'Fat people and bombs':HPA axis cognition, structured stress, and the US obesity epidemic

We examine the accelerating 'obesity epidemic' in the US from the perspective of recently developed theory relating a cognitive hypothalamic-pituitary-adrenal axis to an embedding 'language' of structured psychosocial stress. Using a Rate Distortion argument, the obesity epidemic is found to represent the literal writing of an image of a ratcheting pathological social hierarchy onto the bodies of American adults and children. This process, while stratified by the usual divisions of class and ethnicity, is nonetheless relentlessly engulfing even affluent majority populations. Our perspective places the common explanation that 'obesity occurs when people eat too much and get too little exercise' in the same category as the remark by US President Calvin Coolidge on the eve of the Great Depression that 'unemployment occurs when large numbers of people are out of work'. Both statements ignore profound structural determinants of great population suffering which must be addressed by collective actions of equally great reform

Cancer and the social induction of aging

Age has long been known as the primary population 'risk factor' for cancer. We suggest that the observed disparities in hormonal cancers by ethnicity, gender, and other indices of social structure and power relationships, imply a differential aging by psychosocial and environmental exposures, in the context of cross-generational epigenetic heritage. A relatively simple model of malignancy regulation illuminates the cellular root of induced aging, and explains the decline in cancer rate with extreme old age via telomere shortening. We find that the multifactorial determinants of the disorder cannot be effectively addressed by 'small molecule' interventions at the individual level, but must involve comprehensive prevention strategies that lessen exposures to policies and cultural practices that accelerate senescence in vulnerable or targeted populations

Extending Tlusty's method to the glycome: Tuning the repertoire of glycan determinants

We apply Tlusty's information-theoretic analysis of the genetic code to the glycome, using a cognitive paradigm in which external information sources constrain and tune the glycan code error network, in the context of available metabolic energy. The resulting dynamic model suggests the possibility of observing spontaneous symmetry breaking of the glycan code as a function of metabolic energy intensity. These effects may be currently present, or embedded in evolutionary trajectory, recording large-scale ecosystem resilience shifts in energy availability such as the aerobic transition

Institutional Cognition

We generalize a recent mathematical analysis of Bernard Baars' model of human consciousness to explore analogous, but far more complicated, phenomena of institutional cognition. Individual consciousness is limited to a single, tunable, giant component of interacting cogntivie modules, instantiating a Global Workspace. Human institutions, by contrast, seem able to multitask, supporting several such giant components simultaneously, although their behavior remains constrained to a topology generated by cultural context and by the path-dependence inherent to organizational history. Surprisingly, such multitasking, while clearly limiting the phenomenon of inattentional blindness, does not eliminate it. This suggests that organizations (or machines) explicitly designed along these principles, while highly efficient at certain sets of tasks, would still be subject to analogs of the subtle failure patterns explored in Wallace (2005b, 2006). We compare and contrast our results with recent work on collective efficacy and collective consciousness

The cultural psychology of obesity: diffusion of pathological norms from Western to East Asian societies

We examine the accelerating worldwide obesity epidemic using a mathematical model relating a cognitive hypothalamic-pituitary-adrenal axis tuned by embedding cultural context to a signal of chronic, structured, psychosocial threat. The obesity epidemic emerges as a distorted physiological image of ratcheting social pathology involving massive, policy-driven, economic and social 'structural adjustment' causing increasing individual, family, and community insecurity. The resulting, broadly developmental, disorder, while stratified by expected divisions of class, ethnicity, and culture, is nonetheless relentlessly engulfing even affluent majority populations across the globe. The progression of analogous epidemics in affluent Western and East Asian socieities is particularly noteworthy since these enjoy markedly different cultural structures known to influence even such fundamental psychophysical phenomena as change blindness. Indeed, until recently population patterns of obesity were quite different for these cultures. We attribute the entrainment of East Asian societies into the obesity epidemic to the diffusion of Western socioeconomic practices whose imposed resource uncertainties and exacerbation of social and economic divisions constitute powerful threat signals. We find that individual-oriented 'therapeutic' interventions will be largely ineffective since the therapeutic process itself (e.g. relinace on drug treatments) embodies the very threats causing the epidemic

On the social induction of Alzheimer's disease: An index theorem aging model for amyloid formation

The central 'risk factor' for Alzheimer's disease (AD) is age. From first principles, we construct a mathematical model of protein folding and its in vivo regulation that gives this result in a natural manner. We extend the basic approach using topological information theory methods, and examine a case history of socially-induced premature aging in the United States

Predicting Health Impacts of the World Trade Center Disaster: 1. Halogenated hydrocarbons, symptom syndromes, secondary victimization, and the burdens of history

The recent attack on the World Trade Center, in addition to direct injury and psychological trauma, has exposed a vast population to dioxins, dibenzofurans, related endocrine disruptors, and a multitude of other physiologically active chemicals arising from the decomposition of the massive quantities of halogenated hydrocarbons and other plastics within the affected buildings. The impacts of these chemical species have been compounded by exposure to asbestos, fiberglass, crushed glass, concrete, plastic, and other irritating dusts. To address the manifold complexities of this incident we combine recent theoretical perspectives on immune, CNS, and sociocultural cognition with empirical studies on survivors of past large toxic fires, other community-scale chemical exposure incidents, and the aftereffects of war. Our analysis suggests the appearance of complex, but distinct and characteristic, spectra of synergistically linked social, psychosocial, psychological and physical symptoms among the 100,000 or so persons most directly affected by the WTC attack. The different 'eigenpatterns' should become increasingly comorbid as a function of exposure. The expected outcome greatly transcends a simple 'Post Traumatic Stress Disorder' model, and may resemble a particularly acute form of Gulf War Syndrome. We explore the role of external social factors in subsequent exacerbation of the syndrome -- secondary victimization -- and study the path-dependent influence of individual and community-level historical patterns of stress. We suggest that workplace and other organizations can act as ameliorating intermediaries. Those without acess to such buffering structures appear to face a particularly bleak future

Toward Cultural Oncology: The Evolutionary Information Dynamics of Cancer

'Racial' disparities among cancers, particularly of the breast and prostate, are something of a mystery. For the US, in the face of slavery and its sequelae, centuries of interbreeding have greatly leavened genetic differences between 'Blacks' and 'whites', but marked contrasts in disease prevalence and progression persist. 'Adjustment' for socioeconomic status and lifestyle, while statistically accounting for much of the variance in breast cancer, only begs the question of ultimate causality. Here we propose a more basic biological explanation that extends the theory of immune cognition to include elaborate tumor control mechanisms constituting the principal selection pressure acting on pathologically mutating cell clones. The interplay between them occurs in the context of an embedding, highly structured, system of culturally specific psychosocial stress which we find is able to literally write an image of itself onto disease progression. The dynamics are analogous to punctuated equilibrium in simple evolutionary proces