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We argue that mesoscale ecosystem resilience shifts akin to sudden phase transitions in physical systems can entrain similarly punctuated events of gene expression on more rapid time scales, and, in part through such means, slower changes induced by selection pressure, triggering punctuated equilibrium Darwinian evolutionary transitions on geologic time scales. The approach reduces ecosystem, gene expression, and Darwinian genetic dynamics to a least common denominator of information sources interacting by crosstalk at markedly differing rates. Pettini's 'topological hypothesis', via a homology between information source uncertainty and free energy density, generates a statistical model of sudden coevolutionary phase transition based on the Rate Distortion and Shannon-McMillan Theorems of information theory which links all three levels. Holling's (1992) extended keystone hypothesis regarding the particular role of mesoscale phenomena in entraining both slower and faster dynamical structures produces the result. A main theme is the necessity of a cognitive paradigm for gene expression, mirroring I. Cohen's cognitive approach to immune function. Invocation of the necessary conditions imposed by the asymptotic limit theorems of communication theory enables us to penetrate one layer more deeply before needing to impose a phenomenological system of 'Onsager relation' recursive coevolutionary stochastic differential equations. Extending the development to second order via a large deviations argument may permit modeling the influence of human cultural structures on ecosystems.

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.

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.

We explore the implications of IR Cohen's work on immune cognition for understanding rising rates of asthma morbidity and mortality in the US. Immune cognition is inherently linked with central nervous system cognition, and with the cognitive function of the embedding sociocultural networks by which individuals are acculturated and through which they work with others to meet challenges of threat and opportunity. Externally-imposed patterns of 'structured stress' can, through their effect on a child's socioculture, become synergistic with the development of immune cognition, triggering the persistence of an atopic Th2 phenotype, a necessary precursor to asthma and other immune diseases. Structured stress in the US particularly includes the cross sectional and longitudinal effects of a systematic destruction of minority urban communities occurring since the end of World War II which we characterize as community lynching. Reversal of the rising tide of asthma and related chronic diseases in the US thus seems unlikely without a 21st Century version of the earlier Great Urban Reforms which ended the scourge of infectious diseases, in particular an end to the de-facto ethnic cleansing of minority neighborhood

'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 process

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.

On both empirical and theoretical grounds we find that a particular form of social hierarchy, here characterized as 'pathogenic', can, from the earliest phases of life, exert a formal analog to evolutionary selection pressure, literally writing a permanent image of itself upon immune function as chronic vascular inflammation and its consequences. The staged nature of resulting disease emerges 'naturally' as an analog to punctuated equilibrium in evolutionary theory. Exposure differs according to the social constructs of race, class, and ethnicity, accounting in large measure for observed population-level differences in rates of coronary heart disease affecting industrialized societies. The system of American Apartheid, which enmeshes both majority and minority communities in a construct of pathogenic hierarchy, appears to present a severe biological limit to ultimate possible reductions in rates of coronary heart disease and related disorders for powerful as well as subordinate subgroups.

We explore the implications of IR Cohen's work on immune cognition for understanding rising rates of asthma morbidity and mortality in the US. Immune cognition is conjoined with central nervous system cognition, and with the cognitive function of the embedding sociocultural networks by which individuals are acculturated and through which they work with others to meet challenges of threat and opportunity. Using a mathematical model, we find that externally- imposed patterns of 'structured stress' can, through their effect on a child's socioculture, become synergistic with the development of immune cognition, triggering the persistence of an atopic Th2 phenotype, a necessary precursor to asthma and other immune disease. Reversal of the rising tide of asthma and related chronic diseases in the US thus seems unlikely without a 21st Century version of the earlier Great Urban Reforms which ended the scourge of infectious diseases.

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.

The recent attack on the World Trade Center, in addition to direct injury and psychological trauma, appears to have exposed an exceedingly large 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. Combining recent theoretical perspectives on immune, CNS, and sociocultural cognition with empirical studies of those affected by past toxic fire incidents suggests the appearance of complex, developing spectra of synergistically linked social, pshchosocial, psychological, and physical symptoms among the 100,000 or so persons directly affected by the attack. The expected pattern greatly transcends a simple 'Post Traumatic Stress Disorder' model, and may come to resemble particularly acute forms of Gulf War Syndrome.