a seventh of the nation’s population, travels like water through cracks in ice, and these cracks are the blind spot, the fruit of a canonical inattentional blindness, built in to the very foundations of the United States during its earliest days. The policies and practices of American Apartheid, particularly serial forced displacement, are direct descendants of the slave economy which persisted into the latter half of the 19th century. Just as slavery itself violated human rights then, one of the principal developmental descendants of slavery, serial forced displacement, violates human rights now, and should become the subject of international sanction as well as of continued contention and debate within the US itself. This is a pattern of response which proved critical to the outcome in South Africa, and could well contribute positively to conditions in the United States. We will show below that the canonical inattentional blindness of collective consciousness in the US to the impacts of serial forced displacement of vulnerable communities will likely create concentrations of multiply-drug-resistant HIV within the nation’s permanent refugee populations, resulting in epicenters having great force of infection. This is a classic example of the Paradox of Apartheid, in which brutal dominant groups become chained to those they oppress (Memmi, 1969). Ending policies of serial forced displacement of African-Americans and others would go far in limiting the susceptibility of the nation to emerging infections and to lessening the destabilizing burdens of violence and social decay which threaten to engulf the country.

2 CONSCIOUSNESS AND DISTRIBUTED COGNITION

2.1 Emergence The study of individual consciousness has again become academically acceptable, following nearly a century of ideologically-enforced silence on the topic, the ‘dark night of behaviorism’, as it were. Late 19th Century studies, summarized by William James (1890), have been revived, reinterpreted, and reinvigorated by quite a number of researchers, ranging across a broad intellectual spectrum (e.g. Baars, 1988, 2005; Edelman, 1989; Edelman and Tononi, 2000; Crick and Koch, 2003; Wallace, 2005a; Werner, 2006). The current frontrunner in the Darwinian competition between approaches is Baars’ Global Workspace model (Baars, 1988, 2005; Dehaene and Nacche, 2001), which we will adapt to the problem of collective consciousness and its pathologies, with a special focus on the failure of AIDS control and treatment in the United States. Unfortunately, reaching that focus requires considerable development. Our perspective is consistent with, but slightly more general than, Baars’, concentrating particularly on the many possible mechanisms instantiating the ‘general broadcast’ associated with high order cognitive process. Before presenting the Baars model, however, it seems useful to introduce some parallel ideas. The fundamental concept, is, essentially, of emergent behavior suddenly arising within a set of interacting information systems. To put the cart slightly before the horse, Richter et al.( 2006) describe the phenomenon in contemporary technological terms as follows: “In 1850 more than 700 French soldiers marched lock-step over the rope bridge of Angers. The bridge began to vibrate, collapsed, and 226 soldiers died... This tragedy is often quoted as an example of a resonance catastrophe... Similar phenomena increasingly occur also in informatics... [which is] becoming more and more complex and unmanageable. Our daily life provides various situations where

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we are surrounded by self-organizing, interacting systems showing unknown or emergent behavior... [where] the global behavior of a system appears more coherent and directed than the behavior of individual parts... [T]he question is not whether complexity increases or informatics is confronted with emergence, but how we will design new systems that..[can] cope with the emerging global behavior of self-organizing systems by adequate control actions... [W]e shall be surrounded by large systems of intelligent devices interacting and cooperating in potentially unlimited networks. The design complexity of these systems calls for new design paradigms, and due to the effects of interaction in dynamically changing environments the global behavior of these systems might be unexpected... In particular, to some degree, these systems will organize themselves, independently of initial designs or external interventions.” This perspective has been greatly elaborated by a number of German researchers. Relevant papers include Schmeck, (2005); Muller-Schloer, (2004); Muller-Schloer and Sick; (2006); Branke et. al, (2006); and Mnif and MullerSchloer (2006). The latter paper, in particular, uses a Shannon entropy formalism to characterize information system emergence, and our approach can be considered roughly parallel. One of the most spectacular contemporary examples of a perverse kind of network self-organization is the occurrence of widely-propagating power grid blackouts. Kinney et al. (2005) characterize those as follows: “Today the North American power grid is one of the most complex and interconnected systems of our time, and about one half of all domestic generation is sold over ever-increasing distances on the wholesale market before it is delivered to customers... Unfortunately the same capabilities that allow power to be transferred over hundreds of miles also enable the propagation of local failures into grid-wide events... It is increasingly recognized that understanding the complex emergent behaviors of the power grid can only be understood from a systems perspective, taking advantage of the recent advances in complex network theory...” Dobson (2007) states: “[P]robabalistic models of cascading failure and power system simulations suggest that there is a critical loading at which expected blackout size sharply increases and there is a power law in the distribution of blackout size... There are two attributes of the critical loading: [1] A sharp change in gradient of some quantity such as expected blackout size as one passes through the critical loading. [2] A power law region in probability distribution of blackout size at the critical loading. We use the terminology ‘critical’ because this behavior is analogous to a critical phase transition in statistical physics.”

2.2 Distributed cognition

17

We will find analogous ‘emergent’ high-level behaviors in linked cognitive modules become inevitable once thresholds of information transfer between them – crosstalk – are exceeded. An essential question is how this simple phenomenon is stabilized and harnessed to do useful work: biological (and social) evolution addressed the problem of interacting cognitive modules over literally geological timespans, and, under selection pressures, successfully adapted inverse information blackouts as tools for individual and group survival.

2.2 Distributed cognition Emergent processes in organizations have long been recognized and studied under the rubric of ‘distributed cognition’. Hollan et al. (2000), expanding on previous work by Hutchins and collaborators (e.g. Hutchins, 1994), describe these matters as follows: “The theory of distributed cognition, like any cognitive theory, seeks to understand the organization of cognitive systems. Unlike traditional theories, however, it extends the reach of what is considered cognitive beyond the individual to encompass interactions between people and with resources and materials in the environment. It is important from the outset to understand that distributed cognition refers to a perspective on all of cognition, rather than a particular kind of cognition... Distributed cognition looks for cognitive processes, wherever they may occur, on the basis of the functional relationships of elements that participate together in the process. A process is not cognitive simply because it happens in a brain, nor is a process noncognitive simply because it happens in the interactions between many brains... In distributed cognition one expects to find a system that can dynamically configure itself to bring subsystems into coordination to accomplish various functions. A cognitive process is delimited by the functional relationships among the elements that participate in it, rather than by the spatial colocation of the elements... Whereas traditional views look for cognitive events in the manipulation of symbols inside individual actors, distributed cognition looks for a broader class of cognitive events and does not expect all such events to be encompassed by the skin or skull of an individual... –Cognitive processes may be distributed across the members of a social group. –Cognitive processes may involve coordination between internal and external (material or environmental) structure. –Processes may be distributed through time in such a way that the products of earlier events can transform the nature of later events.” There are many similar perspectives across the literature. One such is Robert Sampson’s ‘collective efficacy’ approach to community function

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2 CONSCIOUSNESS AND DISTRIBUTED COGNITION

(Sampson, Raudenbush and Earls, 1997; Sampson, 2004). A large and growing body of sociological research, beginning with Granovetter (1973), emphasizes the essential role of nondisjunctive ‘weak’ social ties within a community, that is, ties which operate across such classifications as age cohort, ethnicity, religion, occupation, institutional membership, and so on. Collective efficacy is a recent reworking of the basic idea (Sampson, 2004): “...[C]ollective efficacy [means] an emphasis on shared beliefs in a neighborhood’s capability for action to achieve an intended effect, coupled with an active sense of engagement on the part of residents. Some density of social networks is essential... [b]ut the key theoretical point is that networks have to be activated to be ultimately meaningful. Collective efficacy therefore helps to elevate the ‘agentic’ aspect of social life over a perspective centered on the accumulation of stocks of [social capital]. This is consistent with a redefinition of social capital in terms of expectations for action within a collectivity... [in sum] social networks foster the conditions under which collective efficacy may flourish, but they are not sufficient for the exercise of control.” Sampson invokes a vision of community cognition, the ability of a neighborhood to perceive patterns of threat or opportunity, to compare those perceived patterns with an internal, shared, picture of the world, and to choose one or a few collective actions from a much larger repertory of those possible, and to carry them out. Disjunctive or ‘strong’ social ties define some of the underlying cognitive modules – collective and individual – within the neighborhood. Weak ties, then, are those which link such modules – individual or collective – across the community. Individuals, defined subgroups, or formal organizations, may have multiple roles within that community, permitting the formation of multiple working groups, if the strength of the various weak ties linking them is sufficient. Institutional cognition, in the sense of this work, emerges as a dynamic, collective phenomenon. Cultural constraints and developmental trajectory serve to both stabilize and direct the resulting cognitive processes. This phenomenon is, however, constrained, not just by shared culture, but by the path dependent historic development of the community itself. Recent work (e.g. Wallace and Wallace, 1997; D. Wallace and R. Wallace, 1998a, b, 2000; Wallace and Fullilove, 1999; Wallace et al., 1996; Fullilove, 2004) demonstrates that ‘planned shrinkage’, ‘urban renewal’, or other disruptions of weak ties akin to ethnic cleansing, can place neighborhoods onto decades-long irreversible developmental, perhaps evolutionary, trajectories of social disintegration which short-circuit effective community cognition. This is, indeed, a fundamental political purpose of such programs. Thomas Burns and his collaborators have focused particularly on the role of social process in consciousness. Burns and Engdalh (2003) write

2.2 Distributed cognition

19

“What is particularly striking about the academic consciousness industry is the absence of sociology... A collective has the capacity in its collective representations and communications about what it can (and cannot) do, or should do (or should not do). It monitors its activities, its achievements and failures, and... analyzes and discusses itself as a defined and developing collective agent... a collective has potentially a rich basis not only for talking about, discussing, agreeing (or disagreeing) about a variety of objects... but it also has a means to conceptualize and develop alternative types of social relationships, effective forms of leadership, coordination and control, and... new normative orders and institutional arrangements... These potentialities enable systematic, directed problem solving, and the generation of variety and complex strategies. In particular selective environments, these make for major evolutionary advantages... [However]..[c]ollective representations and reflectivity and directed problem-solving based on them may prevent human groups from experiencing or discovering the un-represented or un-named; unrecognized or poorly defined problems cannot be dealt with... Reflective and problem-solving powers may then be distorted, the generation of alternatives and varieties narrow and largely ineffective, and social innovation and transformation misdirected and possibly self-destructive...” Barrett and Henzi (2005) describe parallel phenomena among animal groups: “Physiological studies reveal that the blue fin tuna... should not be able to swim as fast as it actually does. Studies by fluid dynamicists, however, show that tuna are able to find naturally occurring currents in the water, and then use their tails to create additional vortices, which they exploit for extra propulsion.... [T]he ‘real swimming machine’ is not the tuna alone, but the tuna ‘in its proper context’ – the tuna, plus the water, plus the vortices it creates and exploits. As for tuna, so for primates: the real ‘social intelligence machine’ is the primate acting in its proper context – its social group. ...[C]ognition is ‘situated’ and ‘distributed’. Cognition is not limited by the ‘skin and skull’ of the individual... but uses resources and materials in the environment in the same way that tuna use vortices. The dynamic social interactions of primates... can be investigated as cognitive processes in themselves.... A distributed approach... considers all cognitive processes to emerge from the interactions between individuals, and between individuals and their world... Perhaps our greatest opportunistic and prosocial innovation as group-living animals has been to distribute our cognition to an unprecedented level by storing our essential information in other minds, instead merely of our own.”

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As Johnson (2001) puts it: “...[A]... paradigm shift... has been taking place in the study of human cognition... from models that focus on internal mental representations to ones that see cognition as a more distributed process – i.e. a process that occurs not just within but between individuals... [C]ognition is expanded from an individual enterprise to a distributed activity that involves a variety of socio-cultural elements, including the behavior of multiple individuals, their use of objects, and their shared histories.” These and the related ideas of Hutchins et al. cited above, are, in fact, representational models in which the representation itself is distributed. Patel (1998) uses distributed cognition to describe a paradigm shift regarding the role of technology in medicine: “The notion of distributed cognition suggests that the immediate physical and social resources outside the person participate in cognition, not just as a source of input and a receiver of output, but as a vehicle of thought... the individual and the environment should be viewed as dynamically interacting, resulting in cognitive performance and learning... Increasingly, researchers have come to characterize cognition as a distributed process... [I]ntelligence can be seen as distributed in designed artifacts such as computer-user interfaces; in representations, such as diagrams; and through communication in social contexts... The idea of intelligence (i.e. knowledge and cognition) being distributed in a group, or in artifacts, customs, and situations, is interesting because it provides a framework for addressing a number of theoretical and empirical questions.” Patel and colleagues (Cohen et al., 2006 and references therein; Laxmisan et al., 2006) use a distributed cognition model to analyze emergency room process and function, finding what can be interpreted as ‘rate distortion’ error effects at shift change handover of patients between clinical teams, something emergency room personnel have characterized as a ‘telephone game’ (Cohen et al., 2006). This appears to be a prime example of a canonical failure mode involving rate-driven, distorted communication between institutional global workspaces. Hutchins and collaborators have examined aircraft cockpits and naval vessels from similar perspectives, as have Woods and collaborators, and observed similar patterns.

2.3 Baars and Dretske We shall attempt to generalize a class of mathematical treatments of the Baars individual consciousness model to the problem of institutional distributed

2.3 Baars and Dretske

21

cognition, which will then be recognizable as a multiple-workspace collective consciousness. The problems of inattentional blindness and stability inherent to individual consciousness are compounded by questions regarding Rate Distortion limitations on the communication between individual workspaces within a collective consciousness: there are inherent limits to rates at which information may be transferred undistorted. The central ideas of Baars’ Global Workspace Theory of individual consciousness are as follows (Baars and Franklin, 2003): (1) The brain can be viewed as a collection of distributed specialized networks (processors). (2) Consciousness is associated with a global workspace in the brain – a fleeting memory capacity whose focal contents are widely distributed (broadcast) to many unconscious specialized networks. (3) Conversely, a global workspace can also serve to integrate many competing and cooperating input networks. (4) Some unconscious networks, called contexts, shape conscious contents, for example unconscious parietal maps modulate visual feature cells that underlie the perception of color in the ventral stream. (5) Such contexts work together jointly to constrain conscious events. (6) Motives and emotions can be viewed as goal contexts. (7) Executive functions work as hierarchies of goal contexts. Although this basic approach has been the focus of work by many researchers for two decades, consciousness studies has only recently, in the context of a deluge of empirical results from brain imaging experiments, begun digesting the perspective and preparing to move on. Currently popular agent-based and artificial neural network (ANN) treatments of cognition, consciousness and other higher order mental functions, to take Krebs’ (2005) view, are little more than sufficiency arguments, in the same sense that a Fourier series expansion can be empirically fitted to nearly any function over a fixed interval without providing real understanding of the underlying structure. Necessary conditions, as Dretske argues (Dretske, 1981, 1988, 1993, 1994), give considerably more insight. Adams (2003) describes Dretske’s work as follows: “It is not uncommon to think that information is a commodity generated by things with minds. Let’s say that a naturalized account puts matters the other way around, viz. it says that minds are things that come into being by purely natural causal means of exploiting the information in their environments. This is the approach of Dretske as he tried consciously to unite the cognitive sciences around the wellunderstood mathematical theory of communication...” Dretske himself (1994) writes: “Communication theory can be interpreted as telling one something important about the conditions that are needed for the trans-

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mission of information as ordinarily understood, about what it takes for the transmission of semantic information. This has tempted people... to exploit [information theory] in semantic and cognitive studies, and thus in the philosophy of mind. ...Unless there is a statistically reliable channel of communication between [a source and a receiver]... no signal can carry semantic information... [thus] the channel over which the [semantic] signal arrives [must satisfy] the appropriate statistical constraints of communication theory.” Wallace (2005a) addresses Baars’ theme from Dretske’s viewpoint, examining the necessary conditions which the asymptotic limit theorems of information theory impose on the Global Workspace. A central outcome of that work is the incorporation, in a natural manner, of constraints on individual consciousness, i.e. what Baars calls contexts. Information theory methods, extended by an obvious homology between information source uncertainty and free energy density, make it possible to formally account for the effects on individual consciousness of parallel physiological modules like the immune system, embedding structures like the local social network, and, most importantly, the all-encompassing cultural heritage which so uniquely marks human biology (e.g. Richerson and Boyd, 1995, 2004). This embedding evades the mereological fallacy which fatally bedevils brain-only theories of human consciousness (Bennett and Hacker, 2003), i.e the mistake of attributing a property characteristic of a whole to a part. Transfer of phase change methods from statistical physics to information theory via the same homology generates the punctuated nature of accession to consciousness in a similarly natural manner. The necessary renormalization calculation focuses on a phase transition driven by variation in the average strength of nondisjunctive weak ties (Granovetter, 1973) linking unconscious cognitive submodules. A second-order universality class tuning allows for adaptation of conscious attention via rate distortion manifolds which generalize the idea of a retina. The Baars model emerges as an almost exact parallel to hierarchical regression, based, however, on the Shannon-McMillan rather than the Central Limit Theorem. Details are given in the Mathematical Appendix. Wallace (2005b) recently proposed a somewhat different approach, using classic results from random and semirandom network theory (Erdos and Renyi, 1960; Albert and Barabasi, 2002; Newman, 2003) applied to a modular network of cognitive processors. The unconscious modular network structure of the brain is, of course, not random. However, in the spirit of the wag who said “all mathematical models are wrong, but some are useful”, the method serves as the foundation of a different, but roughly parallel, treatment of the Global Workspace to that given in Wallace (2005a), and hence as another basis for a benchmark model against which empirical data can be compared.

2.3 Baars and Dretske

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The first step is to argue for the existence of a network of loosely linked cognitive unconscious modules, and to characterize each of them by the richness of the canonical language – information source – associated with it. This is in some contrast to attempts to explicitly model neural structures themselves using network theory, e.g. the neuropercolation approach of Kozma et al. (2004, 2005), which nonetheless uses many similar mathematical techniques. Here, rather, we look at the necessary conditions imposed by the asymptotic limits of information theory on any realization of a cognitive process, be it biological wetware, silicon dryware, social process, or some direct or systems-level hybrid. All cognitive processes, in this formulation, are to be associated with a canonical dual information source which will be constrained by the Rate Distortion Theorem, or, in the zero-error limit, the Shannon-McMillan Theorem, both of which are described further in the Mathematical Appendix. It is interactions between nodes in this abstractly defined network which will be of interest here, rather than whatever mechanisms, social or biological system, or mixture of them, actually constitute the underlying cognitive modules. The second step is to examine the conditions under which a giant component (GC) suddenly emerges as a kind of phase transition in a network of such linked cognitive modules, to determine how large that component is, and to define the relation between the size of the component and the richness of the cognitive language associated with it. This is the candidate for Baars’ shifting general broadcast of consciousness. While Wallace (2005a) examines the effect of changing the average strength of nondisjunctive weak ties acting across linked unconscious modules, Wallace (2005b) focuses on changing the average number of such ties having a fixed strength, a complementary perspective whose extension via a kind of ‘renormalization’ leads to a far more general approach. The third step is to tune the threshold at which the giant component comes into being, and to tune vigilance, the threshold for accession to consciousness. This modular network treatment can be enriched by introducing a groupoid formalism which is roughly similar to recent analyses of linked dynamic networks described by differential equation models (e.g. Golubitsky and Stewart, 2006; Stewart et al., 2003, Stewart, 2004; Weinstein, 1996; Connes, 1994; Bak et al., 2006). Internal and external linkages between information sources break the underlying groupoid symmetry, and introduce more structure, the shifting general broadcast and the effect of contexts, respectively. The analysis provides a foundation for further mathematical exploration of linked cognitive processes. The crucial generalization is to examine the conditions under which cognitive modules may multitask, engaging in more than one giant component either synchronously or sequentially. This is something which individual consciousness does not permit under normal circumstances. The obvious tradeoff, of course, is the very rapid flow of individual consciousness, a matter of a few hundred milliseconds, as opposed to the much slower, if considerably more comprehensive, operations of institutional distributed cognition.

3 FORMAL THEORY

3.1 Cognition as an information source Cognition is not consciousness. Most mental, and many physiological, functions, while cognitive in a formal sense, hardly ever become entrained into the Global Workspace of individual consciousness: one seldom is able to consciously regulate immune function, blood pressure, or the details of binocular tracking and bipedal motion, except to decide ‘what shall I look at’, ‘where shall I walk’. Nonetheless, many cognitive processes, conscious or unconscious, appear intimately related to language, broadly speaking. The construction is fairly straightforward (Wallace, 2000, 2005a, b). Atlan and Cohen (1998) and Cohen (2000) argue, in the context of immune cognition, that the essence of cognitive function involves comparison of a perceived signal with an internal, learned picture of the world, and then, upon that comparison, choice of one response from a much larger repertoire of possible responses. Cognitive pattern recognition-and-response proceeds by an algorithmic combination of an incoming external sensory signal with an internal ongoing activity – incorporating the learned picture of the world – and triggering an appropriate action based on a decision that the pattern of sensory activity requires a response. More formally, a pattern of sensory input is mixed in an unspecified but systematic algorithmic manner with a pattern of internal ongoing activity to create a path of combined signals x = (a0 , a1 , ..., an , ...). Each ak thus represents some functional composition of internal and external signals. Wallace (2005a) provides neural network examples. This path is fed into a highly nonlinear, but otherwise similarly unspecified, decision oscillator, h, which generates an output h(x) that is an element of one of two disjoint sets B0 and B1 of possible system responses. Let B0 ≡ b0 , ..., bk ,

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B1 ≡ bk+1 , ..., bm . Assume a graded response, supposing that if h(x) ∈ B0 , the pattern is not recognized, and if h(x) ∈ B1 , the pattern is recognized, and some action bj , k + 1 ≤ j ≤ m takes place. The principal objects of formal interest are paths x which trigger pattern recognition-and-response. That is, given a fixed initial state a0 , we examine all possible subsequent paths x beginning with a0 and leading to the event h(x) ∈ B1 . Thus h(a0 , ..., aj ) ∈ B0 for all 0 ≤ j < m, but h(a0 , ..., am ) ∈ B1 . For each positive integer n, let N (n) be the number of high probability grammatical and syntactical paths of length n which begin with some particular a0 and lead to the condition h(x) ∈ B1 . Call such paths ‘meaningful’, assuming, not unreasonably, that N (n) will be considerably less than the number of all possible paths of length n leading from a0 to the condition h(x) ∈ B1 . While the combining algorithm, the form of the nonlinear oscillator, and the details of grammar and syntax, are all unspecified in this model, the critical assumption which permits inference on necessary conditions constrained by the asymptotic limit theorems of information theory is that the finite limit

H ≡ lim

n→∞

log[N (n)] n

(3.1)

both exists and is independent of the path x. We call such a pattern recognition-and-response cognitive process ergodic. Not all cognitive processes are likely to be ergodic, implying that H, if it indeed exists at all, is path dependent, although extension to nearly ergodic processes, in a certain sense, seems possible (Wallace, 2005a). Invoking the spirit of the Shannon-McMillan Theorem, it is possible to define an adiabatically, piecewise stationary, ergodic information source (APSE) X associated with stochastic variates Xj having joint and conditional probabilities P (a0 , ..., an ) and P (an |a0 , ..., an−1 ) such that appropriate joint and conditional Shannon uncertainties satisfy the classic relations H[X] = lim

n→∞

log[N (n)] = n

3.1 Cognition as an information source

27

lim H(Xn |X0 , ..., Xn−1 ) =

n→∞

lim

n→∞

H(X0 , ..., Xn ) . n

This information source is defined as dual to the underlying ergodic cognitive process (Wallace, 2005a). The essence of ‘adiabatic’ is that, when the information source is parametized according to some appropriate scheme, within continuous ‘pieces’ of that parametization, changes in parameters take place slowly enough so that the information source remains as close to stationary and ergodic as is needed to make the fundamental theorems work. By ‘stationary’ we mean that probabilities do not change in time, and by ‘ergodic’ (roughly) that cross-sectional means converge to long-time averages. Between ‘pieces’ one invokes various kinds of phase change formalism, for example, renormalization theory in cases where a mean field approximation is appropriate, as described in the Appendix. The ‘adiabatic’ assumption is analogous to the ‘Born-Oppenheimer Approximation’ (BO) in molecular physics, where, roughly speaking, the rapidly moving electrons closely track the slowly moving molecular nuclei, so that, in first approximation, the two can be treated as independent, interacting structures. Failure of the BO relation introduces richer molucular spectra, but these are difficult to analyze. In essence, our work here is a form of BO approximation, subject to similar complications. Again, not all cognitive processes are likely to have such a dual source, in this formal sense, and the theory is restricted to those which do, and for which our version of the BO approximation holds. This seems quite analogous to the distinction between parametric and nonparametric models in the statistical literature. Recall that the Shannon uncertainties H(...) are cross-sectional law-ofP large-numbers sums of the form − k Pk log[Pk ], where the Pk constitute a probability distribution. See Khinchin (1957), Ash (1990), or Cover and Thomas (1991) for the standard details. For non-ergodic information sources, a function, H(xn ), of each path xn → x, may be defined, such that limn→∞ H(xn ) = H(x), but H will not in general be given by the simple cross-sectional laws-of-large numbers analogs above. Let s ≡ d(x, x ˆ) for high probability paths x and x ˆ, where d is a distortion measure, as described in the Appendix. For ‘nearly’ ergodic systems one might use something of the form H(ˆ x) ≈ H(x) + sdH/ds|s=0 for s sufficiently small. Loosely speaking, the idea is to take a distortion measure as a kind of Finsler metric, imposing a resulting ‘global’ structure

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over an appropriate class of non-ergodic information sources. One possible interesting theorem, then, obviously revolves around what properties are metricindependent, in much the same manner as the Rate Distortion Theorem. This heuristic sketch can be made more precise as follows: Take a set of ‘high probability’ paths xn → x. Suppose, for all such x, there is an open set, U , containing x, on which the following conditions hold: ˆ ∈ U , a distortion measure sn ≡ dU (xn , x ˆn ) exists. (i) For all paths x ˆn → x (ii) For each path xn → x in U there exists a pathwise invariant function H(xn ) → H(x), in the sense of Khinchin (1957, p.72). While such a function will almost always exist, only in the case of an ergodic information source can it be identified as an ‘entropy’ in the usual sense. (iii) A function FU (sn , n) ≡ fn → f exists, for example, fn = sn , log[sn ]/n, sn /n, and so on. (iv) The limit lim

n→∞

H(xn ) − H(ˆ xn ) ≡ ∇F H|x fn

exists and is finite. Under such conditions, various nontrivial standard global atlas/manifold constructions are possible. To reiterate, H is not simply given by the expressions of above if the source is not ergodic, and the phase transition development of subsequent chapters may be correspondingly more complicated. Restriction to high probability paths simplifies matters considerably, although precisely characterizing them may be difficult, requiring extension of the Shannon-McMillan Theorem and its Rate Distortion generalization.

3.2 The cognitive modular network groupoid A formal equivalence class algebra can be constructed by choosing different origin points a0 and defining equivalence of two states by the existence of a high probability meaningful path connecting each of them with the same origin. Disjoint partition by equivalence class, analogous to orbit equivalence classes for dynamical systems, defines the vertices of the proposed network of cognitive dual languages. Each vertex then represents a different information source dual to a cognitive process. This is not a representation of a neural network as such, or of some circuit in silicon. It is, rather, an abstract set of ‘languages’ dual to the cognitive processes instantiated by biological structures, social process, machines, or their hybrids. This structure generates a groupoid, in the sense of Weinstein (1996). States aj , ak in a set A are related by the groupoid morphism if and only

3.2 The cognitive modular network groupoid

29

if there exists a high probability grammatical path individually connecting them to the same base point, and tuning across the various possible ways in which that can happen – the different cognitive languages – parametizes the set of equivalence relations and creates the groupoid. This assertion requires some development. Note that not all possible pairs of states (aj , ak ) can be connected by such a morphism, i.e. by a high probability, grammatical and syntactical path linking them with some given base point, but those that can define the groupoid element, a morphism g = (aj , ak ) having the natural inverse g −1 = (ak , aj ). Given such a pairing, connection by a meaningful path with the same base point, it is possible to define ‘natural’ end-point maps α(g) = aj , β(g) = ak from the set of morphisms G into A, and a formally associative product in the groupoid g1 g2 provided α(g1 g2 ) = α(g1 ), β(g1 g2 ) = β(g2 ), and β(g1 ) = α(g2 ). Then the product is defined, and associative, i.e. (g1 g2 )g3 = g1 (g2 g3 ). In addition there are natural left and right identity elements λg , ρg such that λg g = g = gρg whose characterization is left as an exercise (Weinstein, 1996). An orbit of the groupoid G over A is an equivalence class for the relation aj ∼ Gak if and only if there is a groupoid element g with α(g) = aj and β(g) = ak . A groupoid is called transitive if it has just one orbit. The transitive groupoids are the building blocks of groupoids in that there is a natural decomposition of the base space of a groupoid into orbits. Over each orbit there is a transitive groupoid, and the disjoint union of these transitive groupoids is the original groupoid. Conversely, the disjoint union of groupoids is itself a groupoid. The isotropy group of a ∈ X consists of those g in G with α(g) = a = β(g). These groups prove fundamental to classifying groupoids, as a later example will illustrate. In essence a groupoid is a category in which all morphisms have an inverse, here defined in terms of connection by a meaningful path of an information source dual to a cognitive process. If G is any groupoid over A, the map (α, β) : G → A × A is a morphism from G to the pair groupoid of A. The image of (α, β) is the orbit equivalence relation ∼ G, and the functional kernel is the union of the isotropy groups. If f : X → Y is a function, then the kernel of f , ker(f ) = [(x1 , x2 ) ∈ X × X : f (x1 ) = f (x2 )] defines an equivalence relation. As Weinstein (1996) points out, the morphism (α, β) suggests another way of looking at groupoids. A groupoid over A identifies not only which elements of A are equivalent to one another (isomorphic), but it also parametizes the different ways (isomorphisms) in which two elements can be equivalent, i.e. all possible information sources dual to some cognitive process. Given the information theoretic characterization of cognition presented above, this produces a full modular cognitive network in a highly natural manner. Brown (1987) describes the fundamental structure as follows:

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“A groupoid should be thought of as a group with many objects, or with many identities... A groupoid with one object is essentially just a group. So the notion of groupoid is an extension of that of groups. It gives an additional convenience, flexibility and range of applications... EXAMPLE 1. A disjoint union [of groups] G = ∪λ Gλ , λ ∈ Λ, is a groupoid: the product ab is defined if and only if a, b belong to the same Gλ , and ab is then just the product in the group Gλ . There is an identity 1λ for each λ ∈ Λ. The maps α, β coincide and map Gλ to λ, λ ∈ Λ. EXAMPLE 2. An equivalence relation R on [a set] X becomes a groupoid with α, β : R → X the two projections, and product (x, y)(y, z) = (x, z) whenever (x, y), (y, z) ∈ R. There is an identity, namely (x, x), for each x ∈ X...” Weinstein (1996) makes the following fundamental point: “Almost every interesting equivalence relation on a space B arises in a natural way as the orbit equivalence relation of some groupoid G over B. Instead of dealing directly with the orbit space B/G as an object in the category Smap of sets and mappings, one should consider instead the groupoid G itself as an object in the category Ghtp of groupoids and homotopy classes of morphisms.” Later we will explore homotopy in paths generated by information sources. It is interesting to note that the equivalence class structure which Asanovic et al. (2006) identify for computational problem types can be recast in groupoid language, and may serve as a model for projecting structure onto potential hyperparallel machine architectures. The groupoid approach has become quite popular in the study of networks of coupled dynamical systems which can be defined by differential equation models, (e.g. Golubitsky and Stewart, 2006; Stewart et al. (2003), Stewart (2004)). Here we have outlined how to extend the technique to networks of interacting information sources which, in a dual sense, characterize cognitive processes, and cannot at all be described by the usual differential equation models. These latter, it seems, are much the spiritual offspring of 18th Century mechanical clock models. Cognitive and conscious processes in humans, other animals, and their social assemblies, involve neither computers nor clocks, but remain constrained by the limit theorems of information theory, and these permit scientific inference on necessary conditions.

3.3 Global and local symmetry groupoids Here we follow Weinstein (1996) fairly closely, using his example of a finite tiling.

3.3 Global and local symmetry groupoids

31

Consider a tiling of the euclidean plane R2 by identical 2 by 1 rectangles, specified by the set X (one dimensional) where the grout between tiles is X = H ∪ V , having H = R × Z and V = 2Z × R, where R is the set of real numbers and Z the integers. Call each connected component of R2 \X, i.e. the complement of the two dimensional real plane intersecting X, a tile. Let Γ be the group of those rigid motions of R2 which leave X invariant, i.e. the normal subgroup of translations by elements of the lattice Λ = H ∩V = 2Z × Z (corresponding to corner points of the tiles), together with reflections through each of the points 1/2Λ = Z × 1/2Z, and across the horizontal and vertical lines through those points. As noted by Weinstein (1996), much is lost in this coarse-graining, in particular the same symmetry group would arise if we replaced X entirely by the lattice Λ of corner points. Γ retains no information about the local structure of the tiled plane. In the case of a real tiling, restricted to the finite set B = [0, 2m] × [0, n] the symmetry group shrinks drastically: The subgroup leaving X ∩ B invariant contains just four elements even though a repetitive pattern is clearly visible. A two-stage groupoid approach recovers the lost structure. We define the transformation groupoid of the action of Γ on R2 to be the set G(Γ, R2 ) = {(x, γ, y|x ∈ R2 , y ∈ R2 , γ ∈ Γ, x = γy} with the partially defined binary operation (x, γ, y)(y, ν, z) = (x, γν, z). Here α(x, γ, y) = x, and β(x, γ, y) = y, and the inverses are natural. We can form the restriction of G to B (or any other subset of R2 ) by defining G(Γ, R2 )|B = {g ∈ G(Γ, R2 )|α(g), β(g) ∈ B} 1. An orbit of the groupoid G over B is an equivalence class for the relation x ∼G y if and only if there is a groupoid element g with α(g) = x and β(g) = y. Two points are in the same orbit if they are similarly placed within their tiles or within the grout pattern. 2. The isotropy group of x ∈ B consists of those g in G with α(g) = x = β(g). It is trivial for every point except those in 1/2Λ ∩ B, for which it is Z2 × Z2 , i.e. the direct product of integers modulo two with itself. By contrast, embedding the tiled structure within a larger context permits definition of a much richer structure, i.e. the identification of local symmetries. We construct a second groupoid as follows: Consider the plane R2 as being decomposed as the disjoint union of P1 = B ∩ X (the grout), P2 = B\P1 (the complement of P1 in B, i.e. the tiles), and P3 = R2 \B (the exterior of the tiled room). Let E be the group of all euclidean motions of the plane, and define

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the local symmetry groupoid Gloc as the set of triples (x, γ, y) in B × E × B for which x = γy, and for which y has a neighborhood U in R2 such that γ(U ∩ Pi ) ⊆ Pi for i = 1, 2, 3. The composition is given by the same formula as for G(Γ, R2 ). For this groupoid-in-context there are only a finite number of orbits: O1 = interior points of the tiles. O2 = interior edges of the tiles. O3 = interior crossing points of the grout. O4 = exterior boundary edge points of the tile grout. O5 = boundary ‘T’ points. O6 = boundary corner points. The isotropy group structure is, however, now very rich indeed: The isotropy group of a point in O1 is now isomorphic to the entire rotation group O2 . It is Z2 × Z2 for O2 . For O3 it is the eight-element dihedral group D4 . For O4 , O5 and O6 it is simply Z2 . These are the ‘local symmetries’ of the tile-in-context. Next we begin construction of a ‘biopsychosocial’ model which creates just such a nested hierarchy, and hence splits the simple groupoid modular network into a much more complicated structure. This occurs in two stages.

3.4 Internal symmetry breaking The symmetry groupoid, as we have constructed it for cognitive modules, in a kind of information space, is parametized across that space by the possible ways in which states aj , ak can be equivalent, i.e. connected to some origin by a meaningful path of an information source dual to a cognitive process. These are different, and in this approximation, non-interacting cognitive processes. But symmetry groupoids, like symmetry groups, are made to be broken: by internal cross-talk akin to spin-orbit interactions within a symmetric atom, and by cross-talk with slower, external, information sources, akin to putting a symmetric atom in a powerful magnetic or electric field. As to the first process, suppose that linkages can fleetingly occur between the ordinarily disjoint cognitive modules defined by the network groupoid. This is represented by establishment of a non-zero mutual information measure between them: a cross-talk which breaks the strict groupoid symmetry developed above. Wallace (2005a) describes this structure in terms of fixed magnitude disjunctive strong ties which give the equivalence class partitioning of modules, and nondisjunctive weak ties which link modules across the partition, and parametizes the overall structure by the average strength of the weak ties, to use Granovetter’s (1973) term. The technique is developed at some length in the Mathematical Appendix.

3.4 Internal symmetry breaking

33

By contrast the approach of Wallace (2005b), which we outline here, is to simply look at the average number of fixed-strength nondisjunctive links in the underlying topology. These are obviously two analytically tractable limits of a much more complicated regime. Since we know nothing about how the cross-talk connections can occur, we can – as a first approximation – assume they are random and construct a random graph in the classic Erdos/Renyi manner. Suppose there are M disjoint cognitive modules – M elements of the equivalence class algebra of languages dual to some cognitive process – which we now take to be the vertices of a possible graph. For M very large, following Savante et al. (1993), when edges (defined by establishment of a fixed-strength mutual information measure between the graph vertices) are added at random to M initially disconnected vertices, a remarkable transition occurs when the number of edges becomes approximately M/2. Erdos and Renyi (1960) studied random graphs with M vertices and (M/2)(1+µ) edges as M → ∞, and discovered that such graphs almost surely have the following properties (Molloy and Reed, 1995, 1998; Grimmett and Stacey, 1998; Luczak, 1990; Aiello et al., 200; Albert and Barabasi, 2002): [1] If µ < 0, only small trees and unicyclic components are present, where a unicyclic component is a tree with one additional edge; moreover, the size of the largest tree component is (µ − ln(1 + µ))−1 + O(log log n). [2] If µ = 0, however, the largest component has size of order M 2/3 . [3] If µ > 0, there is a unique giant component (GC) whose size is of order M ; in fact, the size of this component is asymptotically αM , where µ = −α−1 [ln(1 − α) − 1], which has an explicit solution for α in terms of the Lambert W-function. Thus, for example, a random graph with approximately M ln(2) edges will have a giant component containing ≈ M/2 vertices. Such a phase transition initiates a new, collective, cognitive phenomenon. At the level of the individual mind, unconscious cognitive modules link up to become the general broadcast of consciousness, emergently defined by a set of cross-talk mutual information measures between interacting unconscious cognitive submodules. The source uncertainty, H, of the language dual to the collective cognitive process, which characterizes the richness of the cognitive language of the workspace, will grow as some monotonic function of the size of the GC, as more and more unconscious processes are incorporated into it. Wallace (2005b) provides details. Others have taken similar network phase transition approaches to assemblies of neurons, e.g. neuropercolation (Kozma et al., 2004, 2005), but their work has not focused explicitly on modular networks of cognitive processes, which may or may not be instantiated by neurons. Restricting analysis to such modular networks finesses much of the underlying conceptual difficulty, and permits use of the asymptotic limit theorems of information theory and the import of techniques from statistical physics, a matter we will discuss later.

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3.5 External symmetry breaking Just as a higher order information source, associated with the GC of a random or semirandom graph, can be constructed out of the interlinking of unconscious cognitive modules by mutual information, so too external information sources, for example, in humans the cognitive immune and other physiological systems, and embedding sociocultural structures, can be represented as slower-acting information sources whose influence on the GC can be felt in a collective mutual information measure. For machines or institutions these would be the onion-like ‘structured environment’, to be viewed as among Baars’ contexts (Baars, 1988, 2005; Baars and Franklin, 2003). The collective mutual information measure will, through the Joint Asymptotic Equipartition Theorem which generalizes the Shannon-McMillan Theorem, be the splitting criterion for high and low probability joint paths across the entire system. The tool for this is network information theory (Cover and Thomas, 1991, p. 388). Given three interacting information sources, Y1 , Y2 , Z, the splitting criterion, taking Z as the ‘external context’, is given by

I(Y1 , Y2 |Z) = H(Z) + H(Y1 |Z) + H(Y2 |Z) − H(Y1 , Y2 , Z), (3.2)

where H(..|..) and H(.., .., ..) represent conditional and joint uncertainties (Khinchin, 1957; Ash, 1990; Cover and Thomas, 1991). This generalizes to

I(Y1 , ...Yn |Z) = H(Z) +

n X

H(Yj |Z) − H(Y1 , ..., Yn , Z).

j=1

(3.3)

If we assume the Global Workspace/Giant Component to involve a very rapidly shifting, and indeed highly tunable, dual information source X, embedding contextual cognitive modules like the immune system will have a set of significantly slower-responding sources Yj , j = 1..m, and external social, cultural and other environmental processes will be characterized by even

3.6 Information system emergence

35

more slowly-acting sources Zk , k = 1..n. Mathematical induction on equation (3.3) gives a complicated expression for a mutual information splitting criterion which we write as

I(X|Y1 , .., Ym |Z1 , .., Zn ). (3.4)

This encompasses a fully interpenetrating biopsychosociocultural structure for individual consciousness, one in which Baars’ contexts act as important, but flexible, boundary conditions, defining the underlying topology available to the far more rapidly shifting global workspace (Wallace, 2005a, b). This evades the mereological fallacy which Bennett and Hacker (2003) impute to excessively neurocentric perspectives on consciousness in humans, that is, the mistake of imputing to a part of a system the characteristics which require functional completeness. A complete expansion of equation (3.4) appears to require application of the groupoid convolution algebra, a matter we will not pursue further here.

3.6 Information system emergence As a number of researchers have noted, in one way or another, – see Wallace, (2005a) for discussion – equation (3.1), H ≡ lim

n→∞

log[N (n)] , n

is homologous to the thermodynamic limit in the definition of the free energy density of a physical system. This has the form

F (K) = lim

V →∞

log[Z(K)] , V

(3.5)

where F is the free energy density, K the inverse temperature, V the system volume, and Z(K) is the partition function defined by the system Hamiltonian.

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The Appendix shows at some length how this homology permits the natural transfer of renormalization methods from statistical mechanics to information theory, producing phase transitions and analogs to evolutionary punctuation in systems characterized by piecewise, adiabatically stationary, ergodic information sources (Wallace and Wallace, 1998, 1999; S. Gould, 1992). These biological phase changes appear to be ubiquitous in natural systems and can be expected to dominate social and machine behaviors as well. Wallace (2002b) uses these arguments to explore the differences and similarities between evolutionary punctuation in genetic and learning plateaus in neural systems. The mean field approach, described in the Appendix, uses an approximation in which average strength (or probability) of nondisjunctive linkages between cognitive nodes serves as a kind of inverse temperature parameter. Phase transitions can then be described using various ‘biological’ renormalization strategies, in which ‘universality class tuning’ becomes the principal second order mechanism. We have shown above that there is another analytically tractable limit, the giant component, suggesting the possibility of intermediate cases. In the next section we extend the giant component paradigm, so that the mean number of such linkages, above some variable threshold, is the parameter of central interest, and the second order tuning involves topological mechanisms. Whatever scheme is chosen, however, the homology between equations (3.1) and (3.5) ensures that some form of emergent behavior, akin to a physical phase transition, is inevitable for networks of interacting cognitive structures, however instantiated.

3.7 Multiple workspaces The random network development above is predicated on there being a variable average number of fixed-strength linkages between components. Clearly, the mutual information measure of cross-talk is not inherently fixed, but can continuously vary in magnitude. We address this by a parametized renormalization. In essence the modular network structure linked by mutual information interactions has a topology depending on the degree of interaction of interest. Suppose we define an interaction parameter ω, a real positive number, and look at geometric structures defined in terms of linkages which are zero if mutual information is less than, and ‘renormalized’ to unity if greater than, ω. Any given ω will define a regime of giant components of network elements linked by mutual information greater than or equal to it. The fundamental conceptual trick at this point is to invert the argument: A given topology for the giant component will, in turn, define some critical value, ωC , so that network elements interacting by mutual information less than that value will be unable to participate, i.e. will be locked out and not be consciously perceived. We hence are assuming that the ω is a tunable,

3.7 Multiple workspaces

37

syntactically-dependent, detection limit, and depends critically on the instantaneous topology of the giant component defining, for the human mind, the global workspace of consciousness. That topology is, fundamentally, the basic tunable syntactic filter across the underlying modular symmetry groupoid, and variation in ω is only one aspect of a much more general topological shift. More detailed analysis is given below in terms of a topological rate distortion manifold. There is considerable empirical evidence from fMRI brain imaging experiments to show that individual human consciousness involves a single, shifting and tunable, global broadcast, a matter leading necessarily to the phenomenon of inattentional blindness. Cognitive submodules within institutions, – individuals, departments, formal and informal workgroups – by contrast, can do more than one thing, and indeed, are usually required to multitask. Clearly multiple workspaces would lessen the probability of inattentional blindness, but, we will find, do not eliminate it, and introduce other failure modes examined in more detail later. We must postulate a set of crosstalk information measures between cognitive submodules, each associated with its own tunable giant component having its own special topology. Suppose the set of giant components at some ‘time’ k is characterized by k . Fixed parameter values define a para set of parameters Ωk ≡ ω1k , ..., ωm ticular giant component set having a particular set of topological structures. Suppose that, over a sequence of ‘times’ the set of giant components can be characterized by a (possibly coarse-grained) path xn = Ω0 , Ω1 , ..., Ωn−1 having significant serial correlations which, in fact, permit definition of an adiabatically, piecewise stationary, ergodic (APSE) information source. Call that information source X. Suppose that a set of (external or internal) signals impinging on the set of giant components, is also highly structured and forms another APSE information source Y which interacts not only with the system of interest globally, but specifically with the tuning parameters of the set of giant components characterized by X. Y is necessarily associated with a set of paths yn . Pair the two sets of paths into a joint path zn ≡ (xn , yn ), and invoke some inverse coupling parameter, K, between the information sources and their paths. By the arguments of the Section 3.5, generalized in the Appendix, this leads to phase transition punctuation of I[K], the mutual information between X and Y, under either the Joint Asymptotic Equipartition Theorem, or, given a distortion measure, under the Rate Distortion Theorem. I[K] is a splitting criterion between high and low probability pairs of paths, and partakes of the homology with free energy density. Attentional focusing then itself becomes a punctuated event in response to increasing linkage between the structure of interest and an external signal, or some particular system of internal events. This iterated argument parallels the extension of the General Linear Model into the Hierarchical Linear Model of regression theory.

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Call this the Multitasking Hierarchical Cognitive Model (MHCM). For individual consciousness, there is only one giant component. For an institution, there will be a larger, and often very large, set of them. This requirement leads to the possibility of new failure modes related to impaired communication between Giant Components. That is, a complication specific to high order institutional cognition or machine distributed cognition lies in the necessity of information transfer between giant components. The form and function of such interactions will, of course, be determined by the nature of the particular institution or machine, but, synchronous or asynchronous, contact between giant components is circumscribed by the Rate Distortion Theorem. That theorem, reviewed in the Mathematical Appendix, states that, for a given maximum acceptable critical average signal distortion, there is a limiting maximum information transmission rate, such that messages sent at less than that limit are guaranteed to have average distortion less than the critical maximum. Too rapid transmission between parallel global workspaces – information overload – violates that condition, and guarantees large signal distortion. This is a likely failure mode unique to multiple workspace systems which, we will argue, may otherwise have a lessened probability of inattentional blindness.

3.8 The dynamical groupoid A fundamental homology between the information source uncertainty dual to a cognitive process and the free energy density of a physical system arises, in part, from the formal similarity between their definitions in the asymptotic limit. Information source uncertainty, defined as in equation (3.1), is quite analogous to the free energy density of a physical system, equation (3.5). Feynman (1996) provides a series of physical examples, based on Bennett’s work, where this homology is, in fact, an identity, at least for very simple systems. Bennett argues, in terms of idealized irreducibly elementary computing machines, that the information contained in a message can be viewed as the work saved by not needing to recompute what has been transmitted. Feynman explores in some detail Bennett’s ideal microscopic machine designed to extract useful work from a transmitted message. The essential argument is that computing, in any form, takes work. Thus the more complicated a cognitive process, measured by its information source uncertainty, the greater its energy consumption, and our ability to provide energy to the brain is limited: Typically a unit of brain tissue consumes an order of magnitude more energy than a unit of any other tissue. Inattentional blindness, Wallace (2007) argues, emerges as a thermodynamic limit on processing capacity in a topologically-fixed global workspace, i.e. one which has been strongly configured about a particular task. Institutional and machine generalizations seem obvious.

3.8 The dynamical groupoid

39

Understanding the time dynamics of cognitive systems away from phase transition critical points requires a phenomenology similar to the Onsager relations of nonequilibrium thermodynamics. If the dual source uncertainty of a cognitive process is parametized by some vector of quantities K ≡ (K1 , ..., Km ), then, in analogy with nonequilibrium thermodynamics, gradients in the Kj of the disorder, defined as

S ≡ H(K) −

m X

Kj ∂H/∂Kj

j=1

(3.6)

become of central interest. Equation (3.6) is similar to the definition of entropy in terms of the free energy density of a physical system, as suggested by the homology between free energy density and information source uncertainty described above. Pursuing the homology further, the generalized Onsager relations defining temporal dynamics become

dKj /dt =

X

Lj,i ∂S/∂Ki ,

i

(3.7)

where the Lj,i are, in first order, constants reflecting the nature of the underlying cognitive phenomena. The L-matrix is to be viewed empirically, in the same spirit as the slope and intercept of a regression model, and may have structure far different than may be familiar from the usual chemical or physical examples. The ∂S/∂K are analogous to thermodynamic forces in a chemical system, and may be subject to override by external physiological driving mechanisms. Equations (3.6) and (3.7) can be derived in a simple parameter-free covariant manner which relies on the underlying topology of the information source space implicit to the development. Different cognitive phenomena have, according to our development, dual information sources, and we are interested in the local properties of the system near a particular reference state. We impose a topology on the system, so that, near a particular ‘language’ A, dual to an underlying cognitive process, there is (in some sense) an open set U of closely

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ˆ such that A, Aˆ ⊂ U . Note that it may be necessary to similar languages A, coarse-grain the system’s responses to define these information sources. The problem is to proceed in such a way as to preserve the underlying essential topology, while eliminating ‘high frequency noise’. The formal tools for this can be found, e.g., in Chapter 8 of Burago et al. (2001). Since the information sources dual to the cognitive processes are similar, for all pairs of languages A, Aˆ in U , it is possible to: [1] Create an embedding alphabet which includes all symbols allowed to both of them. [2] Define an information-theoretic distortion measure in that extended, joint alphabet between any high probability (i.e. grammatical and syntactical) ˆ which we write as d(Ax, Ax) ˆ (Cover and Thomas, 1991). paths in A and A, Note that these languages do not interact, in this approximation. [3] Define a metric on U , for example,

ˆ A,A

ˆ d(Ax, Ax)

A,A

d(Ax, Aˆ x)

R ˆ = | lim R M(A, A)

− 1|,

(3.8)

using an appropriate integration limit argument over the high probability paths. Note that the integration in the denominator is over different paths within A itself, while in the numerator it is between different paths in A and ˆ A. Consideration suggests M is a formal metric, having M(A, B) ≥ 0, M(A, A) = 0, M(A, B) = M(B, A), M(A, C) ≤ M(A, B) + M(B, C). Other approaches to metric construction on U seem possible. Structures weaker than a conventional metric would be of more general utility, but the mathematical complications are formidable (Glazebrook, 2007). Note that these conditions can be used to define equivalence classes of languages, where previously we defined equivalence classes of states which could be linked by high probability, grammatical and syntactical, paths to some base point. This led to the characterization of different information sources. Here we construct an entity, formally a topological manifold, which is an equivalence class of information sources. This is, provided M is a conventional metric, a classic differentiable manifold. The set of such equivalence

3.8 The dynamical groupoid

41

classes generates the dynamical groupoid , and questions arise regarding mechanisms, internal or external, which can break that groupoid symmetry, as in the previous example. This is, in fact, a critical insight leading to different forms of quasi-stability within, or between, equivalence classes of information sources. The former will be discussed below in terms of directed homotopy theory. This all suggests the possibility of classifying quasistable modes using something like the groupoid generalization of the Seifert-VanKampen theorem (Lee, 2000) or some similar topological argument. Indeed, since H and M are both scalars, a ‘covariant’ derivative can be defined directly as

ˆ H(A) − H(A) , ˆ ˆ A→A M(A, A)

dH/dM = lim (3.9)

where H(A) is the source uncertainty of language A. Suppose the system to be set in some reference configuration A0 . To obtain the unperturbed dynamics of that state, impose a Legendre transform using this derivative, defining another scalar

S ≡ H − MdH/dM. (3.10)

The simplest possible Onsager relation – here seen as an empirical, fitted, equation like a regression model – in this case becomes

dM/dt = LdS/dM, (3.11)

where t is the time and dS/dM represents an analog to the thermodynamic force in a chemical system. This is seen as acting on the reference state A0 . For

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dS/dM|A0 = 0, d2 S/dM2 |A0 > 0 (3.12)

the system is quasistable, a Black hole, if you will, and externally imposed forcing mechanisms will be needed to effect a transition to a different state. We shall explore this circumstance below in terms of topological considerations analogous to the concept of ecosystem resilience. Conversely, changing the direction of the second condition, so that dS 2 /dM2 |A0 < 0, leads to a repulsive peak, a White hole, representing a possibly unattainable realm of states. Explicit parametization of M introduces standard – and quite considerable – notational complications (e.g. Burago et al., 2001; Auslander, 1967): Imposing a metric for different cognitive dual languages parametized by K leads to Riemannian, or even Finsler, geometries, including the usual geodesics. See the Mathematical Appendix for details of the expansion. Weinstein (1996) makes the following important comment: “A groupoid G is a topological groupoid over B if G and B are topological spaces and α, β, and multiplication are continuous maps...[A] notion useful for many purposes... A criticism sometimes applied to the theory of groupoids is that their classification up to isomorphism is nothing other than the classification of equivalence relations (via the orbit equivalence relation) and groups (via the isotropy groups). The imposition of a compatible topological structure produces a nontrivial interaction between the two structures.” Although we cannot pursue such matters here, the famous groupoid convolution algebra, of which matrix algebra is an example, provides the mechanism, presumably via the expansion implicit in equation (3.4). The dynamics, as we have presented them so far, have been noiseless, while neural systems, from which we are abducting theory, are well known to be very noisy, and indeed may be subject to mechanisms of stochastic resonance. Equation (3.11) might be rewritten as dM/dt = LdS/dM + σW (t)

3.8 The dynamical groupoid

43

where σ is a constant and W (t) represents white noise. Again, S is seen as a function of the parameter M. This leads directly to a family of classic stochastic differential equations having the form

dMt = L(t, dS/dM)dt + σ(t, dS/dM)dBt , (3.13)

where L and σ are appropriately regular functions of t and M, and dBt represents the noise structure. In the sense of Emery (1989), this leads into deep realms of stochastic differential geometry and related topics. The obvious inference is that noise, which need not be ‘white’, can serve as a tool to shift the system between various equivalence classes, i.e. as a kind of crosstalk and the source of a generalized stochastic resonance. We have defined a groupoid for the system based on a particular set of equivalence classes of information sources dual to cognitive processes. That groupoid parsimoniously characterizes the available dynamical manifolds, and, in precisely the sense of the earlier development, breaking of the groupoid symmetry creates more complex objects of considerable interest, which will be studied below. This leads to the possibility, indeed, the necessity, of Deus ex Machina mechanisms – some sort of generalized programming, ‘executive decision’, or some analog to noise-induced stochastic resonance – to force transitions between the different possible modes within and across dynamic manifolds. In a machine model a programmer creates the manifold structure, and the computing device hunts within that structure for the ‘solution’ to the problem according to equivalence classes of paths on the manifold. Noise, as with random mutation in evolutionary algorithms, might well be needed to guarantee convergence. Equivalence classes of states gave dual information sources. Equivalence classes of information sources give different characteristic dynamic manifolds Later we will examine equivalence classes of paths, which will produce different directed homotopy topologies characterizing those manifolds. This introduces the possibility of having different quasi-stable resilience modes within individual dynamic manifolds. Pink or white noise might provide a tunable means of creating crosstalk between different topological states within a dynamical manifold, or between different dynamical manifolds altogether. The next important structural iteration, however, is, in some respects, significantly more complicated.

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3.9 The rate distortion manifold The second order iteration above – analogous to expanding the General Linear Model to the Hierarchical Linear Model – which involved paths in parameter space, can itself be significantly extended. This produces a generalized tunable retina model which can be interpreted as a ‘Rate Distortion manifold’, a concept which further opens the way for import of a vast array of tools from geometry and topology. Suppose, now, that threshold behavior for institutional reaction requires some elaborate system of nonlinear relationships defining a set of renormalk . The critical assumption is that there is a ization parameters Ωk ≡ ω1k , ..., ωm tunable zero order state, and that changes about that state are, in first order, relatively small, although their effects on punctuated process may not be at all small. Thus, given an initial m-dimensional vector Ωk , the parameter vector at time k + 1, Ωk+1 , can, in first order, be written as

Ωk+1 ≈ Rk+1 Ωk , (3.14)

where Rt+1 is an m × m matrix, having m2 components. If the initial parameter vector at time k = 0 is Ω0 , then at time k

Ωk = Rk Rk−1 ...R1 Ω0 . (3.15)

The interesting correlates of individual, institutional or machine consciousness are, in this development, now represented by an information-theoretic path defined by the sequence of operators Rk , each member having m2 components. The grammar and syntax of the path defined by these operators is associated with a dual information source, in the usual manner. The effect of an information source of external signals, Y, is now seen in terms of more complex joint paths in Y and R-space whose behavior is, again, governed by a mutual information splitting criterion according to the JAEPT. The complex sequence in m2 -dimensional R-space has, by this construction, been projected down onto a parallel path, the smaller set of m-dimensional ω-parameter vectors Ω0 , ..., Ωk .

3.9 The rate distortion manifold

45

If the punctuated tuning of attention is now characterized by a ‘higher’ dual information source – an embedding generalized language – so that the paths of the operators Rk are autocorrelated, then the autocorrelated paths in Ωk represent output of a parallel information source which is, given Rate Distortion limitations, apparently a grossly simplified, and hence highly distorted, picture of the ‘higher’ conscious process represented by the R-operators, having m as opposed to m × m components. High levels of distortion may not necessarily be the case for such a structure, provided it is properly tuned to the incoming signal. If it is inappropriately tuned, however, then distortion may be extraordinary. Let us examine a single iteration in more detail, assuming now there is a (tunable) zero reference state, R0 , for the sequence of operators Rk , and that

Ωk+1 = (R0 + δRk+1 )Ωk , (3.16)

where δRk is ‘small’ in some sense compared to R0 . Note that in this analysis the operators Rk are, implicitly, determined by linear regression. We thus can invoke a quasi-diagonalization in terms of R0 . Let Q be the matrix of eigenvectors which Jordan-block-diagonalizes R0 . Then

QΩk+1 = (QR0 Q−1 + QδRk+1 Q−1 )QΩk . (3.17)

If QΩk is an eigenvector of R0 , say Yj with eigenvalue λj , it is possible to rewrite this equation as a generalized spectral expansion

Yk+1 = (J + δJk+1 )Yj ≡ λj Yj + δYk+1

= λj Yj +

n X i=1

ai Yi .

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3 FORMAL THEORY

(3.18)

J is a block-diagonal matrix, δJk+1 ≡ QRk+1 Q−1 , and δYk+1 has been expanded in terms of a spectrum of the eigenvectors of R0 , with

|ai |  |λj |, |ai+1 |  |ai |. (3.19)

The point is that, provided R0 has been tuned so that this condition is true, the first few terms in the spectrum of this iteration of the eigenstate will contain most of the essential information about δRk+1 . This appears quite similar to the detection of color in the retina, where three overlapping non-orthogonal eigenmodes of response are sufficient to characterize a huge plethora of color sensation. Here, if such a tuned spectral expansion is possible, a very small number of observed eigenmodes would suffice to permit identification of a vast range of changes, so that the rate-distortion constraints become quite modest. That is, there will not be much distortion in the reduction from paths in R-space to paths in Ω-space. Inappropriate tuning, however, can produce very marked distortion, even inattentional blindness, in spite of multitasking. Note that higher order Rate Distortion Manifolds are likely to give better approximations than lower ones, in the same sense that second order tangent structures give better, if more complicated, approximations in conventional differentiable manifolds (e.g. Pohl, 1962). Indeed, Rate Distortion Manifolds can be quite formally described using standard techniques from topological manifold theory (Glazebrook, 2007). The essential point is that a rate distortion manifold is a topological structure which constrains the ‘multifactorial stream of institutional consciousness’ as well as the pattern of communication between giant components, much the way a riverbank constrains the flow of the river it contains. This is a fundamental insight, which we will pursue further. The Rate Distortion Manifold can, however, also be described in purely information theoretic terms using a ‘tuning theorem’ variant of the Shannon Coding Theorem, which we briefly review. Messages from an information source, seen as symbols xj from some alphabet, each having probabilities Pj associated with a random variable X, are ‘encoded’ into the language of a ‘transmission channel’, a random variable Y with symbols yk , having probabilities Pk , possibly with error. Someone receiving the symbol yk then retranslates it (without error) into some xk , which may or may not be the same as the xj that was sent.

3.9 The rate distortion manifold

47

More formally, the message sent along the channel is characterized by a random variable X having the distribution P (X = xj ) = Pj , j = 1, ..., M. The channel through which the message is sent is characterized by a second random variable Y having the distribution P (Y = yk ) = Pk , k = 1, ..., L. Let the joint probability distribution of X and Y be defined as P (X = xj , Y = yk ) = P (xj , yk ) = Pj,k and the conditional probability of Y given X as P (Y = yk |X = xj ) = P (yk |xj ). Then the Shannon uncertainty of X and Y independently and the joint uncertainty of X and Y together are defined respectively as

H(X) = −

M X

Pj log(Pj )

j=1

H(Y ) = −

L X

Pk log(Pk )

k=1

H(X, Y ) = −

M X L X

Pj,k log(Pj,k ).

j=1 k=1

(3.20)

The conditional uncertainty of Y given X is defined as

H(Y |X) = −

M X L X j=1 k=1

Pj,k log[P (yk |xj )]

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(3.21)

For any two stochastic variates X and Y , H(Y ) ≥ H(Y |X), as knowledge of X generally gives some knowledge of Y . Equality occurs only in the case of stochastic independence. Since P (xj , yk ) = P (xj )P (yk |xj ), we have H(X|Y ) = H(X, Y ) − H(Y ) The information transmitted by translating the variable X into the channel transmission variable Y – possibly with error – and then retranslating without error the transmitted Y back into X is defined as

I(X|Y ) ≡ H(X) − H(X|Y ) = H(X) + H(Y ) − H(X, Y ) (3.22)

See, for example, Ash (1990), Khinchin (1957) or Cover and Thomas (1991) for details. The essential point is that if there is no uncertainty in X given the channel Y , then there is no loss of information through transmission. In general this will not be true, and herein lies the essence of the theory. Given a fixed vocabulary for the transmitted variable X, and a fixed vocabulary and probability distribution for the channel Y , we may vary the probability distribution of X in such a way as to maximize the information sent. The capacity of the channel is defined as

C ≡ max I(X|Y ) P (X)

(3.23)

P subject to the subsidiary condition that P (X) = 1. The critical trick of the Shannon Coding Theorem for sending a message with arbitrarily small error along the channel Y at any rate R < C is to encode it in longer and longer ‘typical’ sequences of the variable X; that is, those sequences whose distribution of symbols approximates the probability distribution P (X) above which maximizes C.

3.9 The rate distortion manifold

49

If S(n) is the number of such ‘typical’ sequences of length n, then log[S(n)] ≈ nH(X) where H(X) is the uncertainty of the stochastic variable defined above. Some consideration shows that S(n) is much less than the total number of possible messages of length n. Thus, as n → ∞, only a vanishingly small fraction of all possible messages is meaningful in this sense. This observation, after some considerable development, is what allows the Coding Theorem to work so well. In sum, the prescription is to encode messages in typical sequences, which are sent at very nearly the capacity of the channel. As the encoded messages become longer and longer, their maximum possible rate of transmission without error approaches channel capacity as a limit. Again, Ash (1990), Khinchin (1957) and Cover and Thomas (1991) provide details. This approach can be, in a sense, inverted to give a tuning theorem which parsimoniously describes the essence of the Rate Distortion Manifold. Telephone lines, optical wave guides and the tenuous plasma through which a planetary probe transmits data to earth may all be viewed in traditional information-theoretic terms as a noisy channel around which we must structure a message so as to attain an optimal error-free transmission rate. Telephone lines, wave guides and interplanetary plasmas are, relatively speaking, fixed on the timescale of most messages, as are most sociogeographic networks. Indeed, the capacity of a channel, is defined by varying the probability distribution of the ‘message’ process X so as to maximize I(X|Y ). Suppose there is some message X so critical that its probability distribution must remain fixed. The trick is to fix the distribution P (x) but modify the channel – i.e. tune it – so as to maximize I(X|Y ). The dual channel capacity C ∗ can be defined as

C∗ ≡

max

I(X|Y )

max

I(Y |X)

P (Y ),P (Y |X)

(3.24)

But C∗ =

P (Y ),P (Y |X)

since I(X|Y ) = H(X) + H(Y ) − H(X, Y ) = I(Y |X).

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Thus, in a purely formal mathematical sense, the message transmits the channel, and there will indeed be, according to the Coding Theorem, a channel distribution P (Y ) which maximizes C ∗ . One may do better than this, however, by modifying the channel matrix P (Y |X). Since P (yj ) =

M X

P (xi )P (yj |xi ),

i=1

P (Y ) is entirely defined by the channel matrix P (Y |X) for fixed P (X) and C∗ =

max

P (Y ),P (Y |X)

I(Y |X) = max I(Y |X). P (Y |X)

Calculating C ∗ requires maximizing the complicated expression I(X|Y ) = H(X) + H(Y ) − H(X, Y ) which contains products of terms and their logs, subject to constraints that the sums of probabilities are 1 and each probability is itself between 0 and 1. Maximization is done by varying the channel matrix terms P (yj |xi ) within the constraints. This is a difficult problem in nonlinear optimization. However, for the special case M = L, C ∗ may be found by inspection: If M = L, then choose P (yj |xi ) = δj,i where δi,j is 1 if i = j and 0 otherwise. For this special case C ∗ ≡ H(X) with P (yk ) = P (xk ) for all k. Information is thus transmitted without error when the channel becomes ‘typical’ with respect to the fixed message distribution P (X). If M < L matters reduce to this case, but for L < M information must be lost, leading to Rate Distortion limitations. Thus modifying the channel may be a far more efficient means of ensuring transmission of an important message than encoding that message in a ‘natural’ language which maximizes the rate of transmission of information on a fixed channel. We have examined the two limits in which either the distributions of P (Y ) or of P (X) are kept fixed. The first provides the usual Shannon Coding Theorem, and the second, hopefully, a tuning theorem variant, i.e. a tunable, retina-like, Rate Distortion Manifold. It seems likely, however, than for many important systems P (X) and P (Y ) will interpenetrate, to use Richard Levins’ terminology. That is, P (X) and P (Y ) will affect each other in characteristic ways, so that some form of mutual tuning may be the most effective strategy.

3.10 Institutional resilience

51

3.10 Institutional resilience The groupoid treatment of modular cognitive networks above defined equivalence classes of states according to whether they could be linked to some origin by grammatical/syntactical high probability meaningful paths, and equivalence classes of languages according to their dynamical properties. One can ask the precisely complementary question regarding paths within a given dynamic manifold: For any two particular given states, is there some sense in which it is possible to define equivalence classes across the set of meaningful paths linking them? This will give rise to the fundamental topological groupoid of a particular cognitive dynamic manifold. This is of particular interest to the second order hierarchical model which, in effect, describes a universality class tuning of the renormalization parameters characterizing the dancing, flowing, tunably punctuated accession to collective consciousness. A closely similar question is central to recent algebraic geometry approaches to concurrent, i.e. highly parallel, computing (e.g. Pratt, 1991; Goubault and Raussen, 2002; Goubault, 2003), which we adapt. For the moment restrict attention to a giant component system characterized by two renormalization parameters, say ω1 and ω2 , and consider the set of meaningful paths connecting two particular points, say a and b, in the two dimensional ω-space plane of figure 3.1. The arguments surrounding equations (3.6), (3.7) and (3.12) suggests that there may be regions of fatal attraction and strong repulsion, Black holes and White holes, which can either trap or deflect the path of institutional cognition. Figures 3.1a and 3.1b show two possible configurations for a Black and a White hole, diagonal and cross-diagonal. If one requires path monotonicity – always increasing or remaining the same – then, following, e.g. Goubault (2003, figs. 6,7), there are, intuitively, two direct ways, without switchbacks, that one can get from a to b in the diagonal geometry of figure 3.1a, without crossing a Black or White hole, but there are three in the cross-diagonal structure of figure 3.1b. Elements of each ‘way’ can be transformed into each other by continuous deformation without crossing either the Black or White hole. Figure 3.1a has two additional possible monotonic ways, involving over/under switchbacks, which are not drawn. Relaxing the monotonicity requirement generates a plethora of other possibilities, e.g. loopings and backwards switchbacks, but it is not clear under what circumstances such complex paths can be meaningful. These ways are the equivalence classes defining the fundamental topological groupoid of the two different ω-spaces, analogs to the fundamental homotopy groups in spaces which admit of loops (e.g. Lee, 2000). The closed loops needed for classical homotopy theory are impossible for this kind of system because of the ‘flow of time’ defining the output of an information source – one goes from a to b, although, for nonmonotonic paths, intermediate looping would seem possible. The theory is thus one of directed homotopy, dihomo-

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Fig. 3.1. a Diagonal Black and White holes in the two dimensional ω-plane. Only two direct paths can link points a and b which are continuously deformable into one another without crossing either hole. There are two additional monotonic switchback paths which are not drawn. Equivalence classes of paths define the fundamental dihomotopy groupoid. b Cross-diagonal Black and White holes as in (a). Three direct equivalence classes of continuously deformable paths can link a and b. Thus the two spaces are topologically distinct, having different dihomotopy groupoids. Here monotonic switchbacks are not possible, although relaxation of that condition can lead to ‘backwards’ switchbacks and intermediate loopings.

3.10 Institutional resilience

53

topy, and the central question revolves around the continuous deformation of paths in ω-space into one another, without crossing Black or White holes. Goubault and Rausssen (2002) provide another introduction to the formalism. Such ideas can, of course, be applied to lower level cognitive modules as well as to the second order hierarchical cognitive model of institutional cognition where they are, perhaps, of more central interest. Empirical study will likely show how the influence of cultural heritage or developmental history defines quite different dihomotopies of attentional focus in human organizations. That is, the topology of blind spots and their associated patterns of perceptual completion in human organizations will be culturally or developmentally modulated. It is this developmental cultural topology of multitasking organization attention which, acting in concert with the inherent limitations of the rate distortion manifold, generates the pattern of organizational inattentional blindness. Such considerations, and indeed the Black Hole development of equation (3.12), suggest that a multitasking organization which becomes trapped in a particular pattern of behavior cannot, in general, expect to emerge from it in the absence of some external forcing mechanism. This form of behavior is central to ecosystem resilience theory, which we will examine at two different scales. The first is at the topology of an individual dynamic manifold. The second emerges when the dynamical groupoid is broken by hierarchical linkages which patch together different manifolds. These may, in fact, simply represent different scales of the same basic phenomenon, i.e. a patching of spaces, leading to topological considerations like the groupoid version of the Siefert-VanKampen Theorem previously mentioned. Ecosystem theorists, in fact, recognize several different kinds of resilience (e.g. Gunderson, 2000). The first, which they call ‘engineering resilience’, since it is particularly characteristic of machines and man-machine interactions, involves the rate at which a disturbed system returns to a presumed single, stable, equilibrium condition, following perturbation. From that limited perspective, a resilient system is one which quickly returns to its one stable state. A slight extension involves asking the degree to which the system amplifies applied perturbations (e.g. Wallace and Wallace, 2000). Biological or social phenomena, however, do not seem limited to this simple pattern. Holling’s (1973) particular contribution was to recognize that sudden transitions between different, at best quasi-stable, domains of relation among ecosystem variates were possible, i.e. that more than one ‘stable’ state was possible for real ecosystems. Gunderson (2000) puts the matter as follows: “One key distinction between these two types of resilience lies in assumptions regarding the existence of multiple [quasi-]stable states. If it is assumed that only one stable state exists or can be designed to exist, then the only possible definition and measures for resilience are near equilibrium ones – such as characteristic return time... The concept of ecological resilience presumes the existence of multiple sta-

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bility domains and the tolerance of the system to perturbations that facilitate transitions among stable states. Hence, ecological resilience refers to the width or limit of a stability domain and is defined by the magnitude of disturbance that a system can absorb before it changes stable states... The presence of multiple [quasi-]stable states and transitions among them [has] been [empirically] described in a [large] range of ecological systems...” The topology of institutional cognition provides a tool for study of resilience in human organizations or social systems. The obvious conjecture is that the set of equivalence classes of directed homotopy described above formally classifies quasi-equilibrium states, and thus characterizes the different possible ecosystem resilience modes by their fundamental topological groupoids within a particular dynamic manifold. However, a shift between dynamical manifolds would represent a qualitatively different kind of resilience transition. This approach generalizes some current work on distributed cognition (e.g. Woods and Hollnagel, 2006) in that it is not restricted to engineering resilience, i.e. graceful degradation, followed by return to equilibrium, but encompasses the idea of pathological states much like the eutrophication of a pristine lake. Changes between orders of these quasi-equilibrium states, in our model, require more than simply the lessening of challenge, but positive, intensive, intervention from outside the system itself to shift domains of quasi-stability. Ultimately, we are invoking the necessity of ‘executive force’ to move organizations between different modes, either within one, or between, dynamic manifolds. If there is an insufficient repertory of possibilities, or insufficient ability to cause transition, then ‘market forces’ may be literally devastating, as was the experience of the Columbia space shuttle disaster (Starbuck and Farjoun, 2005).

3.11 Variation and selection Our finding of two distinctly different analytically tractable models for collective consciousness, the mean number network model given above, and the mean field model explored in the Appendix, suggests the possibility of a spectrum of intermediate, mathematically less tractable, structures instantiating collective consciousness, in much the same sense that R. Wallace and R.G. Wallace (2007) invoked ‘Darwin’s Rainbow’ to describe the vast range of possibilities for animal consciousness. The particular complexity of collective consciousness lies in the possibility of having many global workspaces which communicate with each other. Mixed strategies within institutions and across workspaces seem possible, making the ‘Rainbow’ far more complex than is possible for individual animals.

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This seems analogous to polyphyletic parallelism in biological evolution, where many different responses to similar selection pressures produce similar functional outcomes – for example bird, bat, and insect wings all used for flight. Institutional economics, in fact, takes an explicitly evolutionary view of these matters, (e.g. Hodgson, 1993), abandoning an equilibrium perspective for developmental irreversibility. Selection pressures write distorted images of themselves onto genetic structure through natural selection (Wallace, 2002b). Wallace and Wallace (1998; 1999), in fact, argued that, due to its highly structured nature, an embedding environment constitutes an information source which, as it becomes more closely linked to an organism – as the organism’s homeostatic elasticity fails – writes its distorted genetic image as a phase transition, accounting directly for punctuated equilibrium in the fossil record. Analogs with ecological or institutional resilience seem clear. The essence of evolutionary process, then, is the punctuated occurrence of major innovations in structure and function, which then develop according to an irreversible bush-like branching, that is then pruned by some combination of selection pressure and blind chance. One example is the many mainframe computer companies which flowered and failed, leaving IBM as the principal legacy. Mainframes now face extinction. Another is the many personal computer operating systems that collapsed, leaving Microsoft’s version, which itself now faces strong selection pressure and possible extinction. Thus the various canonical forms of collective consciousness all encounter ‘market’ selection pressures and the vicissitudes of chance, and engage in variation through learning and random change, providing another example of irreversible evolutionary process. Selection pressures – market demands – will write images of themselves onto collectively conscious institutions, which must then homeostatically adjust, structurally adapt, or fail. D. Wallace and R. Wallace (2000), for example, provide an explicit evolutionary perspective on how the ‘South Bronx’ process of policy-driven contagious urban decay constituted a draconian selection pressure for social network structure, the basic skeleton upon which any local collectively conscious institution must be built. Collectively conscious institutions, then, are subject to irreversible evolutionary development, constrained by the intertwining of cultural and historical context which limit adaptability and may well predispose them to characteristic failure modes, which we explore more completely in the next chapter.

3.12 Recapitulation of the formal theory The Global Workspace model We recall the central ideas of Global Workspace theory (Baars and Franklin, 2003):

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(1) The brain can be viewed as a collection of distributed specialized networks (processors). (2) Consciousness is associated with a global workspace in the brain – a fleeting memory capacity whose focal contents are widely distributed (broadcast) to many unconscious specialized networks. (3) Conversely, a global workspace can also serve to integrate many competing and cooperating input networks. (4) Some unconscious networks, called contexts, shape conscious contents. For example, unconscious parietal maps modulate visual feature cells that underlie the perception of color in the ventral stream. (5) Such contexts work together jointly to constrain conscious events. (6) Motives and emotions can be viewed as goal contexts. (7) Executive functions work as hierarchies of goal contexts. Agent-based and artificial neural network (ANN) treatments of cognition, consciousness and other higher order mental functions, taking Krebs’ (2005) view, are sufficiency arguments, mimicking mentality without providing real understanding of the underlying structure in the same way that a Fourier series can approximate a function over a fixed interval. The Ptolemaic theory of the solar system, an Earth-centered paradigm, required epicycle upon epicycle to approximate the dynamic behaviors of the planets. A sun-centered Keplerian system provides instant simplicity. Necessary conditions, as Dretske (1981, 1988, 1993, 1994) argues, give considerably more insight. They are conditions to which all cognitive phenomena must assimilate, and they are in no small part characterized by the asymptotic limit theorems of information theory. Here we study Baars’ theme from Dretske’s viewpoint, finding the necessary conditions which the asymptotic limit theorems of information theory impose on the global workspace. These, it can be shown, impose constraints on individual consciousness – what Baars calls contexts. Information theory methods, extended by a homology between information source uncertainty and the free energy density of a physical system, formally account for the effects on individual consciousness of parallel physiological modules such as the immune system, embedding structures such as the local social network, and, most importantly, the cultural heritages that mark human biology (e.g. Richerson and Boyd, 2004). Neuron firing alone, although certainly a part of the whole, does not comprise the totality of mental function. Consciousness, a higher-order function, is the provenance of an entire animal, including, for many species, its social context. In our effort to link unconscious cognitive submodules we can transfer phase change approaches from statistical physics to information theory via the same homology between information source uncertainty and free energy density. The transfer cleanly generates a punctuated accession to consciousness. The renormalization calculation focuses on a phase transition that arises from a change in the average strength of nondisjunctive weak ties (sensu Granovetter, 1973) linking the unconscious submodules. A second-order univer-

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sality class tuning allows for adaptation of conscious attention via rate distortion manifolds. A version of the Baars model (including contexts) emerges as an almost exact parallel to hierarchical regression, based, however, on the Shannon-McMillan Theorem rather than the Central Limit Theorem on which most modern-day modeling depends. Wallace and colleagues (2005b; 2006; 2007a; Wallace et al., 2007) used classic results from random and semirandom network theory (Erdos and Renyi, 1960; Albert and Barabasi, 2002; Newman, 2003) applied to a modular network of cognitive processors. The method provides a foundation for a different, but roughly parallel, treatment of the global workspace to that given in Wallace (2005a). In fact there can be intermediate models, as well as those acting at very slow rates (Wallace et al., 2007). This suggests an equivalence class structure for global workspace models, and the possibility of a number of different mechanisms which achieve such large-scale structure and dynamics. As the discussions above show, it is possible to use renormalization parameters to tune the threshold at which a giant component, or set of them, emerges, along with its topological structure, by way of an iteration involving a tunable rate distortion manifold retina-analog. The treatment generalizes Newell’s (1990) blackboard model to give a highly flexible, indeed tunable, version of Baars’ broadcast mechanism across many possible underlying neural topologies. Wallace (2005a), by contrast, uses ‘universality class tuning’ to direct the phase transitions associated with changing the average strength of weak ties between modules. Details are in the Appendix. These approaches together offer different analytically tractable asymptotic limits in a much larger domain of possible models. Although both kinds of linkage are sufficient to produce large-scale brain connectivity or general broadcast, another iteration seems required to produce higher mental function. Some second level models may be more amenable to such iteration than others. Again, the essential point is that there are two quite distinct analytically tractable models of this general broadcast mechanism which both instantiate Baars’ global workspace model, the mean field model of nondisjunctive linkage between linked cognitive modules, discussed in great detail in the Appendix, and the mean number model of such linkages, as presented earlier in this chapter. The two contrasting treatments both produce very similar tunable broadcasts comparable to the Baars global workspace model of consciousness. Less mathematically tractable intermediate structures seem possible, in which both average strength and average numbers of crosstalk linkages can vary and tune the broadcast. Evolution, be it Darwinian biological or Lamarckian social, however, does not seem particularly constrained by mathematical tractability. The groupoid approach outlined above permits development of a system which entertains several, even many, simultaneous workspaces which can initiate global broadcasts. An obvious canonical failure mode of such a structure

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involves miscommunication between workspaces: The Rate Distortion Theorem states that there is an inherent limit on the transmission rate for any specified level of average distortion. Too rapid ‘handoff’ at shift change, for example, guarantees great distortion. A second canonical failure mode for such systems is inattentional blindness, i.e. overfocus by the generalized retina of a tunable rate distortion manifold, which might be lessened by the existence of multiple, different, simultaneous workspaces, but would remain acute under policies of enforced institutional or organizational conformity which would eliminate multiple perspectives on incoming ‘sensory’ data. A third involves a pathological ‘lock-in’ to non-adaptive dynamic topological modes similar to the eutrophication of a natural ecosystem: ecological as opposed to engineering resilience. Engineering resilience supposes graceful degradation under stress, followed by return to normal. Ecosystem resilience sees stress causing sudden, relatively permanent, shifts to possibly pathological modes. Such shifts may, indeed, be driven by ‘Red Queen’ effects analogous to competitive failure dynamics in a market economy, particularly inverse ‘Pentagon Ratchet’ mechanisms driven by feedback between institutional distributed cognition and a closely coupled embedding cultural milieu. Further discussion of such failure modes is central to the next chapter.

4 PATHOLOGIES OF COLLECTIVE CONSCIOUSNESS

4.1 Individual consciousness Some insight regarding the depth, breadth, and subtlety of failure mode complexities affecting collective consciousness can be gained from the study of failures in a system having but a single global workspace, i.e. the human mind (Wallace, 2005b). The result is not reassuring. Mental disorders in humans are not well understood. Indeed, such classifications as the Diagnostic and Statistical Manual of Mental Disorders - fourth edition, (DSM-IV, 1994), the standard descriptive nosology in the US, have been characterized as prescientific by Gilbert (2001) and others. JohnsonLaird et al. (2006) put the matter thus: “Current knowledge about psychological illnesses is comparable to the medical understanding of epidemics in the early 19th century. Physicians realized then that cholera, for example, was a specific disease, which killed about a third of the people whom it infected. What they disagreed about was the cause, the pathology, and the communication of the disease. Similarly, most medical professionals these days realize that psychological illnesses occur (cf. [DSMIV]), but they disagree about their cause and pathology. Notwithstanding DSMIV, we doubt whether any satisfactory a priori definition of psychological illness can exist... because it is a matter for theory to elucidate.” Simple arguments from genetic determinism fail, in part because of an apparently draconian population bottleneck which, early in our species’ history, resulted in an overall genetic diversity less than that observed within and between contemporary chimpanzee subgroups. Arguments from psychosocial stress fare better, but are affected by the apparently complex and contingent developmental paths determining the onset of schizophrenia – one of the most prevalent serious mental disorders – dementias, psychoses, and so forth, some of which may be triggered in utero by exposure to infection, low birthweight, or other stressors.

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Gilbert suggests an extended evolutionary perspective, in which evolved mechanisms like the ‘flight-or-fight’ response are inappropriately excited or suppressed, resulting in such conditions as anxiety or post traumatic stress disorders. Nesse (2000) suggests that depression may represent the dysfunction of an evolutionary adaptation which down-regulates foraging activity in the face of unattainable goals. Kleinman and Good, however, (1985, p. 492) have outlined some of the cross cultural subtleties affecting the study of depression which seem to argue against any simple evolutionary interpretation: “When culture is treated as a constant (as is common when studies are conducted in our own society), it is relatively easy to view depression as a biological disorder, triggered by social stressors in the presence of ineffective support, and reflected in a set of symptoms or complaints that map back onto the biological substrate of the disorder... However, when culture is treated as a significant variable, for example, when the researcher seriously confronts the world of meaning and experience of members of non-Western societies, many of our assumptions about the nature of emotions and illness are cast in sharp relief. Dramatic differences are found across cultures in the social organization, personal experience, and consequences of such emotions as sadness, grief, and anger, of behaviors such as withdrawal or aggression, and of psychological characteristics such as passivity and helplessness or the resort to altered states of consciousness. They are organized differently as psychological realities, communicated in a wide range of idioms, related to quite varied local contexts of power relations, and are interpreted, evaluated, and responded to as fundamentally different meaningful realities... Depressive illness and dysphoria are thus not only interpreted differently in non-Western societies and across cultures; they are constituted as fundamentally different forms of social reality.” More generally, Kleinman and Cohen (1997) find that “[S]everal myths... have become central to psychiatry... The first is that the forms of mental illness everywhere display similar degrees of prevalence... [Second is] an excessive adherence to a principle known as the pathogenic/pathoplastic dichotomy, which holds that biology is responsible for the underlying structure of a malaise, whereas cultural beliefs shape the specific ways in which a person experiences it. The third myth maintains that various unusual culture-specific disorders whose biological bases are uncertain occur only in exotic places outside the West... In an effort to base psychiatry in ‘hard’ science and thus raise its status to that of other medical disciplines, psychiatrists have narrowly focused on the biological underpinnings of mental disorders

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while discounting the importance of such ‘soft’ variables as culture and socioeconomic status...” Further, serious mental disorders in humans are often comorbid among themselves – depression and anxiety, compulsive behaviors, psychotic ideation, etc. – and with serious chronic physical conditions such as coronary heart disease, atherosclerosis, diabetes, hypertension, dyslipidemia, and so on. These too are increasingly recognized as developmental in nature (e.g. Wallace, 2005a), and are frequently compounded by behavioral problems like violence or substance use and abuse. Indeed, smoking, alcohol and drug addiction, compulsive eating, and the like, are often done as self-medication for the impacts of psychosocial and other stressors, constituting socially-induced ‘risk behaviors’ which synergistically accelerate a broad spectrum of mental and physical problems. Recent research on schizophrenia, dyslexia, and autism, supports a ‘brain connectivity’ model for these disorders which is of considerable interest from a global workspace perspective, since large-scale brain connectivity is essential for the operation of consciousness, a principal, and very old, evolutionary adaptation in higher animals. Burns et al. (2003), on the basis of sophisticated diffusion tensor magnetic resonance imaging studies, find that schizophrenia is a disorder of large-scale neurocognitive networks rather than specific regions, and that pathological changes in the disorder should be sought at the supra-regional level. Both structural and functional abnormalities in frontoparietal networks have been described and may constitute a basis for the wide range of cognitive functions impaired in the disorder, such as selective attention, language processing and attribution of agency. Silani et al. (2005) find that, for dyslexia, altered activation observed within the reading system is associated with altered density of grey and white matter of specific brain regions, such as the left middle and inferior temporal gyri and left arcuate fasciculus. This supports the view that dyslexia is associated with both local grey matter dysfunction and with altered larger scale connectivity among phonological/reading areas. Villalobos et al. (2005) explore the hypothesis that large-scale abnormalities of the dorsal stream and possibly the mirror neuron system, may be responsible for impairments of joint attention, imitation, and secondarily for language delays in autism. Their empirical study showed that those with autism had significantly reduced connectivity with bilateral inferior frontal area 44, which is compatible with the hypothesis of mirror neuron defects in autism. More generally, their results suggest that dorsal stream connectivity in autism may not be fully functional. Courchesne and Pierce (2005) suggest that, for autism, connectivity within the frontal lobe is excessive, disorganized, and inadequately selective, whereas connectivity between frontal cortex and other systems is poorly synchronized, weakly responsive and information impoverished. Increased local but reduced

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long-distance cortical-cortical reciprocal activity and coupling would impair the fundamental frontal function of integrating information from widespread and diverse systems and providing complex context-rich feedback, guidance and control to lower-level systems. Coplan (2005) has observed a striking pattern of excessive frontal lobe self-connectivity in certain cases of anxiety disorder, and Coplan et al. (2005) find that maternal stress can affect long-term hippocampal neurodevelopment in a primate model. As stated, brain connectivity is the sine qua non of the Global Workspace model of individual human consciousness, and further analysis suggests that these disorders cannot be fully understood in the absence of a functional theory of consciousness, and in particular, of a detailed understanding of the elaborate regulatory mechanisms which must have evolved over the past half billion years to ensure the stability of that most central and most powerful of adaptations. Distortion of consciousness is not simply an epiphenomenon of the emotional dysregulation which many see as the ‘real’ cause of mental disorder. Like the pervasive effects of culture, distortion of consciousness lies at the heart of both the individual experience of mental disorder and the effect of it on the embedding of the individual within both social relationships and cultural or environmental milieu. Distortion of consciousness in mental disorders inhibits both routine social interaction and the ability to meet internalized or expected cultural norms, a potentially destabilizing positive feedback. Distortion of consciousness profoundly affects the ability to learn new, or change old, skills in the face of changing patterns of threat or opportunity, perhaps the most critical purpose of the adaptation itself. Distortion of consciousness, particularly any decoupling from social and cultural context, is usually a threat to long-term individual survival, and those with mental disorders significantly affecting consciousness typically face shortened lifespans.

4.2 Collective consciousness Human communities, as natural as neighborhoods, or as intentional as a multinational corporation or an army, have, according to the perspective of this work, multiple, effectively simultaneous, general broadcast workspaces which must not only function individually, but in concert with, while perhaps in competition for resources with, other similar modules. Granovetter’s (1973) Strength of Weak Ties argument is that nondisjunctive relationships, those which do not disjointly partition a community, are essential for efficient social function. Strong ties are those which do disjointly partition a group, for example religious affiliation, age cohort, ethnicity, national origin, skin color, in some cases, language, and so on. For an institutional setting these might be the classification by Division, Department, Work Group, informal office-politics clique, and so on. From the perspective

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of GWT, Granovetter’s weak ties permit both the formation of individual workspaces, and enable those workspaces to communicate effectively. Understanding failures within and between institutional global workspaces seems predicated on understanding weak tie structure and dynamics, which are themselves embedded in larger social and cultural contexts. Clearly, individual workspace failures will often be subject to monitoring and control by parallel workspaces, limiting the damage, as it were, in a manner impossible for human consciousness. Thus institutions, if of sufficient internal diversity and able to communicate effectively across that diversity, may suffer less inattentional blindness and less consequence from individual workspace failure, by virtue of parallel operations, but these problems will not be eliminated. Powerful subgroups not subject to contextual constraint seem a particular problem. What, then, are the likely failure patterns of such systems, and can they be corrected? Again, collectively conscious institutions, by virtue of their many highly parallel, multitasking global workspaces, can be less prone to errors from inattentional blindness or from misfunction of individual workspaces. Within organizations, several workspaces typically examine a problem, choose possible modes of action, and, essentially, negotiate and reach consensus. If there is a sufficient spectrum of workspace foci – multiple, different R0 ’s – and if cross communication between them is not too distorted, a ‘good’ institutional decision usually emerges. This is not, however, always the case, and the approach of equations (3.6) and (3.7) and their generalization can be used to model some of the myriad possibilities, in particular pathological ecosystem resilience, i.e. institutional ‘lock-in’ to bad procedures, where the system seems to disappear down a black hole, or, conversely, avoids the eight hundred pound gorilla in the livingroom, as it were. Suppose we can operationalize and quantify degrees of both institutional inattentional blindness (IAB) and of Rate Distortion (RD) in communication between different institutional global workspaces. This might be done through surveys, structured interviews, statistical characterization of internal telephone patterns, email logs, or the like. The essential assumption is that the dual information source of a collectively conscious institution which has low levels of both IAB and RD will tend to be richer than that of institutions having greater levels. This is shown in figure 4.1a, where H is the source uncertainty, X = IAB, and Y = RD. Regions of low X, Y , i.e. near the origin, have greater source uncertainty than those nearby, so H(X, Y ) shows a (relatively gentle) peak at the origin, taken as the product of two error functions. The generalized Onsager argument of equations 3.6-3.12 is shown in figure 4.1b, where S = H(X, Y ) − XdH/dX − Y dH/dY is graphed on the Z axis against the X − Y plane, assuming a gentle peak in H at the origin. Peaks in S, according to the arguments of equations 3.6-3.12, constitute repulsive system barriers, which must be overcome by external forces. In figure 4.1b

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there are three quasi-stable topological resilience modes, marked as A, B, and C. The A region is locked in to low levels of both inattentional blindness and rate distortion, as it sits in a pocket. Forcing the system in either direction, that is, increasing either IAB or RD, will, initially, be met by homeostatic attempts to return to the resilience state A, according to this model.

Fig. 4.1. a. Source uncertainty, H, of the dual information source of institutional paraconsciousness, as parametized by degrees of inattentional blindness, X = IAB and rate distortion Y = RD. Note the relatively gentle peak at low values of X, Y . H is generated as the product of two error functions. b. Generalized Onsager treatment of figure 4a. S = H(X, Y ) − XdH/dX − Y dH/dY . The regions marked A, B, and C represent realms of resilient quasi-stablity, divided by barriers defined by the relative peaks in S. Transition among them requires a forcing meachanism. From another perspective, limiting resources or imposing social disintegration from the outside – driving down H in figure 4a, would drive the system to the lower plain of C, in which the system would then become trapped in states having high levels of rate distortion and inattentional blindness.

If, in particular, rate distortion problems become severe in spite of homeostatic mechanisms, the system will then jump to the quasi-stable state B, a second pocket. According to the model, however, once that transition takes place, there will be a tendency for the system to remain in a condition of high

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rate distortion as a matter of institutionalized continued practice. That is, the system will, according to the model, become locked-in to a structure with high distortion in communication between institutional global workspaces, but one having lower overall collective conscious capacity, i.e. a lower value of H in figure 4.1a. The third pocket, marked C, is a broad plain in which both IAB and RD remain high, a highly overfocused, poorly crosslinked, probably pathologically hierarchical, structure which will require significant intervention to alter once it reaches such a quasi-stable resilience mode. Collective conscious capacity, measured by H in figure 4.1a, is the lowest of all for this condition of pathological resilience, and attempts to correct the problem – to return to condition A, will be met with very high barriers in S, according to figure 4.1b. That is, mode C is very highly resilient, although pathologically so, much like the eutrophication of a pure lake by sewage outflow. We can argue that the three quasi-equilibrium configurations of figure 4.1b represent different dynamical manifolds of the system, and that the possibility of transition between them represents the breaking of the associated symmetry groupoid by external forcing mechanisms. That is, three differentiable manifolds representing three different kinds of system dynamics have been patched together by the force of some external executive to create a more complicated topological structure. For cognitive phenomena, this kind of thing is likely to be the rule rather than the exception. ‘Pure’ groupoids are likely to be arbitrary abstractions, and the fundamental questions will involve the systems of linkages which break the underlying symmetry. Matters are, unfortunately, much more complicated than even this example. Figure 4.2 shows a three dimensional version of the X − Y base plane of figures 4.1a and 4.1b. Here we assume that the richness of institutional collective consciousness, as measured by its dual information source, is a function of three parameters, X = IAB, and Y = RD as before, but now introduce a third parameter, Z = P I, where P I represents the degree to which the institution is driven, not by adaptation to externalities, but by fixed internal policy and/or ideology. The assumption is, again, that institutions less constrained by such factors will be more flexible and have ‘richer’ cognitive dual information sources. Thus we could again write H(X, Y, Z), S = H − XdH/dX − Y dH/dY − ZdH/dZ with H ‘denser’ toward the origin of figure 4.2, i.e. near the of lowest X, Y, Z where H has been modeled as the product of three error functions, generalizing figure 4.1. Quite a large number of quasi-stable resilience modes can result from simple variations of this model, but they cannot, unfortunately, be easily represented in three dimensions. The variates PI, IAB, and RD have been represented as orthogonal in figures 4.1 and 4.2. For real systems, however, related empirical indices are not likely to be independent, so that proper analysis would require application of multivariate statistical methods to produce actual orthogonal measures.

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Fig. 4.2. Extension of figure 4.1a, using the product of three error functions. Assume, now, three characteristic parameters, X = IAB and Y = RD as above, with Z = P I representing the degree of policy/ideological rigidity. Again, the fundamental assumption is that H(X, Y, Z) will have a (gentle) peak near the origin. Then S = H(X, Y, Z) − XdH/dX − Y dH/dY − ZdH/dZ has a very complicated system of quasi-stable, locked-in, resilience modes. Again transition between them would require external forcing. Note particularly the nested surfaces with different values of H. Attaining low levels of IAB, RD, and PI requires high values of H, which, in turn, requires high internal channel capacity, i.e. low social disintegration, and, broadly speaking, high use of energy resources. Institutions suffering social disintegration or resource limitation will be confined to the outer shells, and will experience high levels of pathology. Note that low internal channel capacity – high structural rate distortion within the organization – can, in this model, make it virtually impossible to use even available resources effectively.

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Note that attaining low levels of PI, IAB, and RD in this model requires very high levels of H, that is, considerable richness of the dual information source of collective consciousness. Thus one mechanism likely to impose pathologies of IAB, RD, or PI on an institution would be severe resource limitation. Recall the homology between information source uncertainty and free energy density, equation (3.5). The dual information source representing a multiple workspace, collectively conscious institution measures, in one broad sense, available ‘energy’. Limited resources will impose limits on the possible magnitude of that information source. Constraints on H generate structures much like the outer shell of figure 4.2: H < 0.1 generates a system with high rates of the three pathologies. More formally, one might apply Lagrange multiplier or other quantitative constraint/optimization strategies. A second perspective to limits on H, and hence to the imposition of constraints due to RD, IAB, or PI, is derived entirely from communication theory. If one imagines the possibilities for information transmission within the institution to be limited by a maximum channel capacity C, which may well be, but is not necessarily, resource-related, then classical information theory requires that the dual information source transmitting along the channel must satisfy the relation H(X, Y, Z) ≤ C. Invoking the homology with free energy density, again, heuristically speaking, an institution cannot ‘spend energy’ at a rate greater than some limiting value C, which is the (effective) channel capacity of that institution. Institutions embedded in socially disintegrating subcultures, even if they ‘objectively’ have resources comparable to similar institutions in more integrated subcultures, will not be able to operate at cognitive rates greater than their channel capacity C, which is, effectively, the image of imposed cultural, historical, or other externally-imposed constraints. Thus socially disintegrated subcultures will likely impose capacity limits on embedded institutions which will express themselves as pathologies of rate distortion, inattentional blindness, or rigid policy/ideology, even when given supposedly adequate resources. That is, both embedding social disintegration and limited resources act, effectively, to dumb-down collective consciousness, according to this model. From an inverse viewpoint, resource limitation/competition and embedding social disintegration can act synergistically to limit the richness of collective consciousness, thus imposing constraints of rate distortion, inattentional blindness, or policy/ideology on the ability of the organization to recognize patterns of threat or opportunity. That is, imposing limits on maximum H in figures 4.1a or 4.2 drives the system into the dumbed-down, locked-in realms of S – states B and C and their generalization to higher dimension. Thus, within oppressed communities, IAB, RD, and PI can sometimes be viewed as

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responses of institutional triage to social disintegration and/or resource competition/limitation. Within oppressor social structures, however, mechanisms of pathological resilience may simply dominate: Apartheid systems can defend themselves.

4.3 Red Queen and Pentagon Ratchet Recent work in evolutionary economics, particularly analysis of the market economy’s infamous ‘Red Queen’ dilemma, seems adaptable to our analysis of possible pathologies affecting collectively conscious entities which are closely integrated with, and have reciprocal influence on, an embedding cultural milieu. We will focus on a kind of inverse to the Red Queen, a ratchet mechanism that can quickly fracture and fragment cognitive institutional function. Evolutionary economics suggests that firms and technology are closely integrated coevolutionary objects whose time dynamics are very complicated in comparison with the predictions of equilibrium-based models derived from 18th Century analogies with mechanical system. Nelson (1995) finds that, to be effective, a firm, which is a classic example of an enterprise instantiating distributed cognition, needs a package of routines, including those concerned with learning and innovation, which are coherent, imposing a certain rigidity on them. Competencies, according to Nelson (1995), tend to come in strongly intercorrelated complementary packages of traits, and successful firms are difficult to imitate effectively because a competitor must adopt a number of different intercorrelated practices at once. This is a reason why firms that do well in one context may have difficulty in adapting to a new one. Firms must, of course, also persist in time, replicating themselves as coherent patterns of human and organizational behavior. Technology is an integrated body of knowledge and technique passed on from one time and group to others by processes ranging from direct teaching to sociogeographic diffusion, both of which are forms of (approximate) selfreplication. Nelson’s invocation of coevolutionary interaction between firms and technology is similar to recent theorizing in human evolution, which envisions genes and culture as having become a joint coevolutionary object. Durham (1991) summarizes the current opinion: “...[G]enes and culture constitute two distinct but interacting systems of information inheritance within human populations... [and] information of both kinds has influence, actual or potential, over ... behaviors [which] creates a real and unambiguous symmetry between genes and [human] phenotypes on the one hand, and culture and phenotypes on the other... [G]enes and culture are best represented as two parallel lines or ‘tracks’ of hereditary influence on phenotypes...”

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What emerges, in effect, is a description of economic process in terms of a Lamarckian punctuated equilibrium (sensu S. Gould, 1992) in which quasi-equilibria are, essentially, topological resilience modes as we have defined them. Natural systems subject to coevolutionary interaction may become enmeshed in the Red Queen dilemma of Alice in Wonderland, in that they must undergo constant evolutionary change in order to avoid extinction – they must constantly run just to stay in the same place. An example would be a competitive arms race between predator and prey: Each evolutionary advance in predation must be met with a coevolutionary adaptation which allows the prey to avoid the more efficient predator. Otherwise the system will become extinct, since a highly specialized predator can literally eat itself out of house and home. Similarly, each prey defense must be matched by a predator adaptation for the system to persist. While natural populations cannot transmit acquired characteristics, human cultures and organizations are well able to do so, and can sometimes forget more easily than natural systems. Nelson’s perspective suggests the possibility of a Red Queen coevolutionary process affecting firms and technology, but also encompasses the possibility of a rapid inverse, a form of economic ratchet which we will explore at some length. The term Red Queen was used to describe economic interaction as early as 1913 (JMC, 1913), and Hugh-Jones (1955) made explicit use of it to characterize the US economy: “The American firm is like the Red Queen, forced to keep running if it is even to remain in the same place in the economic market, and an increase of productivity of from 3 to 3 1/2 percent a year is necessary to achieve this... A good American executive is one who is divinely discontented with present methods of doing anything and believes that anything he has done, he can do better. It is a state of mind which regards nothing as impossible, but merely taking a little longer than what is only difficult.” Similarly, Krugman (1979) states “Northern [US, Canada, W. Europe, Japan] residents depend in part on the rents from their monopoly of newly developed products. This monopoly is continually eroded by technological borrowing and must be maintained by constant innovation of new products. Like Alice and the Red Queen, the developed region must keep running to stay in the same place.” Thus the macroeconomic Red Queen, in one form or another, has been recognized for the better part of a century. Here we present a fairly elaborate theory of this pathology, which appears to generalize to distributed institutional cognition embedded in a cultural

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context with which it interacts strongly, i.e. engage in a powerful mutual information crosstalk. This may involve contact between internal workspaces, or between the system as a whole and an embedding context. The model is based on the parametization of an information source, which suggests that coevolutionary interactions, their associated Red Queen processes, and related economic extinction/fragmentation events, are all very highly punctuated, subject to sudden phase transitions once a critical point has been passed for driving parameters. More elaborate discussion of such phase transitions is given in the Appendix. An empirical context for this analysis is the massive diversion of capital and technological resources from civilian enterprise in the US, the creation of a Pentagon capitalism (e.g. Melman, 1988, 1997; Tirman, 1984; Ullmann et al., 1988), which has been the distinguishing hallmark of the postwar economy. The failure to civilianize the economy after World War II caused an essentially finite technological capacity – Guns or Butter – to be split in a zero-sum game, Internet and space program spillovers to the contrary. Resulting collapse in the competitiveness of US industry has been catastrophic and is well documented (Melman, 1961, 1971, 1983, 1988, 1997; Dumas, 1987; Ullmann et al., 1988; Ullmann, 1985). The failure to technologically renew heavy manufacturing, consumer electronics, automobile and other industries has cost stable, unionized jobs throughout the Rust Belt, and triggered a balance of payments catastrophe as the US became the dumping ground of choice for the output of Asian Tiger economies, which have themselves become entrained by our precipitate and continuing decline, forming an unstable mutualistic complex. We begin by examining ergodic information sources and their dynamics under the self-similarity of a renormalization transformation near a punctuated phase transition. This calculation recurs repeatedly, with different detail, across a number of problems. We then study the linked interaction of ‘firms’ and ‘technology’, i.e. distributed institutional cognition and its embedding cultural context, in which the richness of the internal language of each affects the other, that is, when firms and technology have become one another’s primary environments. This is a highly special case which leads directly and naturally to a coevolutionary Red Queen, but, when acquired characteristics are inherited, to a rapid inverse, a punctuated Pentagon Ratchet, as well. Wallace and Wallace (1999) examined a more elaborate evolutionary model of firm-technology interaction based on the emergence of a joint meta-language linking these two distinct kinds of information sources, and including them as, essentially, subdialects in a hierarchical structure. While this kind of picture may serve for discussions of biocultural evolution, the simpler treatment we use here – in which each language becomes the other’s primary environment – produces both the Red Queen and the Pentagon Ratchet within the same formalism: Here we opt for Occam’s Razor.

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4.3.1 Firms and technology interact A firm engaging in cognitive process or a coherently organized body of knowledge, i.e. a technology, can be most weakly, and hence universally, described in terms of an adiabatically, piecewise stationary, ergodic information source involving a stochastic variate X which, in some general sense, sends symbols α in correlated sequences α0 , α1 ...αn−1 of length n (which may vary), according to a joint probability distribution, and its associated conditional probability distribution,

P [X0 = α0 , X1 = α1 , ...Xn−1 = αn−1 ], P [Xn−1 = αn−1 |X0 = α0 , ...Xn−2 = αn−2 ]. (4.1)

If the conditional probability distribution depends only on m previous values of X, then the information source is said to be of order m (Ash, 1990). See Wallace and Wallace (1998, 1999) for a more extensive justification of the approach in the context of biological and biocultural evolution. Again, by ‘ergodic’ we mean that, in the long term, correlated sequences of symbols are generated at an average rate equal to their (joint) probabilities. ‘Adiabatic’ means that changes are slow enough to allow the necessary limit theorems to function, much like the Born-Oppenheimer approximation in molecular physics. ‘Stationary’ means that, within pieces, probabilities don’t change (much), and ‘piecewise’ means that these properties hold between phase transitions, which are described using renormalization methods. As the length of the (correlated) sequences increases without limit, the Shannon-McMillan Theorem of Information Theory (Ash, 1990; Khinchin, 1957) – an asymptotic relation as fundamental as the Central Limit Theorem – permits division of all possible streams of symbols into two groups, a relatively small number characterized as meaningful, whose long-time behavior matches the underlying probability distribution, and an increasingly large set of gibberish with vanishingly small probability. Let N (n) be the number of possible meaningful sequences of length n emitted by the source X. The uncertainty of the source, H[X], can be defined by the subadditive relation

H[X] = lim

n→∞

log[N (n)] . n

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(4.2)

The Shannon-McMillan Theorem shows how to characterize H[X] directly in terms of the joint probability distribution of the source X: H[X] is observable and can be calculated from the inferred pattern of joint probabilities. Let P [xi |yj ] be the conditional probability that stochastic variate X = xi given that stochastic variate Y = yj and let P [xi , yj ] be the joint probability that X = xi and Y = yj . Then the joint uncertainty of X and Y , H(X, Y ), is given by

H(X, Y ) = −

XX i

P (xi , yj ) log[P (xi , yj )].

j

(4.3)

The conditional uncertainty of X given Y is defined as (Ash, 1990)

H(X|Y ) = −

XX i

P (xi , yj ) log[P (yj |xi )].

j

(4.4)

The Shannon-McMillan Theorem of states that the subadditive function H[X] defined in equation (4.2) is given by the limits

H[X] = lim H(Xn |X0 , ..., Xn−1 ) = lim n→∞

n→∞

H(X0 , X1 , ..., Xn ) . n+1

(4.5)

Estimating the probabilities of the sequences α0 , ...αn−1 from observation, the ergodic property allows us to use them to estimate the uncertainty of the source, i.e. of the behavioral language X. That is, H[X] is directly measurable (Ash, 1990).

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Some elementary consideration (e.g. Ash, 1990; Cover and Thomas, 1991) shows that source uncertainty has a least upper bound, a supremum, defined by the capacity of the channel along which information is transmitted. That is, there exists a number C defined by externalities such that H[X] ≤ C. C is the maximum rate at which the external world can transmit information originating with the information source. Although we do not do so for pedagogic and historical reasons, much of the subsequent development could, in fact, be expressed using this relation. Similarly, we could recover much of the treatment of evolutionary economics by Nelson and Winter (1982) in terms of Markov chains by noting that the uncertainty of an information source of finite order m, which can be taken as large as needed, can be approximated to any desired accuracy by the uncertainty of a ‘unifilar’ Markov information source, defined uniquely by an underlying Markov process, where the initial state is chosen according to the equilibrium distribution of that process. See Ash (1990, Ch. 6) for the details. We prefer, rather, to use the definition of H[X] from equation (4.2) because of its close analogy with developments from statistical physics. Consider a physical system with volume V which undergoes a phase transition depending on an inverse temperature parameter K = 1/T at a critical temperature TC . The free energy density F (K) of the entire system is defined by the relation

log[Z(K)] V →∞ V

F (K) = lim (4.6)

where V is as above and Z(K) is the partition function defined from the system’s energy distribution. Any good statistical mechanics text will give the details. Imposition of a ‘renormalization symmetry’ on F (K) describes, in the infinite volume limit, the behavior of the system at the phase transition in terms of scaling laws (K. Wilson, 1971). After some development, taking the limit n → ∞ in equation (4.2) as an analog to the infinite volume limit of a physical system, we will apply this approach to a source uncertainty associated with firms or technology. We will examine changes in their structure as a fundamental ‘inverse temperature’ changes across the underlying system. This leads, after some development, to a theory of the interaction of self-replicating information sources which will give our main results. 4.3.2 Punctuated phase transition We use three parameters to describe the relations between an information source and its environment or between different sources. Others might well

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be chosen: recognizably similar results would follow. That is, the information source uncertainty above is taken as an explicit function of three variates. The first, J ≥ 0, measures the inverse degree to which acquired characteristics are transmitted. For systems without memory J = ∞. J ≈ 0 thus represents a high degree of inheritance of acquired characteristics. J will always remain distinguished, a kind of inherent direction or external field strength in the sense of Wilson (1971). The second parameter, Q = 1/C ≥ 0, represents the inverse availability of ‘capital’, i.e. resources. Q ≈ 0 thus represents a high ability to renew and maintain a cognitive enterprise. The third parameter, K = 1/T , is an inverse index of a ‘generalized temperature’ T , which we will more directly specify below. We suppose further that the structure of interest is implicitly embedded in, and operates within the context of, a larger manifold stratified by spatial, behavioral or other ‘distances.’ Take these as multidimensional vector quantities A, B, C.... A may represent location in space, B may be determined through multivariate analysis of a spectrum of observed behavioral or other factors, in the largest sense, etc. It may be possible to reduce the effects of these vectors to a function of their magnitudes a = |A|, b = |B| and c = |C|, etc. Define the generalized distance r as

r2 = a2 + b2 + c2 + .... (4.7)

To be more explicit, we assume an ergodic information source X is associated with the reproduction and/or persistence of a population, organization, language or other structure. The source X, its uncertainty H[J, K, Q, X] and its parameters J, K, Q all are assumed to depend implicitly on the embedding manifold, in particular on the metric r of equation (4.7). There is a fundamental reason for adding this new layer of complexity. Hodgson (1993) provides several extended discussions of the ubiquity of sudden punctuation in evolutionary process, i.e. relatively rapid, seemingly discontinuous fundamental changes in system structure leading to mass extinctions and/or speciation divergences. A particularly elegant and natural formalism for generating such punctuation in our context involves application of Wilson’s (1971) program of renormalization symmetry – invariance under the renormalization transform – to source uncertainty defined on the r-manifold. The results predict that language in the most general sense, which includes the transfer of information

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within a a cognitive enterprise, or between an enterprise and an embedding context, will undergo sudden changes in structure analogous to phase transitions in physical systems. The view is complementary to recent analyses of sudden fragmentation in social networks, seen from the perspective of percolation theory (Wallace, 1993). We must, however, emphasize that this approach is argument by abduction, in Hodgson’s (1993) sense, from physical theory: Much current development surrounding self-organizing physical phenomena is based on the assumption that at phase transition a system looks the same under renormalization. That is, phase transition represents a stationary point for a renormalization transform in the sense that the transformed quantities are related by simple scaling laws to the original values. Renormalization is a clustering semigroup transformation in which individual components of a system are combined according to a particular set of rules into a ‘clumped’ system whose behavior is a simplified average of those components. Since such clumping is a many-to-one condensation, there can be no unique inverse renormalization, and, as the Appendix shows, many possible forms of condensation. Assume it possible to re-define characteristics of the information source X and J, K, Q as functions of averages across the manifold having metric r, which we write as R. That is, ‘renormalize’ by clustering the entire system in terms of blocks of different sized R. Let N (K, J, Q, n) be the number of high probability meaningful correlated sequences of length n across the entire community in the r-manifold of equation (4.7), given parameter values K, J, Q. We study changes in H[K, J, Q, X] ≡ lim

n→∞

log[N (K, J, Q, n)] n

as K → KC and/or Q → QC for critical values KC , QC at which the community begins to undergo a marked transformation from one kind of structure to another. Given the metric of equation (4.7), a correlation length, χ(K, J, Q), can be defined as the average length in r-space over which structures involving a particular phase dominate. Now clump the community into blocks of average size R in the multivariate r-manifold, the ‘space’ in which the cognitive enterprise is implicitly embedded. Following the classic argument of Wilson (1971), reproduced in the Appendix, it is possible to impose renormalization symmetry on the source uncertainty on H and χ by assuming at transition the relations

H[KR , JR , QR , X] = RD H[K, J, Q, X]

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(4.8)

and

χ(KR , JR , QR ) =

χ(K, J, Q) R

(4.9)

hold, where KR , JR and QR are the transformed values of K, J and Q after the clumping of renormalization. We take K1 , J1 , Q1 ≡ K, J, Q and permit the characteristic exponent D to be nonintegral. Equations (4.8) and (4.9) are assumed to hold in a neighborhood of the transition values KC and QC . Differentiating these with respect to R gives complicated expressions for dKR /dR, dJR /dR and dQR /dR depending simply on R which we write as

dKR /dR =

u(KR , JR , QR ) R

dQR /dR =

w(KR , JR , QR ) R

dJR /dR =

v(KR , JR , QR ) JR . R

(4.10)

Solving these differential equations gives KR , JR and QR as functions of J, K, Q and R. Substituting back into equations (4.8) an (4.9) and expanding in a first order Taylor series near the critical values KC and QC gives power laws much like the Widom-Kadanoff relations for physical systems (Wilson, 1971). For example, letting J = Q = 0 and taking κ ≡ (KC − K)/KC gives, in first order near KC ,

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H = κD/y H0 χ = κ−1/y χ0 (4.11)

where y is a constant arising from the series expansion. Note that there are only two fundamental equations – (4.8) and (4.9) – in n > 2 unknowns: The critical ‘point’ is, in this formulation, most likely to be a complicated implicitly defined critical surface in J, K, Q, ...-space. The ‘external field strength’ J remains distinguished in this treatment, i.e. the inverse of the degree to which acquired characteristics are inherited, but neither K, Q nor other parameters are, by themselves, fundamental, rather their joint interaction defines critical behavior along this surface. That surface is a fundamental object, not the particular set of parameters (except for J) used to define it, which may be subject to any set of transformations which leave the surface invariant. Thus ‘inverse generalized temperature,’ ‘resource availability’ or whatever other parameters may be identified as affecting the ‘richness’ of distributed institutional cognition, are inextricably intertwined and mutually interacting, according to the form of this critical evolutionary transition surface. That surface, in turn, is unlikely to remain fixed, and should vary with time or other extrinsic parameters, including, but not likely limited to, J. At the critical surface a Taylor expansion of the renormalization equations (4.8) and (4.9) gives a first order matrix of derivatives whose eigenstructure defines fundamental system behavior. For physical systems the surface is a saddle point (Wilson, 1971), but more complicated behavior seems likely in what we study. See Binney et al., (1986) for some details of this differential geometry. Taking, for the moment, the simplest formulation, (J = Q = 0), that is, a well-capitalized structure with memory, as K increases toward a threshold value KC , the source uncertainty of the reproductive, behavioral or other language common across the community declines and, at KC , the average regime dominated by the ‘other phase’ grows. That is, the system begins to freeze into one having a large correlation length for the second phase. The two phenomena are linked at criticality in physical systems by the scaling exponent y. Assume the rate of change of κ = (KC − K)/KC remains constant, |dκ/dt| = 1/τK . Analogs with physical theory suggest there is a characteristic time constant for the phase transition, τ ≡ τ0 /κ, such that if changes in κ take place on a timescale longer than τ for any given κ, we may expect the

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correlation length χ = χ0 κ−s , s = 1/y, will be in equilibrium with internal changes and result in a very large fragment in r-space. Following Zurek (1985, 1996), the ‘critical’ freezout time, tˆ, will occur at a ‘system time’ tˆ = χ/|dχ/dt| such that tˆ = τ . Taking the derivative dχ/dt, remembering that by definition dκ/dt = 1/τK , gives χ κτK τ0 = = |dχ/dt| s κ so that κ=

p sτ0 /τK .

Substituting this value of κ into the equation for correlation length, the expected size of fragments in r-space, d(tˆ), becomes

d ≈ χ0 (

τK s/2 ) sτ0

(4.12)

with s = 1/y > 0. The more rapidly K approaches KC the smaller is τK and the smaller and more numerous are the resulting r-space fragments. Thus rapid change produces small fragments more likely to risk economic extinction in a system dominated by economies of scale. 4.3.3 Queen and Ratchet Extending the theory above involves envisioning firms and technology as subject to a coevolutionary Red Queen by treating their respective source uncertainties as recursively parametized by each other. That is, assume the internal cultures of a firm and its associated external technology base are each other’s primary environments. These are, respectively, characterized by information sources X and Y, whose uncertainties are parametized [1] by inverse measures of both inheritance and capital – J Q as above – and, most critically, [2] by each others inverse uncertainties, HX ≡ 1/H[X] and HY ≡ 1/H[Y], i.e.

H[X] = H[Q, J, HY , X] H[Y] = H[Q, J, HX , Y].

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(4.13)

Assume a strongly heritable system, i.e. J = 0, with fixed inverse capitalization, Q, for which H[X] follows something like the lower graph in figure 4.3, a reverse S-shaped curve with K ≡ HY = 1/H[Y], and similarly H[Y] depends on HX . That is, increase or decline in the source uncertainty of technology leads to increase or decline in the source uncertainty of the associated firms, and vice versa. The ‘richness’ of the internal cognitive languages of firms and their embedding milieus are closely linked. Start at the right of the graph for H[X] in figure 4.3, the source uncertainty of the firm, but to the left of the critical point KC . Assume some improvement in technology (or the richness of the embedding culture increases) is introduced: H[Y] increases, reflecting the ability to say more things through the increment caused by the new technology (or cultural change), so HY decreases, and thus H[X] increases, walking up the lower curve of figure 4.3 from the right: the richness of the firm’s internal language increases. The increase of H[X] leads, in turn, to an increased capacity of the system to improve its technological base, thus a decline in HX triggers an increase of H[Y], whose increase leads to a further increase of H[X] and vice versa: The Red Queen, taking the system from the right of figure 4.3 to the left, up the lower curve. At the population level, firms undergoing such a dynamic may be expected to become more highly efficient, and thus survive selection by economic competition. Now enlarge the scale of the argument, and consider the possibility of largescale interactions between the overall structure of civilian firms and technology, i.e. the possibility of national-scale Red Queens. Clearly the country with the most efficient such coevolutionary structure gains competitive strength in the global marketplace. Diverting technology and capital from a nation’s civilian to military enterprise, however, slows the national-scale Red Queen, giving a significant advantage to less-militarized economies. Competitive exclusion ensues, with the militarized national economy buying cheaper, more sophisticated civilian goods abroad. This further enervates the domestic coevolutionary linkage, leading in turn to even more dynamic mechanisms of national decline: start with an initially strongly linked coevolutionary civilian economy, a national system with H[X] at the far left of the lower part of figure 4.3. Technological resources are taken from civilian industry and given to the military, causing declines in global competitiveness. Investment in, and indeed maintenance of, the national civilian technology languishes as imports dominate the domestic market. At some point H[Y] actually declines, HY increases and H[X] decreases as firms lose their edge, causing a further fall in H[Y], triggering another rapid decline in H[X], which triggers a further

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Fig. 4.3. A reverse-S-shaped curve for source uncertainty H[X] – measuring language richness – as a function of an inverse temperature parameter K = 1/H[Y], the richness of the embedding technological/cultural base. To the right of the critical point KC the system breaks into fragments in r-space whose size is determined by the rate at which K approaches KC , according to equation (4.12). A collection of fragments already to the right of KC , however, would be seen as condensing into a single unit as K declined below the critical point. If K is an inverse source uncertainty itself, i.e. K = 1/H[Y] for some information source Y, then under such conditions a Red Queen dynamic can become enabled, driving the system strongly to the left. On the other hand, under such circumstances, a decline in H[Y] for a condensed system already to the left of KC would likely trigger a Pentagon Ratchet, driving the condensed system to fragmentation. No intermediate points are asymptotically stable in this development, although the generalized Onsager arguments of chapter 3 suggest that the repulsive peak in S = H − K/dH/dK can serve to create quasi-stable resilience realms. To the right of the critical point KC the system is frozen into disjoint fragments.

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decline in H[Y], and so on until the system reaches the critical point KC , and suddenly shatters. This is the famous Pentagon Ratchet, leading to a high-speed punctuated fragmentation producing many small unlinked pieces likely to suffer very rapid economic extinction under competitive pressures. It is a mechanism likely to affect many forms of distributed institutional cognition which are closely linked to an embedding cultural system: Feedback can drive such a linked human ecosystem rapidly down, as well as up, a ramp of mutual interaction. The Pentagon Ratchet provides a natural model for the punctuated collapse of institutional distributed cognition under increasingly draconian external oppression, for example imposed limits of resource allocation, forced displacement, and the like. The only way to short-circuit such a ratchet mechanism would be to better capitalize the civilian firm-and-technology system, decreasing Q and driving the system back to the left: An industrial policy requiring redeployment of capital and technological resources from the military into the civilian sectors. In a community setting, this would involve reinvestment in place of disinvestment. Unfortunately, reversing the ratchet is also a punctuated process, just like the onset of its results. There is likely to be a significant threshold of reinvestment needed before community reknitting can occur. That is, an initially fragmented system – beginning to the right of the critical point KC in figure 4.3 – would face a similarly punctuated transition before an upwardmoving, technology/culture-driven Red Queen could become enabled. The argument follows the generalized Onsager development of the last chapter: The upper graph of figure 4.3 represents the disorder S = H[K, X] − KdH[K, X]/dK for K = 1/H[Y]. According to the treatment of chapter 3, the peak in S represents a repulsive barrier for transition between high and low values of H[X]. This leads to the expectation of hysteresis in such change: there will be a tendency for the firm to at least attempt to remain at high efficiency as the technological base degrades. By contrast, if the firm is driven beyond the critical point KC , and fragments, then the peak in S represents a barrier to reintegration. The two realms, to the left and right of the peak in S for figure 4.3, thus represent quasi-stable resilience modes, in this model. Relentless decline in ‘technology’, i.e. the embedding richness of culture, H[Y], can, however, simply drive the system from integration to fragmentation – social eutrophication – where it will remain trapped in the absence of a considerable reinvestment of resources.

4.4 Failure of therapeutic intervention Persistent dysfunction by an individual workspace, or a particular subset of them, the effects of inattentional blindness, pathologies of rate-distorted intraworkspace communication, of policy and ideology, or a Pentagon Ratchet,

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can, in theory, be addressed by external correction: therapeutic intervention by other entities, i.e. an interventionist ‘Deus ex Machina’. Pathological context, which is often responsible for global workspace failures of various kinds, can, however, become convoluted with the intervention itself, resulting in therapeutic failure. We model this in some detail. Recall that the essential characteristic of cognition in this formalism involves a mapping, h(x), of a (convolutional) path x = a0 , a1 , ..., an , ... onto a member of one of two disjoint sets, B0 or B1 . Thus respectively, either (1) h(x) ∈ B0 , implying no action taken, or (2), h(x) ∈ B1 , and some particular response is chosen from a large repertoire of possible responses. There is an evident problem in defining these two disjoint sets, suggesting that some higher order, i.e. executive, cognitive module is needed to determine what constitutes B0 , the set of normal actions and procedures, those not constituting explicit intervention. Again, this is because there is no low energy mode for information systems. That is, virtually all states are more or less high energy, high information content or transmission, states. Thus there is no natural way to identify a ground state using the physicist’s favorite variational or other minimization arguments. Suppose that higher order executive cognitive module, which can be described as a kind of Zero Mode Identification, interacts with an embedding, highly structured quasi-language of systemic perturbation – market forces and failures, disasters, structured noise, and the like. Instantiating a Rate Distortion image of that embedding stress, the ZMI begins to include one or more members of the set B1 into the set B0 , or vice versa, when a circumstance requiring action is ignored. Recurrent hits on that aberrant state would be experienced as episodes of institutional pathology, over or under reaction. Empirical tests of this hypothesis quickly involve real-world regression models of the interrelations among measurable markers of success and failure, leading to the Rate Distortion Manifold arguments above. Different eigenmodes Yk of the RDM regression model characterized by the zero mode matrix R0 can be taken to represent the shifting-of-gears between different languages defining the sets B0 and B1 . That is, different eigenmodes of the RDM would correspond to different required (and possibly mixed) characteristic systemic responses. If there is a state (or set of states) Y1 such that R0 Y1 = Y1 , then the unitary kernel Y1 corresponds to the condition ‘no response required’, i.e. the set B0 . Suppose pathology becomes manifest, i.e. ˆ 0, R0 → R0 + δR ≡ R so that some chronic ‘excited state’ becomes the new unitary kernel, and Y1 → Yˆ1 6= Y1

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83

ˆ 0 Yˆ1 = Yˆ1 . R Next, assume other, perhaps embedding, corporate global workspaces induce a sequence of therapeutic counterperturbations – deliberate therapeutic interventions – δTk according to the pattern

ˆ 0 + δT1 ]Yˆ1 = Y 1 , [R ˆ 0 + δT1 , ˆ1 ≡ R R ˆ 1 + δT2 ]Y 1 = Y 2 [R ... (4.14)

so that, in some sense,

Y j → Y1 . (4.15)

That is, the system, as monitored by the RDM, is driven to its original condition. ˆ 0 → R0 . That is, actual remediaIt may or may not be possible to have R tion may not be possible, in which case palliation or control is the therapeutic aim. ˆ 0 and The essential point is that the pathological state represented by R the sequence of therapeutic interventions δTk , k = 1, 2, ... are interactive and reflective, depending on the regression of the set of vectors Y j to the desired state Y1 , much in the same spirit as Jerne’s immunological idiotypic hall of mirrors. The therapeutic problem revolves around minimizing the difference between Y k and Y1 over the course of treatment. That difference represents the inextricable convolution of treatment failure with adverse reactions to the course of treatment itself, and failure of compliance, often attributed through

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social construction by ‘provider’ to ‘patient’, i.e. failure of the therapeutic alliance. It should be obvious that the treatment sequence δTk itself is a cognitive path of interventions which has, in turn, a dual information source in the sense previously invoked. Treatment may, then, interact in the usual Rate Distortion manner with the pathogenic patterns of structured perturbation – market pressures, failures, disasters, resource limitations, embedding channel capacity limits, structured ‘red’ noise, the burdens of history, and the like – which are, themselves, signals from an embedding information source. Thus treatment failure, adverse reactions, and noncompliance will, of necessity, embody a distorted image of embedding structured perturbations which may indeed be responsible for the primary misfunction. This coupling would most likely occur in a highly punctuated manner, depending in a quantitative way on the degree of interlinking of the three-fold system of affected workgroups, therapeutic interaction, and treatment mode, with that perturbation. Clearly this is only one example of a much larger spectrum of possibilities. Empirical study would seem necessary at this point to prune down the search tree, as it were, making further analysis practical. One disturbing implication of this analysis is the apparent difficulty of correcting collective consciousness once it becomes overtly pathological. The general experience of greatly shortened lifespan for most individuals suffering developmental pathologies of global workspace connectivity – schizophrenia, dementia, autism, and the like – suggests that the relentless impact of market forces, which are effectively evolutionary selection pressures, guarantees rapid extinction or merger as the most likely outcome for any systematic, large-scale, organizational cognitive lapses. Western market economies are littered with the corpses of extinct enterprises and economic taxa, and the last century has not been kind to states which possessed, or attempted to gain, colonial empires of various forms, nor to the regions and peoples which suffered occupation under colonial regimes (Memmi, 1969; Fanon, 1966). In particular, contexts of social disintegration and resource limitation, individually and likely synergistically, severely limit the possibilities of therapeutic intervention to correct pathologies of collective consciousness.

5 DISEASE AND COLLECTIVE CONSCIOUSNESS

5.1 Infectious disease Here we explore how public policy and economic practice, which are quintessential expressions of collective consciousness, in synergism with historical trajectory, create an opportunity structure that is a tunable, highly patterned, ‘nonwhite noise’ in a generalized epidemiological stochastic resonance which efficiently amplifies unhealthy living and working conditions to evoke or maintain infectious disease as the projected image of power relations between groups. This is especially true for infections carried by socially-generated ‘risk behaviors’ which are usually adaptations to longstanding resource deprivation or marginalization (e. g. Wallace et al, 1996). A number of local epidemics focused in marginalized communities may subsequently undergo a policy and structure-driven phase transition to become a coherent pandemic, a spreading plague which can entrain more affluent populations into the disease ecology of marginalization. Similarly, policy changes can cause declining endemic infections to rise, likewise enmeshing dominant subgroups. Ecosystem resilience theory suggests that Apartheid and Egalitarian political systems will entertain starkly different modes of epidemic and endemic infections, something of which can be seen in recent outbreaks of AIDS and tuberculosis in and near New York City. Epidemic spread is often viewed as, essentially, a ‘mechanical’ diffusion, in the classic geographic sense (e.g. Abler et al., 1971), little more than a marker for underlying urban structure. For example, Gould and Tornqvist (1971, p. 160) write: “As the urban lattice hardens, and the links between the major centers strengthen, the dominant process is apt to change from a [spatially] contagious to a hierarchical one. We have few examples of this dramatic change in innovation diffusion, but one particularly striking one comes from the early history of the United States (Pyle, 1969). The disease cholera is hardly an

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innovation we would like to spread around, but it does form a useful geographical tracer in a spatial system, rather like a radioactive isotope for many systems studied by the biological sciences. The first great epidemic struck in 1832 at New York and Montreal, and then diffused slowly along the river systems of the Ohio and Great Lakes. A graphical plot of the time the disease was first reported against distance shows a clear distance effect, indicating that basically processes of spatial contagion were operating. A plot of time against city size shows no relationship whatsoever. However, by 1849, the rudimentary urban hierarchy of the United States was just beginning to emerge. The second epidemic struck at New York and New Orleans in the south, and a plot of first reporting times against city size, indicates that a hierarchical effect was beginning to structure innovation flows at this time. Finally, in 1865, when the third epidemic struck, the railways were already strengthening the structure of America’s urban space. The disease jumped rapidly down the urban hierarchy, and a plot of reporting time against city size shows that a very clear hierarchical process was at work.” The first, epidemic, stages of the AIDS pandemic in the US seem to provide an example. The cover of Gould’s 1993 book The Slow Plague, with more detail in Gould (1999), presents a time sequence of maps showing the number of AIDS cases in the US on a logarithmic scale. Cases first appear in the largest US port cities: New York, Los Angeles, San Francisco, Miami and Washington DC. Subsequent spread is by hierarchical hopscotch to smaller urban centers, followed by a spatially contagious winestain-on-a-tablecloth diffusion from city center into the surrounding suburban counties. Figure 5.1a, from Wallace et al. (1999), gives a detailed analytic treatment of the hierarchical hopscotch. Using multivariate analysis of covariance, it shows the log of the number of AIDS cases in each of the 25 largest US metropolitan regions for two periods, (1) through April, 1991 and (2) from April, 1991 through June, 1995, as functions of a composite index defined in terms of a region’s local pattern of susceptibility and its position in the US urban hierarchy. The local indices are (i) the log of the number of violent crimes in the region for 1991, and (ii) an index of ‘rust belt’ deindustrialization, the log of the ratio of manufacturing employment in 1987 to that in 1972. The global index, of position on the US urban hierarchy, is the log of the probability of contact with the New York City metro region, the nation’s largest, determined from a county-by-county analysis of migration carried out by the US Census for the period 1985-1990. Locally, high levels of violence and industrial displacement represent busttown and boom-town social dynamics leading to the loosening of social control. Nationally, the probability of contact with New York represents inverse socio-spatial distance from the principal epicenter of the US AIDS epidemic. Multivariate analysis of covariance finds the lines for the two time periods are

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Fig. 5.1. a. Log number of AIDS cases in the 25 largest US metropolitan regions, through 4/91 and 4/91-6/95. The composite index is X = .764 Log(USVC91) + .827 Log(USME87/USME72) + .299 Log(Prob. NY). USVC91 is the number of violent crimes, USMEnm the number of manufacturing jobs in year nm, and (Prob. NY) the probability of contact with New York City according to Census migration data for 1985-1990. Applying multivariate analysis of covariance, the two lines are parallel with different intercepts: The second is obtained simply by raising the first. This suggests a coherent, national-scale, spatiotemporal stochastic resonance linking marginalized inner-city communities, the Apartheid system which marginalizes them, and the epidemic outbreak which began within them, to the rest of the country. b. Parallel regression lines for 24 counties of the New York Metropolitan Region. Y-axis is the log of the cumulative AIDS cases per 100,000, plotted versus a composite index X = .759 log(PP ) + .197 log(∆µ/∆A). PP is the percent of a county’s population living in poverty and ∆µ/∆A is the area density of the equilibrium commuting intensity. Again, the later period is obtained from the earlier by simple vertical displacement.

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parallel and each accounts for over 90 percent of the variance in the dependent variate. Thus later time periods are obtained from the earlier simply by raising the graph in parallel: As goes the New York Metropolitan Region, so goes the nation. This pattern represents a propagating, spatio-temporally coherent epidemic process which has linked disparate, marginalized ‘core groups’ – inner-city neighborhoods of Gay males, intravenous drug users, and minority youth – across time and space with the rest of the urbanized US, ultimately placing some 3/4 of the nation’s population at increasing risk. See Wallace, Wallace et. al (1999) for details. Analysis of the spread of AIDS in the 24-county New York Metropolitan region – the dominant node in the US urban hierarchy – based on the pattern of commuting into Manhattan, shows an analogous coherence. Figure 5.1b, taken from Wallace et al. (1995), shows the log of AIDS cases per 100,000 population for each of the counties for three periods (1), through 1984, (2) 1985-87, and (3) 1988-1990, as a function of a composite index made up of (i) a local susceptibility factor, the percent of a county’s population living in poverty in 1980, and (ii) the area density of the equilibrium distribution of a Markov process constructed from the 1980 county-to-county commuting pattern, as determined from US Census data. Again, multivariate analysis of covariance finds the three time periods parallel, but displaced vertically, as the disease changed from one of primarily Gay middle-class males into one equally distributed between Gay males and poor, largely minority intravenous drug users. Examination of several other metropolitan regions (Wallace et al. 1997) shows similar coherence in city to suburban spread of disease for the hollowed out urban areas of the US, i.e. those in which policies of planned shrinkage or benign neglect resulted in great devastation of minority voting blocks, for example Detroit, Washington DC, and Philadelphia. Remarkably, however, the San Francisco metropolitan region, which contains one of the principal US AIDS epicenters – the Gay ghetto of the Castro District in San Francisco itself – displayed a far different pattern, in which each of the region’s individual counties seems to have its own independent epidemic, obviously seeded from the center, but with no apparent regional coherence. This difference merits some further discussion, and its explanation is one of the foci of this chapter. Wallace et al. (1997) defined the AIDS outbreak near a central city as ‘regionalized’ in terms of a Markov process inferred from the commuting pattern linking the central city and its suburban counties, and the counties with each other. If a metro region had n counties, an n × n matrix was constructed from Census data of the fraction of the workforce commuting from each county into each other county, including itself. Since the row sums were automatically normalized to unity, an associated Markov process could be defined, and the long-time equilibrium distribution calculated. The essential independent empirical parameter was the equilibrium distribution per unit area for each of the n counties of the metro region.

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The AIDS outbreak was characterized as regionalized if a regression of the log of the AIDS cases per unit population against this independent variate – log of the equilibrium distribution per unit area – was significant in the absence of the commuting center, Manhattan (or New York County) and San Francisco county, respectively. Unlike the analysis of figure 5.1b, local indices were not added to the regression model. The AIDS pattern for the New York Metro Region was highly significant, in this sense, with an associated R2 , the fraction of variance accounted for by the regression model, of 76.3 % through 1990, while that for San Francisco was, remarkably, not significant at all, having an R2 of just 7 %. That is, using this form of analysis, near New York City the early stage of the AIDS epidemic was coherently focused on the commuting center, with the distributions of different years actually obtained from those earlier by simple vertical displacement of the graph, according to multivariate analysis of covariance. For the San Francisco metro region during the same period, however, each county had its own epidemic, and, in spite of the elevated rate for San Francisco itself, no regional coherence, in the sense defined above, was observed. New York City and San Francisco have significantly different patterns of reaction against the Civil Rights Movement of the 1950’s and 60’s, i.e. of the revitalization of the US system of Apartheid, sensu Massey and Denton, (1993). Wallace and Wallace (1990, 1997a, 1998a) describe in great detail how, after 1970, as the Civil Rights Movement turned its attention from its successes in the South to the ghettoized minority urban communities of the North, New York City embarked on a successful program of ethnic cleansing which came to be termed planned shrinkage, and was aimed at dispersing and disempowering ethnic minority voting blocks. Carried out in considerable part through the denial of essential municipal services to neighborhoods on the basis of race, this program resulted in a massive, uncontrollable outbreak of contagious urban decay – fires, building abandonment and forced population displacement – which left vast sectors of the city looking like Dresden after World War II. San Francisco, on the other hand, applied the rapier of development displacement rather than the meat ax of induced contagious urban decay in its dispersal of ethnic minority populations. A gentrification of the Black section of the city was carried out in the context of the expansion of nearby middle class neighborhoods, primarily the Gay ghetto of the Castro District: poor minorities were forced out economically, by relentlessly rising rents, and driven across San Francisco Bay into Oakland and Richmond, rather than displaced by a scorched earth policy as was the case in New York City. Between 2000 and 2005 the African-American population of San Francisco decreased by a quarter. Richmond is now a localized center of both violent crime and infectious disease. New York City’s uncontrolled outbreak of contagious urban desertification during the 1970’s indeed dispersed minority voting blocks, causing a forced

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migration of people of color largely within the city, breaking the back of the neighborhood economies, the churches, local civic associations and other social structures particularly important for the socialization of the young. But the process also served to drive some 1.3 million non-Hispanic Whites – along with much of the Black middle class – from the city into the suburbs at a time when San Francisco’s more delicate approach to resegregation made the central city more attractive to the middle class. Apparently New York’s version of the counterreformation against the Southern-based Civil Rights Movement tightened the ties binding metro regional counties – the commuting field – beyond a critical threshold, creating a unified disease ecosystem, while San Francisco’s more sophisticated version of that counterreformation did not, at least during the early stages of the AIDS pandemic in the US. In both cases, however, extreme marginalization of Gay males, and their resulting hyperconcentration in New York and San Francisco, did serve to create epicenters for AIDS. Different policies of racial apartheid, however, fundamentally altered subsequent metro regional disease spread. Nationally and locally, then, in the US the early diffusion of AIDS was intimately associated with, if not driven by, the patterns and processes of the nation’s system of Apartheid (Massey and Denton, 1993). 5.1.1 Multiple-drug resistant HIV At present, AIDS deaths in the US are, largely, another marker of longstanding patterns of racism and socioeconomic inequity (e.g. Wallace and McCarthy, 2007; Wallace et al., 2007). Those who have economic resources, or reside in stable communities not subject to various forms of ‘redlining’ or de-facto ethnic cleansing, have effective access to HAART, others do not, matters which will be explored further in the next chapter. HIV is, as indeed are most retroviruses, however, an evolution machine (e.g. Rambaut et al., 2004) which, at the individual level, almost always develops multiple drug resistance, resulting in overt AIDS and subsequent premature fatality. Such response to chemical pesticides, as has been the case with myriad other biological pests, is now becoming manifest at the population level. By 2001 in the US some 50 % of patients receiving antiretroviral therapy were infected with viruses that expressed resistance to at least one of the available retroviral drugs, and transmission of drug-resistant strains is a growing concern (Clavel and Hance, 2004; Grant et al., 2002). Multiple drug resistant (MDR) HIV is, in fact, rapidly becoming the norm, and the virus may even develop a far more virulent life history strategy in response to the evolutionary challenges presented by HAART, its successor microbicide strategies, or planned vaccines (R.G. Wallace, 2004; Wallace and Wallace, 2004), a circumstance which may have already been observed (e.g. Simon et al., 2003). The review by Rambaut et al. (2004) puts the matter thus:

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“HIV shows stronger positive selection than any other organism studied so far... [its viral] recombination rate... is one of the highest of all organisms... Within individual hosts, recombination interacts with selection and drift to produce complex population dynamics, and perhaps provide an efficient mechanism for the virus to escape from the accumulation of deleterious mutations or to jump between adaptive peaks. Specifically, recombination might accelerate progression to AIDS and provide an effective mechanism (coupled with mutation) to evade drug therapy, vaccine treatment or immune pressure... More worryingly, there is evidence that some drug-resistant mutants show a greater infectivity, and in some cases a higher replication rate, compared with viruses without drug resistant mutations.” R.G. Wallace (2004) finds that “...HAART may select for... an HIV with a semelparous life history and a precocious senescence... [which] may be embodied by an accelerated time to AIDS or related pathogenesis... Because infection survivorship is physiologically enmeshed with host survivorship the asymptomatic stage becomes under HAART a demographic shield against epidemiological intervention. The results appear to exemplify how pathogens use processes at one level of biological organization to defend themselves against impediments directed at them at another.” Wallace and Wallace (2004) suggest that “As population-level structured stress appears a fundamental part of the biology of disease [including AIDS], we raise the possibility that simplistic individual-oriented magic bullet drug treatments, vaccines, and risk-reduction programs that do not address the fundamental living and working conditions which underlie disease ecology will fail to control many current epidemics. In addition, such reductionist interventions may go so far as to select for more holistic pathogens characterized by processes operating at multiple levels of biocultural organization.” MDR-HIV is already emerging in the very epicenters and epicenter populations where HIV itself first appeared (Clavel and Hance, 2004), since these were the first to benefit from HAART, and thus seems likely to follow diffusion patterns similar to those of the earlier stage of the AIDS epidemic described above. More general evolutionarily-transformed (ET) HIV’s can be expected to follow a similar pattern. 5.1.2 Endemic infection: tuberculosis With regard to endemic infection, Wallace and Wallace (1997a, 1999) explore the role of New York City’s planned shrinkage polices in turning a declining pattern of tuberculosis infection into a rising one, which we outline.

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Figure 5.2 shows the annual numbers of reported tuberculosis cases in Sweden between 1974 and 1990. The fitted line is for an exponential decline, suggesting that a stable, progressive social system with aggressive public health policies and a commitment to social justice is able to produce falling, and ultimately very low, endemic levels of tuberculosis. Figure 5.3, by contrast, examines the number of reported TB cases in New York City from 1959 to 1990. The TB graph, which declines through 1978 and rises sharply thereafter, is superimposed for the same period on that of an annual structural (building) fire damage index, a measure of contagious housing loss and social decay concentrated in poor, overcrowded minority neighborhoods of the city (D. Wallace and R. Wallace, 1998a). Figure 1.1 shows the effect of the 1968-78 peak in the damage index on the Bronx section of New York City. Again, the Bronx map shows the percent change in occupied housing between 1970 and 1980 for the 62 Health Areas of the borough, small aggregates of census tracts by which morbidity and mortality statistics are reported. Large parts of the south-central portion of the Bronx lost over half their housing units in a short time, a degree of devastation unparalleled for an ‘industrialized Western democracy’ in peacetime. Other poor minority neighborhoods of the city suffered similarly (D. Wallace and R. Wallace, 1998a; R. Wallace and D. Wallace, 1990). The devastation, as discussed above, was political in origin, the outcome of a program to disperse minority voting blocks, clear land for redevelopment and rid the housing market of ‘underpriced’ units, a policy characterized as ‘planned shrinkage’ by the popular press, and widely seen as a simple extraconstitutional extension of earlier, leagalized, programs of population displacement characterized as ‘urban renewal’ (Duryea, 1978, Mega, 1978, D. Wallace, and R. Wallace, 1998a; Fullilove, 2004). Figure 5.4 (from Wallace et al., 1995) examines the resulting TB outbreak in the entire New York Metropolitan Region from the same perspective as figure 5.1b, using a similar composite index. The regional outbreak followed upon the resurgence of the disease within the city. The vertical axis shows the natural logs of the reported rates of cases per 100,000 population for the 24 regional counties for the periods 1985-88 and 1989-92. The horizontal axis, again, involves a county’s percent living in poverty and the area density of the equilibrium commuting pattern. According to multivariate analysis of covariance, the two lines are parallel, and differ only in that the latter is higher than the former, i.e. driven by the rise in the central city rate. This is a classic pattern, as Yeomans (1979, p. 366) writes: “Tuberculosis might again become epidemic [in areas where it has been in decline]. It would only require some massive disruption of our social and economic systems, forcing human beings to live under crowded, unsanitary conditions... [Historically] incidence and mortality from tuberculosis increased markedly in those countries suffering the greatest dislocations in their economy and social structures... Cer-

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Fig. 5.2. Annual numbers of reported tuberculosis cases in Sweden, 1974-1990. The fitted line is that of an exponential decay.

tain... areas... may become almost free of the diseae, but the accumulation... of large numbers of susceptible persons may provide the basic requirements for future epidemics that, in turn, will restore tuberculosis as ‘Captain of All the Men of Death’.” Planned shrinkage, in the words of a public offical who must remain anonymous, served to ‘shotgun AIDS all over the Bronx’. It also served to shotgun tuberculosis over the New York Metropolitan Area and appears to have significantly accelerated the national diffusion of HIV.

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Fig. 5.3. Coupled epidemic outbreaks of contagious urban decay and tuberculosis in New York City. The fire damage index is a composite of number and seriousness of building fires and is an environmental index of an embedding process of contagious urban decay.

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Fig. 5.4. Tuberculosis rates in the 24 county New York Metropolitan Region. The vertical axis is the log of the TB rate per 100,000 population. The horizontal axis is a composite determined by multivariate analysis of covariance: x = 0.759 ln(Pp ) + 0.197 ln(δµ/δa), where Pp is the percentage of a county’s population living in poverty, δµ is the county’s fraction of the equilibrium distribution of the commuting Markov process, and δa is the county area. Manhattan is the uppermost right-hand point. See Wallace et al 1995 for details. Raise the upper right hand point, and the entire system follows, in parallel.

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There is, it seems, far more to the diffusion of infectious disease than the dispersal of a dye marker along travel pathways, although that is clearly one part of the story. Here we will focus on the other part, uncovering a populationlevel epidemic quasi-language reflecting power relationships between groups within the underlying society. Different resilience modes of the infectious disease ecosystem will emerge as qualitative differences between Apartheid and Egalitarian polities, and can be taken as projected images of those different systems. 5.1.3 Reconsidering infection The formal approach is somewhat counterintuitive: One must, in essence, address generalized stochastic resonance in a spatial array of nonlinear components from an information theory perspective, a hard technical problem (e.g. R. Wallace, 2000). The central idea of stochastic resonance is that the addition of noise to a weak input signal, usually taken as some repeated train of excitations, can raise the amplitude of the combined signal so as to exceed the trigger of a relatively powerful but highly nonlinear oscillator, resulting in an amplified train of output signals. Proper choice of the amplitude of the noise can maximize the signal-to-noise ratio of the combined system. See, for example, Gammaitoni et al. (1998) for a review. Explicit applications of a stochastic resonance viewpoint have been recently made to the triggering of epidemics by the noise of regressive social policies affecting the underlying signal of a marginalized community (e.g. Wallace et al. 1997; Wallace and Wallace, 1997a, b; Wallace et al., 1997; Wallace et al. 1999). Such treatments are inherently limited by the fact that long trains of output are not easily observed: Historically, multiple plague outbreaks, repeated economic catastrophes, episodes of mass slaughter and such like are self-limiting in the most Darwinian manner. Each case history required a different elaborate mathematical attack. Wallace and Wallace (1997a), for example, studied the ongoing tuberculosis crisis in New York City from this viewpoint. Their analysis required the coupling of a model of contagious urban decay triggered by ‘planned shrinkage’ cuts in fire service provided racial minority voting blocks to a TB model, both having numerous simultaneous nonlinear differential equations. Wallace and Wallace (1999) used the Martingale Theorem to greatly simplify examination of coupled, spatially nested epidemics. Rather than seeking detailed time dynamics, such a treatment asks whether overall disease patterns are approaching higher or lower limiting states of endemicity or recurrence. Here we will ask similarly generic questions about stochastic resonators and the distribution of fluctuational paths leading to the triggering of a resonance, and, in fact, generalize the nested Martingale example accordingly. McClintock and Luchinsky (1999) suggest a unifying perspective, looking at the prehistory probability density of the ensemble of pathways by which a

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system susceptible to stochastic resonance approaches the trigger. This leads directly to a formal development in the spirit of the Onsager and Machlup (1953) study of the distribution of fluctuational paths. The analysis, however, is carried out in terms of the Shannon-McMillan Theorem, one of the two basic foundations of information theory, and itself an asymptotic relation of probability as fundamental as the Martingale Theorem. Others have, indeed, used a maximization of noise-dependent mutual information between input and amplifier output to characterize stochastic resonance (e.g. Deco and Schurmann, 1998; Henegan et al., 1996; Godivier and Chapeau-Blondeau, 1998; Schimansky-Geier et al., 1996). Here we attempt a more extensive analysis using these methods, focusing on the role of the highly strucured signal of public policy rather than on random noise. The modern mathematical context for such extension is a branch of applied probability theory known as large deviation theory (e.g. Dembo and Zeitouni, 1998; Ellis, 1985) which seeks to unite analysis of fluctuations, statistical mechanics and information theory under a single formalism. The first real step in this direction was taken by Cramer (1938). Subsequent proofs of the ergodic theorem, in the context of generalizations of Cramer’s results by Gartner and Ellis, permit derivation of the Shannon-McMillan Theorem as the zero error limit of rate distortion theory (Dembo and Zeitouni, 1998). Next, two mathematical infectious disease models are restated as generalized stochastic resonances, in which the ‘noise’ is, in fact, the highly structured output of an information source representing public policy and economic practice. These are, of course, primary outcomes of institutional collective consciousness. 5.1.4 The simple epidemic with removal We first take a simple epidemic outbreak, with removal, to represent a large fluctuation in an otherwise relatively normal public health system. To paraphrase the paper by Dykman et al., (1996), large fluctuations, although infrequent, are fundamental in a broad range of processes, and it was recognized by Onsager and Machlup (1953) that insight into the problem could be gained from studying the distribution of fluctuational paths along which the system moves to a given state. This distribution is a fundamental characteristic of the fluctuation dynamics, and its understanding leads toward control of the fluctuations. Again following Dyckman et al. (1996), fluctuational motion from the vicinity of a stable state may occur along different paths. For large fluctuations, the distribution of these paths peaks sharply at along an optimal, i.e. most probable, path. In the theory of large fluctuations, the pattern of optimal paths plays a role similar to that of the phase portrait in nonlinear dynamics. In this context we restate the problem of the simple epidemic with removal as a stochastic resonance. More complicated models could be chosen, as in the next section, but similar results follow.

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Let X be the number of susceptible individuals in a population, Y the number of infectives and Z the number removed, by death or immunity. Let t be the time. The simple epidemic with removal has the form

dX/dt = −βXY, dY /dt = βXY − γY = Y (βX − γ), dZ/dt = γY, N = X + Y + Z. (5.1)

β is the infectivity of the disease, and γ the rate of removal of infective individuals, and N is the total population. Let ρ ≡ γ/β. Suppose at time t = 0 there are X0 susceptible individuals. From the second of these expressions it becomes clear that no epidemic outbreak takes place if X0 < ρ. If X0 = ρ + δ, 0 < δ  ρ, then a simple calculation (e.g. Bailey, 1975) shows that the total number infected over the course of the epidemic, and the final number of susceptibles after it, will be approximately

Z∞ ≈ 2δ X∞ ≈ ρ − δ. (5.2)

We suppose the epidemic process has a natural time frame relatively short with respect to periods of observation, ∆T , so that epidemic outbreaks have time to equilibrate – another ‘adiabatic’ approximation.

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We look at the system at times i = 0, 1, ...n normalized to multiples of ∆T , with initial conditions (X0i , ρi ). These we write as points on a two dimensional graph labeled as ai . We will call ai the ‘state’ of the system at time i. The total number infected during an epidemic outbreak at time i will be i ≈ 2(X0i − ρi ) if X0i > ρi , and 0 otherwise. Z∞ For marginalized communities – the epicenter of most disease outbreaks in developed countries – the state of the system at time i, ai = (X0i , ρi ), is the result of the interaction between the socioeconomic opportunity structure available to it, i.e. the strictures of our Apartheid system, and the patterns of compensatory behavior developed by the community to address the impacts of those strictures. Coping strategies in marginalized communities are often characterized as risk behaviors by researchers based in the marginalizing superstructure, regardless of their inevitability under the pressure of constraint. There is much research on the topic, some from an information theory viewpoint (e.g. Wallace, Fullilove and Flisher, 1996; Wallace, Flisher and Fullilove, 1997; Wallace and Fullilove, 1999). Figure 5.5 illustrates a revision of the simple epidemic with removal from this perspective. The community structure and the externally-defined opportunity structure in which it is embedded are convoluted together at times i = 0, 1, ...n to create the distinctly nonrandom serially correlated sequence of states a0 , a1 , ...an , which we will call a path x. That path enters the nonlinear amplifier of the epidemic process, producing an output sequence of epidemics of final sizes Z0 , Z1 , ...Zn .

Fig. 5.5. Restatement of the simple epidemic with removal as a stochastic resonance. The community structure and opportunity structure are convoluted at time i into a ‘state’ ai defined by the initial conditions (X0i , ρi = γi /βi ). If X0i > ρi then the nonlinear amplifier of the epidemic process produces an output Zi ≈ 2(X0i − ρi ). Otherwise Zi = 0. The nested Martingale argument is somewhat more complex, with an = (An ∆Yn , Bn ).

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Figure 5.6 shows several such paths x = a0 , a1 , ...an in the two-dimensional parameter space defined by the points (X0i , ρi ). Those for which X0i < ρi do not lead to epidemic outbreaks, the region below the line X = ρ. We shall be particularly concerned with paths starting from an initial state a0 below the line, and leading to some state an above it. That is, here we primarily focus on the properties of the nonrandomly structured paths which lead to large fluctuations in Z rather than on the technical details of the nonlinear oscillator. Most current research in mathematical epidemiology appears limited to study of that oscillator, seemingly independent of larger, and indeed determining, contexts by design. See Wallace and Wallace (1997b) for a more detailed criticism. To reemphasize the change in perspective, we note that the states constituting the paths of interest do not, in general, undergo simple uncorrelated Brownian motion: these paths have internal structure, serial correlations which contain essential information on systematic changes in community, constraints and their interactions. These are much the outcomes of institutional deliberation and decisions of resource allocation, i.e. of collective consciousness. Thus Monte Carlo sensitivity analysis which randomly varies the parameters of some large array of simultaneous nonlinear differential equations modeling an epidemic is rather beside the point. We have, with some difficulty, now rephrased the simple epidemic with removal as a generalized stochastic resonance: The community structure is the signal, the opportunity structure the noise, and their convolution produces paths which can then trigger a nonlinear amplifier whose output is the outbreak of infection. To reiterate, opportunity structures are matters of policy and practice which are essential expressions of collective consciousness, as we have conceived it. 5.1.5 Endemic infection Rather than examining infection rates or processes in detail, a more sophisticated approach involves, again counterintuitively, asking a simpler question; does an established endemic infection remain the same, grow larger, or decline in time. The central tool for this is the Martingale Theorem, another of the fundamental asymptotic limit theorems of probability. Suppose a player begins a game of chance with an initial fortune of some given amount, and bets n times (n = 1, 2, ...) according to a stochastic process in which a stochastic variable Xn , which represents the size of the player’s fortune at play n, takes values Xn = xn,i with probabilities Pn,i such that X

Pn,i = 1,

i

where i represents a particular outcome at step n.

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Fig. 5.6. ‘Paths’ in the state space defined by X0 and ρ of figure 5.5. These all start at a0 and terminate when the line X = ρ is crossed and an outbreak occurs. The states a0 , a1 , ...an constituting a path are not undergoing uncorrelated Brownian motion, and indeed the internal correlation properties of paths are very much the focus of interest. Similarly, for the nested Martingale example, the (coarse-grained) x = (a0 , ..., an ) are also subject to a complex grammar and syntax defined by the power relations between marginalized and dominant subgroups.

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Assume for all n there exists a value 0 < C < ∞ such that the expectation of Xn ,

E(Xn ) ≡

X

xn,i Pn,i < C

i

(5.3)

for all n. That is, no infinite or endlessly increasing fortunes are permitted. We note that the state Xn = 0, having probability Pn0 , i.e. the loss of all a player’s funds, terminates the game. Regarding endemic infectious disease, the particular ‘game’ to which we will eventually apply this theory, for the foreseeable future, Pn0 → 0. That is, once an infection with a long latent period becomes established in a sufficiently large population, its probability of extinction is essentially zero on the timescale of real events defined by the sequence n. We will assume the games played in our casino have this property. Indeed, the only global-scale epidemic game to terminate in this century is smallpox, which had a two hundred year prior history of safe, cheap, universally effective vaccination. We suppose it possible to define conditional probabilities at step n + 1 which depend on the way in which the value of Xn was reached, so that we can define the conditional expectation of Xn+1 : E(Xn+1 |X1 , X2 , ...Xn ) ≡ E(Xn+1 |n) The ‘sample space’ for the probabilities defining this conditional expectation is the set of different possible sequences of the xm,i > 0: x1,i , x2,j , x3,k ...xn,q We call the sequence of stochastic variables Xn defining the game: a Submartingale if, at each step n, E(Xn+1 |n) ≥ Xn , a Martingale if E(Xn+1 |n) = Xn and

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a Supermartingale if E(Xn+1 |n) ≤ Xn . Xn is, remember, the player’s fortune at step n. Clearly a submartingale is favorable to the player, a Martingale is an absolutely fair game, and a supermartingale is favorable to the house. Regardless of the complexity of the game, the details of the playing instruments, the ways of determining gains or loss or their amounts, or any other structural factors of the underlying stochastic process, the essential content of the Martingale Limit Theorem is that in all three cases the sequence of stochastic variables Xn converges in probability ‘almost everywhere’ to a welldefined stochastic variable X as n → ∞. That is, for each kind of Martingale, no matter the actual sequence of winnings x1,i , x2,j , ...xn,k , xn+1,m , ..., you get to the same limiting stochastic variable X. Sequences for which this does not happen have zero probability. A simple proof of this result (e.g. Petersen, 1995) runs to several pages of dense mathematics using modern theories of abstract integration on sets. To put these matters in perspective, we claim that the socioeconomic system is the house, the player is a long established infectious agent like tuberculosis, and the player’s fortune at step n, Xn , is the number of people infected. Each ‘step’ n is determined by the recurrent patterns which structure our lives; the daily journey-to-work, the weekly ceremonies of worship or binge behavior, and the annual cycles of ritual and other gatherings, including those driven by the weather, which often determines the fraction of time spent indoors. Other inherent characteristic times may require aggregation of these ‘natural’ cycles, i.e. ‘coarse graining’. A supermartingale is a declining infection, a submartingale is a spreading infection. Both, according to this theorem – one of the most powerful and subtle results of 20th century mathematics – will inevitably attain a limiting state of endemicity. This may fluctuate considerably and in a structured or serially correlated manner, but will do so about a mean value, E(X), regardless of the complexity of the rules of the game. Industrialized social systems are, of course, not simple analogs to gambling casinos, but reflect the large-scale patterns of nested hierarchy defined by their underlying economic engines (Abler, Adams and Gould, 1971). We therefore propose a ‘nested Martingale’ model for epidemic spread in a hierarchically-structured social system. This will be a compound stochastic process in which the winnings at the smaller scale, played by one set of rules, contribute, in some sense, to a quite different game having completely different rules on a larger scale. These games are bounded, as we have discussed, by the conditions E(Xn ) < C, for some finite positive C, and Pn0 → 0. The essential point is that a proportion of the winnings from the smaller game are duplicated by a benefactor and directly raise the magnitude of the player’s fortune for the larger, embedding game.

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If the inner game is characterized at step n by the random variable Yn , then the real winnings at step n + 1 for the embedding game, associated with the random variable Xn+1 , become, for some function fn , which may involve additional stochastic variables,

Xn+1 = fn (Xn , Yn , Yn+1 ). (5.4)

A slightly different approach would involve conditional expectations in the convolution of scales:

E(Xn+1 |n) = Fn (Xn , Yn , E(Yn+1 |n)) (5.5)

for some function Fn . The simplest version of this extension assumes that the compound game is merely a subset of the original. In our context this would be to envision, for example, a suburban county connected to an inner city by the commuting field (Wallace, et al., 1997) as functioning according to its own self-conception; an entity separated by social and geographic distance from the troubles of the deteriorating inner city, and having little of the kind of internal structure which would spread disease within its own borders. In this case the diseases of the suburb are entirely those of the larger city center, attenuated by segregation:

Xn+1 = Xn + An (Yn+1 − Yn ). (5.6)

We assume An ≥ 0 is a non-negative stochastic variable, which can indeed take the value 0. The model states that the number of outlying cases at time n + 1 will be the number at time n, augmented or decremented by the change in case numbers within the city center, as attenuated by the segregation filter

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An . This may, for example, be greater than zero only one time in ten or a hundred, on average. Taking the conditional expectation gives

E(Xn+1 |n) = Xn + An (E(Yn+1 |n) − Yn ) (5.7)

where we recognize the conditional expectation of any variate Zn at step n is just its value. Since An ≥ 0, the game described by the attenuated sequence Xn has the same martingale classification as does the nested central city game described by Yn . The X-process in equation (5.6) is the Martingale transform of Yn (Taylor, 1996, p.232; Billingsley, 1968, p. 412), and the result is classic, representing the impossibility of a successful betting system. That is, the betting system of moving to the suburbs to get away from urban problems, in the long run, can’t win if the city center is itself losing. Note that the basic Martingale transform can be rewritten as

Xn+1 − Xn ∆Xn ≡ = An , Yn+1 − Yn ∆Yn or ∆Xn = An ∆Yn . (5.8)

Induction gives

Xn+1 = X0 +

n X j=1

(5.9)

Aj ∆Yj .

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This notation is suggestive: in fact the Martingale transform is the discrete analog of Ito’s stochastic integral relative to a sequence of stopping times, (Taylor, 1996, p. 232; Protter, 1990, p. 44; Ikeda and Watanabe, 1989, p. 48). In the stochastic integral context the Y -process is called the integrator and the A-process the integrand. Further development leads toward generalizations of Brownian motion, the Poisson process, and so on (Meyer, 1989; Protter, 1990). The basic picture is, thus, of another generalized stochastic resonance: the transmission of a signal, Yn , convoluted with a noise, An . This ‘noise’ is, however, defined in our context by powerful factors of socioeconomic structure and public policy. As described above, however, detailed examination of the spread of AIDS and other pathologies in a number of metropolitan regions shows this is not always simple (Wallace et al., 1997). A more realistic extension of the elementary denumerable Martingale transform for our purposes is

Xn+1 = Xn + (Bn+1 − Bn )Xn + An (Yn+1 − Yn ), (5.10)

where Bn is a stochastic variable representing, for example, the balance between the growth and removal of infection, for example within a suburban county, while An again measures, for example, the coupling of the suburb to the central city. A positive difference, ∆Bn = Bn+1 − Bn > 0, represents the local spread of infection. Using the more suggestive notation of equations (5.8) and (5.9) this becomes the fundamental stochastic differential equation

∆Xn = Xn ∆Bn + An ∆Yn . (5.11)

Taking conditional expectations gives

E(Xn+1 |n) − Xn =

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Xn (E(Bn+1 |n) − Bn ) + An (E(Yn+1 |n) − Yn ). (5.12)

We can assume Xn , An ≥ 0. The Martingale classification of suburban infection X thus depends on those of B and Y. If the suburb has a stagnant public health system, so that B is a Martingale, then a growing infection within the city center – Y a submartingale – will express itself as a growing submartingale of disease within the suburb. In general, however, the social deterioration within the city can be expected to express itself as neglect of the poor within nearby suburbs, if only from an outward diffusion of social disintegration which overwhelms local social and public health programs. That is, B is itself likely to become a submartingale, resulting in a very rapid spread of suburban disease. Even if the suburb has a highly effective public health system, so that B is a supermartingale, the terms An ∆Yn > 0 will cause an increase in the endemic level of infection within the suburb, above what it had been. If the terms An ∆Yn > 0 are sufficiently large, however, infection within the city center may overwhelm even the best suburban public health programs, turning local disease supermartingales into submartingales strongly linked to the central epidemic outbreak. The ‘paths’ for this process as a stochastic resonance which are analogous to those shown in figure 5.6 are sequences x = (a0 , a1 , ..., an ) with aj = (Aj ∆Yj , Bj ). The policy-driven changes of tuberculosis infection rates in and near New York City – figures 5.3 and 5.4 – appear quite consistent with this model: The policy of planned shrinkage directed against minority voting blocks in New York City, in addition to dispersing political capital, succeeded in transforming a declining regional endemic infection into a rising one. 5.1.6 Coherence Thus far we have restricted our attention to a single nonlinear oscillator and its properties as a stochastic resonance involving structures signals when the two inputs are algorithmically mixed. Here we attempt to expand the development to systems coupled socio-spatially, in the largest sense. The approach is a simplified version of the method used in the last chapter, as expanded in the Appendix. We assume there are two kinds of coupling between individual simple oscillators, defining a two-stage hierarchy of organization. The first we will take as reflexive, symmetric and transitive, permitting the division of the array into disjoint equivalence classes (Wallace and Wallace, 1998, 1999). We will call this a strong tie, in the tradition of sociology (Granovetter, 1973). The second

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coupling, which we characterize as weak, operates across all possible subdivisions of the array, and does not permit identification of disjoint equivalence classes. A physicist might call these local and mean field forces, respectively. We assume the index of strong ties remains constant, and permit the index of weak tie coupling, which we will call T , to vary and to characterize the array as a whole. More details are given in the Appendix. We again assume the array, signal, and noise depend on three parameters, two explicit and one implicit. The explicit are an external field strength analog J which gives a direction to the phenomenon, and an inverse disorder parameter K defined as K = 1/T , where T is an index of the strength of the ‘weak’ ties which couple elements of the array without disjointly partitioning them. We may, in the limit, set J = 0. Other explicit parameters can be added, of course, at the expense of complicating the analysis. The implicit parameter, which we call r, is an inherent generalized length on which the phenomenon – including its direction and temperature-analog – is defined. That is, we can write J and K as functions of averages of the parameter r, which may be quite complex, having nothing to do with conventional ideas of space. For example Wallace and Wallace (1998) examine the role of social as well as of spatial separation within a population in determining the probability of weak ties between individuals or subgroups. Rather than specify complicated patterns of individual dependence or interaction for signal, noise and elements of the array, we follow the direction of the previous sections and instead work entirely within the domain of the uncertainty of the ergodic information source dual to the large-scale stochastic resonance defined by the entirety of the coupled array, H[K, J, X]. This draconian simplification enables us to directly obtain certain general results. Taking only K as significant for the moment, the fundamental relation H(K) = lim

n→∞

log[N (K)] n

has, as we showed above, the same form as the free energy density of a physical system. If Z(K) is the partition function defined by the system’s energy distribution, then, again, the free energy density F (K) is F (K) = lim

V →∞

log[Z(K)] , V

where V is the system volume. Generalizing in the spirit of the large deviations program of applied probability (e.g. Dembo and Zeitouni, 1998), imposition of invariance under a renormalization transform in the implicit parameter r on the dual information source of the generalized ergodic stochastic resonance characterizing the array as a whole leads to expectation of both a critical point in K, KC , reflecting a phase transition to or from collective behavior across the entire array,

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and of power laws for system behavior near KC . See Wilson (1971) for calculational details, which are standard, and the Mathematical Appendix for a more complete application to information sources. Let κ = (KC − K)/KC and take χ as the correlation length defining the average domain in r-space for which the dual information source is primarily characterized by strong ties. We begin averaging across r-space in terms of ‘clumps’ of length R, defining JR , KR as J, K for R = 1. Then, following the physical analog of Wilson (1971), we choose the renormalization symmetry relations as

H[KR , JR , X] = RD H[K, J, X]

χ(KR , JR ) =

χ(K, J) , R

(5.13)

where D is a nonnegative real constant, possibly reflecting a fractal network structure. Other symmetry relations – not necessarily based on simple physical analogs – seem possible, as described in the Mathematical Appendix, permitting the grouping of stochastic resonances into disjoint equivalence classes, leading to complicated topological phenomena. For example discussion of the phase transition to instability in quasiperiodic orbits leads to renormalization relations of the form f (x) = α2 f (α−1 f (α−1 x)) and f (x) = αf (αf (α−2 x)). McCauley (1993, p. 168) provides details. Then near KC , for J = 0, some clever development, and a simple series expansion of equation (5.13) (Wilson, 1971; Binney et al., 1995; Wallace and Wallace, 1998, 1999; Wallace, 2005a), as described in the Appendix, gives

H = H0 κsD

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χ = χ0 κ−s (5.14)

where s is a positive real constant. Again, H is the dual source uncertainty of the entire array as a stochastic resonance and χ the average size the region dominated by ‘strong’ ties. Further from the critical point matters are more complicated, as in the v arious treatments of the dynamical groupoid. Using the developlment of the last chapter, we estimate the size of the disjoint partition of the array into strongly interacting subsets. Assume K < KC and that the rate of change of κ remains constant as K → KC , so that |dκ/dt| = 1/τK . Further analogs with physical theory suggest there is a characteristic time constant for the phase transition, τ ≡ τ0 /κ, such that if changes in κ take place on a timescale longer than τ for any given κ, we may expect the correlation length to remain in equilibrium with internal changes, resulting in very large fragment sizes in r-space. Following Zurek (1985, 1990, 1996), as in the last chapter, we again argue that the critical freezeout time tˆ, will occur at a system time tˆ = χ/|dχ/dt| such that tˆ = τ . Taking the derivative dχ/dt, remembering that by definition dκ/dt = 1/τK , gives χ κτK τ0 = = |dχ/dt| s κ so that κ=

p sτ0 /τK .

Substituting this value of κ into the equation for correlation length, the expected size of fragments of the spatially distributed generalized stochastic resonance in r-space, d(tˆ), becomes

d ≈ χ0 (

τK s/2 ) . sτ0

(5.15)

The more rapid the changes, the smaller τK and the smaller, and more numerous, on average, the resulting fragments.

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Different renormalization symmetry relations than equation (5.13) would, of course, lead to different universal power laws. See the Mathematical Appendix for details. Now invert the argument: It is clear that sudden critical point transition is possible in the opposite direction for this model. That is, the system can suddenly go from a set of independent, isolated and spatially fragmented strongly interacting resonators of some average diameter, d, firing more or less at random, into a single large, coherent, tightly interlinked and (socio)spatially extended system. That is, disjoint, incoherent, strongly coupled subregions having independent and isolated epidemic outbreaks can become a single, massively coherent spatiotemporal structure – a spreading pandemic – if the probability of weak ties between the components increases beyond a threshold. 5.1.7 Resilience of infectious disease ecosystems Figure 5.7 examines an epidemic with removal within Egalitarian and Apartheid political systems, using the format of figure 5.5. The horizontal dotted line represents a fixed critical X0 and is a repulsive barrier. An Aparthied system is confined above the line, and Egalitarian system below it, in this model. An Apartheid system would perceive a fall in susceptible population, a decline in X0 consequent on increases in social, political, and economic capital within a marginalized subgroup, as a political threat, and would most likely engage in some program (or pogrom) of forced displacement or ethnic cleansing. Over the last sixty years in the US, such programs have had names like ‘redlining’, ‘urban renewal’, ‘planned shrinkage’, and ‘Hope Six’ (Fullilove, 2004; Wallace and Wallace, 1998a). Their primary impact has been the repeated and relentless dispersal of economic, political and social capital concentrations in communities of color, which seems to account for a good portion of the supposedly mysterious health disparities that have recently become an academic research cash cow. By contrast, an Egalitarian system would see an increase in susceptible population, a rise in X0 , as a threat, and would act to raise the social, political, and economic capital of vulnerable subgroups in an attempt to improve the living and working conditions which are the ecological foundation of individual and group resistance to infectious disease. It is clear that transformation of an Apartheid social system into an Egalitarian one, or vice versa, cannot be done in the absence of some forcing mechanism, and that each kind of system would attempt to return to its ‘natural’ state in the face of such a mechanism. This kind of behavior is central to ecosystem resilience theory, as discussed above. Thus infectious diseases do not, according to our arguments, simply constitute a dye marker for urban sociogeography, although the overall pattern

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Fig. 5.7. Epidemic topology of Egalitarian and Apartheid states. The dotted line represents a highly repulsive barrier. An Egalitarian social system, absent catastrophe, would be largely confined to the region below the dotted line, while an Apartheid state would be confined to the region above it. The Apartheid state would perceive decline in susceptible population consequent on the amassing of social, political, and economic capital by marginalized subgroups as a threat against the dominant polity, to be answered by ethnic cleansing. An Egalitarian state, in contrast, would perceive a rise in susceptible population as a general social threat to be met by programs aimed at improving social, economic, and political capital within vulnerable subgroups. Some external forcing mechanism seems required to move from one kind of system to the other, for example progressive regime change, or, by contrast, globalization into the neoliberal market economy. The two directed homotopy equivalence classes of possible paths serve to identify the two quasi-equilibrium domains of ecological resilience in this disease ecosystem.

of social and geographic spread is certainly constrained by, and must be consistent with, that underlying sociogeography. Consideration of the prehistory probability distribution and the distribution of fluctuational paths suggests understanding the spread of infectious disease in terms of a generalized stochastic resonance having a dual ergodic information source, a kind of language. Paths of signal – community structure – convoluted with (highly patterned) noise – the embedding opportunity structure – which are not consistent with the grammar and syntax of

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that language cannot trigger simple epidemic outbreaks, or, taking the nested Martingale perspective, turn a declining infection into a rising one. Conversely, for a given fixed signal – community structure – there will be an optimal noise – opportunity structure – whose convolution, analogous to coding, permits the system to approach a channel capacity measure arbitrarily closely. That is, certain patterns of constricted opportunity will most efficiently trigger repeated outbreaks of infectious epidemic disease in marginalized communities, or turn a falling endemic infection into a growing one. Further development suggests that spatially (or socio-spatially) distributed systems undergoing such generalized stochastic resonance can be subject to phase transition at critical values of driving parameters, which may encompass signal and non-linear amplifier as well as noise. These transitions should follow ‘universal’ power laws, depending on the appropriate renormalization symmetry, which is itself related to the underlying sociogeographic architecture. Thus isolated, incoherent, spatiotemporal infectious epidemic resonators – individual neighborhoods, counties, or metropolitan regions – may suddenly coalesce into a single powerful and coherent amplifier, a spatially contagious or hierarchically spreading pandemic, under the influence of particular constrained opportunity structures. This result strongly implies that diseases of marginalization, and their control, are very much creatures of collective consciousness and its pathologies, related to overt decisions regarding allocation of resources and their historical impacts. In fact endemic and epidemic states of infectious disease represent Rate Distortion Manifolds in which complex processes of institutional cognition reflecting the power relations between groups are projected down onto starkly simple patterns of illness and death. Across markedly different scales, powerful and dominant population subgroups can become entrained into the disease ecology of marginalization which their policies tolerate or actively maintain. This has sometimes been called the Paradox of Apartheid. The analysis by Wallace et al. (1997) on the regional conformations of the early stages of AIDS in eight US metropolitan areas provides a case history. As discussed, the two principal US AIDS epicenters of San Francisco and New York City showed, in the early stages, markedly different forms of regionalization. New York had a coherent disease pattern across the entire metropolitan area, strongly dominated by the commuting center of Manhattan, while the San Francisco metro area, at least for the period studied, remained a patchwork of several individual outbreaks. Again, the two cities took significantly different approaches to reinforcement of the system of US Apartheid following the challenges of the Southernbased Civil Rights Movement. San Francisco made the city center attractive to White middle class residents, while New York drove some 1.3 million nonHispanic Whites and other middle class residents from the city to the suburbs,

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tightening the weak ties linking counties of the metro region beyond threshold, and creating a unified disease ecosystem. As described above, figures 5.3 and 5.4 detail the change of tuberculosis infection pattern in and near New York City, from declining to rising, as a consequence of the same set of policies. From these examples, and from the formal considerations above, it becomes clear that the synergistic unification of community, policy, and infectious disease into a language of power relations defining the generalized stochastic resonance of a pandemic means that public health interventions against plague must be similarly synergistic and hierarchical to bring the system below coherent threshold. Our analysis particularly suggests that marginalized subgroups constitute keystone populations for the ecology of infectious disease, especially AIDS and TB. The most marginalized groups in the largest cities become the most central: For the US, as go New York City’s South Bronx and Los Angeles’ South Central, so goes the nation. Thus victim and victimizer within the highly patterned, indeed, Manichean, structures of an Apartheid system (Fanon, 1966) or other colonial social structure, will become jointly enmeshed in pandemic infectious disease. Pestilence is thus a part of the image that a colonial relationship writes upon the bodies of those it entrains, both the powerful and the powerless (Memmi, 1969). This perspective washes out confusing model-dependent behaviors which have been the focus of previous study, leaving behind a starkly simple structure in which the concentration of disease resulting from policies of marginalization represents, not containment, but intensification of the Paradox of Apartheid, where the powerful are ever more closely bound to their victims. This suggests that controlling emerging infections in the United States, particularly multiple drug resistant (MDR) HIV and tuberculosis, which undergoing policy-driven evolution in the dominant metropolitan regions of the nation’s urban hierarchy (Wallace and Wallace, 2004), will require resurrection of traditional public health practices, but this will be difficult because so much of the discipline’s history has been lost in favor of the blame-the-victim, medicalized, and individual-oriented perspectives now popular with the current crop of major funding agencies and their client organizations. Many resulting projects are characterized as ‘fundable trivialities’ or ‘planting a tree in a desert’ by even those providing financial support. MDR-HIV is poised to spread from present HIV epicenters to the rest of the US in much the same manner the early stages of the pandemic spread nationally. By contrast, evidence exists that, for at least one more egalitarian social system – Amsterdam – there is a declining trend in transmission of drug-resistant HIV (Bezemer et al., 2004). MDR-TB seems likely to follow. Unfortunately, the nation’s response to the hurricane Katrina disaster which devastated New Orleans provides a sentinel case history for the likely outcome. The US system of Apartheid has proven highly, if pathologically, resilient in the sense of this work, and the very real and serious threats posed by mul-

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tiple drug resistant emerging infections may not be sufficient to alter deeply entrenched, although highly damaging, public policies, socioeconomic structures, and their historical trajectories. From Redlining and Urban Renewal to Planned Shrinkage and Hope Six, and now the aftermath of Hurricane Katrina, serial forced displacement of minority communities remains a firm cornerstone of American Apartheid. Even the rich may now reap the harvest of these deeply-planted dragons’ teeth.

5.2 Chronic disease Consciousness is not the only cognitive physiological or psychological phenomenon entertained by an individual, and much of what we have done can be applied to other – interacting – cognitive modules of interest, and in particular to their interaction with embedding psychosocial stressors which are largely determined by processes of collective consciousness, i.e. public policy. We begin with a brief listing of a few of them, and then explore how policy-driven structured psychosocial stress can impose an image of itself upon human development, entraining not only consciousness, but other cognitive modules into characteristic patterns of comorbid mind/body dysfunction carried upon tides of collective consciousness and its outfalls. 5.2.1 Immune function Atlan and Cohen (1998) have proposed an information-theoretic cognitive model of immune function and process, a paradigm incorporating cognitive pattern recognition-and-response behaviors analogous to those of the central nervous system. This work follows in a very long tradition of speculation on the cognitive properties of the immune system (Tauber, 1998; Podolsky and Tauber, 1998; Grossman, 1989, 1992, 1993a, b, 2000). From the Atlan/Cohen perspective, the meaning of an antigen can be reduced to the type of response the antigen generates. That is, the meaning of an antigen is functionally defined by the response of the immune system. The meaning of an antigen to the system is discernible in the type of immune response produced, not merely whether or not the antigen is perceived by the receptor repertoire. Because the meaning is defined by the type of response there is indeed a response repertoire and not only a receptor repertoire. To account for immune interpretation Cohen (1992, 2000) has reformulated the cognitive paradigm for the immune system. The immune system can respond to a given antigen in various ways. It has ‘options’. Thus the particular response we observe is the outcome of internal processes of weighing and integrating information about the antigen. In contrast to Burnet’s view of the immune response as a simple reflex, it is seen to exercise cognition by the interpolation of a level of information processing between the antigen stimulus and the immune response. A cognitive immune system organizes the

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information borne by the antigen stimulus within a given context and creates a format suitable for internal processing; the antigen and its context are transcribed internally into the ‘chemical language’ of the immune system. The cognitive paradigm suggests a language metaphor to describe immune communication by a string of chemical signals. This metaphor is apt because the human and immune languages can be seen to manifest several similarities such as syntax and abstraction. Syntax, for example, enhances both linguistic and immune meaning. Although individual words and even letters can have their own meanings, an unconnected subject or an unconnected predicate will tend to mean less than does the sentence generated by their connection. The immune system creates a ‘language’ by linking two ontogenetically different classes of molecules in a syntactical fashion. One class of molecules are the T and B cell receptors for antigens. These molecules are not inherited, but are somatically generated in each individual. The other class of molecules responsible for internal information processing is encoded in the individual’s germline. Meaning, the chosen type of immune response, is the outcome of the concrete connection between the antigen subject and the germline predicate signals. The transcription of the antigens into processed peptides embedded in a context of germline ancillary signals constitutes the functional ‘language’ of the immune system. Despite the logic of clonal selection, the immune system does not respond to antigens as they are, but to abstractions of antigens-incontext. From the perspectives of this work a kind of attentional focus – a Rate Distortion Manifold – must be inherent to immune response. Energy considerations require such a cognitive fovia, and tuning, via adaptive immunity, is already a fundamental mechanism by which the immune system learns to respond to new infections. This supplements the limited spectrum of inherited innate immune mechanisms. It can perhaps be argued that AIDS emerges when the retina of adaptive immunity is blinded by persistent HIV attack. 5.2.2 Tumor control Reflection shows the next cognitive submodule after the immune system is necessarily a tumor control mechanism that may include ‘immune surveillance’, but certainly transcends it. Nunney (1999) has explored cancer occurrence as a function of animal size, suggesting that in larger animals, whose lifespan grows as about the 4/10 power of their cell count, prevention of cancer in rapidly proliferating tissues becomes more difficult in proportion to size. Cancer control requires the development of additional mechanisms and systems to address tumorigenesis as body size increases – a synergistic effect of cell number and organism longevity. Nunney concludes

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“This pattern may represent a real barrier to the evolution of large, long-lived animals and predicts that those that do evolve ... have recruited additional controls [over those of smaller animals] to prevent cancer.” Different tissues may have evolved markedly different tumor control strategies. All of these, however, are likely to be energetically expensive, permeated with different complex signaling strategies, and subject to a multiplicity of reactions to signals, including those related to psychosocial stress. Forlenza and Baum (2000) explore the effects of stress on the full spectrum of tumor control, ranging from DNA damage and control, to apoptosis, immune surveillance, and mutation rate. Elsewhere (Wallace et al., 2003) we argue that this elaborate tumor control strategy, particularly in large animals, must be at least as cognitive as the immune system itself, which is one of its components: some comparison must be made with an internal picture of a ‘healthy’ cell, and a choice made as to response: none, attempt DNA repair, trigger programmed cell death, engage in full-blown immune attack. This is, from the Atlan/Cohen perspective, the essence of cognition. 5.2.3 The HPA axis The hypothalamic-pituitary-adrenal (HPA) axis, the ‘flight-or-fight’ system, is cognitive in the Atlan/Cohen sense. Upon recognition of a new perturbation in the surrounding environment, memory and brain or emotional cognition evaluate and choose from several possible responses: no action needed, flight, fight, helplessness (flight or fight needed, but not possible). Upon appropriate conditioning, the HPA axis is able to accelerate the decision process, much as the immune system has a more efficient response to second pathogenic challenge once the initial infection has become encoded in immune memory. Certainly ‘hyperreactivity’ in the context of post-traumatic stress disorder (PTSD) is a well known example. Chronic HPA axis activation is deeply implicated in visceral obesity leading to diabetes and heart disease, via the leptin/cortisol diurnal cycle (Bjorntorp, 2001). 5.2.4 Blood pressure regulation Rau and Elbert (2001) review much of the literature on blood pressure regulation, particularly the interaction between baroreceptor activation and central nervous function. We paraphrase something of their analysis. The essential point, of course, is that unregulated blood pressure would be quickly fatal in any animal with a circulatory system, a matter as physiologically fundamental as tumor control. Much work over the years has elucidated some of the mechanisms involved: increase in arterial blood pressure stimulates the arterial baroreceptors which in turn elicit the baroreceptor reflex, causing a reduction in cardiac output and in peripheral resistance, returning pressure

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to its original level. The reflex, however, is not actually this simple: it may be inhibited through peripheral processes, for example under conditions of high metabolic demand. In addition, higher brain structures modulate this reflex arc, for instance when threat is detected and fight or flight responses are being prepared. Thus blood pressure control cannot be a simple reflex. It is, rather, a broad and actively cognitive modular system which compares a set of incoming signals with an internal reference configuration, and then chooses an appropriate physiological level of blood pressure from a large repertory of possible levels – a cognitive process in the Atlan/Cohen sense. The baroreceptors and the baroreceptor reflex are, from this perspective, only one set of a complex array of components making up a larger and more comprehensive cognitive blood pressure regulatory module. 5.2.5 Emotion Thayer and Lane (2000) summarize the case for what can be described as a cognitive emotional process. Emotions, in their view, are an integrative index of individual adjustment to changing environmental demands, an organismal response to an environmental event that allows rapid mobilization of multiple subsystems. Emotions are the moment-to-moment output of a continuous sequence of behavior, organized around biologically important functions. These ‘lawful’ sequences have been termed ‘behavioral systems’ by Timberlake (1994). Emotions are self-regulatory responses that allow the efficient coordination of the organism for goal-directed behavior. Specific emotions imply specific eliciting stimuli, specific action tendencies (including selective attention to relevant stimuli), and specific reinforcers. When the system works properly, it allows for flexible adaptation of the organism to changing environmental demands, so that an emotional response represents a selection of an appropriate response and the inhibition of other less appropriate responses from a more or less broad behavioral repertoire of possible responses. Such ‘choice’ leads directly to something closely analogous to the Atlan and Cohen language metaphor. Damasio (1998) concludes that emotion is the most complex expression of homeostatic regulatory systems. The results of emotion serve the purpose of survival even in nonminded organisms, operating along dimensions of approach or aversion, of appetition or withdrawal. Emotions protect the subject organism by avoiding predators or scaring them away, or by leading the organism to food and sex. Emotions often operate as a basic mechanism for making decisions without the labors of reason; that is, without resorting to deliberated considerations of facts, options, outcomes, and rules of logic. In humans learning can pair emotion with facts which describe the premises of a situation, the option taken relative to solving the problems inherent in a situation, and, perhaps most importantly, the outcomes of choosing a certain option, both immediately and in the future. The pairing of emotion and fact

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remains in memory in such a way that when the facts are considered in deliberate reasoning when a similar situation is revisited, the paired emotion or some aspect of it can be reactivated. The recall, according to Damasio, allows emotion to exert its pairwise qualification effect, either as a conscious signal or as nonconscious bias, or both. In both types of action the emotions and the machinery underlying them play an important regulatory role in the life of the organism. This higher order role for emotion is still related to the needs of survival, albeit less apparently. Thayer and Friedman (2002) argue, from a dynamic systems perspective, that failure of what they term ‘inhibitory processes’ which, among other things, direct emotional responses to environmental signals, is an important aspect of psychological and other disorder. Sensitization and inhibition, they claim, ‘sculpt’ the behavior of an organism to meet changing environmental demands. When these inhibitory processes are dysfunctional – choice fails – pathology appears at numerous levels of system function, from the cellular to the cognitive. Thayer and Lane (2000) also take a dynamic systems perspective on emotion and behavioral subsystems. In the service of goal-directed behavior and in the context of a behavioral system, they see these organized into coordinated assemblages that can be described by a small number of control parameters. This is much like the factors of factor analysis, which reveal the latent structure among a set of questionnaire items thereby reducing or mapping the higher dimensional item space into a lower dimensional factor space. In their view, emotions may represent preferred configurations in a larger ‘state-space’ of a possible behavioral repertoire of the organism. From their perspective, disorders of affect represent a condition in which the individual is unable to select the appropriate response, or to inhibit the inappropriate response, so that the response selection mechanism is somehow corrupted. Gilbert (2001) suggests that a canonical form of such ‘corruption’ is the excitation of modes that, in other circumstances, represent ‘normal’ evolutionary adaptations, a matter to which we will return. Panskepp (2003) has argued that emotion represents a primary form of consciousness, based in early-evolved brain structures, which has become convoluted with what we here describe as a later-developed global neuronal workspace. To anticipate the argument somewhat, we are going to suggest that the convolution with GNW consciousness involves quite a large number of other cognitive biological and social submodules as well. 5.2.6 Sociocultural network Humans are particularly noted for a hypersociality that inevitably enmeshes us all in group processes of decision and a collective cognitive behavior within a social network, tinged by an embedding shared culture. For humans, culture is truly fundamental. Durham (1991) argues that genes and culture are two distinct but interacting systems of inheritance within human populations.

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Information of both kinds has influence, actual or potential, over behaviors, which creates a real and unambiguous symmetry between genes and phenotypes on the one hand, and culture and phenotypes on the other. Genes and culture are best represented as two parallel lines or tracks of hereditary influence on phenotypes. Much of hominid evolution can be characterized as an interweaving of genetic and cultural systems. Genes came to encode for increasing hypersociality, learning, and language skills. The most successful populations displayed increasingly complex structures that better aided in buffering the local environment (e.g. Bonner, 1980). Successful human populations seem to have a core of tool usage, sophisticated language, oral tradition, mythology, music, and decision making skills focused on relatively small family/extended family social network groupings. More complex social structures are built on the periphery of this basic object (e.g. Richerson and Boyd, 1995, 2004). The human species’ very identity may rest on its unique evolved capacities for social mediation and cultural transmission. These are particularly expressed through the cognitive decision making of small groups facing changing patterns of threat and opportunity, processes in which we are all embedded and all participate. This listing, in concert with our general focus on consciousness, suggests a more comprehensive picture of chronic mental and physical disorder than is current. 5.2.7 Comorbidity We briefly discussed the problem of dividing the full set of possible responses of a cognitive process into resting and active sets, respectively labeled B0 and B1 . Like the ‘second order selection’ we proposed for the dynamic threshold of individual or collective consciousness, it seems likely that a higher order cognitive module must act to define which states of acognitive physiological or psychological system are to be labeled as resting and active. This is because, depending on the patterns of threat or opportunity facing the organism, different ‘languages of thought’ are appropriate at different times. Perceived threat, for example, requires activation of the HPA axis as ‘normal’ for the duration of that threat. This suggests existence of, in addition to consciousness as a higher order function, a ‘zero mode identification’ cognitive module (ZMI), whose dysfunction through improper identification of a typically excited mode as a resting mode, can result in chronic disease. See Wallace (2003, 2004) for an extended discussion. The idea is, basically, a generalization of Gilbert’s (2001) mechanism for emotional disorder, i.e. having some ‘normal’ evolutionary adaptation become pathologically persistent or inappropriately activated. An example might be long-lasting emergency hypervigilance in anxiety disorder. We suppose most cognitive modules subject to similar problems, likely with mutually-reinforcing ‘crosstalk’ between them: comorbidity.

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If Y represents the information source dual to ZMI in generalized cognition, and if Z is the information source characterizing ‘structured psychosocial stress’, an embedding context, the mutual information between them I(Y ; Z) = H(Y ) − H(Y |Z), serves as a splitting criterion for pairs of linked paths of states. Structured psychosocial stress is usually long-term, continually affecting individuals, families, and communities at all stages of life. Certain physiologically excited modes are thus likely to be continually activated during the life course, from gestation, birth, and growth, through senesence. A typical example would be growing up or living under an Apartheid system, a Manichean world, divided into ‘good’ and ‘bad’, ‘black’ and ‘white’ (Fanon, 1966; Massey and Denton, 1998; Memmi, 1969). Other examples would include Americanstyle ‘regulated poverty’, the British ‘class’ system, nonunionized workplaces, prisons, the military during combat, and so on. Parametize the coupling between these interacting information sources, writing I(Y ; Z) = I[K], with structured psychosocial stress as the embedding context. Invocation of the mathematical homology between free energy density and information source uncertainty permits imposition of a renormalization formalism resulting in punctuated phase transition depending on K. Socioculturally constructed and structured psychosocial stress, in this model having both ‘grammar’ and ‘syntax’, can be viewed as entraining the function of zero mode identification when the coupling with stress exceeds a threshold. More than one threshold appears likely, accounting, perhaps, for the often staged nature of ‘environmentally caused’ disorders. These should result in a series of collective, but highly systematic, ‘tuning failures’ in the Rate Distortion Manifold sense, that represent a literal image of the structure of imposed psychosocial stress written upon the ability of the ZMI system to characterize a ‘normal’ mode of excitation. This causes a mixed atypical and usually transient state to become permanent, producing comorbid mental and chronic physical disorder. The process may have both cross-sectional and longitudinal structure, with the latter accounting for ‘critical periods’ in the onset of developmental disorders. Coronary heart disease (CHD) is already understood as a disease of development which begins in utero. Work by Barker and colleagues (Barker, 2000; Barker et al., 2002; Eriksson et al., 2000; Godfrey and Barker, 2001; Osmond and Barker, 2000) suggests that those who develop CHD grow differently from others, both in utero and during childhood. Slow growth during fetal life and infancy is followed by accelerated weight gain in childhood, setting a life history trajectory for CHD, type II diabetes, hypertension, and, of course, obesity. Barker (2002) concludes that slow fetal growth might also heighten the body’s stress responses and increase vulnerability to poor living conditions later in life. Thus, in his view, CHD is a developmental disorder that originates through two widespread biological phenomena, developmental plasticity and compensatory growth, a conclusion consistent with the work of

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Smith et al. (1998), who found that deprivation in childhood influences risk of mortality from CHD in adulthood, although an additive influence of adult circumstances is seen in such cases. Much of the CHD work particularly implicates certain kinds of hypertension as a developmental disorder. As Eriksson et al. (2000) put the matter, “The association between low birth weight and raised blood pressure in later life has now been reported in more than 50 published studies of men, women, and children. It has been shown to result from retarded fetal growth rather than premature birth. The ‘fetal origins’ hypothesis proposes that the association reflects permanent resetting of blood pressure by undernutrition in utero.” Asthma fits within a similar perspective. Wright et al. (1998) describe how prospective epidemiological studies show the newborn period is dominated by Th2 reactivity in response to allergens. It is also evident that Th1 memory cells selectively develop shortly after birth, and persist into adulthood in non-atopic subjects. For most children who become allergic or asthmatic, the polarization of their immune systems into an atopic phenotype probably occurs during early childhood. It has been speculated that stress triggers hormones in the early months of life which may influence Th2 cell predominance, perhaps through a direct influence of stress hormones on the production of cytokines that are thought to modulate the direction of immune cell differentiation. There is evidence that parental reports of life stress are associated with subsequent onset of wheezing in children between birth and one year. Recent work by Collins et al. (2004) explores how the experience of racism can express itself as very low birthweight among African-Americans. They conclude that “Our study adds to the small but growing evidence of a relation between African American women’s exposure to interpersonal racial discrimination and pregnancy outcomes. We found that African American mothers who delivered [very low birthweight] preterm infants were more likely to report discrimination during their lifetime than African American mothers who delivered [normal birthweight] infants at term...the reported lifelong accumulated experiences of interpersonal racial discrimination by African American women constitute an independent risk factor for infant [very low birthweight].” Work by Hirsch (2003) suggests that obesity, which is also seriously epidemic in the USA, is a developmental disorder with roots in utero or early childhood. Hirsch and others have developed a ‘set point’ or homeostatic theory of body weight, finding that it is the process which determines that ‘set point’ which needs examination, rather than the homeostasis itself, which is now fairly well understood. Hirsch concludes that the truly relevant question is not why obese people fail treatment, it is how their level of fat storage

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became elevated, a matter, he concludes, is probably rooted in infancy and childhood, when strong genetic determinants are shaping a still-plastic organism. In this regard, Bjorntorp (2001) finds that embedding psychosocial stress is a principal determinant of obesity at both the individual and population levels, as do Wallace and Wallace (2005). Somewhat less conclusively, a lively debate rages regarding various possible subforms of psychopathy, a mental disorder characterized by a long history of manipulative, impulsive, and callous antisocial ‘cheating’ behavior. Mealey (1995) places the disorder in an evolutionary perspective as either a genetically determined or an acquired ‘life history strategy’ very similar to Nunney’s (1999) analysis of cancer, albeit at the social rather than cellular level of interaction. Paris (1993) attempts to provide a comprehensive, integrative, biopsychosocial perturbed ‘condition-development’ model for personality disorders. Lalumiere et al. (2001), by contrast, find evidence for a strict life-history strategy model, concluding, as a result of studies on children and adolescents, that “If psychopathy is a result of condition-development, the environmental triggers are likely to operate very early”. The review by Herpertz et al. (2000) examines the hypothesis that pathologically neglectful parenting and early social rejection contribute to onset of the disorder, particularly in the context of ‘individualistic’ social structures (Cooke, 1996). We speculate that it is possible to place the ‘social cheating’ of psychopathy in the same context as Nunney’s cellular cheating for cancer, consequently being subject to the standard pattern of gene-environment ‘norms of reaction’ emerging as structured psychosocial stress acts over the course of child development, probably beginning in utero. The diagnosis of psychopathy (like other ‘personality disorders’) is very much concentrated in prison subpopulations. These always have marked ethnic and ‘racial’ structure as a consequence of formal patterns of discrimination, economic deprivation, and various forms of Apartheid – all constituting structured psychosocial stressors which write literal images of themselves upon their victims either through induction of developmental disorders or as adaptation pressures. Anxiety disorders have a long history of attribution to developmental factors and early childhood exposures (Bandelow et al., 2002). More generally, Egle et al. (2002) find evidence that early biological and psychosocial stress in childhood is associated with long-term vulnerability to various mental and physical diseases. Research findings have, in their view, accumulated on those emotional, behavioral and psychobiological factors responsible for the mediation of lifelong consequences including increased risk of somatization and other mental disorders such as anxiety, depression and personality disorders. These often result in high-risk behaviors that are associated with physical disease – cardiovascular disorders, stroke, hepatitis C, type 2 diabetes, chronic lung disease, as well as with aggressive behavior. These case histories appear to present specific instances of a comprehensive general phenomenon affecting the etiology of the larger spectrum of chronic

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and comorbid mental and physical disorders, in the sense that structured psychosocial stress can literally write an image of itself upon the developing child, and if acute enough, on the adult, initiating trajectories to comorbid mental and chronic physical disorder. Such disorder must inevitably constitute a powerful context for individual consciousness: mind-body dysfunction will always have profound impact on conscious experience and the possibilities for voluntary action. The next example suggests that such interactions may involve ‘second order’ as well as direct effects. 5.2.8 Schizophrenia Schizophrenia appears to fall broadly within the paradigm of a developmental cognitive disorder (Lewis and Levitt, 2002; Allin and Murray, 2002). Within the United Kingdom schizophrenia is, however, significantly more prevalent among Afro-Caribbean immigrants subject to chronic unemployment, early separation from parents, and perhaps racial discrimination, when compared with non-migrants of either majority or minority ethnicity (Mallett et al., 2002). For the U.S. there is some controversy as to the propensity of majority clinicians to overdiagnose schizophrenia among minority patients, perhaps masking underlying demographic patterns. As Gaughran et al. (2002) note, however, there is good evidence of immune activation in schizophrenia. Up to a third of patients has an autoimmune condition clinically unrelated to their psychiatric illness, and first degree relatives of people with schizophrenia also have increased incidence of autoimmune disease. Torrey and Yolken (2001) note the similarities and contrasts between schizophrenia and rheumatoid arthritis. Both are chronic, persistent diseases displaying lifelong prevalence and a relapsing and remitting course. Both are felt to involve environmental insults occurring in genetically susceptible individuals, and their diagnosis depends upon syndromal diagnostic criteria which have been developed by committees and have changed over time. Many studies, however, have observed a striking inverse correlation – an ‘anticomorbidity’ – between the two diseases, although both are believed to run in families, with a population prevalence of about one percent. That is, people with schizophrenia seem less likely to suffer from rheumatoid arthritis, although perhaps more likely to suffer autoimmune disease in general. This begins to resemble the retinal ‘nonorthogonal eigenmode’ patterns discussed in terms of the Rate Distortion Manifold. Grossman et al. (2003) describe how the recent emphasis on schizophrenia as a developmental disorder has focused on characterizing the role of nongenetic factors in the development of symptom patterns. Certain prenatal and perinatal environmental exposures, including maternal stress and malnourishment, and obstetric complications such as low birth weight, have been reported to be associated with increased susceptibility to the disorder. Increased incidence has also been reported in children born to mothers who

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experienced infection from influenza or rubella during the second trimester of pregnancy. Thus early neurodevelopmental processes may be compromised, laying groundwork for disorder when taxed by later developmental demands, for example those associated with the stressful periods of social development in childhood and adolescence. Rothermundt et al. (2001) further summarize at some length the case for both the infection and autoimmune hypotheses regarding onset of schizophrenia. Torrey and Yolken (2001) conclude that the negative association between schizophrenia and rheumatoid arthritis may depend on the timing of some critical exposure, e.g. that exposure in utero or childhood produces schizophrenia, while exposure in adulthood produces rheumatoid arthritis. A slightly different hypothesis, consistent with the mathematical exercises above, is that rheumatoid arthritis and schizophrenia characterize different atypical mixed eigenmodes falsely and recurrently identified as zero states by the progressive failure of the ZMI module. Such would tend to be mutually exclusive, although not absolutely so since the eigenmodes are not orthogonal. A broadly similar pattern has been commented on by Karlsson et al. (2001), who found homologous sequences of the HERV-W family of endogenous retroviruses in the cerebro-spinal fluid of newly-diagnosed individuals with schizophrenia and in other subjects having multiple sclerosis. Karlsson et al. (2001) speculate it is possible that individuals with schizophrenia and multiple sclerosis undergo the activation of similar retroviral sequences but differ in terms of genetically determined responses to the retroviral activation. Schizophrenia and multiple sclerosis are distinct clinical entities and have different pathological manifestations, gender ratios, and clinical courses, but share a number of epidemiological features including age of onset, seasons of birth, and geographic distributions. In addition, however, some patients display clinical manifestations of both diseases. Similarly, rigorous studies by Dupont et al. (1986), Gulbinat et al. (1992) and Mortinsen (1989, 1994) followed large Danish and Dutch cohorts of patients with schizophrenia. When adjusted for smoking patterns, these showed marked and highly significant reduction in a broad variety of cancers. More recent work by Cohen et al. (2002) adjusted for age, race, gender, marital status, education, net worth, smoking, and hospitalization in the year before death, for a large US sample likewise found greatly reduced risk of cancer among persons diagnosed with schizophrenia. Catts and Catts (2000) speculate that such results are driven by hyperactivation of the p53 tumor suppressor/apoptosis gene during neurodevelopment, causing long-term developmental dysfunction, while Teunis et al. (2002) suggest, from animal model studies, that the hyperreactive dopaminergic system characteristic of schizophrenia inhibits tumor vascularization. These examples, again, strongly suggest a ‘nonorthogonal eigenmode’ pattern in which the ZMI module, including both immune function and the larger system of tumor control mechanisms within a unified and broadly cognitive

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structure, fails in a systematic manner, producing characteristic spectra of coand antico- morbidities among different dysfunctions. It appears that, at the population level, structured psychosocial stress can also exert a ‘higher order effect,’ producing different spectra of co- and antico- morbidities between schizophrenia and other disorders within powerful and marginalized subgroups. 5.2.9 Reconsidering Zero mode identification An essential characteristic of cognition in this formalism involves a function h(x) which maps a (convolutional) path x = a0 , a1 , ..., an , ... onto a member of one of two disjoint sets, B0 or B1 . Thus respectively, either (1) h(x) ∈ B0 , implying no action taken, or (2), h(x) ∈ B1 , and some particular response is chosen from a large repertoire of possible responses. The problem of defining these two disjoint sets arises, and a ‘higher order cognitive module’ seems needed to identify what constituted B0 (the set of ‘normal’ states), a matter which may vary according to the challenges faced by the organism. We suppose that higher order cognitive module, Zero Mode Identification, much like that inferred above in the discussion of the pathologies of therapeutic intervention regarding collective consciousness, interacts with an embedding language of structured psychosocial stress and, instantiating a Rate Distortion image of that embedding stress, begins to include one or more members of the set B1 into the set B0 . Recurrent ‘hits’ on that aberrant state would be experienced as episodes of highly structured comorbid mind/body pathology. Empirical tests of this hypothesis, again, all quickly generate real-world regression models or their time series variants, involving the interrelations of measurable biomarkers, beliefs, behaviors, neural correlates, reported thoughts and feelings, and so on. These considerations also lead directly to an analysis of therapeutic failure essentially similar to that given above for institutions. that is, the system of psychosocial stressors initiating a developmental trajectory to individual comorbid mind/body dysfunction may also preclude effective therapeutic intervention against those dysfunctions (Wallace and Wallace, 2005). 5.2.10 Chronic disease and collective consciousness Collective consciousness plays multiple roles in the production and distribution of structured psychosocial stress. Public policies instituting and maintaining Apartheid, segregation, discrimination according to gender or sexual orientation, workplace disempowerment, the permanent war economy resulting in deindustrialization (sensu Melman, 2001, etc.; Ullmann 1988, etc.), serial forced displacement of African-Americans and other populations (sensu Fullilove, 2004 or Wallace and Wallace, 1998), the prison-industrial complex, and the like, create the underlying system of stressors. Risk behaviors emerge as structured adaptations to persistent structured stress (e.g. Wallace et al.,

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1996). These may include cultural patterns of overeating and/or substance abuse and sexual excess, violent behaviors, including gun use, and so on. Risk behaviors are, in turn, contagious learned adaptations which can diffuse socially and spatially according to the epidemic and endemic models developed above, in which public policy plays a central role. Thus the spread of new, or reactivation of old, risk behaviors, is shaped by the very collective consciousness responsible for creating pathogenic stress in the first place. Our conclusion that a pattern of co- and antico- morbid mental and chronic physical disorder represents a pathological, ordinarily atypical or transient, state is consistent with theorizing in both autoimmune disease and mental disorder. Gilbert (2001), for example, uses an evolutionary approach to conclude that the relatively small number of evolved adaptive defense mechanisms, for example the flight-or-fight hypothalamic-pituitary-adrenal (HPA) axis, may become pathologically activated to produce mental disorder. He suggests that such evolved defenses, of which there is a limited number, can become pathological when they are too easily aroused or prolonged, are arrested (i.e. aroused but not expressed), or are ineffective. These might involve depression, anxious arousal, or heightened vigilance to threat, with the type of defense (e.g. flight, fight, submit, help seeking) being mirrored in particular symptom presentations. Jones and Blackshaw (2000) likewise argue that behavioral similarities between humans and animals show that many psychiatric states are distortions of evolved behavior, a perspective which provides, in their view, a new etiological approach to psychiatry transcending current mainstream empirical and phenomenological approaches which are principally forms of symptom classification. Although individual pathologies of both mind and body may predominate in particular cases, our work here encompasses a broad spectrum of chronic diseases, emotional disorders, and classic cognitive dysfunction, in the context of the local sociocultural network so important in human biology. We particularly emphasize the effects of structured psychosocial stess as an expression of embedding collective consciousness in the development of comorbid mind/body symptom patterns over the full life course. Typically such developmental disorders are characterized by particular critical periods for exposure to pathogenic agencies. Gestation and early childhood are usually times of special sensitivity. The model which emerged focuses on the ‘eigenstructure’ of a rate distortion manifold, and particularly on failure of a higher cognitive module which permits identification of the ‘zero mode’ of the manifold. We conclude that, for certain classes of mind/body symptomatology, early experiences of exposure to structured psychosocial stress – particularly childhood poverty – can trigger identification of a highly atypical mode as the ‘normal’ zero-reference state. This will often initiate a life course of co- or antico- morbid psychiatric and physical disorders. The characteristic pattern we have in mind would involve individual and population-level comorbidity among obesity, asthma,

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diabetes, hypertension, depression, anxiety, substance abuse, ruthless or violent behaviors, coronary heart disease, certain cancers, and asthma or lupus – what might well be characterized as ‘oppression disorder’ at the individual level. We find that historical patterns of discrimination, deprivation, and injustice – fundamental expressions of collective consciousness – are a determining feature in population-level expression of comorbid psychiatric and chronic physical disorder, patterns which are literally an image of that system imposed upon children, beginning in their mothers’ wombs. To reiterate, our modeling exercise implies that maternal/child poverty is a principal determinant of an unexpectedly broad and characteristic life-course spectrum of population-level patterns of comorbid psychiatric and chronic physical disorder in the US. This is an empirically testable hypothesis. The works of Memmi (e.g. 1969) and Fanon (e.g. 1966), however, show clearly that, for such systems as ours, the reflective nature of structured psychosocial stress ensures that the health and welfare of both dominant and dominated populations will be closely linked through a wide variety of mechanisms. We conclude that, while generalized developmental disorders may be concentrated in populations of color in the USA, they cannot be contained there, and will inevitably diffuse up the social hierarchy, entraining even affluent populations (e.g. Wallace and Wallace, 2004, 2005).

6 THE FAILURE OF AIDS CONTROL AND TREATMENT IN THE US

6.1 Introduction A particularly striking example of canonical failure in public health, and a clear dysfunction of distributed institutional cognition/collective consciousness, involves systematic and widespread inadequate response to AIDS in the United States. Here we examine that pattern from the perspectives of this analysis, first for a geographic region near the principal West Coast epicenter, and then for African-American religious groups in and near New York City, the principal East Coast epicenter. We will end with a broad case study examining systematic inadequacy in medical care provided HIV positive women of color. In 1998, while conducting a study of community leaders’ response to the AIDS epidemic, Mindy Fullilove and colleagues gained first-hand experience of society’s hesitance to engage epidemic response (Morales and Fullilove 1992). No matter that AIDS was a deadly killer, nor that this attack on the immune system posed nearly imponderable implications for human survival. Because the illness was associated with intravenous drug use and sex – particularly male homosexual acts – community leaders backed away from providing care or engaging in prevention efforts. That stigma could trump death was remarkable. In order to understand this phenomenon better, a model of epidemic response was developed by examining reports of rapid epidemic control, such as that of a 1993 epidemic of pertussis in Cincinnati, Ohio (Christie et al, 1994). Fullilove was able to identify three phases of epidemic control. In the first phase, recognition, society must decide if a disease poses a significant threat to social functioning and merits the appellation “epidemic”. In the second phase, which concerns resources, society must decide to commit resources to epidemic control. In the third phase, realignment, society must promote social organization for mounting and sustaining the epidemic response. In the case of the Cincinnati pertussis epidemic, the Health Department recognized in July that there had been a rise in pertussis cases over base-

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line. The Department issued a “pertussis alert” and started an information campaign. Those measures proved insufficient, and in August more extensive controls were put in place. Cooperation among a broad group of providers, ranging from schools to hospitals, ensured the success of the initiative. By October of that year, the number of cases had returned to baseline and the epidemic was over. Though the example used here is of a known disease, these phases apply equally well to an emerging condition, such as AIDS, albeit the recognition phase is considerably extended. This model of ideal epidemic response was then used as a yardstick in three cases studies of response to AIDS. The first was conducted in 1989, the second in 1994 and the third in 1999. These studies examine different groups in different settings, yet each documents the ways in which stigma and other marginalizing processes derailed effective action against AIDS. Furthermore, reading the cases side by side permits one to examine how failure in the initial effort accumulated over time, creating a deepening crisis of AIDS management, a path dependence characteristic of dysfunction in collective consciousness.

6.2 CASE STUDY 1: Epidemic Response in Alameda County Alameda County lies on the east side of the San Francisco Bay from San Francisco, a virulent focus of the US AIDS pandemic, and is closely connected to it by the commuting field defined by the daily journey-to-work. Despite its proximity, Alameda County had very low rates of AIDS throughout the first decade of the epidemic, thus creating the opportunity for epidemic preparedness. The Epidemic Response in Alameda Study (Gracia-Soto et al., 1998) was designed to learn how health care organizations just outside a major epicenter of the American AIDS epidemic had responded to growing numbers of cases. Here we follow closely the argument presented in that paper. Health care agencies in Alameda County were enumerated using a variety of methods, including examination of lists maintained by the County Department of Health, reviewing brochures of existing services and consulting telephone books. A total of 51 agencies were identified, ranging from local hospitals to small community-based organizations. Directors of 31 agencies participated in the study by completing a semi-structured interview and filling out an agency information sheet. Interviews were carried out between March and September, 1989, well before introduction of antiretroviral drugs. The recognition of the epidemic was slow and tortuous, slowed by stigma, lack of resources and lack of central leadership from federal, state or county agencies. Rather than the rapid mobilization of a system of organizations, what the study documented was the individual response of organizations that integrated new services as a result of a push-pull process, that is, a social process in which a hierarchical system is acted on from the top (pull) and the

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bottom (push). Among the pushes were: loss of key members of the organization to AIDS; growth of cases in the organization’s service area; and the expansion of acknowledged ‘affected’ groups from gay men and intravenous drugs to include women, the elderly, and many others. Among the pulls were: new regulations imposed by government agencies, and new monies allotted for AIDS care. The directors were highly critical of the push-pull process, which acted spasmodically on the individual organizations that formed the health care system. Indeed, providers in Alameda County used the term ‘system’ as a euphemism for the complex set of relatively autonomous agencies that provided care. Although most aspects of patient need could be met by some part of the health care industry, the agencies were not subunits of a whole that might be easily mobilized in recognition of new health threats. Each autonomous unit was responsive to its own set of funders and clients. There was no regional planning authority that set direction and tone. Though a substantial proportion of health care funding came through the County Health Department, it would be a great overstatement to suggest that that agency provided direction for the entire system. Thus, response to AIDS lay largely in the purview of the individual organizations and there was a great variation in the moment in time at which each agency had initiated such work. Agencies characteristics contributed to manner in which social pressures to respond to AIDS acted on each organization. Large organizations were likely to be ordered to act by outside governing bodies. They were likely to respond early the epidemic. Mid-size organizations followed social concern and funding opportunities. Those organizations tended to follow the large hospitals and small advocacy organizations. Because of their reasonably large resource base and high adaptability, they played a major role in the evolution of AIDS services once they had become engaged. Small activist organizations acted on their political and social commitments. To the degree that AIDS was consonant with their mission, these groups could move swiftly to address the epidemic. Thus, the push and pull of outside forces-such as government, larger social concerns and political commitments-worked on each agency in complex ways. We will examine this push/pull in more detail through the lens of the three phases of epidemic response. 6.2.1 Epidemic recognition The slow pace of the recognition phase may be largely attributed on the one hand to the enormous effort it took to overcome fear and stigma, and, on the other hand, the relative lack of strong central leadership guiding and funding the process. Push came from affected and infected individuals and communities. At times, the affected individual was a key member of the agency. A director described: “We actually started around January or February of 1988. I think it grew out of two things really. As the national epidemic grew and

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being in a high-risk area, it became more and more obvious to us that we needed to be doing something in this area. And there was an employee in the upper management level in the city who developed and died of AIDS, who I think had a tremendous impact on people’s lives, so that people said we’ve got to do something. I think that was a very motivating factor”. In other instances, the affected individuals were the population served by the agency. One director described this experience of the push: “Yes, what happened to us, this was before we ever moved into our clinic. We still had our clinic over at —. At that time, the blood bank was doing a scary thing here. They were testing people when they went to give blood, and they would find something funny and that’s exactly how they would characterize it, something funny in their blood. And they would write these little notes about this person Joe Blow had something funny in their blood, so we’re sending them down to you. So here comes this guy in our clinic over there, totally hysterical, because they haven’t told him anything, but they’re telling his there is ‘something funny’ in his blood, ‘They told me I should come and see you.’ By the time he gets to our doorstep, he is ready to go bonkers, and we have to take this person off into a room and spend an hour trying to calm him down.” A striking feature of the push process was the slow expansion of “affected groups”. This category was largely confined to gay men and intravenous drug users early in the epidemic. Gradually, agencies serving blacks, the elderly, and women came to see their clientele as being “at risk”. One director commented: “I think those of us in health care have been very sensitive to the epidemic over the last, what, 5, 9 years. And have watched with helplessness on the sideline that this would eventually hit our population. But at what point do you sound the call? About 3 years ago we started realizing that no one else was going to take on the work, and that as a health care organization, we really had to address it”. Pull for AIDS services came from several levels of government: federal (largely the US Centers for Disease Control), state (State Department of Health) and county (Department of Health). Agency directors reported several actions that led to new AIDS-related activities. First, new regulations were set-for example, for the management of contaminated waste-that led to the need for staff training. Second, funds were made available for new services. Third, new activities were included under new or existing contracts. Pull also came from private funders and from peer agencies. One director described the pull exerted within a hospital by the existence of an AIDS education team:

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“Generally, we’ve offered [AIDS education] before it’s requested. There’s been that kind of historic resistance-you’ve probably encountered it-particular departments within a hospital have had more difficulty with HIV issues than other departments, and they have actively solicited providing education and classes for them. So there was basic AIDS 101 that’s being done, and then we try to provide more current updates, and those are aimed primarily at nurses: current diseases that they’re going to be seeing on an inpatient setting, experimental drugs, research protocols that we’re doing, to stay contemporary with the disease process of AIDS.” Directors were critical actors in the push/pull process. All of the directors interviewed felt they had a role in the agency decision-making and could provide direction for new initiatives. The leader’s willingness to tackle AIDS was a rate-setting factor determining the speed of response to the epidemic. One director described personal efforts to get an AIDS program started: “Just barely two years ago, I was coming over to [a community organization in San Francisco] and I was stealing buttons from [the director] and pamphlets and anything else I could steal. And I said, I have no shame because I have no money for AIDS and I wanted to bring that information back to my community here. So I did and, in fact, somebody interviewed me for the newspaper once and I said that I ran around and stole from everybody in San Francisco that I could steal from to bring information back to our community, until I got funding to do that. ” As a result of the push/pull process, agencies came to ‘own’ AIDS as their issue. Over and over, agency leaders pointed out that discovering the link between the agency’s historical sense of itself and the AIDS epidemic was critical in the initiation of AIDS services. At that point, agency leaders recognized a ‘fit’ between the traditional mission and the new service needs. The leader of a hospice described this realization in this manner: “One of the things that happened is that we have nondiscriminatory statements in our policies and procedures... So when the issue of AIDS came up, the immediate decision of the staff managers was, ‘We don’t discriminate. We don’t run a hospice for just sixty-five year-old cancer patients, we run a hospice program for terminally ill people’... There really wasn’t a decision that needed to be made... it was covered by existing policy... So what happened then in terms of the board of directors, we reaffirmed that with them... it was simply a reaffirmation.”

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6.2.2 Resources for fighting the epidemic Garnering resources, the second stage of epidemic response, involved getting money as well as many other kinds of resources, like knowledge and connections. All of the organizations used existing resources at the beginning of their response to AIDS. Particularly in resource-poor community agencies, people were adept at making a little go even further, as described in the following quote: “Let me try to trace what we’ve been doing in the past years before we even got funding. We created an internal AIDS subcommittee, [including] our sociomedical director, our clinical coordinator who’s a [registered nurse], myself, our health education department head, and from time to time the department head who supervises medical records... So about three years ago we formed and started investigating all the different things that have to be investigated: how to develop protocols, confidentiality issues, the logistics around testing, what health education needs there are, doing these assessments, what resources already exist locale and around the country for Asians.” As they began to understand the epidemic and carve out a path of action, all of the organizations looked for new resources to support new activities. At the level of the local hospitals, this involved massive expenditure for new forms of care. But even small organizations faced serious challenges relative to their existing and potential resources. Central to the problems in garnering resources was the inadequate epidemic response by the society in general. “I, who could have worked on policy development, instead had to concentrate on funding. And spent a good year and half writing proposals and find funding sources and that kind of stuff. That’s part and parcel of doing business in the nonprofit world, but it took a year and a half to do that, whereas if we had been funded at the very start, I could have spent a lot more time trying to push forward our AIDS services as opposed to, first of all trying to educate funders about the Asian community, and then trying to find money for AIDS.” Insufficient monies could not meet growing demands. Therefore, the monies were shifted from one group to another, using competition for funding to shift blame from government to providers. After all, if an agency failed to win a grant, the problem was the weakness of the application, not the overall lack of resources. In a funding-version of a lazy susan, money moved among the interest groups, creating unnecessary strife and tension. Maintenance funds were particularly difficult to find. One director described the funding situation in this way: “It’s positive and negative. It’s positive in that the funding is there, but it’s haphazard. Like right now in order to fund one of my positions,

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I have to get funding from two different sources because there’s not adequate funding from either one. And need more funding and more positions than we have. Unfortunately, the state is not as organized as I think it needs to be and one of the concerns I’ve had is we’ve had a three-year proposal to subcontract with the county, and the state has chosen not to give us additional funds, even though we have a good track record. Instead they’re giving new places funding and cutting our funding... I believe we need the diversification, obviously, but you still need to say, how can we support the organizations who are out there and been struggling from the beginning and obviously have learned a lot. They need support also.” 6.2.3 Social realignment The new demands of the AIDS epidemic called for extensive social organization to develop and sustain an adequate response to the epidemic. This took two forms among health care agencies. First, some new agencies were developed in response to the AIDS epidemic. Second, agencies related to each other and to their funding and client audiences in new ways. Networking was an important tool, especially for the community-based health care agencies. Directors participated in a large number of groups organized by services, race or ethnicity, geographic region, or other shared characteristics. A partial list of relevant organizations and networks included: Alameda AIDS Action Committee, East Bay AIDS Interfaith Network, Black AIDS Coalition, the South Bay AIDS Task Force, and the East Bay AIDS Response Organization. An important fact about the AIDS epidemic was that it brought together groups and individuals that had had no previous relationships. Because these groups did not know each other, effective partnerships depended on the development of mutual trust and respect. AIDS provided an effective testing ground, as groups had many opportunities to work and struggle together, forging deep and lasting bonds. One director illustrated this with a story about a co-worker: “There’s a way in which it’s helped people on my staff personally grow. To be more comfortable with gay people. I’ve one employee who’s just the sweetest, most wonderful person, she’s in her late 20s, has a wonderful home up in the Castro Valley hills. We were talking one day about the story about the guy taking them out to the gay bar. She looked at me and she said, ‘There’s gay bars in Hayward? Really?’ she says. She was shocked. She didn’t know that. She’d never thought about it... It’s gratifying to see people’s openness and ability to be comfortable and welcoming, and to be touched by people’s stories and people’s lives as much as they are by the homeless. ” These new social relationships were meaningful at a very personal level, as echoed in the reactions of another director:

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“It’s had a tremendous impact on me personally and on the people I work with. I chose to go into infectious diseases because most infections in children you can, with some detective work, identify, treat, and with a little effort and a lot of observation, you can make sure your treatment is working and you can cure kids of diseases that they would otherwise die from. So it’s a field that I went into because there’s a lot of optimism and hope ... And then came the AIDS epidemic, and suddenly you’re dealing with kids and families who deal with chronic illness, and you know, you’ve heard the story of what impact it has... I think it’s given all of us who participated in the care of kids here a better perspective on living with chronic illness. I think that we recognize these families have tremendous ongoing stresses, even when their children may be relatively healthy and going to camp and going to school and participating in sports and feeling good, the emotional impact is still devastating. So for me, I developed a closeness with families where normally there’s a fairly transient relationship, when you can cure their kids fairly quickly.” Personal experience was an important factor in the growth of ‘ownership’ of the epidemic, and in turn, as more and more individuals and groups ‘owned’ the epidemic, the base of advocacy became larger and more diverse. This had important implications for the ways in which social realignment proceeded. As one director noted: “There have been black programs for ages. Nobody documents Latinos. In Alameda County, until 1987, we were lumped in with whites. So that when AIDS money comes out, for example, from the County, they automatically target 60 % for Oakland. The rest of the money, the other 40 %, everybody in the South County, all the way down to Pleasanton and Livermore, we all have to go in for the last 40 %. And it’s one bone, $ 10, for the Hispanics. When we wrote the United Way applying, throughout the application, I used SIDA. They called back and wanted to know if that was a typographical error. That, if nothing else, made my point, and I’m sure that’s why they gave us money last year and this year. If you don’t know the way we call it, then you don’t know anything about how to reach Latinos” Yet these important personal and social transformations were undermined by the larger society which shifted money from one organization to another. Ideal response to an epidemic demands cooperation among a large number of groups. Epidemic response in Alameda County demanded successful competition among groups. In a zero sum game, blacks had to get less money in order for Latinos to get more money. As Asians entered the fray, they took money from both blacks and Latinos. As the epidemic expanded, the intergroup competition became more and more severe, limiting the cooperation that was needed to manage the steadily growing epidemic.

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6.2.4 Overall assessment of epidemic response Though Alameda County was minutes from a major epicenter of the AIDS epidemics, the opportunity to learn and prepare was largely lost. These data suggest that the process of epidemic response in Alameda County was halting and inadequate. The study identified a large number of vulnerabilities that undermined epidemic response, including failure of multiple levels of government to provide leadership, widespread stigma, perhaps representing ideological rigidity associated with certain ‘risk behaviors’, and lack of an organized system of disease management that could easily incorporate new demands. Vulnerabilities of this sort are not typically considered in the planning of disaster response, yet it seems evident that this needs to be reconsidered. In fact, evidence from case studies of the crack epidemic, fatal school shooting, the violence epidemic, and the response to Hurricanes Katrina and Rita suggest that such vulnerabilities can easily derail response. Given the cost in human suffering - indeed, the potential implications for all human existence - organizational non-response to disaster should be given much more detailed examination. Rather than integrating into a more comprehensive working unit, Alameda County’s AIDS treatment and prevention organizations were forced to compete for resources. Other organizations’ fundraising, rather than the threat of AIDS, became a principal embedding context, in the sense of Chapter 4, locking the system into fragmentation – social eutrophication. Inadequate resources appear to have imposed a kind of collective inattentional blindness and a systematic failure of interorganizational cooperation and collaboration.

6.3 CASE STUDY 2: Black clergy respond to AIDS Despite their excess risk for HIV/AIDS, African American communities have not developed a united response to this epidemic. Community-based organizations, especially those that provide additional treatment services, have played an active role in developing HIV prevention and treatment services. Other organizations, however, have been more reticent, among those, churches and other worship centers. In one study in San Francisco, religious leaders were significantly less likely than other community leaders to participate in an AIDS education intervention (Morales and Fullilove, 1992). In that study among 4 categories of community leaders, religious leaders were most difficult to contact, least likely to participate and least likely to complete the intervention. This finding stands in marked contrast to the social activism that is commonly attributed to African American clergy (Walls, 1991; Billingsley, 1991). The limited response of African American clergy has great salience for epidemic control because African Americans are closely linked to their clergy: 70% of those interviewed in a national survey reported they belonged to a

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church and 71% reported regular church attendance (Billingsley, 1991). Furthermore, African American churches and their clergy have historically played a substantial role in building and supporting African American communities. Churches are the oldest social institutions in those communities. Their stability was underscored by Lincoln and Mamiya (1990) who noted that, in a survey of rural and urban black churches, the median age of the 2,150 churches studied was 100 years. The churches had been physically stable through their history: 47.6% had moved once, while an additional 23.9% had moved only twice. As in any community closely linked to its church, the role of pastors in setting social agendas reaches into nearly every aspect of life. As noted in Case Study 1, stigma surrounding AIDS, because of its links to sex and drug use, has had a marked effect on epidemic response across American society. These issues have particular importance for religious leaders. Defert (1996), in discussing the issues surrounding the mobilization of religious organizations, has defined the relevant vulnerability in this fashion: “Most religions underline the importance of charity towards the weak, the poor, the infirm, the sick, which they justify philosophically in different ways. Religious communities also have the responsibility to enforce obedience to their rules and commandments, and they can be intolerant when faced with their violation. This reaction to errors, infractions, or sins normalized various forms of exclusion. The severity with which moral or religious taboos are regarded reflects the perceived threats to various boundaries, and defenders of religious values greatly fear breaches of such rules” (p. 447). This case study of African American clergy was conducted by the Community Research Group, led by Mindy Fullilove. It examined the ways in which the two roles of the clergy-community support and rule enforcement-came into conflict around the problem of response to the AIDS epidemic. Fiftyone members of the clergy took part in semi-structured interviews, conducted in 1995. They represented 14 denominations and 11 communities, all in the greater New York metropolitan area. Both men and women participated, though for the most part, for purposes of maintaining confidentiality, they are referred to here as ‘clergyperson’. In general, three characteristics may be said to describe the clergy interviewed for this study. The first is that the group was diverse. There was a great range of opinions and experiences described by those we interviewed. There was no single experience of church or religion, but rather many different experiences, and this represented the complexity of the black religious tradition. Second, the group prized its ability to interpret holy writ. There was a great spirit of independence and deep investment in providing theological leadership of the community. Third, the clergy varied greatly in their response to AIDS. AIDS had joined a long list of threats to community survival, including problems of poor education, loss of jobs, massive destruction of housing and drug epidemics. The clergy talked of the new challenge in dire tones. The epidemic had

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hit a community ‘already under siege,’ and it was described as ‘a staggering blow,’ ‘an insurmountable problem,’ ‘devastating,’ and ‘a tragedy’. That said, the sense of peril had not consistently led to action. As anticipated, the clergy were torn between secular and religious imperatives. 6.3.1 Being right with God All the clergy wanted to help their flock to ‘be right with God,’ but they did not share a common vision as to how that was to be accomplished. Rather, they can be divided into roughly three groups. The first group, which was quite small, made a sharp distinction between the problems of sin-which they saw as central to their ministry-and the problems of AIDS-which had to do with community health. In their view, AIDS was the result of a virus spreading through the community. They supported all efforts to contain the virus-including the distribution of condoms and clean needles-and to care for those stricken with illness. The second group, which was also small, was composed of the fundamentalists, both Muslim and Christian, who believed in a very strict reading of their holy books. They viewed the use of drugs or participation in homosexual acts as sins which were inextricably linked to the spread of infection. They were willing to provide support for those with AIDS who had recanted their sins and were currently living a sin-free life. However, they were unable to support any prevention activities that enable sin. The third group, which included the vast majority of the people interviewed in this study, found themselves in a middle position, concerned about both the ‘sin’ and the ‘sinner’. The clergy in this group tended to be those who viewed sin as universal, and included themselves among the sinners. This did not prohibit them from preaching against sin, but it did lead them to have compassion for others who had ‘strayed.’ AIDS was strongly associated with sin, but the compassion for the individual often overrode the condemnation of what they perceived as a sinful act that might have led to infection. Thus, except for a handful who saw this as a public health crisis, those interviewed linked HIV infection with sinful behavior. They saw it as their duty to condemn sin; they might or might not display condemnation for the sinner. One commented: “It’s a moral issue and it’s a health issue. You can’t separate the two. It’s a moral issue in the fact that they’re involved in activities that’s y’know, against the rule. Ethical values that we have whether you happen to be Protestant, Catholic or Jewish or Muslims. It’s a health problem in terms of the amount of Black people that are involved, you know, contacting this particular, you know, AIDS virus. So you do have, you know, moral and ethical problems, you know.” Another expressed the dilemma in this fashion:

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“I still hold to the responsibility as a pastor, an ordained elder of the church, to preach the gospel, and teach the word of God as it is set forth, but to be, but to show compassion, and love, to people who are in need... I will not in any way, shape or form, I do not feel I can in my heart, ah, condone, the gay life style, ah, and say it’s okay, you know, the Bible endorses it, God approves it, I could never say that. But on the other hand, I could not say that because people are engaged in that life style, they need to be, ah, if they contract AIDS or if they are sick, that we should cast them off and ignore them off and don’t bother with them. I don’t, I don’t feel that that’s the case.” The co-mingling of health and morality was at the heart of the hobbled effort to respond to AIDS. Clergy were ambivalent about what to do. Further, they were unwilling to take a stand that might be controversial within their groups, including their congregations and their fellow clergy. As one minister noted, pastors were reluctant to undertake AIDS activities because they feared others would say to them, ”Why are you on the bandwagon for the gays?” One minister explained: “The church has tried to be the moral agent of our community and so the idea of any kind of sexual activity that is not within the confines of marriage is always frowned upon generally and most of our churches do a lot to trying to even deny that it takes place. I think that that basic idea is what stops us from being able to kind of talk openly about the issues related to HIV.” Though respondents perceived themselves to be acting as moral agents condemning sinful acts, those acts still occurred. The condemnation, in effect, placed a blanket of silence over the matter. AIDS, because it was linked to sin, was shameful, and hence could not be discussed. A minister illustrated this by recounting, ‘I have discovered that almost all, there is shame, when we have people that I know who have died of AIDS, ah, that’s the last thing [the families] want brought up’. Action or discussion implied tolerance, perhaps even acceptance; it implied that the respondent was getting ‘on the bandwagon with the gays’. Silence was rigorously enforced. After speaking boldly of these constraints on speech, a minister told us, ‘If you tell anyone I said that, I’ll make you out of a liar’. 6.3.2 Addiction to drugs Drug addiction was widespread in the African American communities represented in this study. Heroin epidemics of the 1960s and 1970s had subsided into endemic states, to be followed by the crack epidemic of the 1980s, which many viewed as an even greater scourge. The presence of drugs in the community meant that drugs affected church members as well. As one clergyperson noted:

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“I know of one instance in my own congregation where the daughter who is about eighteen, seventeen or eighteen, became a victim of drugs and her boyfriend of course also. The parents are out at work and she invited her boyfriend into the home and they literally took the television, took other valuables and literally sold them from her own home - from her own home -to purchase drugs... The church is not exempt, see. The church is made up of people and the people bring all those conditions to church. I’m deeply aware that people come to church have the same problems as persons who are not in church.” After years of discussion about the disease model of addiction, that view had gained wide, if not complete, acceptance. ‘An IV drug user is a person in great trouble, and in need of help,’ one noted. The ascendancy of the ‘disease model’ created a form of acceptance. Stories of non-acceptance - rushing an addicted person of church, for example - were related as signs of the struggle between compassion and disdain, acceptance and rejection. Threaded in a hopeful manner through the interviews was the knowledge that spirituality was a potent force in recovery from addiction. One clergyperson observed: “I have people in the church now they are standing like 8 years clean. You know, 5 and 6 years clean. These are people who use to go in and out of the revolving door. Because we give them a hope, it’s that mission element, and they talk about a Higher Power and all that as they go through the revolving door, but they need a connection on the outside, a spiritual connection and that’s what we try to be to them.” The choice between God and drugs was a very real one for the clergy and one that frames many of the worst crises in the community. One clergy person described a neighborhood drug dealer who was, he said, a kind of Robin Hood helping those in need. The man’s funeral was attended by a thousand people-“this church can squeeze in about 450 and it was almost a 1000 people here, old ladies, old men”-and brought home the moral ambiguity introduced by the drug trade. At one and the same time drug trafficking was bringing life, because it was a major employer, and death, because of the havoc of addiction. The minister went on to connecting the crisis of the community to the international financial markets: “Look at NAFTA. You sign an agreement to move capital into Mexico and Canada, you know, and you desert the inner city. Capital’s taking flight. Major corporations can hold the city hostage, all they got to do is say ‘We’re going to leave.’ They get all kinds of tax breaks... these brothers are intuitively picking up on that saying, ‘Man, the economic system is rigged. This is what got happen: it’s every man for himself, you know, I gon git mine.’ ”

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That clergyperson’s own stance, which was to condemn his local Robin Hood as a ‘dope dealer, liar and murderer,’ accentuated one side of what he knew to be a more nuanced situation. It was often apparent that African American clergy took rigid positions. For some, taking such a stance did not indicate lack of knowledge about an issue, but rather served as a way of reminding people of ‘God’s side’ of the argument. It is this effort, perhaps, that underlies the fervor of the following statement: “I cannot divorce myself from making people accountable for their actions or being responsible for the actions... I would rather see a billion bodies dead to have their souls saved and I have no qualms about saying something like that.” On one level this comment might simply be read as the view of a fundamentalist minister. But, viewed in context of the community’s struggle against the influence of a powerful drug culture, it can also be understood as one of many sides in a complex debate. The common expression, ‘Somebody’s got to say it, so it might as well be me,’ might be used to describe an important motivation for many of the comments we heard. In this, the clergy were exercising the role of religious rule enforcement that they hold in the community. 6.3.3 Homosexuality Attitudes towards homosexuality have presented a separate, and nearly insurmountable, barrier to response to AIDS. For the most part, the clergy agreed that homosexuality was a sin and an ‘abomination’. The clergy felt that it was their responsibility to preach against the sin of homosexuality. Such views were especially common among older ministers with a literal interpretation of the Bible. One explained, “I just give them the God said word and if they can take it, they can make it. They either gonna change or they leaving here. I’m not puttin’ them out. They’re not going stay with that, they’re not going stay with that but we have some homosexuals in our church, not openly homosexuals but you know. I’ve witnessed hard on that as I am they would be worse, but they try they to, men try to act like men and don’t let you see nothing.” Yet many, in using the phrase, ‘Love the sinner, hate the sin,’ attempted to distinguish between the individual and the act. One minister whose remarks were echoed by many in the study, explained: “It’s okay, okay. I say ain’t nothing private here. They come, they come, and when they come I don’t turn them away. We, y’know, I’ve had one of my ministers whose child admitted to being gay and I have had to counsel with that child, young boy, and try to direct, but yet and still leave the decision up to him because y’know, he still has

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some idea which, where he wishes to go. We counsel, we do pastoral work, ah, and he brought his friend in for counseling as well. But, as, they’re still gay. But I think they find that we have a love for them that says that they’re not an outcast, they they’re not somebody to walk on and trample on and that they are still God’s creatures. And as I said before, we love the person, but we hate the sin, ah that’s, we do that.” The limited acceptance described here was based on a very unequal relationship: the homosexuals gave their gifts to the church but were accepted only on the basis of maintaining a strict silence about their ‘lifestyle’. When the silence was broken, it could take an even more stigmatizing form. One story described a pastor who felt that the way to stop the AIDS epidemic was to shame the young gay men in his congregation. He called the ‘whole names’ of 125 young men and demanded that they come to the altar and confess their sins. In essence, the pastor blamed them for creating AIDS. The storyteller related, “They came to the altar and cried at the altar like they in fact were guilty. It shocked me, and it shocked me double so, that the deep self hate in victimized communities is so deep, until someone can blame you and you will accept it and not fight back.” The ambiguous relationship between homosexuals and their clergy was described by another in these words: “I think that an, the Black church has had it, a, what I call the du-, what I would call dubious kind of relationship with issues of homosexuality. They have been throughout time, you know, ah, homosexuals who have been present within the Black church, and but there’s never been open discussion about what that really means. Musicians, preachers, administrators, ah people in leadership, where the talk-you know folk know, that the person is, you know, a bit effeminate and most of them have been males. I mean I haven’t heard a lot of discussions about lesbians, you know, in the church. Certainly a lot of effeminate males within the church, and ah, there has been a kind of tolerance, but not acceptance which means, cause acceptance to me means that you recognize the individual for who the individual is.” The irony of the situation was not lost on those involved. As one minister noted, ‘If I put all the sinners out, we all got to get out, me, too’. Another pointed out that, at least for Baptists like himself, there was no doctrinal distinction among sins. Yet, clearly, homosexuality was much worse than other sins. This special status of homosexuality as more heinous than other sins created a heavy burden of stigma and shame for gays and lesbians in the church. One clergyperson pointed out that those men and women were denied the benefits of the faith community in which they had invested so much. Specifically, if they fell ill or needed counseling, they were afraid to ask for

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help from the clergy or the church. Indeed, the complex reality created by the clergy preaching against homosexuality in between hymns sung by gay men can best be described as an ‘open closet’: ‘open’ because the presence of homosexuals in the church is acknowledged by all, but a ‘closet’ because there exists no way to address this fact other than religious condemnation. The weight of stigma and shame created distance between homosexuals and their clergy. A poignant story of hiding was told by a clergyperson. He had counseled a bereaved family, and had come to feel quite close to them. He was shocked to learn, some months later, that a son of the family had died. They family would not tell him the cause, but he learned from others that the young man had died of AIDS. He pointed out: “What really hurt me was nobody in the family told me to go to the hospital to see him. They would rather wait until he died and then come to me and say, ‘Well, Reverend, you bury him’. Not thinking that not only was that bad for him, to not have pastoral care and not be able to talk about God and dealing with AIDS, but it’s bad for me ’cause I considered him a friend.” There was little question but that, for some, the ambiguity of the situation was a cause for unease. One clergyperson, himself a recovering addict, voiced the view that love of God could make homosexuals new, as he, himself, had been delivered from his addiction and made new. That view, clearly in line with the mainstream of fundamentalist thought, was tempered by another line of concern that had to do with not hurting anyone. “I acknowledge there’s a split here, but I don’t know how to split it. I would not be offended that someone would be angry at me for what I stand for if they listen to me preach about sin and homosexuality is included in that. But if they listen to me talk about life and helping people, and community and stuff like that, I think that they’ll get a different picture. But how to bring it all together, I don’t know, and maybe out of this research you might be able to help me, to tell you the truth, cause I don’t want to, like I said I’m the humanitarian, I don’t want to hurt anyone deliberately... this is too serious of the issue to be playing mental gymnastics with one another and playing games with people dying.” Finally, a small group expressed a clear break with the older tradition. One pointed to experiences in seminary that had opened up new ways of understanding the injunctions in the Bible. ‘In the laws of the Old Testament you have a very strong condemnation of [homosexuality] but you know the Old Testament law say a lot of things, condemn a lot of people, because those laws also say that if you disobey your parents you ought to be stoned. So I think the church needs to think more creatively about how we work with these sacred texts.’ That such critique of the doctrine was most likely to come from

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outside the core of its tradition is suggested by one of the women interviewed. She pointed out, “As a female, you can’t stand in a structure that is male dominated, and accept uncritically the theology and the ethics. You can’t do that because if you do that you wouldn’t be a leader in the structure, you would a church sister baking cakes.” 6.3.4 Personal transformation Stories of personal transformation stood out in the data set, partly because they were emotional episodes, and partly because they represented occasions during which the storyteller had moved to embrace a new position in AIDSrelated work. AIDS was linked, on the one hand, to the ‘two boo boo’s of the church-intravenous drug use and homosexuality’, and on the other hand to death penetrating the community’s religious home. One respondent noted that, out of a congregation of 500, he had buried 34 people with AIDS. Several remarkable stories emerged describing what it was like to have to face AIDS. One clergyperson described going to the hospital to visit a young man who was ill with AIDS. He went to the room assigned to the young man, but he was not there. On inquiring, he was told again that the young man was in the room. He then realized that the rail-thin, wizened person lying in the hospital bed was the vigorous, athletic young man he had known. This ‘traumatic experience’ opened his eyes to the effects of AIDS. ‘I never related AIDS with being so close my family, my church family. It registered to me I was dumb and ignorant’. He was overwhelmed by a sense of inadequacy, and in that state of guilt stumbled into the room of another parishioner, a woman dying of cancer. He said: “She was dying, she knew she was dying as much as the guy upstairs was dying and she had to remind me what I was about, you know. ‘This is what you were called on to do, Reverend,’ you know, ‘You have to do it.’ And she talked me, I said, ‘Well, I, you know, I’m supposed to come in and minister to you but there are times when we must minister to each other’.” The woman offered him a seat and continued to comfort him. He swore to himself that he would no longer be a ‘slouch’ but would minister with greater awareness and sensitivity to the effects of AIDS on his church family. In a second example of personal transformation, a clergyperson described attending a retreat organized by the Black Leadership Commission on AIDS. He went on the retreat thinking that AIDS was problem of gay, white men but learned differently. At the retreat, a Black woman with AIDS told her story of being rejected by her church because of her illness. He said: “Her husband had given her the AIDS virus. He had died and when the church learned that she had it they did not embrace her. They stood off from her, nobody would shake her hand anymore. She

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was isolated and my heart went out and when that woman finished talking I got up from my seat and for the first time in my life knowingly got up and embraced a person that I knew had AIDS. And I knew this today was something that I had to deal with from that day on. We came back and put together a package and we began to work on developing the scatter site housing for people with AIDS.” A third clergyperson described a transformation that altered previously unchallenged beliefs. He related the story of how this transformation occurred, beginning with the comment: “I was very young and I didn’t know a lot of the world and at that time homelessness was a big issue and AIDS was little itty bitty issue and I didn’t know absolutely anything about it. And I remember my pastor-I’ll never forget my pastor getting on the pulpit many Sundays and saying this new disease they have out there is killing people who are homosexuals and who are drug abusers and you need to change your way of life and this is why you have to come to the Lord and stuff like that. And I was sitting there and it never, y’know, to my mind, I said, yeah, he’s right. And it never crossed my mind to give it any further thought. Scripture said this wrong, that was it.” One day, when newly ordained as a hospital chaplain, he went on rounds with his colleagues. He noted that everyone was passing by one of the rooms. He decided that his calling to minister to the sick did not permit such selectivity and he advanced towards the door, pausing at the sill in recognition that inside was a person with AIDS. He related: “I opened the door to this man’s room and literally I went through a whole spiritual transformation. I knew without a doubt as soon as I opened up the door that this man had this thing called AIDS. But I talked to him and I introduced myself and I came to give him communion. He was so shocked that he didn’t know what to do. He wanted me to just sit down and talk to him about how I got to his room and stuff and after I gave him communion as I was giving it to him I felt such a feeling of overwhelming love for this human beoing, I mean literally, I understand love, I understand unconditional love.” In the aftermath of that transformation experience, the clergy person began to question the teaching of his denomination. Eventually, he decided to join a different religious group, giving up the status and position he had attained in his former denomination. In reflecting on the nature of the transformation, the clergyperson pinpointed his choice to confront prejudice: “I had to examine myself, and when I realized that I was prejudiced, that was the hardest thing for me to do y’know that Sunday [at the hospital] was to go past my prejudice and walk across that

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door stop. To this day I don’t know how to explain it. To this day, I don’t know how to explain my moral integrity, my spirituality, and my prejudice. All I know is that when I confronted my prejudice, it was such a itty bitty thing that it wasn’t even worth having, okay, because the man was sick. He wanted Holy Communion. He wanted prayer. He wanted us to release him so his spirit could be free, case closed. That was it. My prejudice could have said, ‘No, I can’t give communion because he has sinned so bad.’ But I was ordained to do just that for any person... and I had to do just that, regardless. And the prejudice I felt, I have to deal with that myself.” 6.3.5 Approaches to AIDS The complex struggle between death and sin led to an array of actions. One clergyperson said he’d never been aware of any AIDS-related issues in his congregation. Overall, one-third of the 51 interviewees were convinced that condemning homosexuality and drug use from the pulpit was the way to fight the spread of AIDS, what we might call the ”religion only” group. The rest had undertaken some form of AIDS activity into addition to preaching against sin. These included: providing housing for people with AIDS, offering hospital and home visits, and sponsoring or sheltering AIDS programs. One church had erected a sign that read, ‘This is an AIDS friendly congregation’. Response to AIDS had opened up new relationships and new ideas for clergy and their congregations. One clergyperson described: “I’ve seen a lot of growth... the majority of the congregation has, has, we’ve done some drastic things that really challenged people’s thinking about that and being more inclusive of, of who we are. We are our brother’s keeper, and those people are our people, and so we’ve opened the gate. And those little kids are now members of our church and usher and sing in the choir and are very much a part of us, and people are receiving a new understanding of who they are as a result of that.” Similarly, among the clergy, new alliances had been formed, which created new dialogue and new relationships. One pastor had worked for three years to form a local clerical alliance. Although progress had been slow, he felt that breaking the isolation of individual clergy was essential to progress on a broad social agenda. He concluded, ‘We’re at that point where dialogue is really happening’. The progress, however, was generally rated as slow, as in this assessment: “I mean there’s coalitions here and there by name anyway. I’ve not been everywhere, I don’t know everything, but I do not, I wouldn’t say that, I couldn’t give the church, as a general rule, much credit for

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its role in AIDS awareness, prevention or anything else, even to the fact that, us, various times, you’ll have symposiums or whatever, you know supported by the churches, whatever, but the people don’t come to it.” 6.3.6 Overall assessment of epidemic response The data presented here have significant implications for the theory of epidemic response. Public health workers assume that, in the face of clear and present danger, people will lay aside their differences. But the findings reported here underscore the extent to which ideology can become a ratelimiting factor for epidemic response, as we have argued above in the theory of Chapter 4, and with regard to the response to AIDS in Alameda. Ideological struggles are rarely considered within the purview of public health. It is often quite difficult for public health officials in the employ of a divided society to respond to threat. As we learn more about the political nature of the spread of disease, we must alter and extend the practice of public health to take account of these realities. Equally important, these findings suggest that what is operating is a cultural injunction: religious rule enforcement is more important than preventing epidemic spread. This strength of this imperative becomes obfuscated by the appearance of activity: symposia, ministries and the like. But the ‘enforce first’ rule is quite powerful, as Denfert (1996) suggested (see above). Action in the face of such a rule has to challenge the rule itself. It is apparent in the stories of transformation that the breaking through the appellation ‘sinner’ to reveal the hurting person is one powerful way to undo the enforcement rule. But others way also needed, such as direct protest directed at ‘The Black Church’ as a unit. It is, in any event, clear that ideologicial rigidity can markedly constrain the course of collective cognition in responding to a serious epidemic. Theory suggests, however, that for oppressed populations such ideology may constitute a socially evolved response to historic patterns of deprivation and injustice, i.e. the need to hold fast to deep core values defining collective self-image and self-worth in the context of the Manichean perspectives of a powerfully imposed Apartheid system (e.g. Fanon, 1966).

6.4 CASE STUDY 3: Women’s Equity in AIDS Resources Treatment of HIV disease is an essential part of a prevention agenda. As effective treatments became available in the mid-1990s, patients and their providers were heartened that lives could be prolonged and suffering reduced. In order to achieve this goal, patients, providers, advocates and government

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workers collaborated to improve the ‘system’ of care. By 1999, the disorganized, inadequately funded services described in Alameda County in 1989 had counterparts, albeit somewhat more mature, all across the United States. A major source of funding for HIV-related health care was the special federal program funded under the Ryan White Comprehensive AIDS Resources Emergency (CARE) Act. In 1999, as the US Health Services Resources Administration prepared for reauthorization of the Ryan White program, five research teams were asked to assess the effectiveness of the program. The Community Research Group was asked to examine Ryan White programs meeting the needs of minority women, a project CRG dubbed ‘Women’s Access to AIDS Resources’ or the WEAR study. It had been established by previous research (Shapiro et al, 1999) that minority women were at a disadvantage in obtaining medical care for their HIV infection. Therefore, the WEAR study focused on trying to understand: 1) how people understood this failure of access to care and 2) how people rated access to other kinds of services, such a mental health and substance abuse treatment. In order to learn about these issues, the CRG team utilized ‘situation analysis,’ a theoretically-derived form a qualitative research in which a complex interpersonal episode is analyzed via interviewing participants in key roles, observing interactions and obtaining information about the local setting and the larger embedding context (Green, at al, in press). Five cities were selected: New York, Miami, San Antonio, St. Louis, and Los Angeles. A diverse group of 120 people-including patients, providers, administrators and advocates-were interviewed and meetings were observed. This report of the case study follows closely on the CRG Report to HRSA (Fullilove, et al, 1999; see also Fullilove 2000) and benefits from Madoff’s further analysis (2002). 6.4.1 The central antithesis: life vs health Minority women with HIV/AIDS had limited financial or societal resources with which to meet their personal and family responsibilities. As one physician who specialized in AIDS care put it: “Our patients are operating with so many weights hanging off them, that [HIV] would be just one more. So in a very practical, dayto-day kind of thing, you can understand their approach. There is a certain hopelessness about this. A woman’s philosophy, and I think this cuts across all classes, is generally to do the thing that is in front of you. It is not necessarily a powerless position: it is powerful in that you know how to manage all of these things. That is a life approach that is very antithetical to preventive primary health care.” This antithesis between fulfilling one’s life duties and benefiting from health care was the fundamental issue raised with the CRG team during WEAR fieldwork. Interviewees agreed that this was the central problem, and had a range of experiences with this issue. One administrator emphasized,

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“Minority women in treatment have a lot going on besides their HIV status. Most women [at our clinic] are the primary care takers of their families and the primary income earners. They are undereducated and underemployed. They not only have to face disclosure issues, but also issues related to race and poverty. Daily, they have to stack all these issues on top of one another and sort out what they will address.” A psychiatrist offered a particularly vivid example of this antithesis: “If you are a woman who is infected and you have two kids, one is infected and one is not, but both are under the age of six, you have to go to provider A for your primary care for your HIV. You might have to go to provider B for your outpatient substance abuse treatment that is on the west side of the county. Your infected child has to come here to the clinic for infected kids. But your affected child needs to go to a different provider, maybe the health department clinic, for his immunizations. One of those kids needs psychological services and is being tested for developmental delay. A perfect example: The infected kid has a developmental delay secondary to viral invasion of the central nervous system. You as a woman have to orchestrate all of your service providers and all of the service providers for your kids and you’ve got to haul them around almost every day. Plus you’ve got to go to the store, plus you’re got to get your meds, plus you’ve got to go to the welfare department, plus, plus, plus... It’s mind-boggling.” Another provider hypothesized a very similar scenario, “As a black woman with children, and I am trying to do the best I can, but I have 3 children who are not in daycare. And if I am trying to keep the appointment for one, I have to take everybody. And I can’t take the 2 because they are affected and not infected, so I am not going to go. This is difficult and these issues need to be addressed.” This basic contradiction was exacerbated by illness. One woman living with HIV/AIDS said, ‘We need someone that we can call up and say can you just help me today? Not an ongoing thing, but something in place to help me today. I have energy today, but I do have those days’. Another struck a similar note when she said, ‘On good days you want to participate and do you own thing, but you have bad days or months and that contributes to your state of mind and then you get depressed and don’t go out of your house and you isolate’. A third was even more emphatic about how difficult it was to keep all the balls in the air. She said, ‘I am not real sick, but I am not well. Some days I don’t have good days. I will get pulled from Pasadena all over the universe and I am so damn tired of trying to get from Point A to Point B that I just say the hell with it’.

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The solution to the antithesis was generally held to be the provision of intermediary resources. As explained by one provider: “If you don’t attend and put a disproportionate amount of resources into that nexus of psychosocial and mental health needs, they can’t access care consistently, they can’t utilize health care appropriately, and they can’t adhere to the complex treatment regimens we force upon them.” What were these resources? A long list of items were mentioned by the 120 interviewees, including, but not limited to, these: * Supportive social environments in churches and neighborhoods * Early training in empowerment * Places to solidify and unite as women * New ways of discussing AIDS in communities * Ways to learn about changing risk environments * Improved cross-cultural training for providers * Care centers that were relaxed and brought many providers under one roof * Better local treatment * Better transportation to major HIV care centers * Easy access to housing * Easy access to childcare and other supportive services for children * Access to counseling for domestic violence * Enough basic education to follow instructions on managing HIV * Easy access to substance abuse treatment * Easy access to mental health care * Education in advocating for appropriate services. This list corresponds to what Reed, writing about women in substance abuse treatment (1989), called the ‘web of needs’. 6.4.2 Care in Combat While the web of needs was evident to all-and the utility of meeting the needs was not in dispute-the needs were not met. How was this understood? Obviously the driving problem was the intersection of race, class and gender that served to marginalize poor women of color. This societally-driven marginalization had created their excess risk for infection and then created their risk for early death from poorly managed disease. These structural forces were apparent in obvious ways that interviewees related with great irony. For example, in one city there was a $2 parking fee required at the place where impoverished clients had to go to register for low-cost HIV/AIDS care. In that same city, there was no substance abuse treatment for women except in the jail, therefore, women in urgent need of detoxification were urged to commit a minor crime.

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But the system of marginalization was fundamentally divisive and this laid a layer of internal bickering over the discussion of the issue. The divisions among the marginalized threaded through the every day of the AIDS world in ways that pitted groups against each other and successfully distracted them from the larger fight for adequate resources for all. AIDS was highly stigmatized in these cities and in the minority communities. One director said she was grateful to her staff for doing anything about AIDS, given how stigmatized it was in the community. Gay white men were often seen as acting inimically to the needs of minority women. A woman with HIV complained: “So much of your money [is] going to agencies that have programs that are basically for the gay white male, and the male population and you are giving money to them that have little programs within their programs that help women. But you are not giving money specifically for agencies that are women specific and the programs that are created by women, and run by women who are actually living with HIV. And who else better than those of us who are actually living with HIV can actually say what we need” Men of color were also a source of anger and frustration because of the collapse of communication about sexuality. In particular, at the time of the fieldwork for this project, the subject of men’s hidden bisexual behavior, particularly in prison, was frequently cited as a source of trouble. One woman noted: “So many of the African American supposedly heterosexual males [are] in jail, doing their thing, and they are writing this woman out here, [and] she is sending them the money. And when they get out, they never say, well you know I did this, we’d better use protection. They jump right into bed, the woman is so glad to have her man home, they go right into having unprotected sex. Women just don’t know. They know but they just don’t want to believe it. It is a whole completely different life [in jail]. [The men] are not honest and they do not tell these girlfriends and these wives.” Finally, the minority communities were often at odds with each other. In one city, discord over the implementation of a program to report names of sexual contacts of people with HIV infection, as is done in the management of other sexually transmitted diseases, was offered as an example of intercommunity conflict. A community leader said: “There has been a split between the African American women in their community and Latinas in our community. Part of that split has arisen over the issue of HIV surveillance and names reporting. What the African American women did is say basically that it is bisexual men, primarily, who have been in prison, who come out and infect

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their African American women. In the Latino community we felt that the issue of names reporting was tied directly to immigration issues for us, issues tied to domestic violence, tied to HIV and condom use among Latinos. And we were not going to allow anyone to split the men and women in our community. We decided to hang tough as a community. We have enough cultural issues, whether they be male or female, that we have to deal with in the community.” These splits-and others that we will not detail here-had a major impact on the Ryan White funding process, because local planning boards had responsibility for distributing funds. White gay men with well-honed political skills and a long track record of HIV/AIDS advocacy were at a major advantage in the planning process. Women were arriving late, ill-prepared, and unable to devote the necessary time and energy to the process. A women’s advocate put it this way: “Our funding bodies were started by gay white men and they funded service categories such as housing and food but not the other services we provide for women, and people do not want to give up their money.” Yet the deeper absurdity of the situation was evident in the fact that funding for AIDS services was at best a zero sum game. Although groups struggled to hold on to their money, in the Ryan White competition there were no permanent winners. As had been the case in Alameda County in the 1980s, funds rotated in lazy-susan fashion from organization to organization, playing off demands from competing communities and constituencies, but never satisfying anyone. 6.4.3 Out of harm’s way Under such conditions astute leaders could, at least temporarily, work the lazy-susan system to put together exemplary programs. Thus, in each of the five cities visited for the WEAR study, exemplary programs were identified. In general, these were services designed with women’s web of needs in mind. The most successful programs made women feel at home, were easy to negotiate, and had enough staff that women could get help when they needed it. These programs offered the necessary bridging services. As one administrator noted, “At [our clinic] the women are allowed to incorporate [all their issues] whereas if they were just going to their doctor’s office, they would not mention they don’t have a phone. The staff at [our clinic] wants to know about things that are going on in their clients’ daily lives and wants to assist them in day-to-day activities. There are a lot of things that keep infected women from taking care of themselves. [Our clinic] tries to put daily living up front while helping women take time our for themselves.”

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Being exceptional was no protection from the vagaries of the funding system. One of the best programs we visited was defunded just after the WEAR study ended. These shifts in funding posed serious problems for continuity of care, most often by taking away the supports that made access possible. A client at an exemplary clinic described losing funds for family gatherings that had been an important source of social support: “The women would get together, we would be in the kitchen all day long and the kids would come out. One Easter we had over 100 people. The whole families come. That used to be a monthly thing and we are not able to do that even on a quarterly basis now. And that is something that brought women out... and it would bring the family in. They would be exposed to what I was dealing with on a daily basis. That different types of women would be infected and that these different types of women had different types of family backgrounds. By bringing them in we were educating. It is a social function, but if you really get down to the nitty gritty of it, it was an educational process, educating people on how to deal with that and learn how other families were coping.” 6.4.4 Can demoralization be overcome? The gap between needs and services was large enough to produce frustration, irritation and demoralization. There was marked tension in the tone of the interviews which is reflected in quotes included in this report. But the sense that there was no way out was widespread. Interviewees knew that in a system that required political action, women were not able to act politically. Fighting a disease that required doctors’ visits, they were not able to get to care. One Ryan White administrator complained: “Women don’t take the initiative with what they don’t receive and they don’t see themselves as having the power to. It would be ideal for Hispanic women to go to their providers and ask for help because of their partners’ activities but this just doesn’t happen. This would be a form of betrayal in their minds. There is instead a victim mentality whereby they are numb to what is happening to them.” Conversely, a woman with HIV expressed a certain despair that she would ever get the care she needed: “I am a intravenous drug user, I have full blown AIDS, and also terminal cancer. The life changes I have experienced is being seen by so many doctors, being told by them what I must do, not given any explanations or options about the medications, and just trying to deal with feelings that these doctors don’t give a damn about me. I am presently seeing a psychiatrist to help me deal with these feelings

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I have of just wanting to give up. I know that I’m dying, but I hope I live long enough to see a change as far as sensitivity mainly among the professionals who are suppose to service my needs.” The frustration was expressed as annoyance that a growing crisis was being ignored by the larger society. One leader said, ‘I bet you it is true that in different cultural groups you could measure how long the denial period is to certain crises. Maybe we have just reached the limit on how long we deny that we have a very serious problem that we would rather not have’. Her optimism was not shared by all. Another leader said, ‘We’re sitting on top of a volcano and not really doing very much to meet the explosive need that we are sitting on top of’. A third leader weighed the consequences of denial versus action: “If you won’t own diabetes and you won’t own hypertension as a community plague, how do you think you’ll get to owning HIV? Outreach can change that but I think you have to persuade people politically. You have to persuade people that this is connected to the whole political posture of minority people in America. Recognizing it and holding on to it and saying this is ours and we can solve it is empowering. It is not a negative thing.” 6.4.5 Overall assessment of epidemic response Given an inadequately organized care system, women’s web of needs was unlikely to be adequately addressed. This was not ameliorated by the system of community governance, which simply served to pit underserved communities against one another, triggering Red Queen competition instead of larger scale cooperation and higher order institutional cognition. In that system, women were at a great disadvantage, which worsened their situation. Here resource limitation and competition, in concert with community disintegration, policy-driven limits causing service fragmentation, and very traditional, culturally-induced, inattentional blindness to the needs of poor women of color, combined synergistically to greatly undercut distributed institutional cognition affecting the provision of medical care and other essential services needed by this population.

6.5 Epidemic Response and Collective Consciousness As is shown in these three cases studies of response to the AIDS epidemic in diverse settings and over the decade 1989-1999, epidemic response is social in nature. At all three phases-recognition, resources and realignment-groups are required to agree on and implement actions. In a society operating on rules of exclusion and abandonment, illness among so-called outsiders triggers epidemic redlining, an aberrant and dysfunctional response to spreading disease that threatens the well-being of the body politic.

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The attendant vulnerabilities, in particular resource limitations and structurally imposed Darwinian competition for available resources, have contributed to inattentional blindness/group denial, breakdown of interworkspace communication (i.e. collaboration between different groups), and, ultimately, a systematic failure of engagement, possibly exacerbated by ideological constraints regarding ‘unacceptable’ risk behaviors. Instead of creating a larger, cooperating umbrella organization, the individual groups appear to have engaged in a Red Queen competition for resources under a declining zero-sum game, as more and more groups entered competition for a basically fixed resource base: ‘competitive renewals’ for AIDS treatment and control funding. Although the weaknesses were clearly recognized, ‘therapeutic’ interventions against this pattern seem to have largely been ineffective for the very same reasons. These case histories represent, paradoxically, an example of a pathological resilience-institutional inertia in which deep-seated structural factors prevented effective recognition of, and response to, a significant threat. Epidemic redlining has been identified in other epidemics, such as the response to the crack epidemic. In that case, the epidemic was entirely located in politically disenfranchised poor communities, a marked difference from the AIDS epidemic which was shaped by the fact that white men, albeit homosexual, were among those affected first. Their political skills created a better situation for AIDS control than for crack control, although they have not yet (as of 2007) won the battle against prejudice. Driven by structural exclusion, AIDS and other redlined epidemics will continue to ravage people all over the world, including those in the United States.

7 FINAL REMARKS

The ‘real world’ is always perceived through one’s cultural and developmental blinders, and assigned meaning from that context. Those who have endured the 20th century – the consequences of two World Wars, preparations for Global Thermonuclear War, the aftermath of a closely associated colonialism, and its rebirth as neocolonialism – have observed and participated in the grossest failures of regulation of collective consciousness. Those of us who dwell within the Belly of the Beast particularly experience the ways in which the madness of the collective is expressed in the lives of the individuals who constitute it. The regulation and stabilization of individual and collective consciousness, which, for humans, are particularly linked, is not well understood in current scientific terms. That regulation has, certainly, been the focus of religious and legal attention since the invention of agriculture allowed humans to live in large groups. While human biocultural evolution has produced relatively effective, if poorly understood, systems for stabilizing individual consciousness, constraining the collective variety seems far more difficult. This may, in part, be a consequence of its fundamental variability, as it is not subject to the biological limitations of the individual mind. Institutions are cultural artifacts, and we can, at least in theory, make them what we want them to be. The force of history, however, provides a Lamarckian constraint on our plans and interventions. The examples we have examined here provide a case history of the consequences of a spectrum of failure in collective consciousness. More explicitly, several powerful, intertwined, and mutually reinforcing policy-driven processes of social decay and structural violence now shape patterns of health, illness, and behavioral pathology in the United States: [1] Massive deindustrialization consequent on wholesale diversion of scientific and engineering resources from civilian enterprise into the excesses of the Cold War, and its continuation as the ‘war on terror’, has disrupted individual lives and entire communities, and markedly lessened the power of organized labor. A dispersal of accumulated social, economic, and political

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capital has followed, along with a correlated increase in the concentration of income within the top five percent of the population (e.g. Wallace and Wallace, 2004, fig. 4; Wallace et al., 1999, and references therein, particularly Ullmann 1985, 1988, etc. and Melman, 1971, 1983, 2001, etc.; Pappas, 1989). [2] Deurbanization amounting to the abandonment of numerous central cities, some of which came to resemble the bombed-out sections of Dresden and Hiroshima after World War II, has, in effect, turned many urban neighborhoods into virtual refugee camps, triggering a spectrum of health and behavior problems associated with long-term displacement and social isolation (e.g. Wallace and Wallace, 1997, 1998; Fullilove, 2004; Klinenberg, 2002). The effects have not been limited to minority populations. Destruction of neighborhoods by deliberate policy or by initiation of contagious urban decay has usually resulted in the demise of nearby majority communities overwhelmed by refugee displacement, creating a long-term and very general sense of ‘grieving for a lost home’ among diverse sectors of the population. [3] ‘American Apartheid’ (sensu Massey and Denton, 1993, and Charles, 2003), the lineal descendant of the US slave economy that persisted into the latter half of the 19th Century, has exacerbated many of the effects of deindustrialization and deurbanization. In addition to the ‘last hired, first fired’ syndrome of manufacturing job loss, a relentless subtheme to deurbanization has been the recurrent and systematic demolition and dispersal of AfricanAmerican urban neighborhoods since the end of World War II, through the many official and semiofficial programs described in the Introduction. An implicit cultural tenet of American Apartheid – true of many such systems (Fanon, 1966; Memmi, 1969) – is the assumption of a frozen, Manichean division of the world which effectively separates ‘them’ from ‘us’. The unvoiced question then becomes ‘which side are you on’, and the unvoiced response of the powerful and their political clientele – effectively a US Nomenklatura – becomes ‘whatever happens, we will remain insulated’. Attempts to transcend such culturally-induced tunnel vision have indeed been made within the public health literature: Figure 5.8 of Wilkinson’s (1996) classic analysis Unhealthy Societies displays age-standardized death rates as a function of social class for England/Wales and Sweden, societies with vastly different patterns of intra-national social equality. For all occupational levels, including the highest, England and Wales have greatly elevated death rates compared with Sweden. The inference from this, and similar work focused particularly on the US, is that Apartheid or ‘Class’ societies are inherently unhealthy: the health of both relatively more and relatively less powerful populations within such systems is constrained when compared with more egalitarian social structures. Figures 2 and 3 of Wallace and Wallace (2004) show Black vs. White diabetes and hypertension death rates in the US between 1979 and 1997. Both display marked rise, with Black rates significantly higher than white, but the square correlations of the increases over the period are, respectively, 0.99 and 0.85: strong coupling indeed.

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Much of our previous work, at the levels of the US national urban hierarchy and of the urban/suburban commuting field, has been aimed at understanding the large-scale longitudinal public health dynamics of American Apartheid in the context of deindustrialization, deurbanization, and serial forced displacement: how changes in patterns of contagious disease and violence are propagated across the system, engulfing and coupling both dominant and subordinate populations in the spread of pathology. A principal finding has been, in conflict with powerful American cultural assumptions, that the system is far indeed from static. Near ‘hollowing out’ cities in particular, the dynamics of spreading disease and disorder in the suburbs are strongly driven by those of the central city. In essence, the policy-driven serial displacement of urban minority areas over the last decades of the 20th Century, in concert with deindustrialization, has greatly accelerated long-studied mechanisms for the rapid national dispersal of contagious disease and behavioral pathology, from larger to smaller urban centers along the national travel network, and from central cities to outlying suburbs along paths defined by the daily journey-to-work (Wallace et al., 1997, 1999). This conclusion is consistent with a large body of past work on geographic diffusion (e.g. Abler, Adams and Gould, 1971; Gould and Wallace, 1994). A main, and not unexpected, finding of our analysis has been the strongly determining role played by the very largest urban area, the New York Metropolitan Region (NYMR), in driving the overall national diffusion of AIDS. Ever since the development of the railroad network in the latter part of the 19th century, contagious processes have spread nationally, as opposed to regionally, by hierarchical diffusion, from larger central places to smaller, along travel routes. We suggest in particular that the dysfunction of collective consciousness represented by policies leading to the continued forced displacement of African-American and other vulnerable populations now constitutes a serious national threat. Collective consciousness is, from the perspective of this work, far more complex than the individual variety, which is widely regarded as a major unsolved scientific problem. Collective consciousness involves, at the very least, a multiple-workspace, highly distributed, generalization of individual consciousness whose complexity dwarfs that of the human mind. If individual consciousness is the Great White Shark of science, then collective consciousness is the Great White Whale, the Moby Dick, which haunts the frail ships of our individual lives. Current scientific conundrums surrounding individual consciousness are largely a consequence of the ideological ‘dark night of behaviorism’ which suppressed research on the topic for the better part of a century. Problems of collective consciousness have, under different names, long been recognized and of central concern to religious and legal thought from ancient times, with only marginal success. Most often religion and law are made the servants of

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ruling elites, which exempt themselves from all strictures. One is reminded of the true story of a US draft resister serving time in a Federal prison who elicited gales of laughter from fellow inmates – including leaders of organized crime – when he explained that he was in jail for refusing to kill. The discontents of collective consciousness are not the discontents of ‘civilization’ as viewed through late 19th Century eyes. Collective consciousness has made humans and their predecessors the most efficient predators on the planet for half a million years. Collective consciousness in small groups, like the emergency room staff, or the cockpit crews studied by distributed cognition researchers, seems to have undergone something much like the biocultural evolution which stabilized individual minds, and their dysfunctions seem subject to simple corrective interventions. The larger entities into which we are all entrained – corporations, nations, and so on – seem caught in the very act of a massive evolutionary process whose outcome appears very much in doubt. Again, our theoretical development has been intertwined with a particular case history, the relations between public health and the American ‘peculiar institution’, the system of Apartheid which evolved from the slavery of earlier times. At this writing the evident socioeconomic trajectory for that system involves either the forced displacement of people of color from urban centers to a suburban periphery where they will be abandoned, as in New York City, or their further de-facto abandonment within devastated central cities, as in St. Louis and Detroit. For the United States, traditions of law and religion are failing to alter deeply embedded historical patterns of injustice and exploitation. The synergism of these patterns with the ecology of infectious and chronic disease has produced a relentlessly rising tied of pathology now enmeshing even powerful subgoups. Past recognition of such dynamics has sometimes led to significant improvements in living and working conditions which greatly reduced the burden of disease, proving that policy drives health in a modern state. Hopefully our work here will contribute to the eventual rediscovery of that fundamental reality. Beyond that hope, we have presented a formal model of distributed cognition, indeed what appears to be the first such, which can provide managerial and engineering insight across a variety of disciplines. Our mathematical characterization of failure modes involving both rate distortion and inattentional blindness could aid in the address of varous institutional pathologies. The larger model seems adaptable to designing strategies for the programming of massively parallel multi-core machines. Perhaps the most signal contribution, however, is recognition that stabilizing such machines may be as inherently hard as programming them. The theory has implications for understanding the evolution of animal consciousness: Our recognition that many different kinds of mathematical structures can describe both individual and collective consciousness suggests that biological and biocultural evolution have had a vast playing field. Current

7 FINAL REMARKS

161

taxa of conscious animals are the chance survivors of an evolutionary branching process which seems likely to have explored many exotic pathways. The once-burgeoning discipline of astrobiology might do well to adopt something of our approach. Evolution elsewhere in the universe may have produced forms of individual or collective consciousness far different from what has survived on Earth. Our adaptation of topological methods and structures to information theory should be of independent mathematical interest: Rate distortion manifolds, and their dynamical groupoids, may provide useful starting models for many currently intractable practical and theoretical problems. Hopefully, the readers of this book will be encouraged to begin their own journeys of exploration and discovery.

8 Mathematical appendix

8.1 Two basic theorems 8.1.1 The Shannon-McMillan Theorem According to the structure of the underlying language of which a message is a particular expression, some messages are more ‘meaningful’ than others, that is, are in accord with the grammar and syntax of the language. The Shannon-McMillan or Asymptotic Equipartition Theorem, describes how messages themselves are to be classified. Suppose a long sequence of symbols is chosen, using the output of the random variable X above, so that an output sequence of length n, with the form xn = (α0 , α1 , ..., αn−1 ) has joint and conditional probabilities

P (X0 = α0 , X1 = α1 , ..., Xn−1 = αn−1 ) P (Xn = αn |X0 = α0 , ..., Xn−1 = αn−1 ). (8.1)

Using these probabilities we may calculate the conditional uncertainty H(Xn |X0 , X1 , ..., Xn−1 ). The uncertainty of the information source, H[X], is defined as

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8 Mathematical appendix

H[X] ≡ lim H(Xn |X0 , X1 , ..., Xn−1 ). n→∞

(8.2)

In general H(Xn |X0 , X1 , ..., Xn−1 ) ≤ H(Xn ). Only if the random variables Xj are all stochastically independent does equality hold. If there is a maximum n such that, for all m > 0 H(Xn+m |X0 , ..., Xn+m−1 ) = H(Xn |X0 , ..., Xn−1 ), then the source is said to be of order n. It is easy to show that H(X0 , ...Xn ) . n→∞ n+1

H[X] = lim

In general the outputs of the Xj , j = 0, 1, ..., n are dependent. That is, the output of the communication process at step n depends on previous steps. Such serial correlation, in fact, is the very structure which enables most of what is done in this book. Here, however, the processes are all assumed stationary in time, that is, the probabilities and serial correlations do not change in time. A very broad class of such self-correlated, stationary, information sources, the so-called ergodic sources for which the long-run relative frequency of a sequence converges stochastically to the probability assigned to it, have a particularly interesting property: It is possible, in the limit of large n, to divide all sequences of outputs of an ergodic information source into two distinct sets, S1 and S2 , having, respectively, very high and very low probabilities of occurrence, with the source uncertainty providing the splitting criterion. In particular the Shannon-McMillan Theorem states that, for a (long) sequence having n (serially correlated) elements, the number of ‘meaningful’ sequences, N (n) – those belonging to set S1 – will satisfy the relation

log[N (n)] ≈ H[X]. n (8.3)

8.1 Two basic theorems

165

More formally,

log[N (n)] = H[X] n→∞ n lim

= lim H(Xn |X0 , ..., Xn−1 ) n→∞

= lim

n→∞

H(X0 , ..., Xn ) . n+1

(8.4)

Using the internal structures of the information source permits limiting attention only to high probability ‘meaningful’ sequences of symbols. 8.1.2 The Rate Distortion Theorem The Shannon-McMillan Theorem can be expressed as the ‘zero error limit’ of the Rate Distortion Theorem (Dembo and Zeitouni, 1998; Cover and Thomas, 1991), which defines a splitting criterion that identifies high probability pairs of sequences. We follow closely the treatment of Cover and Thomas (1991). The origin of the problem is the question of representing one information source by a simpler one in such a way that the least information is lost. For example we might have a continuous variate between 0 and 100, and wish to represent it in terms of a small set of integral segments in a way that minimizes the inevitable distortion that process creates. Typically, for example, an analog audio signal will be replaced by a ‘digital’ one. The problem is to do this in a way which least distorts the reconstructed audio waveform. Suppose the original stationary, ergodic information source Y with output from a particular alphabet generates sequences of the form y n = y1 , ..., yn . These are ‘digitized,’ in some sense, producing a chain of ‘digitized values’ bn = b1 , ..., bn , where the b-alphabet is much more restricted than the y-alphabet.

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8 Mathematical appendix

bn is, in turn, deterministically retranslated into a reproduction of the original signal y n . That is, each bm is mapped on to a unique n-length ysequence in the alphabet of the information source Y : bm → yˆn = yˆ1 , ..., yˆn . Note, however, that many y n sequences may be mapped onto the same retranslation sequence yˆn , so that information will, in general, be lost. The central problem is to explicitly minimize that loss. The retranslation process defines a new stationary, ergodic information source, Yˆ . The next step is to define a distortion measure, d(y, yˆ), which compares the original to the retranslated path. For example the Hamming distortion is

d(y, yˆ) = 1, y 6= yˆ d(y, yˆ) = 0, y = yˆ. (8.5)

For continuous variates the Squared error distortion is

d(y, yˆ) = (y − yˆ)2 . (8.6)

There are many possibilities. The distortion between paths y n and yˆn is defined as

n

d(y n , yˆn ) = (8.7)

1X d(yj , yˆj ). n j=1

8.1 Two basic theorems

167

Suppose that with each path y n and bn -path retranslation into the ylanguage and denoted y n , there are associated individual, joint, and conditional probability distributions y n ), p(y n |ˆ y n ). p(y n ), p(ˆ The average distortion is defined as

D=

X

p(y n )d(y n , yˆn ).

yn

(8.8)

It is possible, using the distributions given above, to define the information transmitted from the incoming Y to the outgoing Yˆ process in the usual manner, using the Shannon source uncertainty of the strings: I(Y, Yˆ ) ≡ H(Y ) − H(Y |Yˆ ) = H(Y ) + H(Yˆ ) − H(Y, Yˆ ). If there is no uncertainty in Y given the retranslation Yˆ , then no information is lost. In general, this will not be true. The information rate distortion function R(D) for a source Y with a distortion measure d(y, yˆ) is defined as

R(D) = p(y,ˆ y );

P (y,y) ˆ

min

I(Y, Yˆ ).

p(y)p(y|ˆ y )d(y,ˆ y )≤D

(8.9)

The minimization is over all conditional distributions p(y|ˆ y ) for which the joint distribution p(y, yˆ) = p(y)p(y|ˆ y ) satisfies the average distortion constraint (i.e. average distortion ≤ D). The Rate Distortion Theorem states that R(D) is the maximum achievable rate of information transmission which does not exceed the average distortion D. Cover and Thomas (1991) or Dembo and Zeitouni (1998) provide details. More to the point, however, is the following: Pairs of sequences (y n , yˆn ) can be defined as distortion typical ; that is, for a given average distortion D, defined in terms of a particular measure, pairs of sequences can be divided

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8 Mathematical appendix

into two sets, a high probability one containing a relatively small number of (matched) pairs with d(y n , yˆn ) ≤ D, and a low probability one containing most pairs. As n → ∞, the smaller set approaches unit probability, and, for those pairs,

y n |y n ) exp[−nI(Y, Yˆ )]. p(y n ) ≥ p(ˆ (8.10)

Thus, roughly speaking, I(Y, Yˆ ) embodies the splitting criterion between high and low probability pairs of paths. For the theory of interacting information sources, then, I(Y, Yˆ ) can play the role of H in the dynamic ‘Onsager’ treatment. The rate distortion function can actually be calculated in many cases by using a Lagrange multiplier method – see Section 13.7 of Cover and Thomas (1991).

8.2 The mean field approximation Wallace and Wallace (1998; 1999) have addressed how a language, in a large sense, ‘spoken’ on a network structure, responds as properties of the network change. The language might be speech, pattern recognition, or cognition. The network might be social, chemical, or neural. The properties of interest were the magnitude of ‘strong’ or ‘weak’ ties which, respectively, either disjointly partitioned the network or linked it across such partitioning. These would be analogous to local and mean-field couplings in physical systems. Fix the magnitude of strong ties – again, those which disjointly partition the underlying network into cognitive or other submodules – but vary the index of nondisjunctive weak ties, P , between components, taking K = 1/P . Assume the piecewise, adiabatically stationary ergodic information source (or sources) dual to cognitive process depends on three parameters, two explicit and one implicit. The explicit are K as above and, as a calculational device, an ‘external field strength’ analog J, which gives a ‘direction’ to the system. We will, in the limit, set J = 0. Note that many other approaches may well be possible, since renormalization techniques are more philosophy than prescription. The implicit parameter, r, is an inherent generalized ‘length’ characteristic of the phenomenon, on which J and K are defined. That is, J and K are written as functions of averages of the parameter r, which may be quite complex, having nothing at all to do with conventional ideas of space. For

8.2 The mean field approximation

169

example r may be defined by the degree of niche partitioning in ecosystems or separation in social structures. For a given generalized language of interest having a well defined (adiabatically, piecewise stationary) ergodic source uncertainty, H = H[K, J, X]. To summarize a long train of standard argument (Binney et al., 1986; Wilson, 1971), imposition of invariance of H under a renormalization transform in the implicit parameter r leads to expectation of both a critical point in K, written KC , reflecting a phase transition to or from collective behavior across the entire array, and of power laws for system behavior near KC . Addition of other parameters to the system results in a ‘critical line’ or surface. Let κ ≡ (KC − K)/KC and take χ as the ‘correlation length’ defining the average domain in r-space for which the information source is primarily dominated by ‘strong’ ties. The first step is to average across r-space in terms of ‘clumps’ of length R =< r >. Then H[J, K, X] → H[JR , KR , X]. Taking Wilson’s (1971) analysis as a starting point – not the only way to proceed – the ‘renormalization relations’ used here are:

H[KR , JR , X] = f (R)H[K, J, X]

χ(KR , JR ) =

χ(K, J) , R

(8.11)

with f (1) = 1 and J1 = J, K1 = K. The first equation significantly extends Wilson’s treatment. It states that ‘processing capacity,’ as indexed by the source uncertainty of the system, representing the ‘richness’ of the generalized language, grows monotonically as f (R), which must itself be a dimensionless function in R, since both H[KR , JR ] and H[K, J] are themselves dimensionless. Most simply, this requires replacing R by R/R0 , where R0 is the ‘characteristic length’ for the system over which renormalization procedures are reasonable, then setting R0 ≡ 1, hence measuring length in units of R0 . Wilson’s original analysis focused on free energy density. Under ‘clumping,’ densities must remain the same, so that if F [KR , JR ] is the free energy of the clumped system, and F [K, J] is the free energy density before clumping, then Wilson’s equation (4) is F [K, J] = R−3 F [KR , JR ], F [KR , JR ] = R3 F [K, J]. Remarkably, the renormalization equations are solvable for a broad class of functions f (R), or more precisely, f (R/R0 ), R0 ≡ 1.

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8 Mathematical appendix

The second equation just states that the correlation length simply scales as R. Again, the central feature of renormalization in this context is the assumption that, at criticality, the system looks the same at all scales, that is, it is invariant under renormalization at the critical point. All else flows from this. There is no unique renormalization procedure for information sources: other, very subtle, symmetry relations – not necessarily based on the elementary physical analog we use here – may well be possible. For example, McCauley (1993, p.168) describes the highly counterintuitive renormalizations needed to understand phase transition in simple ‘chaotic’ systems. This is important, since biological or social systems may well alter their renormalization properties – equivalent to tuning their phase transition dynamics – in response to external signals. We will make much use of a simple version of this possibility, termed ‘universality class tuning,’ below. To begin, following Wilson, take f (R) = Rd , d some real number d > 0, and restrict K to near the ‘critical value’ KC . If J → 0, a simple series expansion and some clever algebra (Wilson, 1971; Binney et al., 1986) gives

H = H0 κα χ=

χ0 , κs

(8.12)

where α, s are positive constants. More biologically relevant examples appear below. Further from the critical point, matters are more complicated, appearing to involve Generalized Onsager Relations, ‘dynamical groupoids’, and a kind of thermodynamics associated with a Legendre transform of H: S ≡ H − KdH/dK. Although this extension is quite important to describing behaviors away from criticality, the mathematical detail is cumbersome. An essential insight is that regardless of the particular renormalization properties, sudden critical point transition is possible in the opposite direction for this model. That is, going from a number of independent, isolated and fragmented systems operating individually and more or less at random, into a single large, interlocked, coherent structure, once the parameter K, the inverse strength of weak ties, falls below threshold, or, conversely, once the strength of weak ties parameter P = 1/K becomes large enough. Thus, increasing nondisjunctive weak ties between them can bind several different cognitive ‘language’ functions into a single, embedding hierarchical

8.2 The mean field approximation

171

metalanguage containing each as a linked subdialect, and do so in an inherently punctuated manner. This could be a dynamic process, creating a shifting, ever-changing pattern of linked cognitive submodules, according to the challenges or opportunities faced by the organism or institution. This heuristic insight can be made more exact using a rate distortion argument (or, more generally, using the Joint Asymptotic Equipartition Theorem) as follows (Wallace, 2002a, b): Suppose that two ergodic information sources Y and B begin to interact, to ‘talk’ to each other, to influence each other in some way so that it is possible, for example, to look at the output of B – strings b – and infer something about the behavior of Y from it – strings y. We suppose it possible to define a retranslation from the B-language into the Y-language through ˆ the translated information source, as a deterministic code book, and call Y mirrored by B. Define some distortion measure comparing paths y to paths yˆ, d(y, yˆ). Invoke the Rate Distortion Theorem’s mutual information I(Y, Yˆ ), which is the splitting criterion between high and low probability pairs of paths. Impose, now, a parametization by an inverse coupling strength K, and a renormalization representing the global structure of the system coupling. This may be much different from the renormalization behavior of the individual components. If K < KC , where KC is a critical point (or surface), the two information sources will be closely coupled enough to be characterized as condensed. In the absence of a distortion measure, the Joint Asymptotic Equipartition Theorem gives a similar result. Detailed coupling mechanisms will be sharply constrained through regularities of grammar and syntax imposed by limit theorems associated with phase transition. 8.2.1 Biological renormalization Next the mathematical detail concealed by the invocation of the asymptotic limit theorems emerges with a vengeance. Equation (8.11) states that the information source and the correlation length, the degree of coherence on the underlying network, scale under renormalization clustering in chunks of size R as H[KR , JR ]/f (R) = H[J, K] χ[KR , JR ]R = χ(K, J), with f (1) = 1, K1 = K, J1 = J, where we have slightly rearranged terms. Differentiating these two equations with respect to R, so that the right hand sides are zero, and solving for dKR /dR and dJR /dR gives, after some consolidation, expressions of the form

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8 Mathematical appendix

dKR /dR = u1 d log(f )/dR + u2 /R dJR /dR = v1 JR d log(f )/dR +

v2 JR . R

(8.13)

The ui , vi , i = 1, 2 are functions of KR , JR , but not explicitly of R itself. We expand these equations about the critical value KR = KC and about JR = 0, obtaining

dKR /dR = (KR − KC )yd log(f )/dR + (KR − KC )z/R dJR /dR = wJR d log(f )/dR + xJR /R. (8.14)

The terms y = du1 /dKR |KR =KC , z = du2 /dKR |KR =KC , w = v1 (KC , 0), x = v2 (KC , 0) are constants. Solving the first of these equations gives

KR = KC + (K − KC )Rz f (R)y , (8.15)

again remembering that K1 = K, J1 = J, f (1) = 1. Wilson’s essential trick is to iterate on this relation, which is supposed to converge rapidly near the critical point (Binney et al., 1986), assuming that for KR near KC , we have

8.2 The mean field approximation

173

KC /2 ≈ KC + (K − KC )Rz f (R)y . (8.16)

We iterate in two steps, first solving this for f (R) in terms of known values, and then solving for R, finding a value RC that we then substitute into the first of equations (8.11) to obtain an expression for H[K, 0] in terms of known functions and parameter values. The first step gives the general result

f (RC ) ≈

[KC /(KC − K)]1/y z/y

21/y RC

.

(8.17)

Solving this for RC and substituting into the first expression of equation (8.11) gives, as a first iteration of a far more general procedure (Shirkov and Kovalev, 2001), the result

H[K, 0] ≈

H[KC /2, 0] H0 = f (RC ) f (RC )

χ(K, 0) ≈ χ(KC /2, 0)RC = χ0 RC , (8.18)

which are the essential relationships. Note that a power law of the form f (R) = Rm , m = 3, which is the direct physical analog, may not be biologically reasonable, since it says that ‘language richness’ can grow very rapidly as a function of increased network size. Such rapid growth is simply not observed. Taking the biologically realistic example of non-integral ‘fractal’ exponential growth,

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8 Mathematical appendix

f (R) = Rδ , (8.19)

where δ > 0 is a real number which may be quite small, equation (8.17) can be solved for RC , obtaining

RC =

[KC /(KC − K)][1/(δy+z)] 21/(δy+z)

(8.20)

for K near KC . Note that, for a given value of y, one might characterize the relation α ≡ δy + z = constant as a ‘tunable universality class relation’ in the sense of Albert and Barabasi (2002). Substituting this value for RC back into equation (8.17) gives a complex expression for H, having three parameters: δ, y, z. A more biologically interesting choice for f (R) is a logarithmic curve that ‘tops out’, for example

f (R) = m log(R) + 1. (8.21)

Again f (1) = 1. Using Mathematica 4.2 or above to solve equation (8.17) for RC gives

RC = [ (8.22)

where

Q ]y/z , LambertW [Q exp(z/my)]

8.2 The mean field approximation

175

Q ≡ (z/my)2−1/y [KC /(KC − K)]1/y . The transcendental function LambertW(x) is defined by the relation LambertW (x) exp(LambertW (x)) = x. It arises in the theory of random networks and in renormalization strategies for quantum field theories. An asymptotic relation for f (R) would be of particular biological interest, implying that ‘language richness’ increases to a limiting value with population growth. Such a pattern is broadly consistent with calculations of the degree of allelic heterozygosity as a function of population size under a balance between genetic drift and neutral mutation (Hartl and Clark, 1997; Ridley, 1996). Taking

f (R) = exp[m(R − 1)/R] (8.23)

gives a system which begins at 1 when R = 1, and approaches the asymptotic limit exp(m) as R → ∞. Mathematica 4.2 finds

RC =

my/z , LambertW [A]

(8.24)

where A ≡ (my/z) exp(my/z)[21/y [KC /(KC − K)]−1/y ]y/z . These developments indicate the possibility of taking the theory significantly beyond arguments by abduction from simple physical models, although the notorious difficulty of implementing information theory existence arguments will undoubtedly persist.

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8 Mathematical appendix

8.2.2 Universality class distribution Physical systems undergoing phase transition usually have relatively pure renormalization properties, with quite different systems clumped into the same ‘universality class,’ having fixed exponents at transition (Binney et al., 1986). Biological and social phenomena may be far more complicated: If the system of interest is a mix of subgroups with different values of some significant renormalization parameter m in the expression for f (R, m), according to a distribution ρ(m), then the first expression in equation (8.11) should generalize, at least to first order, as

H[KR , JR ] =< f (R, m) > H[K, J] Z ≡ H[K, J]

f (R, m)ρ(m)dm.

(8.25)

If f (R) = 1 + m log(R) then, given any distribution for m,

< f (R) >= 1+ < m > log(R) (8.26)

where < m > is simply the mean of m over that distribution. Other forms of f (R) having more complicated dependencies on the distributed parameter or parameters, like the power law Rδ , do not produce such a simple result. Taking ρ(δ) as a normal distribution, for example, gives

< Rδ >= R<δ> exp[(1/2)(log(Rσ ))2 ], (8.27)

8.2 The mean field approximation

177

where σ 2 is the distribution variance. The renormalization properties of this function can be determined from equation (8.17), and the calculation is left to the reader as an exercise, best done in Mathematica 4.2 or above. Thus the information dynamic phase transition properties of mixed systems will not in general be simply related to those of a single subcomponent, a matter of possible empirical importance: If sets of relevant parameters defining renormalization universality classes are indeed distributed, experiments observing pure phase changes may be very difficult. Tuning among different possible renormalization strategies in response to external signals would result in even greater ambiguity in recognizing and classifying information dynamic phase transitions. Important aspects of mechanism may be reflected in the combination of renormalization properties and the details of their distribution across subsystems. In sum, real biological, social, or interacting biopsychosocial systems are likely to have very rich patterns of phase transition which may not display the simplistic, indeed, literally elemental, purity familiar to physicists. Overall mechanisms will, however, still remain significantly constrained by the theory, in the general sense of probability limit theorems. 8.2.3 Punctuated universality class tuning The next step is to iterate the general argument onto the process of phase transition itself, producing a tunable workspace subject to inherent punctuated detection of external events. As described above, an essential character of physical systems subject to phase transition is that they belong to particular ‘universality classes’. Again, this means that the exponents of power laws describing behavior at phase transition will be the same for large groups of markedly different systems, with ‘natural’ aggregations representing fundamental class properties (Binney et al., 1986). It appears that biological or social systems undergoing phase transition analogs need not be constrained to such classes, and that ‘universality class tuning’, meaning the strategic alteration of parameters characterizing the renormalization properties of punctuation, might well be possible. Here we focus on the tuning of parameters within a single, given, renormalization relation. Clearly, however, wholesale shifts of renormalization properties must ultimately be considered as well, a matter for future work. Universality class tuning has been observed in models of ‘real world’ networks. As Albert and Barabasi (2002) put it, The inseparability of the topology and dynamics of evolving networks is shown by the fact that [the exponents defining universality class] are related by [a] scaling relation..., underlying the fact that a network’s assembly uniquely determines its topology. However, in no case are these exponents unique. They can be tuned continuously...

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8 Mathematical appendix

Suppose that a structured external environment, itself an appropriately regular information source Y, ‘engages’ a modifiable cognitive system. The environment begins to write an image of itself on the cognitive system in a distorted manner permitting definition of a mutual information I[K] splitting criterion according to the Rate Distortion or Joint Asymptotic Equipartition Theorems. K is an inverse coupling parameter between system and environment. At punctuation – near some critical point KC – the systems begin to interact very strongly indeed, and, near KC , using the simple physical model of equation (8.12), I[K] ≈ I0 [

KC − K α ] . KC

For a physical system α is fixed, determined by the underlying ‘universality class.’ Here we will allow α to vary, and, in the section below, to itself respond explicitly to signals. Normalizing KC and I0 to 1,

I[K] ≈ (1 − K)α . (8.28)

The horizontal line I[K] = 1 corresponds to α = 0, while α = 1 gives a declining straight line with unit slope which passes through 0 at K = 1. Consideration shows there are progressively sharper transitions between the necessary zero value at K = 1 and the values defined by this relation for 0 < K, α < 1. The rapidly rising slope of transition with declining α is of considerable significance: The instability associated with the splitting criterion I[K] is defined by

Q[K] ≡ −KdI[K]/dK = αK(1 − K)α−1 , (8.29)

and is singular at K = KC = 1 for 0 < α < 1. Following earlier work (Wallace and Wallace, 1998, 1999; Wallace and Fullilove, 1999; Wallace, 2002a), we interpret this to mean that values of 0 < α  1 are highly unlikely for real systems, since Q[K], in this model, represents a kind of barrier for ‘social’

8.2 The mean field approximation

179

information systems, in particular interacting cognitive modules, a matter explored further below. On the other hand, smaller values of α mean that the system is far more efficient at responding to the adaptive demands imposed by the embedding structured environment, since the mutual information which tracks the matching of internal response to external demands, I[K], rises more and more quickly toward the maximum for smaller and smaller α as the inverse coupling parameter K declines below KC = 1. That is, systems able to attain smaller α are more responsive to external signals than those characterized by larger values, in this model, but smaller values will be harder to reach, probably only at some considerable physiological or opportunity cost. Focused conscious action takes resources, of one form or another. The more biologically realistic renormalization strategies given above produce sets of several parameters defining the universality class, whose tuning gives behavior much like that of α in this simple example. Formal iteration of the phase transition argument on this calculation gives tunable consciousness, focusing on paths of universality class parameters. Suppose the renormalization properties of a language-on-a network system at some ‘time’ k are characterized by a set of (possibly coarse-grained) k . Fixed parameter values define a particular uniparameters Ak ≡ α1k , ..., αm versality class for the renormalization. We suppose that, over a sequence of ‘times,’ the universality class properties can be characterized by a path xn = A0 , A1 , ..., An−1 having significant serial correlations which, in fact, permit definition of an adiabatically piecewise stationary ergodic information source associated with the paths xn . We call that source X. Suppose also, in the now-usual manner, that the set of external (or internal, systemic) signals impinging on consciousness is also highly structured and forms another information source Y which interacts not only with the system of interest globally, but specifically with its universality class properties as characterized by X. Y is necessarily associated with a set of paths yn . Pair the two sets of paths into a joint path, zn ≡ (xn , yy ) and invoke an inverse coupling parameter, K, between the information sources and their paths. This leads, by the arguments above, to phase transition punctuation of I[K], the mutual information between X and Y, under either the Joint Asymptotic Equipartition Theorem or under limitation by a distortion measure, through the Rate Distortion Theorem. The essential point is that I[K] is a splitting criterion under these theorems, and thus partakes of the homology with free energy density which we have invoked above. Activation of universality class tuning, the mean field model’s version of attentional focusing, then becomes itself a punctuated event in response to increasing linkage between the organism and an external structured signal or some particular system of internal events. This iterated argument exactly parallels the extension of the General Linear Model to the Hierarchical Linear Model in regression theory (Byrk and Raudenbusch, 2001).

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8 Mathematical appendix

Another path to the fluctuating dynamic threshold might be through a second order iteration similar to that just above, but focused on the parameters defining the universality class distributions given above.

8.3 Toward a stochastic differential geometry of cognition Explicit parametization of M of Section 3.7, for example by X and Y in figure 3.1, introduces standard – and quite considerable – notational complications (e.g. Burago et al., 2001; Auslander, 1967). Letting the parameters be a vector K having components Kj , j = 1..m, we can write M in terms of a ‘metric tensor’ gi,j (K) as

Z M(A0 , A) =

ˆ X m A

[

A

i,j

gi,j (K)

dKi dKj 1/2 ] dt dt dt

(8.30)

where the integral is taken over some parametized curve from the reference state A0 to some other state A. Then equation (8.30) becomes

[

X

gi,j (K)

i,j

dKi dKj 1/2 dS ] . =L dt dt dM

(8.31)

This states that the ‘velocity’ dK/dt has a magnitude determined by the local gradient in S at A0 , since the summation term on the left is the square root of an inner product of a vector with itself. The first condition of equation (3.12), i.e. setting dS/dM|A0 = 0, gives

X i,j

gi,j

dKi dKj = 0. dt dt

8.3 Toward a stochastic differential geometry of cognition

181

(8.32)

Thus the initial velocity is again zero, in the coordinates K. To go much beyond this obvious tautology we must, ultimately, generate a parametized version of equation (8.30) and its dynamics, but expressing the metric tensor, and hence redefining the geometry, in terms of derivatives of S by the Ki . The result requires some development. Write now, for parameters Ki – analogous to X and Y in figure 3.1 – the Onsager relation

dKi /dt = L∂S/∂Ki , (8.33)

where the Ki have been appropriately scaled. Again place the system in a reference configuration A0 , having a vector of parameters K0 , so that

dK/dt|K0 = L∇S|K0 ≡ 0. (8.34)

Deviations from this state, δK ≡ K − K0 , to first order, obey the relation

dδKi /dt ≈ L

m X ( j=1

∂2S |K )δKj . ∂Ki ∂Kj 0

(8.35)

In matrix form, writing Ui,j = Uj,i for the partials in S, this becomes

182

8 Mathematical appendix

dδK/dt = LUδK. (8.36)

Assume appropriate regularity conditions on S and U, and expand the deviations vector δK in terms of the m eigenvectors ei of the symmetric Pm matrix U, having Uei = λi ei , so that δK = i=1 δai ei . Equation (8.36) then has the solution

δK(t) =

m X

δai exp(Lλi t)ei .

i=1

(8.37)

If all λi ≤ 0, then the system is bounded quasistable, and a physiological forcing mechanism will be required to change status. Next let dδKi /dt ≡ δVi . In first order the magnitude of the vector δV is

|δV|2 =

L2 X X [ Ui,k Uk,j ]δKi δKj 2 i,j k

(8.38)

Redefining

gi,j ≡

L2 X Ui,k Uk,j 2 k

(8.39)

gives, after some notational shift, the symmetric Riemannian metric

8.3 Toward a stochastic differential geometry of cognition

dV 2 =

X

183

gi,j (Ki , Kj )dKi dKj ,

i,j

(8.40)

so that the metric, and hence the geometry, is now defined in terms of derivatives of S by the Kj . The ‘distance’ between points a and b along some dynamic path in this geometry is, again,

Z

B

s(A, B) =

[ A

X

gi,j

i,j

dKi dKj 1/2 ] dt. dt dt

(8.41)

Application of the calculus of variations to minimize this expression produces a geodesic equation for the slowest dynamical path, and hence the most physiologically stable configuration. This has the traditional component-bycomponent form

d2 Ki /dt2 +

X j,m

i Γj,m

dKj dKm = 0, dt dt

(8.42)

i are the famous Christoffel symbols involving sums and where the Γj,k products of gi,j and ∂gi,j /∂Km (e.g. Auslander, 1967; Burago et al., 2001; Wald, 1984, etc.). The analog to equation (8.31) in this new geometry, defining a quasi-stable state, is that there exists a positive number K  R, where R is the maximal possible number characteristic of the entire system, such that, for all geodesics K(t) which solve equation (8.42),

184

8 Mathematical appendix

|K(t)| ≤ K. (8.43)

at all times t. Under such circumstances geodesics sufficiently near the reference state A0 are all bound, and external physiological forcing must be imposed to cause a transition to a different condition. This result is analogous to the ‘Black Hole’ solution in General Relativity: recall that, within a critical radius near a sufficiently massive point source – the ‘event horizon’ – all geodesics, representing possible paths of light, are gravitationally bound without, however, the possible grace of a physiological deus ex machina. Note that the repulsive version of equation (8.43) might well be characterized as an unattainable White Hole. Extending these considerations to the stochastic differential equation formulation of equation 3.13 leads quickly and decidedly into realms of stochastic differential geometry much like those of Emery (1989).

9 References

Abler R., J. Adams, and P. Gould, 1971, Spatial Organization: The Geographer’s View of the World, Prentice-Hall, Englewood, NJ. Adams F., 2003, The informational turn in philosophy, Minds and Machines, 13:471-501. Ademi C., C. Ofria, and T. Collier, 2000, Evolution of biological complexity, Proceedings of the National Academy of Sciences, 97:4463-4468. Aiello W., F. Chung, and L. Lu, 2000, A random graph model for massive graphs, in Proceedings of the 32nd Annual ACM Symposium on the Theory of Computing. Albert R., and A. Barabasi, 2002, Statistical mechanics of complex networks, Reviews of Modern Physics, 74:47-97. Allin M., and R. Murray, 2002, Schizophrenia: a neurodevelopmental or neurodegenerative disorder?, Current Opinion in Psychiatry, 15:9-15. Arnold V., 1989, Mathematical Methods of Classical Mechanics, SpringerVerlag, New York. Asanovic K, R. Bokik, B. Catanzaro, J. Gebis, P. Husbands, K. Keutzer, D. Patterson, W. Plishker, J. Shalf, S. Williams, and K. Yellick, 2006, The landscape of parallel computing research: a view from Berkeley, http://www.eecs.berkeley.edu/Pubs/TechRpts/2006/EECS-2006-183.pdf. Ash R., 1990, Information Theory, Dover Publications, New York. Atlan H., and I. Cohen, 1998, Immune information, self-organization and meaning, International Immunology, 10:711-717. Atmanspacher H., 2006, Review of Consciousness: A Mathematical Treatment of the Global Neuronal Workspace Model, Acti Biorheoretica, 54:157-160. Auslander L., 1967, Differential Geometry, Harper and Row, New York. Baars B., 1988, A Cognitive Theory of Consciousness, Cambridge University Press, New York. Baars B., and S. Franklin, 2003, How conscious experience and working memory interact, Trends in Cognitive Science, doi:10.1016/S1364-6613(03)00056-1.

186

9 References

Baars, B., 2005, Global workspace theory of consciousness: toward a cognitive neuroscience of human experience, Progress in Brain Research, 150:45-53. Bak A., R. Brown, G. Minian and T. Porter, 2006, Global actions, groupoid atlases and related topics, Journal of Homotopy and Related Structures, 1:154. Available from ArXiv depository. Bailey, N., 1975, The Mathematical Theory of Infectious Diseases and its Applications, Hafner Press, New York. Bandelow B., C. Spath, G. Tichauer, A. Broocks, G. Hajak, and E. Ruther, 2002, Early traumatic life events, parental attitudes, family history, and birth risk factors in patients with panic disorder, Comprehensive Psychiatry, 43:269278. Barker D., 2002, Fetal programming of coronary heart disease, Trends in Endocrinology and Metabolism, 13:364-372. Barker D., T. Forsen, A Uutela, C. Osmond, and J. Erikson, 2002, Size at birth and resilience to effects of poor living conditions in adult life: longitudinal study, British Medical Journal, 323:1261-1262. Barrett L., and P. Henzi, 2005, The social nature of primate cognition, Proceedings of the Royal Society, B, 272:1865-1875. Bennett C., 1988, Logical depth and physical complexity, in The Universal Turing Machine: A Half-Century Survey, R. Herkin, ed., pp. 227-257. Oxford University Press. Bennett M., and P. Hacker, 2003, Philosophical Foundations of Neuroscience, Blackwell Publishing. Bezemer D., S. Jurriaans, M. Prins, L. van der Hoek, J. Prins, F. de Wolr, B. Berkhout, R. Countinho, and N. Back, 2004, Declining trends in transmission of drug resistand HIV-1 in Amsterdam, AIDS, 18:1571-1577. Billingsly P., 1968, Convergence of Probability Measures, Wilen and Sons, New York. Binney J., N. Dowrick, A. Fisher, and M. Newman, 1986, The theory of critical phenomena, Clarendon Press, Oxford. Bjorntorp P., 2001, Do stress reactions cause abdominal obesity and comorbidities? Obesity Reviews, 2:73-86. Branke J., M. Mnif, C. Muller-Schloer, H. Prothmann, U. Richter, F. Rochner, and H. Schmeck, 2006, Organic computing - addressing complexity by controlled self-organization. In Tiziana M., A Philippou and B. Steffen, Proceedings of ISoLA2006, 200-206, Paphos, Cyprus, November, 2006. Brown R., 1987, From groups to groupoids, Bulletin of the London Mathematical Society, 19:113-134. Burago D., Y. Burago, and S. Ivanov, 2001, A Course in Metric Geometry, American Mathematical Society, Providence, RI. Burns J., D. Job, M. Bastin, H. Whalley, T. Macgillivary, E. Johnstone, and S. Lawrie, 2003, Structural disconnectivity in schizophrenia: a diffusion tensor magnetic resonance imaging study, British Journal of Psychiatry, 182:439-443.

9 References

187

Burns T., and E. Engdahl, 2003, Toward a social theory of human consciousness, Karl Jaspers Forum, http://www.kjf.ca/N-61-BUR.htm. Burns T., and E. Engdahl, 1998a, Collective consciousness and its sociocultural foundations, Journal of Consciousness Studies, 5:67-85. Burns T., and E. Engdahl, 1998b, Individual selves, self-awareness and reflectivity, Journal of Consciousness Studies, 5:166-184. Byrk A., and S. Raudenbusch, 2001, Hierarchical Linear Models: Applications and Data Analysis Methods, Sage Publications, New York. Catts V., and S. Catts, (2000), Apoptosis and schizophrenia: is the tumor suppressor gene p53 a candidate susceptibility gene? Schizophrenia Research, 41:405-415. Charles C., 2003, The dynamics of racial segregation, Annual Reviews of Sociology, 29:167-207. Christie C., M. Marx, C. Marchant, and S. Reising, 1994, The 1993 epidemic of pertussis in Cincinnati: resurgence of disease in a highly immunized population of children, New England Journal of Medicine, 331:16-21. Clavel F., and A. Hance, 2004, HIV drug resistance, New England Journal of Medicine, 350:1023-1035. Cohen I., 1992, The cognitive principle challenges clonal selection, Immunology Today, 13:441-444. Cohen I., 2000, Tending Adam’s Garden: Evolving the Cognitive Immune Self, Academic Press, New York. Cohen M., B. Dembling, and J. Schorling, (2002), The association between schizophrenia and cancer: a population-based mortality study, Schizophrenia Research, 57:139-146. Cohen T., B. Blatter, C. Almeida, E. Shortliffe, and V. Patel, 2006, A cognitive blueprint of collaboration in context: Distributed cognition in the psychiatric emergency department, Artificial Intelligence in Medicine, 37:7383. Collins J., R. David, A. Handler, S. Wall, and S. Andes, (2004), Very low birthweight in African American infants: the role of maternal exposure to interpersonal racial discrimination, American Journal of Public Health, 94:21322138. Cooke D., 1996, Psychopathic personality in different cultures: what do we know?, Journal of Personality Disorders, 10:23-40. Coplan J., 2005, Personal communication. Coplan J., M. Altemus, S. Matthew, E. Smith, B. Scharf. P. Coplan, J. Kral, J. Gorman, M. Owens, C. Nemeroff, and L. Rosenblum, 2005, Synchronized maternal-infant elevations of primate CSF CRF concentrations in response to variable foraging demand, CNS Spectrums, 10:530-536. Connes A., 1994, Noncommutative Geometry, Academic Press, San Diego. Corless R., G. Gonnet, D. Hare, D. Jeffrey, and D. Knuth, 1996, On the Lambert W function, Advances in Computational Mathematics, 4:329-359. Courchesne E., and K. Pierce, 2005, Current Opinion in Neurobiology, 15:225-230.

188

9 References

Cover T., and J. Thomas, 1991, Elements of Information Theory, John Wiley and Sons, New York. Cramer H., 1939, Sur un nouveau theoreme-limite de la theorie des probabilities, in Actualaties Scientifiques et Industrielles, No. 736 in Colloque consacre a la theorie des probabilities, pp. 5-23, Hermann, Paris. Crick J., and C. Koch, 2003, A framework for consciousness, Nature Neuroscience, 6:119-126. Damasio, A., (1989), Time-locked multiregional retroactivation: a systemslevel proposal for the neural substrates of recall and recognition, Cognition, 33:25-62. Damasio A., 1998, Emotion in the perspective of an integrated nervous system, Brain Research Reviews, 26:83-86. Darden, J., 1973,Afro-Americans in Pittsburgh: The Residential Segregation of a People, Heath and Company, Lexington, MA. Deco G., and B. Schurmann, 1998, Stochastic resonance in the mutual information between input and output spike trains of noisy central neurons, Physica D, 117:276-282. Defert D., 1996, AIDS as a challenge to religion, in Mann J., and D. Tarantola (eds.), AIDS in the World II: Global Dimensions, Social Roots and Responses, Oxford Uinversity Press, New York, pp. 447-452. Dehaene S., and L. Naccache, 2001, Towards a cognitive neuroscience of consciousness: basic evidence and a workspace framework, Cognition, 79:1-37. Dehaene S., and J. Changeux, 2005, Ongoing spontaneous activity controls access to consciousness: a neuronal model for inattentional blindness, PLOS Biology, 3:e141. Dembo A., and O. Zeitouni, 1998, Large Deviations: Techniques and Applications, Second edition, Springer, New York. Dobson I., 2007, Where is the edge for cascading failure?: challenges and opportunities for quantifying blackout risk. IEEE Power Engineering Society General Meeting. Tampa, Fl., USA, June, 2007. Available from [email protected]. Dretske F., 1981, Knowledge and the Flow of Information, MIT Press, Cambridge, MA. Dretske F., 1988, Explaining Behavior, MIT Press, Cambridge, MA. Dretske, F., 1993, Mental events as structuring causes of behavior, in Mental Causation (ed. by A. Mele and J. Heil), pp. 121-136, Oxford University Press. Dretske F., 1994, The explanatory role of information, Philosophical Transactions of the Royal Society A, 349:59-70. Dumas L., 1987, The Over-Burdened Economy, UCLA Press, Los Angeles. Durham W., 1991, Coevolution: Genes, Culture and Human Diversity, Stanford University Press, Stanford, CA. DSMIV, 1994, Diagnostic and Statistical Manual, fourth edition, American Psychiatric Association, Washington, DC.

9 References

189

Dupont A., O. Jensen, E. Stromgren, and A. Jablonsky, (1986), Incidence of cancer in patients diagnosed as schizophrenic in Denmark, in: ten Horn, G., R. Giel, W. Gulbinat, and W. Henderson (eds.), Psychiatric Case Registers in Public Health, Elsevier, Amsterdam, 229-239. Durham W., 1991, Coevolution: Genes, Culture, and Human Diversity, Stanford University Press, Palo Alto, CA. Duryea P., 1978, Press release from the office of the New York State Assembly Republican Leader. Dykman M., D. Luchinsky, P. McClintock and V. Smelyansky, 1996, Corrals and critical behavior of the distribution of fluctuational paths, Physical Review Letters, 77:5229-5232. Edelman G., 1989, The Remembered Present, Basic Books, New York. Edelman G. and G. Tononi, 2000, A Universe of Consciousness, Basic Books, New York. Egle U., J. Hardt, R. Nickel, B. Kappis, and S. Hoffmann, 2002, Longterm effects of adverse childhood experiences – actual evidence and needs for research, Zeitshrift fur Psychosomatische Medizin und Psychotherapie, 48:411434. Eldredge N., 1995, Reinventing Darwin, John Wiley and Sons, New York. Emery M., 1989, Stochastic calculus in manifolds, Universitext series, Springer-Verlag, New York. Erdos P., and A. Renyi, 1960, On the evolution of random graphs, reprinted in The Art of Counting, 1973, 574-618 and in Selected Papers of Alfred Renyi, 1976, 482-525. Eriksson J., T. Forsen, J. Tuomilehto, C. Osmons, and D. Barker, 2000, Fetal and childhood growth and hypertension in adult life, Hypertension, 39:790794. Fanon F., 1966, The Wretched of the Earth, Grove Press, Boston. Feynman R., and A. Hibbs, 1965, Quantum Mechanics and Path Integrals, McGraw-Hill, New York, NY. Feynman R., 1996, Feynman Lectures on Computation, Addison-Wesley, Reading, MA. Feynman R., 1998, Statistical Mechanics, Perseus Books, Reading, MA. Forlenza M. and A. Baum, 2000, Psychosocial influences on cancer progression: alternative cellular and molecular mechanisms, Current Opinion in Psychiatry, 13:639-645. Freeman, W., 2003, The wave packet: an action potential of the 21st Century, Journal of Integrative Neurosciences, 2:3-30. Fullilove M.T. and R. Fullilove, 1999, Women’s Equity in AIDS Resources: A report to the Health Resources and Services Administration HIV/AIDS Bureau. Community Research Group, Colubmia University, December 6, 1999. Fullilove M.T., R. Fullilove, J. Stevens, and L. Green, 2000, Women’s Equity in AIDS resources, in C. Ryan (ed.), Directions in HIV Service Delivery and Care: A Policy Brief, Office of Policy and Program Development,

190

9 References

HIV/AIDS Bureayu, Health Resources and Services Administration, Washington, DC¿ Fullilove, M., 2004, Root Shock: How Tearing up City Neighborhoods Hurts America and What we can do About it, Ballantine Books, New York. Gamarekian B. 1986. ‘Where Have All the Inventors Gone? New York Times, June 20. Gammaitoni A., P. Hanggi, P. Jung, and F. Marchesoni, 1998, Stochastic resonance, Reviews of Modern Physics, 70:223-287. Garcia-Soto M., K. Haynes-Sanstad, R. Fullilove, and M. Fullilove, 1998, The peculiar epidemic, part 1: Social response to AIDS in Alameda County, Environment and Planning A, 30:731-746. Garud R. and M. Rappa 1994. A socio-cognitive model of technology evolution: the case of cochlear implants, Organization Science, 5, 344-362. Gaughran F., E. O’Neill, P. Sham, R. Daly, and F. Shanahan, 2002, Soluble Il-2 receptor levels in families of people with schizophrenia, Schizophrenia Research, 56:235-239. Geertz C., 1973, The growth of culture and the evolution of mind. In C. Geertz, The interpretation of cultures (pp. 55-87), Basic Books, New York. Gilbert P., 2001, Evolutionary approaches to psychopathology: the role of natural defenses, Austrailian and New Zealand Journal of Psychiatry, 35:1727. Glazebrook, J., 2007, Rate distortion manifolds as model spaces for cognitive information. In preparation. Godfrey K, and D. Barker, 2001, Fetal programming and adult health, Public Health and Nutrition, 4:611-624. Godivier X., and F. Chapeau-Blondeau, 1998, Stochastic resonance in the information capacity of a nonlinear dynamic system, International Journal of Bifurcation and Chaos, 8:581-589. Golembeski C., and R. Fullilove, 2005, Criminal (In)justice in the city and its associated health consequences, American Journal of Public Health, 95:1701-1706. Golubitsky M., and I. Stewart, 2006, Nonlinear dynamics and networks: the groupoid formalism, Bulletin of the American Mathematical Society, 43:305-364. Goubault, E., and M. Raussen, 2002, Dihomotopty as a tool in state space analysis, Lecture Notes in Computer Science, Vol. 2286, April, 2002, pp. 16-37, Springer, New York. Goubault E., 2003, Some geometric perspectives in concurrency theory, Homology, Homotopy, and Applications, 5:95-136. Gould P., and G. Tornqvist, 1971, Information, innovation and acceptance, in T. Hagerstrand and A. Kuklinskui (eds.), Information Systems for Regional Development, Lund series in Geography, Ser. B., Human Geography, No. 37, 149-168. Gould P., 1993, The Slow Plague, Blackwell, Oxford. Gould P., 1999, Becoming a Geographer, Syracuse University Press.

9 References

191

Gould P., and R. Wallace, 1994, Spatial structures and scientific paradoxes in the AIDS pandemic, Geografiska Annaler, 76B, 105-116. Gould, S. and N. Eldredge 1977, Punctuated equilibria: the tempo and mode of evolution reconsidered, Paleobiology, 3:115-151. Gould, S., 1992, The Structure of Evolutionary Theory, Harvard University Press, Cambridge, MA. Granovetter M., 1973, The strength of weak ties, American Journal of Sociology, 78:1360-1380. Grant R., F. Hect, M. Warmerdam, et al., 2002, Time trends in primary HIV-1 drug resistance among recently infected persons, Journal of the American Medical Association, 288:181-188. Green-Rennis, L., L. Hernandez-Cordero, K. Schmitz, and M. Fullilove, (in press), ‘We have a situation here’: Using situation analysis for health and social research. Chapter in Miller R., (ed.), Qualitative Research Methods for Social Work Research, Columbia University Press, New York. Grimmett G., and A. Stacey, 1998, Critical probabilities for site and bond percolation models, The Annals of Probability, 4:1788-1812. Grossman A., J. Churchill, B. McKinney, I. Kodish, S. Otte, and W. Greenough, (2003), Experience effects on brain development: possible contributions to psychopathology, Journal of Child Pschology and Psychiatry, 44:33-63. Grossman Z., 1989, The concept of idiotypic network: deficient or premature? In: H. Atlan and I.R. Cohen (eds.), Theories of Immune Networks, Springer Verlag, Berlin, p. 3852. Grossman Z., 1992a, Contextual discrimination of antigens by the immune system: towards a unifying hypothesis, in: A. Perelson and G. Weisbch, (eds.), Theoretical and Experimental Insights into Immunology, Springer-Verlag, New York. Grossman Z., 1992b International Journal of Neuroscience, 64:275. Grossman Z., 1993 Cellular tolerance as a dynamic state of the adaptable lymphocyte, Immunology Reviews, 133:45-73. Grossman Z., 2000, Round 3, Seminars in Immunology, 12:313-318. Gulbinat W., A. Dupont, A. Jabolinsky, O. Jensen, A. Marsella, Y. Nakane, and N. Sartorius, 1992, Cancer incidence of schizophrenia patients. Results of record linkage studies in three countries. British Journal of Psychiatry, 161 Suppl. 18:75-85. Gunderson L., 2000, Ecological resilience - in theory and application, Annual Reviews of Ecological Systematics, 31:425-439. Heine S., 2001, Self as cultural product: an examination of East Asian and North American selves, Journal of Personality, 69:881-906. Henegan C., C. Chow, J. Collins, T. Imhoff, S. Lowen, and M. Teich, 1996, Information measures quantifying aperiodic stochastic resonance, Physical Review A, 54:2366-2377. Herpertz S. and H. Sass, 2000, Emotional deficiency and psychopathy, Behavioral Sciences and thye Law, 18:567-580. Hirsch J., 2003, Obesity: matter over mind? Cerebrum, 5:7-18.

192

9 References

Hodgson G., 1993. Economics and Evolution: Bringing Life Back into Economics, University of Michigan Press, Ann Arbor. Hong B., 1979. Inflation under Cost Pass-along Management, Prager, New York. Hollan J., J. Hutchins, and D. Kirsch, 2000, Distributed cognition: toward a new foundation for human-computer interaction research, ACM Transactions on Computer-Human Interaction, 7:174-196. Holling C., 1973, Resilience and stability of ecological systems, Annual Reviews of Ecological Systematics, 4:1-23. Hugh-Jones E., 1955. Industrial productivity: The lessons of Fawley, Journal of Industrial Economics, 3:173-183. Hutchins E., 1994, Cognition in the Wild, MIT Press, Cambridge, MA. Ikeda N., and S. Watanabe, 1989, Stochastic Differential Equations and DIffusion Processes, North Holland, Amsterdam. J.M.C., 1913. Possible complications of the compensated dollar, The American Economic Review, 3:576-588. James, William, 1890, The Principles of Psychology, Cosimo Classics, New York, NY, 2007. Johnson C., 2001, Distributed primate cognition: a review, Animal Cognition, 4:167-183. Johnson-Laird P., F. Mancini, and A. Gangemi, 2006, A hyper-emotion theory of psychological illness, Psychological Review, 113:822-841. Jones I. and J. Blackshaw, 2000, An evolutionary approach to psychiatry, Australian and New Zealand Journal of Psychiatry, 34:8-13. Karlsson H., S. Bachmann, J. Schroder, J. McArthur, E. Torrey, and R. Yolken, 2001, Retroviral RNA identified in the cerebrospinal fluids and brains of individuals with schizophrenia, Proceedings of the National Academy of Sciences, 98:4634-4639. Khinchin A., 1957, The Mathematical Foundations of Information Theory, Dover Publications, New York. Kinney R., P. Crucitti, R. Albert, and V. Latora, 2005, Modeling cascading failures in the North American power grid, European Physics Journal, B, 46:101-107. Kleinenberg, E., 2002, Heat Wave, University of Chicago Press. Kleinman A. and B. Good, 1985, Culture and Depression: Studies in the Anthropology of Cross-Cultural Psychiatry of Affect and Depression, University of California Press, Berkeley, CA. Kleinman A., and A. Cohen, 1997, Psychiatry’s global challenge, Scientific American, xx:86-89. Kozma R., M. Puljic, P. Balister, B. Bollobas, and W. Freeman, 2004, Neuropercolation: a random cellular automata approach to spatio-temporal neurodynamics, Lecture Notes in Computer Science, 3305:435-443. Kozma R., M. Puljic, P. Balister, and B. Bollobas, 2005, Phase transitions in the neuropercolation model of neural populations with mixed local and non-local interactions, Biological Cybernetics, 92:367-379.

9 References

193

Krebs, P., 2005, Models of cognition: neurological possibility does not indicate neurological plausibility, in Bara, B., L. Barsalou, and M. Bucciarelli (eds.), Proceedings of CogSci 2005, pp. 1184-1189, Stresa, Italy. Available at http://cogprints.org/4498/. Krugman P., 1979. A model of innovation, technology transfer, and the world distribution of income, The Journal of Political Economy, 87:253-266. Lalumiere M., G. Harris, and M. Rice, 2001, Psycopathy and developmental instability, Evolution and Human Behavior, 22:75-92. Laxmisan A., F. Hakimzada, O. Sayan, R. Green, J. Zhang, V. Patel, 2006, The multitasking clinician; Decision-making and cognitive demand during and after team handoffs in emergency care, International Journal of Medical Informatics. Epub ahead of print. Lee J., 2000, Introduction to Topological Manifolds, Springer, New York. Lewis D. and P. Levitt, 2002, Schizophrenia as a disorder of neurodevelopment, Annual Reviews of Neuroscience, 25:409-432. Lincold C., and L. Mamiya, 1990, The Black Church in the African American Experience, Rutgers University Press, New Brunswick, NJ. Luchinsky, D., 1997, On the nature of large fluctuations in equilibrium systems: observations of an optimal force, Journal of Physics A Letters, 30:L577L583. Luczak T., 1990, Random Structures and Algorithms, 1:287. Mack A., 1998, Inattentional Blindness, MIT Press, Cambridge, MA. Madoff J., 2002, Islands of success in the midst of inequality: The situation of AIDS care for women of color. Dissertation, Mailman School of Public Health, Columbia University. Maia T., and A. Cleeremans, 2005, Consciousness: converging insights from connectionist modeling and neuroscience, Trends in Cognitive Sciences, 9:397404. Mallett R., J. Leff, D. Bhugara, D. Pang, and J. Zhao, 2002, Social environment, ethnicity, and schizophrenia: a case-control study, Social Psychiatry and Epidemiology, 37:329-335. Markus H., and S. Kitayama, 1991, Culture and the self: implications for cognition, emotion, and motivation, Psychological Review, 98:224-253. Massey, D., and N. Denton, 1998, American Apartheid, Harvard University Press, Cambridge, MA. Masuda T., and R. Nisbett, 2006, Culture and change blindness, Cognitive Science: A Multidisciplinary Journal, 30:381-399. McCauley L., 1993, Chaos, Dynamics, and Fractals: An Algorithmic Approach to Deterministic Chaos, Cambridge University Press, UK. McClintock M., and D. Luchinsky, 1999, Glorious Noise! The New Scientist, 161, No. 2168, January, pp. 36-39. Mealey L., 1995, The sociobiology of sociopathy: an integrated evolutionary model, Behavioral and Brain Sciences, 18:523-599. Mega C., 1978, Report of the New York State Assembly Republican Task Force on Urban Fire Protection.

194

9 References

Melman S., 1961, The Peace Race, Ballantine Books, New York. Melman S., 1971, The War Economy of the United States: Readings in military industry and economy, St. Martins Press, New York. Melman S., 1983, Profits Without Production, Knopf, New York. Melman S., 1988, Economic consequences of the arms race: the second-rate economy, AEA Papers and Proceedings, 78, 55-59. Melman S. 1993. What Else Is There To Do?, National Commission for Economic Conversion and Disarmament (ECD, Washington DC, October). Melman S., 1997, From private to state capitalism: how the permanent war economy transformed the institutions of American capitalism, Journal of Economic Issues, 31:311. Melman S., 2001, After Capitalism: From Managerialism to Workplace Democracy, Knopf, New York. Memmi A., 1969, Dominated Man, Beacon Press, Boston, MA. Meyer P., 1989, Appendix: a short presentation of stochastic calculus, in Stochastic Calculus on Manifolds. Ed. by M. Emer, Springer, New York. Mnif M., and C. Muller-Schloer, 2006, Quantitative Emergence. In Proceedings of the 2006 IEEE Mountain Workshop on Adaptive and Learning Systems, IEEE SMCals2006, 78-84. . Molloy M., and B. Reed, 1995, A critical point for random graphs with a given degree sequence, Random Structures and Algorithms, 6:161-179. Molloy M., and B. Reed, 1998, The size of the giant component of a random graph with a given degree sequence, Combinatorics, Probability, and Computing, 7:295-305. Morales E., and M. Fullilove, 1992, ‘Many are called’: Participation by minority leaders in an AIDS intervention in San Francisco, Ethnicity and Disease, 21:389-401. Mortensen P., 1989, The incidence of cancer in schizophrenic patients, Journal of Epidemiolgy and Community Health, 43:43-47. Mortensen P., 1994, The occurrence of cancer in first admitted schizophrenic patients, Schizophrenia Research, 12:185-194. Muller-Schloer C., 2004, Organic computing - on the feasibility of controlled emergence, CODES+OSSS’04, ACM 1-58113-937-3/04/0009. Muller-Schloer C. and B. Sick, 2006, Emergence in organic computing systems: discussion of a controversial concept, Yang et al. (eds.), ATC 2006, LNCS 4158, pp.1-16. Nelson R., 1995. ‘Recent evolutionary theorizing about economic change,’ Journal of Economic Literature, 33, 48-90. Nelson R. and S. Winter, 1982. An Evolutionary Theory of Economic Change, Harvard University Press, Cambridge. Nesse R., 2000, Is depression an adaptation? Archives of General Psychiatry, 57:14-20. Newell A., 1990, Unified Theories of Cognition, Harvard University Press, Cambridge, MA.

9 References

195

Newman M., S. Strogatz, and D. Watts, 2001, Random graphs with arbitrary degree distributions and their applications, Physical Review E, 64:026118, 1-17. Newman M., 2003, Properties of highly clustered networks, arXiv:condmat/0303183v1. Nisbett R., K. Peng, C. Incheol, and A. Norenzayan, 2001, Culture and systems of thought: holistic vs. analytic cognition, Psychological Review, 108:291310. Nisbett R., and T. Masuda, 2003, Culture and point of view, Proceedings of the National Academy of Sciences, 100:11163-11170. Norenzayan A., and S. Heine, 2004, Psychological universals across cultures: what are they and how can we know? Submitted. Nunney, L., 1999, Lineage selection and the evolution of multistage carcinogenesis, Proceedings of the Royal Society, B, 266:493-498. Onsager L. and S. Machlup, 1953, Fluctuations and irreversible processes, Physical Review, 91:1505-1512. Osmond C. and D. Barker, 2000, Environmental Health Perspectives, 108, Suppl 3:545-553. Panskepp J., 2003, At the interface of the affective, behavioral, and cognitive neurosciences: Decoding the emotional feelings of the brain, Brain and Cognition, 52:4-14. Pappas G., 1989, The Magic City, Cornell University Press, Ithaca, NY. Paris J., 1993, Personality disorders: a biopsychosocial model, Journal of Personality Disorders, 7:53-99. Patel, V., 1998, Individual to collaborative cognition: a paradigm shift? Artificial Intelligence in Medicine, 12:93-96. Petersen K., 1995, Cambridge Studies in Advanced Mathematics 2: Ergodic Theory, Cambridge University Press, UK. Pielou, E., 1977, Mathematical Ecology, John Wiley and Sons, New York. Podolsky S. and A. Tauber, 1997, The generation of diversity: Clonal selection theory and the rise of molecular biology, Harvard University Press, Cambridge, MA. Pohl W., 1962, Differential geometry of higher order, Topology 1:169-211. Pratt V., 1991, Modeling concurrency with geometry, Proceedings of the 18th ACM SIGPLAN-SIGACT Symposium on Principles of Programming Languages, 311-322. Protter P., 1990, Stochastic Integration and Differential Equations: A New Approach, Springer, New York. Pyle G., 1969, Diffusion of cholera in the United States, Geographical Analysis, 1:59-75. Rambaut A., D. Posada, K. Crandall, and E. Holmes, 2004, The causes and consequences of HIV evolution, Nature Reviews/Genetics, 5:52-61. Rau H. and T. Elbert, 2001, Psychophysiology of arterial baroreceptors and the etiology of hypertension, Biological Psychology, 57:179-201.

196

9 References

Reed B., 1987, Developing women-sensitive drug dependence treatment services: why so difficult?, Journal of Psychoactive Drugs, 19:151-164. Repetti R., S. Taylor, and T. Seeman, 2002, Risky families: family social environments and the mental and physical health of offspring, Psychological Bulletin, 128:330-366. Richerson P. and R. Boyd, 1995, The evolution of human hypersociality. Paper for Ringberg Castle Symposium on Ideology, Warfare and Indoctrinability (January, 1995), and for HBES meeting. Richerson P., and R. Boyd, 2004, Not by Genes Alone: How Culture Transformed Human Evolution, Chicago University Press. Richter U., M. Mnif, J. Branke, C. Muller-Schloer, and H. Schmeck, 2006, Towards a generic observer/controller architecture for Organic Computing, p. 112 in INFORMATIK 2006, Lecture Notes in Informatics Hochberger and Liskowsky, (eds.), Gesllschaft fur Informatik, Bonn, Germany. Rothermundt M., V. Arolt, and T. Bayer, 2001, Review of immunological and immunopathological findings in schizophrenia, Brain, Behavior, and Immunity, 15:319-339. Sampson R., S. Raudenbush, and F. Earls, 1997, Neighborhoods and violent crime: A multilevel study of collective efficacy, Science, 277:918-924. Sampson R., 2004, Networks and neighborhoods, in Network Logic: Who Governs in an Interconnected World?, ed. by H. McCarthy, P. Miller, and R. Skidmore, Demos, London. Savante J., D. Knuth, T. Luczak, and B. Pittel, 1993, The birth of the giant component, arXiv:math.PR/9310236v1. Schimansky-Gier L., J. Freund, U. Siewert and A. Nieman, 1996, Stochastic resonance: informational aspects and distributed systems, ICND-96 book of abstracts. Schmeck H., 2005, Organic computing - a new vision for distributed embedded systems, Proceedings of the Eighth IEEE International Symposium on Object-Oriented Real-Time Distributed Computing (ISORC’05), 0-76952356-0/05. Schwartz J., 1993, The New York Approach: Robert Moses, Urban Liberals, and Redevelopment of the Inner City, Ohio State Press, Columbus, OH. Sclar, E., 1990, Homelesness and housing policy: a game of musical chairs, American Journal of Public Health, 80:1049-1052. Shannon C., and W. Weaver, 1949, The Mathematical Theory of Communication, University of Illinois Press, Chicago, IL. Shirkov D. and V. Kovalev, 2001, The Bogoliubov renormalization group and solution symmetry in mathematical physics. Physics Reports 352:219-249. Siliani G., U. Frith, J. Demonet, F. Fazio, D. Perani, C. Price, C. Frith, and E. Paulesu, 2005, Brain abnormalities underlying altered activation in dyslexia: a voxel based morphometry study, Brain, 128(Pt.10):2453-2461. Simon V., et al., 2003, Infectivity and replication capacity of drug resistant HIV-1 variants isolated during primary infection, Journal of Virology, 77:77367745.

9 References

197

Simons, D., and C. Chabris, 1999, Gorillas in our midst: sustained inattentional blindness for dynamic events, Perception, 28:1059-1074. Simons D., 2000, Attentional capture and inattentional blindness, Trends in Cognitive Sciences, 4:147-155. Smith G. C. Hart, D. Blane, and D. Hole, 1998, Adverse socioeconomic conditions in childhood and cause-speciofic adult mortality: prospective observational study, British Medical Journal, 317:1631-1635. Smith T. and J. Ruiz, 2002, Psychosocial influences on the development and course of coronary heart disease: current status and implications for research and practice, Journal of Consulting and Clinical Psychology, 70:548568. Starbuck W., and M. Farjoun, 2005, Lessons from the Columbia Accident, Blackwell, Malden, MA. Stewart I., M. Golubitsky, and M. Pivato, 2003, Symmetry groupoids and patterns of synchrony in coupled cell networks, SIAM Journal of Applied Dynamical Systems, 2:609-646. Stewart I., 2004, Networking opportunity, Nature, 427:601-604. Tauber A., 1998, Conceptual shifts in immunology: Comments on the ‘twoway paradigm.’ In K. Schaffner and T. Starzl (eds.), Paradigm changes in organ transplantation, Theoretical Medicine and Bioethics, 19:457-473. Taylor J., 1996, Introduction to Measure and Probability, Springer, New York. Teunis M., A Kavelaars, E. Voest, J. Bakker, B. Ellenborek, A. Cools, and C Heijnen, 2002, Reduced tumor growth, experimental metastasis formation, and angiogenesis in rats with a hyperreactive dopaminergid system, FASEB Journal express article 10.1096/fj.02-014fje. Thayer J. and R. Lane, 2000, A model of neurovisceral integration in emotion regulation and dysregulation, Journal of Affective Disorders, 61:201216. Thayer J., and B. Friedman, 2002, Stop that! Inhibition, sensitization, and their neurovisceral concomitants, Scandinavian Journal of Psychology, 43:123-130. Timberlake W., 1994, Behavior systems, associationism, and Pavlovian conditioning, Psychonomic Bulletin, Rev. 1, 405-420. Tirman J., 1984, The Militarization of High Technology, Ballinger, Cambridge, MA. US Congress, Joint Economic Committee 1986. the US Trade Position in High Technology, 1980-1986 US Government Printing Office, Washington DC. Tononi G., and G. Edelman, 1998, Consciousness and complexity, Science, 282:1846-1851. Tononi G., 2004, An information integration theory of consciousness, BMC Neuroscience, 5:42. Torrey E. and R. Yolken, 2001, The schizophrenia-rheumatoid arthritis connection: infectious, immune, or both? Brain, Behavior, and Immunity, 15:401-410.

198

9 References

Toth G., C. Lent, P. Tougaw, Y. Brazhnik, W. Weng, W. Porod, R. Liu, and Y. Huang, 1996, Quantum cellular neural networks, Superlattices and Microstructures, 20:473-478. Ullmann J. 1970. Conversion and the Import Problem: A Confluence of Opportunities, IEEE Spectrum, April, 55. Ullmann J. 1978. Tides and Shallows, in Management for the Future, L. Benton (ed.), McGraw-Hill, New York. Ullmann J., 1985, The Prospects of American Industrial Recovery, Quorum Books, Westport, CT. Ullmann J. et al. 1988. The Anatomy of Industrial Decline, GreenwoodQuorum, Westport, CT. Ullmann J. 1989. Economic Conversion: Indispensable for America’s Economic Recovery, Briefing Paper 3, National Commission for Economic Conversion and Disarmament (ECD, Washington DC, October). Ullmann J. 1993. A National High Speed Rail System: The Task for Engineers, IEEE Technology and Society, Winter, 13-20. Ullmann J. 1994. Conversion: The Prospects for Long Island, Hofstra Business Review, April, 1. Ullmann J. 1997a. Ronald Reagan and the Illusion of Victory in the Cold War, in President Reagan and the World, A Ugrinsky, E Schmertz and N Datlof, (eds.), Greenwood Press, Westport CT, 109ff. Ullmann J. 1997b. Defense Cuts, Base Closings and Conversion: Slow Reaction and Missed Opportunities, Paper at Conference on ‘George Bush: Leading in a New World,’ 10th Presidential Conference, Hofstra University, April 17-19. UNHCHR, 1993, Fact Sheet 25: forced evictions and human rights. http://unhchr.ch/html/menu6/fs25.htm. Villalobos M., A. Mizuno, B. Dahl, N. Kemmotsu and R. Muller, 2005, Reduced functional connectivity between VI and Inferior frontal cortex associated with visumotor performance in autism, Neuroimage, 25:916-925. Waddington C., 1972, Epilog, in Towards a Theoretical Biology 4: Essays, CH Waddington (ed.), Aldine-Atherton, Chicago, IL. Wald R., 1984, General Relativity, University of Chicago Press, Chicago, IL. Wall C., and S. Zarit, 1991, Informal support from black churches and the well-being of elderly blacks, The Gerontologist, 31:490-495. Wallace D., and R. Wallace, 1998a, A Plague on Your Houses, Verso, New York. Wallace D. and R. Wallace, 1998b, Scales of geography, time, and population: the study of violence as a public health problem, American Journal of Public Health, 88:1853-1858. Wallace D., and R. Wallace, 2000, Life and death in Upper Manhattan and the Bronx: toward evolutionary perspectives on catastrophic social change, Environment and Planning A, 32:1245-1266.

9 References

199

Wallace R., 1990, Urban desertification, public health and public order: planned shrinkage, contagious housing destruction and AIDS in the Bronx, Social Science and Medicine, 31:801-816. Wallace R., 1993, Social disintegration and the spread of AIDS II: meltdown of sociogeographic structure in urban minority neighborhoods, Social Science and Medicine, 37:887-896. Wallace R., 2000, Language and coherent neural amplification in hierarchical systems: renormalization and the dual information source of a generalized spatiotemporal stochastic resonance, International Journal of Bifurcation and Chaos, 10:493-502. Wallace R., 2002a, Immune cognition and vaccine strategy: pathogenic challenge and ecological resilience, Open Systems and Information Dynamics 9:51-83. Wallace R., 2002b, Adaptation, punctuation and rate distortion: noncognitive ‘learning plateaus’ in evolutionary process, Acta Biotheoretica, 50:101116. Wallace R., 2004, Comorbidity and anticomorbidity: autocognitive developmental disorders of structured psychosocial stress. Acta Biotheoretica, 52:71-93. Wallace R., 2005a, Consciousness: A Mathematical Treatment of the Global Neuronal Workspace Model, Springer, New York. Wallace R., 2005b, A global workspace perspective on mental disorders, Theoretical Biology and Medical Modelling, 2:49. Wallace R., 2005c, The sleep cycle: a mathematical analysis from a global workspace perspective, http://cogprints.org/4517/ Wallace R., 2006, Pitfalls in biological computing: canonical and idiosyncratic dysfunction of conscious machines, Mind and Matter, 4:91-113. Wallace R., 2007, Culture and inattentional blindness: a global workspace perspective, Journal of Theoretical Biology, 245:378-390. Wallace R., and D. Wallace, 1990, Origins of public health collapse in New York City: The dynamics of planned shrinkage, contagious urban decay and social disintegration, Bulletin of the New York Academy of Medicine, 66:391426. Wallace R., M. Fullilove, and A. Flisher, 1996, AIDS, violence and behavioral coding: information theory, risk behavior, and dynamic process on core-group sociogeographic networks, Social Science and Medicine, 47:339352. Wallace R., and D. Wallace, 1997a, Community marginalization and the diffusion of disease and disorder in the United States, British Medical Journal, 314:1341-1345. Wallace R., and D. Wallace, 1997b, The destruction of US minority urban communities and the resurgence of tuberculosis: ecosystem dynamics of the white plague in the de-developing world, Environment and Planning A, 29:269-291.

200

9 References

Wallace R., D. Wallace, H. Andrews, R. Fullilove and M. Fullilove, 1995, The spatiotemporal dynamics of AIDS and TB in the New York metropolotan region from a sociogeographic perspective, Environment and Planning A, 27:1085-1108. Wallace R., Wallace D., and H. Andrews, 1997, AIDS, tuberculosis, violent crime and low birthweight in eight US metropolitan areas: public policy, stochastic resonance, and the regional diffusion of iiner-city markers, Environment and Planning A, 29:525-555. Wallace R. and R.G. Wallace, 1998, Information theory, scaling laws and the thermodynamics of evolution, Journal of Theoretical Biology 192:545-559. Wallace R. and R.G. Wallace, 1999, Organisms, organizations and interactions: an information theory approach to biocultural evolution, BioSystems 51:101-119. Wallace R., and R. Fullilove, 1999, Why simple regression models work so well describing risk behaviors in the USA, Environment and Planning A, 31:719-734. Wallace R., J. Ullmann, D. Wallace and H. Andrews, 1999, Deindustrialization, inner city decay and the hierarchical diffusion of AIDS in the US: how neoliberal and cold war policies magnified the ecological niche for emerging infections and created a national security crisis, Environment and Planning A,31:113-139. Wallace D. and R. Wallace, 2000, Life and death in Upper Manhattan and the Bronx: toward an evolutionary perspective on catastrophic social change, Environment and Planning A, 32:1245-1266. Wallace R. and R.G. Wallace, 2002, Immune cognition and vaccine strategy: beyond genomics, Microbes and Infection 4:521-527. Wallace R., R.G. Wallace and D. Wallace, 2003, Toward cultural oncology: the evolutionary information dynamics of cancer, Open Systems and Information Dynamics 10:159-181. Wallace R., and R.G. Wallace, 2004, Adaptive chronic infection, structured stress, and medical magic bullets: Do reductionist cures selcet for holistic diseases? BioSystems, 77:93-108. Wallace R., and R.G. Wallace, 2007, Darwin’s rainbow: Evolutionary radiation and the spectrum of consciousness, http://cogprints.org/5170/. Wallace R., and D. Wallace, 2004, Structured psychosocial stress and therapeutic failure, Journal of Biological Systems, 12:335-369. Wallace R., D. Wallace, 2005, Structured psychosocial stress and the US obesity epidemic, Journal of Biological Systems, 13:363-384. Wallace R., D. Wallace and R.G. Wallace, 2004, Biological limits to reduction in rates of coronary heart disease: a punctuated equilibrium approach to immune cognition, chronic inflammation, and pathogenic social hierarchy, Journal of the National Medical Association, 96:609-619. Wallace R., M. Fullilove, R. Fullilove, and D. Wallace, 2007, Collective consciousness and its pathologies: understanding the failure of AIDS control and

9 References

201

treatment in the United States, Theoretical Biology and Medical Modelling, 4:10. Wallace, R.G., 2004, Projecting the impact of HAART on the evolution of HIV’s life history, Ecological Modelling, 176:227-253. Wayand J., D. Levin and D. Alexander Varakin, 2005, Inattentional blindness for a noxious multimodal stimulus, American Journal of Psychology, 118:339-352. Weinstein A., 1996, Groupoids: unifying internal and external symmetry, Notices of the American Mathematical Association, 43:744-752. Weiss, M., 1985, The origins and legacy of urban renewal. In Mitchell, J. (ed.), Federal Housing Policy and Programs: Past and Present, Rutgers University Press, New Brunswick, 253-276. Werner G., 2006, Metastability, criticality and phase transitions in brain and its models, BioSystems, Dec. 8 (epub ahead of print). Wilkinson R., 1996, Unhealthy Societies: The Afflictions of Inequality, Routledge, London and New York. Wilson K., 1971, Renormalization group and critical phenomena. I Renormalization group and the Kadanoff scaling picture. Physical Review B, 4:31743183. Woods D., and E. Hollnagel, 2006, Joint Cognitive Systems: Patterns in Cognitive Systems Engineering, Taylor and Francis, Boca Raton, FL. Wright R., M. Rodriguez, and S. Cohen, (1998), Review of psychosocial stress and asthma, Thorax, 53:1066-1074. Youmans, G., 1979, Tuberculosis, Saunders, Philadelphia. Zurek W., 1985, Cosmological experiments in superfluid helium?, Nature, 317:505-508. Zurek W. (Ed.), 1990, Complexity, Entropy and the Physics of Information, SFI Studies in the Science of Complexity, Volume VII, Addison-Wesley, New York. Zurek W., 1996, The shards of broken symmetry, Nature, 382:296-298.

Index

Adams, F., 21 AIDS, 1, 129 Alameda County, 130 Albert, R., 22 American Apartheid, 158 American Revolution, 3 anxiety, 61 anxiety disorders, 123 Apartheid, 111 APSE, 26, 168 arms race, 69 asthma, 122 atherosclerosis, 61 Atlan, H., 25, 115 autism, 61 Baars, B., 15 Bennett, C., 38 Bennett, M., 35 biocultural evolution, 157 biological renormalization, 171 Black clergy, 137 Black hole, 42 blood pressure, 117 Born-Oppenheimer, 27 Boyd, R., 2 Branke, J., 16 Bronx, 92 Brownian motion, 100 Burns, T., 18 cancer, 116 category, 29 chronic disease, 115

Civil Rights Movement, 89 coevolutionary, 68 cognitive paradigm, 116 Cohen, I., 25, 115 Cohen, T., 20 Cold War, 157 collective efficacy, 17 Collins, C., 122 comorbidity, 120 compulsion, 61 contagious urban desertification, 89 contexts, 56 Coplan, J., 62 coronary heart disease, 61, 121 Crick, J., 15 critical point, 39 Darwin’s Rainbow, 54 decision oscillator, 25 Dehaene, S., 15 depression, 61 diabetes, 61 Distributed cognition, 17 Dretske, F., 21, 56 drugs, 140 DSMIV, 59 dual information source, 27 dynamical groupoid, 38, 41 dyslexia, 61 Edelman, G., 15 emotion, 118 emotional dysregulation, 62 endemic infection, 100

204

Index

equivalence class, 28, 40 Erdos, P., 22 ergodic, 26 ergodic theorem, 97 eutrophication, 54 evolution, 55 evolutionary economics, 68 Fanon, F., 128 Feynman, R., 38 Finsler geometry, 42 fluctuations, 97 free energy density, 35 general broadcast, 33 genetic determinism, 59 Gentrification, 8 geodesic, 42, 183 giant component, 33 Gilbert, P., 59 Global Workspace Theory, 21 Golubitsky, M., 30 Goubault, E., 51 Gould, P., 85 Granovetter, M., 62 Grossman, Z., 115 groupoid, 23, 28 Gunderson, L., 53 HAART, 90 Hacker, P., 35 Hamiltonian, 35 Hill District, 4 Hirsch, J., 122 HIV, 1 Hodgson, G., 55 Hollan, J., 17 Holling, C., 53 homology, 36 homotopy, 30, 51 Hope VI, 10 HPA axis, 117 Hutchins, E., 17 hypertension, 61, 122 immune function, 115 inattentional blindness, 37, 58, 63 infectivity, 98 International law, 13

isotropy group, 29 Ito stochastic integral, 106 James, W., 15 Johnson-Laird, P., 59 Kinney, R., 16 Kleinman, A., 60 Koch, C., 15 Kozma, R., 23, 33 Krebs, P., 56 Lamarckian, 69 large deviation theory, 97 martingale, 103 Martingale Theorem, 96, 100 Martingale transform, 105 MDR-HIV, 91, 114 meaningful, 26 Melman, S., 70, 158 Memmi, A., 128 metric, 40 Mnif, M., 16 modular network, 22 morphism, 29 Muller-Schloer, C., 16 multiple workspaces, 37 Multitasking Hierarchical Cognitive Model, 38 nested Martingale, 103 network information theory, 34 neuropercolation, 33 New York Metropolitan Region, 88 Newark, 8 Nunney, L., 116 obesity, 122 Onsager relations, 39 opportunity structure, 85, 113 pandemic, 85 Panskepp, J., 119 Patel, V, 20 Pentagon Ratchet, 70, 81 phase transition, 39, 73 planned shrinkage, 4 polyphyletic parallelism, 55 population bottleneck, 59

Index power relations, 85 Pratt, V., 51 prehistory probability density, 96 psychopathy, 123 psychotic, 61 punctuated fragmentation, 81 racism, 122 Rand Corporation, 6 rate distortion manifold, 37, 44 Reconstruction, 3 Red Queen, 68 Redlining, 5 refugee, 13 renormalization, 36, 74, 170, 179 resilience, 51, 53, 111 resource limitation, 67 Richter, U., 15 Riemannian geometry, 42 right with God, 139 Rust Belt, 70 Sampson, R., 17 San Francisco, 88, 130 schizophrenia, 61, 124 Schmeck, H., 16 Seifert-VanKampen theorem, 41 serial forced displacement, 3 set point, 122 simple epidemic with removal, 97 slave, 3 social decay, 157 social disintegration, 67

South Africa, 14 splitting criterion, 37 Starr, R., 6 Stewart, I., 30 stochastic differential geometry, 43 stochastic resonance, 96 Strength of Weak Ties, 62 structural violence, 157 submartingale, 103 supermartingale, 103 susceptible, 98 TB, 92 Thayer, J., 119 The Slow Plague, 86 therapeutic intervention, 81 thermodynamic limit, 35 tiling, 30 Tononi, G., 15 topology, 36, 39, 54 tuberculosis, 2 Ullmann, J., 70, 158 universality class, 36 universality class tuning, 177 weak ties, 23 Weinstein, A., 28 Werner, G., 15 Wilson, K., 75, 109 zero mode identification, 120, 126 Zurek, W., 110

205