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Mismatch: the lifestyle diseases timebomb

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Abstract

We have built a world that no longer fits our bodies. Our genes - selected through our evolution - and the many processes by which our development is tuned within the womb, limit our capacity to adapt to the modern urban lifestyle. There is a mismatch. We are seeing the impact of this mismatch in the explosion of diabetes, heart disease and obesity. But it also has consequences in earlier puberty and old age. Bringing together the latest scientific research in evolutionary biology, development, medicine, anthropology and ecology, Peter Gluckman and Mark Hanson, both leading medical scientists, argue that many of our problems as modern-day humans can be understood in terms of this fundamental and growing mismatch. It is an insight that we ignore at our peril.
... As a result of this natural selection, humans are bestowed with genes that program thrifty and proinflammatory characteristics. [7][8][9][10] Western populations have passed through a transition from adverse to affluent environments over multiple generations. This transition has minimized the burden of malnutrition and infectious diseases, improved survival of individuals with wasteful and anti-inflammatory characteristics, and consequently, relaxed the selection of genetic variants that program thrifty and proinflammatory characteristics. ...
... The thrifty and proinflammatory genetic variants expressed in an environment with abundance and hygiene contribute to noncommunicable diseases. [7][8][9][10] In developing populations, the transition from adverse to affluent environments has started only recently and is completed within one generation. Here, the selection of thrifty and proinflammatory genetic variants has acted on generations up to those born today. ...
... The epigenetic programming is attuned to the environment experienced in early life and continues to have its effects in later life. 10,16 Western populations are hardly exposed to food shortage and infections early in life. Several generations have been epigenetically attuned to abundance and hygiene, which matches the affluent environments being present throughout their later lives. ...
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With their transition from adverse to affluent environments, developing populations experience a rapid increase in the number of individuals with noncommunicable diseases. Here, we emphasize that developing populations are more susceptible than western populations to acquire these chronic diseases, because their genetic, cultural, and epigenetic characteristics do not match with the eagerly awaited affluent environments. In regard to this, there is an urgent need for public health organizations to reorganize current environments in developing populations so as to fit their inherited characteristics. Unfortunately, this need is neglected as an essential part of the Sustainable Development Goals that form the core of the United Nations' Post-2015 Development Agenda. Only through global collaborative efforts can the environments in developing populations be reorganized and, thereby, the emerging epidemic of noncommunicable diseases be stalled.
... (See e.g. Williams and Nesse (1991); Nesse and Williams (1994); Trevathan (1999); Gluckman and Hanson (2006); Trevathan et al. (2008); Gluckman et al. (2009);Lindeberg (2010).) ...
... In 1 Much evolutionary medicine and mismatch-oriented work (e.g. Eaton and Konner (1985), Nesse and Williams (1994), Gluckman and Hanson (2006), and Lindeberg (2010)) are interested in major environmental changes experienced by the human species, and point to the transition from foraging to agriculture-with its alterations in diet, social structure, activity levels, and so forth-as a particularly significant change. ...
... Nesse and Williams (1994);Gluckman and Hanson (2006);Gluckman et al. (2009) all advance mismatch hypotheses of myopia as well, though their proposed mechanisms of action differ.4 Other discussions of so-called 'ancestral' or 'Paleolithic' diets includeShatin (1964),Shatin (1967),Eaton and Konner (1985),,Lindeberg et al. (1997),Lindeberg et al. (2001),Lindeberg et al. (2007). ...
Article
Evolutionary mismatch is, roughly, poor fit between an organism and its environment. Researchers in evolutionary medicine have proposed mismatch as a possible cause for morbidity and mortality in contemporary Homo sapiens populations. Mismatch hypotheses are often taken to provide an evolutionary explanation for the health outcome in question, while simultaneously offering possible interventions for researchers and clinicians to pursue. A problem: fitness outcomes and health outcomes are distinct. Natural selection operates on fitness, not on health per se. There are cases where increased health may not contribute to fitness in the modern environment. I propose an approach for using evolutionary mismatch in clinical research which sidesteps this problem. The gist of the proposal: given structural analogies between environmental causes of morbidity and environmental causes of fitness reductions, evolutionary mismatch can be used as a heuristic to shrink the space through which clinical and public health researchers must search for possible interventions in response to contemporary health problems.
... It remains unclear, however, why these phenotypic adjustments should persist into adulthood. According to one family of explanations, collectively called Predictive Adaptive Response (PAR) models, relationships between small birth size and adult phenotypes reflect evolutionarily adaptive adjustments made by an energy-limited fetus in expectation of an energy-limited future environment, and so persist because they confer selective advantages in post-natal life (Gluckman and Hanson, 2006;Kuzawa 2005;Kuzawa, 2008;Kuzawa et al., 2007). One PAR model proposes that phenotypes induced by fetal energy scarcity serve the specific adaptive function of down-regulating somatic energy requirements within energy-scarce adult environments : ...
... In keeping with previous research, birth weight (reported to the nearest ounce then converted to grams) was used to indicate fetal energy balance (Gluckman and Hanson, 2006;Gluckman et al., 2007). Participants were asked to contact their mother or to reference a birth record in order to accurately report their own birth weights. ...
... Prenatal growth conditions reflected in birth weight did not predict the sensitivity of metabolic demands to fasting. Because reduced birth weight is the diagnostic indicator employed by PAR models to assess fetal energy scarcity (Gluckman and Hanson, 2006;Gluckman et al., 2007), our PAR-motivated hypothesis predicts that adults of smaller birth size should display relatively enhanced sensitivity of metabolic demands in response to current energy scarcity, conferring relative energetic savings. Energetic savings are generally considered advantageous because they allow redistribution of scarce resources to meet the needs of competing fitness-enhancing functions (Zera and Harshman, 2001). ...
Article
OBJECTIVES: Aiming to test the evolutionary significance of relationships linking prenatal growth conditions to adult phenotypes, this study examined whether birth size predicts energetic savings during fasting. We specifically tested a Predictive Adaptive Response model that predicts greater energetic saving among adults who were born small. METHODS: Data were collected from a convenience sample of young adults living in Albuquerque, NM (n=34). Indirect calorimetry quantified changes in resting energy expenditure (REE) and active muscular efficiency that occurred in response to a 29-hour fast. Multiple regression analyses linked birth weight to baseline and post-fast metabolic values while controlling for appropriate confounders (e.g., sex, body mass). RESULTS: Birth weight did not moderate the relationship between body size and energy expenditure, nor did it predict the magnitude change in REE or muscular efficiency observed from baseline to after fasting. Alternative indicators of birth size were also examined (e.g., low v. normal birth weight, comparison of tertiles), with no effects found. However, baseline muscular efficiency improved by 1.1% per 725 g (S.D.) increase in birth weight (p=0.037). CONCLUSIONS: Birth size did not influence the sensitivity of metabolic demands to fasting—neither at rest nor during activity. Moreover, small birth size predicted a reduction in the efficiency with which muscles convert energy expended into work accomplished. These results do not support the ascription of adaptive function to phenotypes associated with small birth size.
... It remains unclear, however, why these phenotypic adjustments should persist into adulthood. According to one family of explanations, collectively called PAR models, relationships between small birth size and adult phenotypes reflect evolutionarily adaptive adjustments made by an energy-limited fetus in expectation of an energylimited future environment, and so persist because they confer selective advantages in postnatal life (Gluckman and Hanson, 2006;Kuzawa 2005;Kuzawa, 2008;Kuzawa et al., 2007). One PAR model proposes that phenotypes induced by fetal energy scarcity serve the specific adaptive function of down-regulating somatic energy requirements within energy-scarce adult environments : ...
... In keeping with previous research, birth weight (reported to the nearest ounce then converted to grams) was used to indicate fetal energy balance (Gluckman and Hanson, 2006;Gluckman et al., 2007). Participants were asked to contact their mother or to reference a birth record in order to accurately report their own birth weights. ...
... Prenatal growth conditions reflected in birth weight did not predict the sensitivity of metabolic demands to fasting. Because reduced birth weight is the diagnostic indicator employed by PAR models to assess fetal energy scarcity (Gluckman and Hanson, 2006;Gluckman et al., 2007), our PAR-motivated hypothesis predicts that adults of smaller birth size should display relatively enhanced sensitivity of metabolic demands in response to current energy scarcity, conferring relative energetic savings. Energetic savings are generally considered advantageous Efficiency baseline, R 2 5 13% Efficiency after fast, R 2 5 60% ...
Article
Full-text available
OBJECTIVES Aiming to test the evolutionary significance of relationships linking prenatal growth conditions to adult phenotypes, this study examined whether birth size predicts energetic savings during fasting. We specifically tested a Predictive Adaptive Response (PAR) model that predicts greater energetic saving among adults who were born small. METHODS Data were collected from a convenience sample of young adults living in Albuquerque, NM (n = 34). Indirect calorimetry quantified changes in resting energy expenditure (REE) and active muscular efficiency that occurred in response to a 29-h fast. Multiple regression analyses linked birth weight to baseline and post-fast metabolic values while controlling for appropriate confounders (e.g., sex, body mass). RESULTS Birth weight did not moderate the relationship between body size and energy expenditure, nor did it predict the magnitude change in REE or muscular efficiency observed from baseline to after fasting. Alternative indicators of birth size were also examined (e.g., low v. normal birth weight, comparison of tertiles), with no effects found. However, baseline muscular efficiency improved by 1.1% per 725 g (S.D.) increase in birth weight (P = 0.037). CONCLUSIONS Birth size did not influence the sensitivity of metabolic demands to fasting—neither at rest nor during activity. Moreover, small birth size predicted a reduction in the efficiency with which muscles convert energy expended into work accomplished. These results do not support the ascription of adaptive function to phenotypes associated with small birth size.
... In the decade since the fi rst edition of the Handbook of the Life Course was published, life course scholarship has benefited from new analytical tools and expanded data sources, both national and international (see Bynner, this volume), and has expanded its scope across multiple substantive domains, within and beyond the discipline of sociology (Alexander et al. 2014 ;Dannefer 2013 ;Gluckman and Hanson 2008 ;Smith 2005 ;Priestley 2001 ;Laub and Sampson 2003 ); And in this decade, a journal devoted specifi cally to the life course, Advances In Life Course Research , was launched as was an international society dedicated solely to life course scholarship, the Society for Longitudinal and Life Course Studies (SLLS). Clearly, the life course has become an established domain of study in contemporary sociology. ...
... Now famously called the Barker hypothesis, this study helped launch a rich line of inquiry in epidemiology and biology referred to as Fetal Origins of Adult Disease (FOAD). Drawing from the critical or sensitive period model in epidemiology whereby an early-life exposure may be more infl uential on later-life health outcomes because it occurs during a period of vulnerability or rapid development, early origins hypotheses started to appear in epidemiology, sociology, and public health (Gluckman and Hanson 2008 ;Kuh and Ben-Shlomo 2004 ;Doblhammer 2004 ). [see Skogen and Overland ( 2012 ) for a review of the development of FOAD research.] ...
... Instead, gene expression at the molecular level is recognized as conditional on forces external to the cell, including forces in the social environment. Thus, it is increasingly recognized that "… social experiences regulate genetic activity" at the level of intracellular chemistry (Shanahan 2013 : 1;see also Cole 2009 ;Dannefer 2011 ;Gluckman and Hanson 2008 ). The growing recognition of the extent the chemistry of the cell itself is regulated by the environment has led to a suggestion that the study of G-E interactions has entered what some scholars have called a "postgenomic" (Plomin et al. 2002 ) or "neogenomic" (Charney 2012 ) era, and the emergence of several new subfi elds of research, including environmental epigenetics and social genomics. ...
Chapter
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The life course perspective originated with the recognition that an adequate understanding of “lives through time” requires attention to the importance of social context. Since those origins, extensive evidence of ways in which context shapes and organizes life course outcomes has been presented. Yet the problem of formulating an adequate theoretical understanding of context’s role in life course processes and outcomes persists, and remains unresolved. This paper suggests that life course scholarship, even while paying attention to context, has frequently relied on theoretical assumptions based in functionalism that restrict exploration of the full explanatory power of social forces. Contextual factors are “contained” through what we term a functional-developmental nexus. We illustrate this tension by examining three domains of life course inquiry: (1) a consideration of the place of agency in life course studies, (2) research on the early life influences on the life course and (3) the study of gene-environment interactions over the life course.
... Scurvy is a disease resulting from a lack of adequate vitamin C, and is particularly well-known for historically afflicting sailors on long ocean voyages, who typically 2 Credit for coining the term is typically given to Bowlby (1982), cf. Barr (1999), Tooby and Cosmides (2005), Gluckman and Hanson (2006) and Taylor (2015). A related term is 'ancestral environment', preferred by Lloyd et al. (2011) but treated as roughly equivalent to EEA. ...
... 3 See, e.g., Lindeberg (2010, p. 30). As I said in footnote 2, for the sake of brevity I am eliding the full set of views here: some theorists prefer to think of each trait or mechanism as having a specific EEA. 4 See, e.g., Nesse and Williams (1994), Trevathan (1999), Tooby and Cosmides (2005), Gluckman and Hanson (2006), Keller and Nesse (2006), Gluckman et al. (2009), Lindeberg (2010, Lieberman (2013) and Aktipis et al. (2015). 5 Whether we are being given a story about fitness outcomes or health outcomes can sometimes be a bit fuzzy. ...
... As noted in footnote 16, I take it that this sense of optimal environment is not too different from the sense of optimal environments described in Gluckman and Hanson (2006) and Levins (1962Levins ( , 1968. A particular variant's optimal environment is that in which its "best performance" (with respect to fitness) occurs. ...
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In evolutionary medicine, researchers characterize some outcomes as evolutionary mismatch. Mismatch problems arise as the result of organisms living in environments to which they are poorly adapted, typically as the result of some rapid environmental change. Depression, anxiety, obesity, myopia, insomnia, breast cancer, dental problems, and numerous other negative health outcomes have all been characterized as mismatch problems. The exact nature of evolutionary mismatch itself is unclear, however. This leads to a lack of clarity about the sorts of problems that evolutionary mismatch can actually explain. Resolving this challenge is important not only for the evolutionary health literature, but also because the notion of evolutionary mismatch involves central concepts in evolutionary biology: fitness, evolution in changing environments, and so forth. In this paper, I examine two characterizations of mismatch currently in the literature. I propose that we conceptualize mismatch as a relation between an optimal environment and an actual environment. Given an organism and its particular physiology, the optimal environment is the environment in which the organism's fitness is maximized: in other words, the optimal environment is that in which the organism's fitness is as high as it can possibly be. The actual environment is the environment in which the organism actually finds itself. To the extent that there is a discordance between the organism's actual and optimal environments, there is an evolutionary mismatch. In the paper, I show that this account of mismatch gives us the right result when other accounts fail, and provides useful targets for investigation.
... These changes are likely to be mediated by epigenetic mechanisms (Demetriou et al., 2013). In addition, as explained by Gluckman and Hanson in their book, Mismatch (Gluckman and Hanson, 2006), the earlier and earlier sexual maturation of girls is mismatched with psychosocial maturation, which is more and more delayed in both girls and boys. The global market exploits both the 'infantilisation' of society and earlier sexual maturation to increase consumerism and target the marketing of commodities for pre-teens. ...
... One of the problems with intentional exercise as a form of PA is that it often has no immediate purpose other than to expend energy. Although energy expenditure, for its own sake, has positive long-term health consequences in most modern environments, it was not adaptive throughout the vast majority of evolutionary history stretching back to human hunter/gatherers, protohumans, and beyond (Gluckman and Hanson, 2008). Although some types of exercise, such as sports, may serve an additional purpose, many types of exercise, such as running on a treadmill or walking around a track, exemplify PA that would have been unnecessary and thus maladaptive in ancestral times (Lieberman, 2015). ...
Article
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The low rates of regular exercise and overall physical activity (PA) in the general population represent a significant public health challenge. Previous research suggests that, for many people, exercise leads to a negative affective response and, in turn, reduced likelihood of future exercise. The purpose of this paper is to examine this exercise–affect–adherence relationship from an evolutionary perspective. Specifically, we argue that low rates of physical exercise in the general population are a function of the evolved human tendency to avoid unnecessary physical exertion. This innate tendency evolved because it allowed our evolutionary ancestors to conserve energy for physical activities that had immediate adaptive utility such as pursuing prey, escaping predators, and engaging in social and reproductive behaviors. The commonly observed negative affective response to exercise is an evolved proximate psychological mechanism through which humans avoid unnecessary energy expenditure. The fact that the human tendencies toward negative affective response to and avoidance of unnecessary physical activities are innate does not mean that they are unchangeable. Indeed, it is only because of human-engineered changes in our environmental conditions (i.e., it is no longer necessary for us to work for our food) that our predisposition to avoid unnecessary physical exertion has become a liability. Thus, it is well within our capabilities to reengineer our environments to once again make PA necessary or, at least, to serve an immediate functional purpose. We propose a two-pronged approach to PA promotion based on this evolutionary functional perspective: first, to promote exercise and other physical activities that are perceived to have an immediate purpose, and second, to instill greater perceived purpose for a wider range of physical activities. We posit that these strategies are more likely to result in more positive (or less negative) affective responses to exercise, better adherence to exercise programs, and higher rates of overall PA.
... In most cases, this programming is beneficial for health and survival, because the offspring are likely to live in a nutritionally poor environment. On the other hand, if they live in an affluent society later in life, there will likely be a mismatch with this programming, 24) which could lead to metabolic abnormalities such as diabetes mellitus, obesity, and vascular diseases. From an evolutionary viewpoint, this programming can be considered as developmental plasticity (change of phenotype or organ function) for better adapting to adverse living conditions. ...
Article
Non-communicable diseases (NCDs), such as diabetes mellitus and coronary heart disease, are chronic, non-infectious diseases of long duration. NCDs are increasingly widespread worldwide and are becoming a serious health and economic burden. NCDs arise from complex interactions between the genetic make-up of an individual and environmental factors. Several epidemiological studies have revealed that the perinatal environment influences health later in life, and have proposed the concept of developmental programming or developmental origin of health and disease (DOHaD). These studies suggest the importance of life course health care from fetal life, early childhood, adulthood, and through to old age. Recent progress in genomics, proteomics and diagnostic modalities holds promise for identifying high risk groups, predicting latent diseases, and allowing early intervention. Preemptive medicine is the ultimate goal of medicine, but to achieve it, the full participation of the public and all sectors of society is imperative.(Contributed by Hiroo IMURA, M.J.A.).
... It has been suggested that it is the mismatch between the pre-and postnatal environment that renders the offspring susceptible to developing disease at adulthood. 72 In the present study, the environmental condition of hypoxia occurs in ovo and persists after hatching. In this context, it is of interest that significant alterations in blood pressure homoeostasis were evident in male and female adult chickens despite matching of the incubation and post-hatching environments. ...
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Although it is accepted that impaired placental perfusion in complicated pregnancy can slow fetal growth and programme an increased risk of cardiovascular dysfunction at adulthood, the relative contribution of reductions in fetal nutrition and in fetal oxygenation as the triggering stimulus remains unclear. By combining high altitude (HA) with the chick embryo model, we have previously isolated the direct effects of HA hypoxia on embryonic growth and cardiovascular development before hatching. This study isolated the effects of developmental hypoxia on cardiovascular function measured in vivo in conscious adult male and female chickens. Chick embryos were incubated, hatched and raised at sea level (SL, nine males and nine females) or incubated, hatched and raised at HA (seven males and seven females). At 6 months of age, vascular catheters were inserted under general anaesthesia. Five days later, basal blood gas status, basal cardiovascular function and cardiac baroreflex responses were investigated. HA chickens had significantly lower basal arterial PO2 and haemoglobin saturation, and significantly higher haematocrit than SL chickens, independent of the sex of the animal. HA chickens had significantly lower arterial blood pressure than SL chickens, independent of the sex of the animal. Although the gain of the arterial baroreflex was decreased in HA relative to SL male chickens, it was increased in HA relative to SL female chickens. We show that development at HA lowers basal arterial blood pressure and alters baroreflex sensitivity in a sex-dependent manner at adulthood.
... doi:10.1371/journal.pone.0041759.g004 Fetal Liver Blood Flow Distribution strategy has brought with it a predisposition to obesity and later diabetes in contemporary societies with abundant nutrition in later postnatal life [32]. Because the strategy is a fundamental aspect of human biology, it occurs to a degree across the range of infant growth and development, and could be an important determinant of the risk of obesity at the population level. ...
... In humans, with much longer life spans, it is hypothesized that adjustments made by the fetus to maternal cues will confer a survival advantage in the short term, to get through gestation and early life and weaning -but perhaps won't help or will be outright detrimental to health in the long term. Thus the idea of a "mismatch" between uterine or early life milieu, in which the nutritive milieu is encoded by epigenetic controls on gene expression, and the resulting physiology proves ill adapted to the world of plenty in which the individual lives (Gluckman and Hanson 2008). It is an adaptive response that turns out to be out of sync with the actual conditions -in this case, overabundance, sedentary life, and knowledge work, as in the above example. ...
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Through examination of four examples from contemporary metabolic sciences, this article characterizes the rise of a post-industrial metabolism. Concerned with regulation, timing, and information, this understanding of metabolism is analyzed as a shift away from the factory or motor model of classic metabolism, in which food was fuel, providing energy and building blocks to the body. Accordingly, metabolic disorders - treatments for which are the explicit aim of much of this research - are increasingly explained and intervened in as regulatory crises, asynchronies, or instances of misinformation. Close empirical examination of the explanatory frameworks and experimental design of the metabolic sciences answers, with some specificity, the question of the knowledge effects of the demand to translate directly from research to treatments for obesity and diabetes; or, fat knowledge.
... The philosopher of biology Kim Sterelny (2014) focuses on the positive benefits of human intergenerational knowledge transmission but downplays the many negatives. Nested within us are many animal instincts, and also many evolutionary mismatch problems which we cannot simply shake off (Clack, 2009;Gluckman & Hanson, 2008). Dean (1997) applies genetic, neurobiological, and chaos theory to individual lives of substance misuse, suggesting many unpredictable, fractal outcomes. ...
Book
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This review of recent evolutionary theories on psychopathology takes on controversies and contradictions both with established psychological thought and within the evolutionary field itself. Opening with the ancestral origins of the familiar biopsychosocial model of psychological conditions, the book traces distinctive biological and cultural pathways shaping human development and their critical impact on psychiatric and medical disorders. Analyses of disparate phenomena such as jealousy, social anxiety, depressive symptoms, and antisocial behavior describe adaptive functions that have far outlasted their usefulness, or that require further study and perhaps new directions for treatment. In addition, the book’s compelling explorations of violence, greed, addiction, and suicide challenge us to revisit many of our assumptions regarding what it means to be human. Included in the coverage: · Evolutionary foundations of psychiatric compared to non-psychiatric disorders.· Evolutionary psychopathology, uncomplicated depression, and the distinction between normal and disordered sadness. · Depression: is rumination really adaptive? · A CBT approach to coping with sexual betrayal and the green-eyed monster. · Criminology’s modern synthesis: remaking the science of crime with Darwinian insight. · Anthropathology: the abiding malady of the species. With its wealth of interdisciplinary viewpoints, The Evolution of Psychopathology makes an appropriate supplementary text for advanced graduate courses in the evolutionary sciences, particularly in psychology, biology, anthropology, sociology, and philosophy.
... The notion of a mismatch between the environment in which the human body evolved and that in which we live today has been invoked to explain the recent rise in chronic disease prevalence (Gluckman and Hanson 2006), a concept that was earlier an underlying feature of several developmental biology frameworks. The idea of diseases emerging across time as legacies from once useful genes, later interacting with novel environments, was originally tagged as the thrifty gene hypothesis (Neel 1962). ...
Chapter
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Physical growth is an emergent process integrating a complex network of social, biological, and environmental interactions. The global diversity of body shapes and sizes reflects developmental plasticity in response to environmental exposures, both advantageous and adverse, and depicts an evolutionarily robust strategy for species’ survival. Epidemiologic surveillance efforts demonstrate that early life skeletal growth and body composition trajectories are associated with and predict adult chronic disease risks. Both human and animal studies have provided an evidentiary base for the physiological mechanisms by which differences in growth processes manifest as cell- and organ-level changes that influence disease susceptibility across the life course. This chapter leverages a systems biology approach to describe macro- and micropathways affecting growth from a global perspective, reflecting on auxology’s place in theoretical frameworks that help us to understanding past, present, and future health trends. Methodological challenges that face the field are considered, and recommendations to guide future research and policy efforts are offered with the aim of advancing the science of growth biology and its contributions to life course health development.
... Of course, attention to interactions with forces in the domains of biology is warranted, as made clear by the explosion of interest in the ways in which gene expression is itself sensitive to the environment (e.g., Shanahan, 2013;Slavich & Cole, 2013). Indeed, biologists are now seeking out social scientists to understand better how the social and experiential factors regulating epigenetics and related mechanisms are organized (e.g., Dannefer, Kelley-Moore, & Huang, 2015;Gilbert & Epel, 2008;Gluckman & Hanson, 2008). An enhanced understanding of biological and social processes and their interaction are required if the objective is to achieve an adequate understanding of human development. ...
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The need to pay attention to context has been a prominent theme in research on human development. Nevertheless, the empirical reality of the immediate context within which individuals develop has been largely ignored in research on human development. Therefore, my “one wish” is that the field begin to take seriously the processes that operate in the everyday social world. Doing so will help clarify three key principles: advance understanding: 1) diversity in developmental outcomes is largely socially organized; 2) “bi-directional” individual-context interactions are generally asymmetrical; 3) individuals are producers not only of themselves but also of the social world. While it shapes the development of individuals, the social world is also a human creation. These insights can assist developmental research in efforts to broaden its concern to focus on issues of social justice and the analysis of science itself as part of the social world, with cultural, political and ideological dimensions.
... Humans evolved over millennia in egalitarian indigenous cultures that nurtured and revered the young [72]. However, modern society is mismatched with how homo sapiens are biologically designed to live; the result is a breakdown in health, emotional well-being, and social stability [73]. In contrast, Indigenous peoples created cultures of respect that meet the needs of all members of the community. ...
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While there are many “trauma-informed” training programs for professionals, youth are the leading players on the trauma stage. In contemporary cultures of coercion, youth battle adults and become bullies or victims of peers. But Indigenous cultures of respect view children as contributors to the community, not problems to be controlled. This article describes how “trauma-wise youth” can respond to the needs of their peers in pain. Strategies drawn from the circle of courage resilience model and positive peer culture are used to engage youth in helping roles. These developmental relationships heal trauma and build resilience.
... It is unlikely that a significant proportion of our genotype has changed since then, but our lifestyles have [45]. Examining the potential consequences of the incongruities between some human lifestyles and environments today from the conditions under which we originally evolved is growing in popularity by practitioners and advocates of evolutionary (or Darwinian) medicine [46]. " Evolutionary mismatch " is the term typically applied to the negative consequences of the incompatibilities between modern lifestyles/environments and the conditions under which traits originally evolved. ...
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Stress and disease. Although psychological stress is an adaptive phenotypic state necessary for survival, chronic psychological stress in developed, industrialized human populations can be characterized as an immune-altering factor associated with a wide range of allergic, autoimmune, and other inflammatory-related diseases. Modern lifestyles, chronic disease, and psychological stress. Here we present a synopsis of factors in industrialized populations which might increase or decrease psychological stress compared with preindustrialized populations. Several sources are identified which might increase chronic stress in postindustrialized society, although the stress induced by half of those is counterbalanced to some degree by decreasing the likelihood that individuals will be consigned to undesirable social roles that developed following the agricultural revolution. The environment of evolutionary adaptedness and disease. It is hypothesized that chronic stress in industrialized society might exceed that found in our environment of evolutionary adaptedness, particularly for those individuals who, for whatever reason, have not found satisfying social roles among the wide range of options available.
... As such, we can be certain that there are in-built mechanisms that mitigate for such circumstances. This notion also helps point to the cause of such injuries as not being unfortunate happenstance vulnerabilities, but a mismatch between how people live today versus how they lived in the 99% of our species' history, known as the Paleolithic Age (Gluckman and Hanson, 2008). ...
... We address the origins of chronic stress and insomnia here largely from the basis of an evolutionary perspective, namely the evolutionary mismatch hypothesis. This hypothesis identifies the pathophysiology of many human diseases as resulting from traits that were once advantageous to our cave dwelling and primal ancestors but that are maladaptive in modern life, thus a mismatch between environments exists [46] [47]. For instance, we have evolved over millions of years to crave high calorie (sugars and fats) foods due to the scarcity of food in our ancestor's environments, however today we have large surpluses of food and these primal cravings have led us to ever increasing rates of obesity [47]. ...
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Excessive distress and insomnia are much too common in the modern world and often lead to a myriad of detrimental effects including loss of cognitive ability and even physical ailments such as cancer. Current pharmaceutical treatments can be addictive, detrimental to health, and in the case of insomnia don’t produce naturalistic sleep. We present a viewpoint on a potential adjunctive treatment of distress and insomnia that harnesses specific mental imagery as a component of mind/body relaxation technique. Via our perspective on the modern nature of stress and insomnia, our theoretical perspective on how specific guided mental imagery can be used to treat these ailments, and our review on the current literature on treatment with mental imagery, we hope to stimulate further research into mental health treatment with mental imagery which has traditionally been neglected. This perspective on the pathology of insomnia and distress is founded in prevailing “dysevolution” and hyper-arousal theories. Hyper-arousal is characterized in part by a vicious cycle of chronic physiological and emotional stimulation/distress. We argue for spatially based mental imagery in the form of nighttime-sky imagery to attenuate such pathology by breaking one away from a vicious cycle of stimulation and distress and discuss neuropsychological bases for its potential treatment mechanisms which include the autonomic nervous system and a phenomenal foundation of conscious cognition.
... Indeed, some scholars have long called attention to the importance of biology for life course studies (e.g., Dannefer, 1999, Riley & Bond, 1983 and more recently, the study of gene-environment interactions has become an active field of life course scholarship (e.g., Dannefer, 2011;Douthit, Dannefer, & Kelley-Moore, 2011;Shanahan & Hofer, 2005;Shanahan, Hofer, & Shanahan, 2003). Specifically related to later life health and well-being, there is increasing attention to social conditions both in prenatal and early childhood environments (e.g., nutrition, toxicity) that may fix with some permanence hormonal and metabolic parameters (Adair, 2007(Adair, , 2008Barker, 1990;Dannefer, 2011;Gluckman & Hanson, 2006;Gluckman, Hanson, Cooper, & Thornburg, 2008). Along with additive and accumulative processes over the life course, such factors may have a direct impact on adult health (Ferraro & Kelley-Moore, 2003;Ferraro, Shippee, & Schafer, 2009). ...
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UANE Alwin is to be thanked for an ambitious effort to provide a systematic review of the diverse array of meanings of “life course” and related terms and to contrib-ute to the discussion of the possibilities of integration of this important but often unwieldy literature. It is an undertaking that invites reaction at many points. Of course, space pre-cludes a comprehensive response to the full range of ideas and issues Alwin presents. I limit my comment to three top-ics that warrant further attention: (a) the importance of the life course as a social institution, (b) the relation of the “life span” and “life course” concepts, and (c) the need to address what I have earlier identified as theoretical deficiencies that are common to both life span and life course perspectives.At the beginning of his essay “Integrating Varieties of Life-Course Concepts” (hereafter termed “IVLC”), Alwin counter-poses the risks that may be present when a single term is used to connote “a multiplicity of meanings that are at variance with one another” with the benefits that may come from a concept whose breadth offers “rich tapestry of different emphases.” I am sympathetic to Alwin’s caution of the dangers inherent in requiring a single term—life course—to carry a “multiplicity of meanings,” which is the more worrisome when the use of the term is accompanied by unexamined assumptions and a lack of consistency in explanatory objectives. In attempting to bring some order to this unwieldy domain, I applaud and appreciate the taxonomic and integrative objectives of IVLC. In this comment, I will note some significant arenas in which the formulation offered in IVLC needs to be extended in terms of conceptual scope, precision, and critical analysis.Although the array of terms, concepts, and issues intro-duced in IVLC do indeed represent quite a varied collec-tion, I must begin by taking note of the need to add yet even more “richness to the tapestry.” The task of integration pre-supposes that the components essential to the integrative ef-fort have been identified, and it is necessary to begin by pointing out at least one omitted but essential class of phe-nomena, which revolve around the concept of the life course as a social institution.
... This concept of 'mismatch' is crucial for understanding and explaining the existence of many diseases and disorders of modernity such as obesity, metabolic syndrome, Type 2 diabetes, eating disorders, and many others. Evolutionary mismatch occurs when the environment changes too rapidly for selection to be able to track it, resulting in residual traits that are no longer suited to the (Gluckman and Hanson, 2006). Furthermore, the extreme ends of functional adaptations can become maladaptive e.g. when adaptive personality traits are magnified (Trull and Widiger, 2013). ...
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In an ideal world, psychiatry would be appropriately informed by evolutionary theory and we expect that this will happen one day. In this chapter salient evolutionary contributions regarding the definition and demarcation of mental disorder are considered as well as evolutionary proposals for rethinking the classification of mental disorder. Although evolutionary analysis of mental disorders rests on a set of principles shared with the rest of medicine, these principles remain unfamiliar to the majority of psychiatrists. We examine these principles and advocate consideration of the phylogenetic or ultimate causes of disorders and how Tinbergen’s four questions may be applied to psychiatry. Leading evolutionary literature on a number of psychiatric conditions is explored including: schizophrenia spectrum disorders, depression, alcohol and drug addictions, eating disorders and others. Some preliminary evolutionary thoughts on placebo responses, pharmacological treatments and future research are also presented in brief. Mainstream psychiatry, like the rest of medicine, continues to focus on proximate causation of disease and disorder. Evolutionary science has not permeated the syllabus of most undergraduate or postgraduate medical and psychiatric education, with a few notable exceptions. Consequently, most psychiatrists have scant understanding of even the basics of evolution let alone its impact on the behavioural sciences. Therefore, the majority of psychiatrists and other mental health professionals remain largely unaware of the potential of Darwinian theory to further our understanding of human vulnerability to mental disorder. Evolutionary work consequently has not yet significantly influenced the mainstream research agenda in mental health nor has it had much impact on clinical practice. Various barriers to the incorporation and dissemination of evolutionary thinking into psychiatry are discussed, some of which are shared by the rest of medicine. Finally, we contemplate the potential contributions evolutionary science can generate for both theory and practice of psychiatry and advocate for pertinent areas of evolutionary biology to be taught at both the undergraduate and postgraduate levels as a basic science.
... However, the recent publication from the Centre for Global Development stressed the importance of a focus on adolescence in addressing a range of widespread problems including NCD (26). We previously pointed out that puberty and adolescence are good examples of life history plasticity, evolutionary mismatch and its adverse consequences (22,6). Tanner (27) showed the secular trend in the falling age at menarche in many Western countries since 1850. ...
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... There is only space for brief review of these topics. Other, more extensive reviews of various aspects of the fetal programming hypothesis and its implications may be found in (Bateson et al., 2004; Gluckman, Hanson, Cooper, and Thornburg, 2008). ...
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Human Evolutionary Biology The introduction of the ‘fetal programming hypothesis’, first in epidemiology, subsequently in a broad range of disciplines concerned with developmental biology, has generated new interest in phenotypic plasticity, the mechanisms that govern it, and its place in evolutionary biology. A number of epidemiological studies link small size at birth, assumed to be a consequence of constrained prenatal energy availability, with adverse effects on the risk of chronic diseases later in life. The cluster of chronic diseases associated with the metabolic syndrome and alterations of glucose metabolism are particularly implicated. Recent evidence suggests that epigenetic modification of gene expression affecting the hypothalamic-pituitary-adrenal (HPA) axis may be involved in these effects. In animal studies epigenetic alteration of HPA axis activity and responsiveness is associated with changes in adult behaviour and stress responsiveness. The potential for similar effects to contribute to psychological and psychiatric outcomes in humans has been explored in a number of contexts, including famine exposure, observed covariance with birth weight, and prenatal dexamethasone treatment of fetuses at risk of congenital adrenal hyperplasia. While fetal programming effects have now been widely demonstrated across species and human populations, the adaptive significance of these effects is still a matter of debate.
... It is beyond my expertise to review the possible effects of epigenesis, processes through which environments contribute to inherited modes of gene expression across multiple generations without modification of DNA. The extent and durability of these effects in humans is the subject of ongoing debate and research (e.g., Gluckman and Hanson 2006; Jablonka and Lamb 2005). A related but distinct set of mechanisms may arise through grandparent effects on genetic transmission and expression in the female line. ...
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The study of intergenerational mobility and most population research are governed by a two-generation (parent-to-offspring) view of intergenerational influence, to the neglect of the effects of grandparents and other ancestors and nonresident contemporary kin. While appropriate for some populations in some periods, this perspective may omit important sources of intergenerational continuity of family-based social inequality. Social institutions, which transcend individual lives, help support multigenerational influence, particularly at the extreme top and bottom of the social hierarchy, but to some extent in the middle as well. Multigenerational influence also works through demographic processes because families influence subsequent generations through differential fertility and survival, migration, and marriage patterns, as well as through direct transmission of socioeconomic rewards, statuses, and positions. Future research should attend more closely to multigenerational effects; to the tandem nature of demographic and socioeconomic reproduction; and to data, measures, and models that transcend co-resident nuclear families.
... doi:10.1371/journal.pone.0041759.g004 Fetal Liver Blood Flow Distribution strategy has brought with it a predisposition to obesity and later diabetes in contemporary societies with abundant nutrition in later postnatal life [32]. Because the strategy is a fundamental aspect of human biology, it occurs to a degree across the range of infant growth and development, and could be an important determinant of the risk of obesity at the population level. ...
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Thesis
As the past decade built toward today’s crisis, Scandinavian social democracy was frequently suggested as a model that could reform capitalism. The Nordic region’s income equality, gender equality, low-conflict politics, and prosperous economies with generous benefits contribute to high levels of happiness and social cohesion. Leading politicians on the American Left, as well as a majority of young Americans, express that they would prefer such outcomes. But is the Nordic Model suitable for cross-cultural export? This study examines the cultural origins of Scandinavian egalitarianism by applying an evolutionary perspective to ten influential works of fiction. These criticisms—ranging from an Icelandic saga to Swedish posthumanist TV—align to trace the emergence of modernity in the Nordic region. These works illustrate how fiction can be an evolutionary tool when environmental change requires that communities update the story they live by, their master-narrative. This study analyzes the ideological evolution from the polytheistic beliefs of Viking kinship societies, to Christian monotheism, to religious and later secular humanism, the master-narrative of the modern world. With each of these transitions, communities face a narrative abyss. The unquestionable story that had provided meaning, informed their cooperation, and dictated which future to strive for becomes transparent to them. Homo sapiens need such stories, or their larger communities come unglued. Reading these Nordic case studies through an evolutionary lens illuminates the brain mechanisms that make us factionalize, fall prey to anxiety, double down on orthodoxy, or even kill our neighbors during these master-narrative transitions. This study proposes that the West entered into such a transition in the 2010s. No longer convinced by liberal humanism, some populations have reverted to older stories of nationalism or tribal belonging. Until people are able to unite around a new master-narrative, things could get worse. The tenth work of fiction points to the leading candidate for becoming tomorrow’s uniting story: dataism. This study concludes that social democracy arose from uniquely Nordic experiences, which makes the political model unlikely to work well elsewhere. But insights from this journey through a millennium of cultural change illuminate the challenges humanity faces in the twenty-first century.
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Hereditary, environmental, and stochastic factors determine a child's growth in his unique environment, but their relative contribution to the phenotypic outcome and the extent of stochastic programming that is required to alter human phenotypes is not known because few data are available. This is an attempt to use evolutionary life-history theory in understanding child growth in a broad evolutionary perspective, using the data and theory of evolutionary predictive adaptive growth-related strategies. Transitions from one life-history phase to the next have inherent adaptive plasticity in their timing. Humans evolved to withstand energy crises by decreasing their body size, and evolutionary short-term adaptations to energy crises utilize a plasticity that modifies the timing of transition from infancy into childhood, culminating in short stature in times of energy crisis. Transition to juvenility is part of a strategy of conversion from a period of total dependence on the family and tribe for provision and security to self-supply, and a degree of adaptive plasticity is provided and determines body composition. Transition to adolescence entails plasticity in adapting to energy resources, other environmental cues, and the social needs of the maturing adolescent to determine life-span and the period of fecundity and fertility. Fundamental questions are raised by a life-history approach to the unique growth pattern of each child in his given genetic background and current environment.
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Epidemiological studies demonstrated a clear phenomenological association between low birth weight and increased cardiometabolic risk later in life, very similar to that in high birth weight subjects. Pre- and/or neonatal overfeeding appears to be an etiological clue. In animal studies, irrespective of birth weight neonatal over-nutrition leads to later overweight, impaired glucose tolerance and cardiometabolic alterations. Probably, perinatally acquired alterations of DNA methylation patterns of gene promoters of central nervous regulators of body weight and metabolism play a key role in mediating these relationships. In humans, the long-term impact of neonatal nutrition is conclusively demonstrated by studies on the consequences of breastfeeding vs. formula-feeding. Taken together, the quantity and quality of nutrition during neonatal life plays a critical role, beyond prenatal development, in the long-term programming of health and disease. This opens a variety of opportunities and challenges to primarily prevent chronic diseases, e.g. the metabolic syndrome.
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Objective: Modern immunology has been extremely successful in elucidating many features of the immune system, but not in stemming pandemics of non-infectious, immune-related disease associated with industrialized populations. These pandemics involve a broad range of allergic, autoimmune, and inflammatory diseases, potentially including neuroinflammatory-associated disorders. It is the purpose of this review to outline the literature pointing toward the causes and potential treatments of these problems. Conclusions: A wide range of evidence from the fields of clinical medicine, biomedical research, evolutionary biology, anthropology, epidemiology, immunology, and ecology point to the conclusion that pandemics of non-infectious, immune-related conditions arise from consequences of industrialization. Primary among these consequences is the loss of helminths from the ecosystem of the human body, the 'human biome'. In this view, helminths comprise a 'keystone species' of the human biome, and their loss is profoundly felt as pandemics of non-infectious, immune-related disease. Fortunately, evidence indicates that the consequences of industrialization that cause immune disease, such as helminth depletion, can be effectively avoided. Using this approach, it is expected that further pandemics of immune disease may be prevented, although it remains to be established whether prophylaxis rather than treatment of disease is required for some disorders. Thus, it is predicted that those who will succeed in curing and preventing immune-related disease will focus on addressing 'evolutionary mismatches' rather than simply on the molecular and genetic underpinnings of immunological disorders.
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Background: By combining the chick embryo model with incubation at high altitude (HA), the effects of chronic hypoxia on fetal growth, fetal cardiac and aortic wall remodeling and systemic arterial blood pressure at adulthood were reported. Using non-invasive functional echocardiography, here we investigated the in vivo effects of HA hypoxia on the pulmonary circulation at adulthood in male and female chickens. Methods and results: Chick embryos were incubated, hatched and raised at sea level (SL) or at HA. At 6 months of age, functional echocardiography was performed and the body and heart weights were taken. Heart weight was heavier in males but not in female HA chickens compared to their same sex SL counterparts. Similarly, male but not female HA chickens had greater in vivo right ventricular wall thickness compared to their same sex SL counterparts. The tricuspid pressure gradient was greatly enhanced in HA male and HA female chickens. However, the increment in the tricuspid pressure gradient was greater in HA males than in HA females. The pulmonary artery diameter was also enhanced in HA males than in SL males. In contrast, HA did not affect this variable in female chickens. Conclusions: The data show that chronic hypoxia during development at HA is associated with echocardiocraphic indices of pulmonary hypertension at adulthood in a highly sex-dependent manner.
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Background Following wider acceptance of “the thrifty phenotype” hypothesis and the convincing evidence that early life exposures can influence adult health even decades after the exposure, much interest has been placed on the mechanisms through which early life exposures become biologically embedded.Methods In this review, we summarize the current literature regarding biological embedding of early life experiences. To this end we conducted a literature search to identify studies investigating early life exposures in relation to DNA methylation changes. In addition, we summarize the challenges faced in investigations of epigenetic effects, stemming from the peculiarities of this emergent and complex field. A proper systematic review and meta-analyses were not feasible given the nature of the evidence.ResultsWe identified 7 studies on early life socioeconomic circumstances, 10 studies on childhood obesity, and 6 studies on early life nutrition all relating to DNA methylation changes that met the stipulated inclusion criteria. The pool of evidence gathered, albeit small, favours a role of epigenetics and DNA methylation in biological embedding, but replication of findings, multiple comparison corrections, publication bias, and causality are concerns remaining to be addressed in future investigations.Conclusions Based on these results, we hypothesize that epigenetics, in particular DNA methylation, is a plausible mechanism through which early life exposures are biologically embedded. This review describes the current status of the field and acts as a stepping stone for future, better designed investigations on how early life exposures might become biologically embedded through epigenetic effects.This article is protected by copyright. All rights reserved.
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Life is principally a process of permanent environment-dependent development. Developmental origins of health and diseases are particularly sustainable if shaped during critical periods in prenatal and early postnatal life. The key to the approach is an environment-dependent epigenomic and microstructural conditioning of the organism, leading to a homeostatic calibration of functional and tolerance ranges from the subcellular up to the organismic levels (vegetative imprinting). This process, in terms of a developmental vegetative “training”, serves to optimize the self-organization of an organism in order to cope with the environmental conditions during later life. It generally occurs normatively as a basic mechanism of ontogenesis. Through alterations of the prenatal and neonatal environment it may become disadvantageous or even harmful for long-term individual health. Most important and sustainable effects occur if the main regulatory instances of the organism are affected, i.e. the genome and/or the brain. For instance, perinatal overfeeding, suggesting an affluent environment, has been shown epidemiologically, clinically and experimentally to induce epigenomic and microstructural malprogramming of the hypothalamo-adipo-pancreatic system, leading to long-term increased “diabesity” risk. Similar mechanisms have been identified for conditioning of stress responsiveness and other fundamental life functions. In general, distress, disnutrition and disruptors (unfavorable xenobiotics) appear to be the fundamental risk factors of regular vegetative programming (distress-disnutrition hypothesis and 3-D concept on perinatal malimprinting), potentially leading to acquired health risks throughout later life. In the future this opens up multiple chances and challenges for a genuine, lasting, primary prevention in developmental medicine through the recognition, avoidance and/or adequate treatment of maternofetal and/or early postnatal malexposures.
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This chapter presents a new conceptual framework to characterize the interactions between modern environments and ancestral physiology that can influence health over the life course. Although the human body was not designed by natural selection to maximize health, it was nonetheless designed to function within certain environmental parameters. Physiology serves as the essential interface between genes and environment not only during life history transitions but also during short-term responses needed to regulate the impact of environmental variation on the internal state. Here, I argue that the contemporary habitat has become an “extreme environment” in the sense that, much like climbing Mount Everest, it requires the human body (and psyche) to function beyond the limits of its adaptive capacity, with potential dire consequences to health. Adaptive mechanisms that have become dysfunctional in an extreme environment show three distinct features: (1) gradient effects, often without overt signs of dysfunction, whereby (2) compensatory mechanisms themselves become the source of illness, and (3) involve systemic repercussions. I present an analysis of altitude hypoxia to illustrate an extreme environmental condition and then apply the same framework to a consideration of metabolic disorders. A conceptual framework that identifies lifestyle factors as being equivalent to entering an extreme environment conveys an immediate, intuitive sense of urgency and an implicit recognition that the human organism has strayed into a habitat for which it is ill equipped.
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In recent years, an overwhelming number of epidemiological, clinical, and experimental data have shown that exposures during prenatal and early postnatal life influence the risk of developing chronic diseases during childhood and adulthood (e.g., obesity, type 2 diabetes, cardiovascular disease).
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This chapter focuses on the evidence that early life under or overnutrition can exert powerful effects, termed 'programming', upon the development of organs and systems. These programming effects are an important risk factor for disease. It reviews some proposed mechanisms that link nutrition during fetal life to diseases such as coronary heart disease and diabetes in the older adult. Rapid catch-up growth in infancy, following fetal growth restriction, increases the disease risk associated with a poor maternal diet in pregnancy. Animal studies show that restricted intakes or excessive intakes of a variety of macro- and micronutrients in pregnancy programme obesity, glucose intolerance and high blood pressure in the developing fetus. Candidate mechanisms proposed to explain the association between maternal nutrition and disease in the offspring include disturbance of maternal-fetal hormone exchange across the placenta, specific nutrient-gene interactions that impact on tissue development and disruption of epigenetic regulation of gene expression.
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A view of negative human evolution is put forward here by way of balance against the many positive, sometimes romantic, ‘ascent of man’, or academically cautious and narrow accounts.¹ Anthropathology is advanced as a hypothetical, quasi-singular entity with multiple roots and micro-manifestations, with some attempt being made to suggest a chronology and a speculative aetiology. Anthropathology is characterised by damaging features such as violence, greed, deception, extended niche construction, and complex suffering on a scale never been known among other species. This is an interdisciplinary endeavour that will probably not satisfy readers with demands for detailed, specialist, and evidence-based prose. No attempt is made to proffer solutions to the existential problem of anthropathology. Given certain controversial aspects, a look at cognate disciplines and epistemological tensions is included.
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In this study some typical aspects of human behavior are reconsidered in a new evolutionary perspective. Firstly, a theoretical paradigm is introduced, according to which animals show a natural propensity to maintain behavior far beyond the time when the triggering motivation has been removed;, these drifting conducts are defined as Vestigial Drifting Drives or (VDDs). Such a paradigm is then applied to those human attitudes that once conferred an adaptive advantage on our species but have now become dysfunctional within the framework of the current ecological crisis. In this context, human beings are considered the repository of VDDs that may play out as evolutionary threats. This thesis is supported by many examples and references that, hopefully, could stimulate scientific debate and further research in evolutionary anthropology, psychology, and related disciplines.
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en Geologists have declared an epochal transition to the Anthropocene, formally recognizing humans as the driving force of destructive global change; a distinction can no longer be made between human history and natural history. Certain commentators argue that Capitalocene better characterizes the situation, given that the effects of planetary decimation and global warming are not equally distributed among humans. A second conceptual change has recently taken place in which genomes are recognized as reactive to environmental stimuli both external and internal to the human body. In the post‐genomic era, genes neither initiate life nor drive human development. The science of the bourgeoning field of behavioural epigenetics is introduced, followed by illustrative examples of environmentally caused epigenetic changes that impact negatively on health. Epigeneticists routinely delimit their attention to detecting measurable changes at the molecular level. It is argued that anthropological contributions that incorporate subjective accounts of embodiment involving past and present events are crucial in order to better situate and account for biological differences and health outcomes historically, ecologically, and politically. Discussion of the microbiome provides a cautionary reminder that microbes are the ultimate driving force of health and illness. In conclusion, the Earth Optimism movement is briefly introduced, as is the concept of resilience, but alone these positive moves will not curb unremitting global warming. Abstrait fr Environnements mutables et corps humains perméables Résumé Les géologues ont défini une transition d’ère vers l'Anthropocène, reconnaissant ainsi formellement le rôle moteur des humains dans les changements destructeurs à l’échelle mondiale : il n'y a désormais plus de distinction entre histoire humaine et histoire naturelle. Certains commentateurs estiment cependant que le terme de « Capitalocène » décrit mieux la situation, puisque les effets de la décimation planétaire et du réchauffement climatique ne sont pas également répartis entre les humains. Un deuxième changement conceptuel s'est récemment produit, avec la reconnaissance du fait que le génome réagit à des stimuli environnementaux extérieurs aussi bien qu'intérieurs au corps humain. Dans l’ère postgénomique, les gènes ne sont pas à l'origine de la vie et ne sont pas non plus les moteurs du développement humain. L'auteure présente ici le domaine naissant de l’épigénétique comportementale, qu'elle illustre d'exemples de changements épigénétiques néfastes pour la santé causés par l'environnement. Les épigénéticiens limitent habituellement leur objet à la détection des changements décelables au niveau moléculaire. L'auteure avance que l'apport anthropologique de récits subjectifs d'incorporation, relatifs à des événements présents et passés, est indispensable pour mieux situer et expliquer les différences biologiques et l’évolution des paramètres de santé du point de vue historique, écologique et politique. La discussion du microbiome rappelle que les micro‐organismes sont, en dernier recours, la force qui fait la santé et la maladie. En conclusion, l'auteure présente rapidement le mouvement « Earth Optimist » et le concept de résilience, tout en précisant que ces mouvements positifs ne suffiront pas à enrayer l'implacable réchauffement climatique.
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I test the Developmental Origins of Health and Disease hypothesis using a cohort perspective on mortality. I combine data from the National Health Interview Survey Linked Mortality Files, 1986–2006, and U.S. economic data between 1902 and 1956 (403,746 respondents and 39,439 deaths), to estimate how exposures to adverse economic conditions in utero and during the first three years of life affect circulatory disease mortality risk in adulthood. I also examine cohort‐based variation in these associations. Findings suggest that in utero exposures to poor economic conditions increased risk of death from circulatory diseases. Results are consistent with theory and evidence suggesting that developmental processes early in life are strongly associated with circulatory disease susceptibility in older adulthood. However, findings indicate that the mortality effects of these early‐life exposures have likely weakened across birth cohorts.
Article
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Mental Illnesses, particularly anxiety, insomnia, and depression often involve vicious cycles which are self-perpetuating and can trap one into a more chronic state. For example in the case of insomnia, sympathetic overactivity, intrusive thoughts, and emotional instability due to sleep loss can perpetuate further sleep loss the next night and so on. In this article, we put forward a perspective on breaking these vicious cycles based on preeminent theories in global and spatial cognition, that the foundation of the conscious mind is a spatial coordinate system. Based on this we discuss the potential and future of virtual reality therapeutic applications which utilize massive virtual spaces along with biofeedback designed to help break perpetual cycles in depression, anxiety, and insomnia. “Massive spaces” are those which are truly expansive such as when looking to the clear night sky. These virtual realities may take the form of a night sky, fantastical cosmic scenes, or other scenes such as mountain tops. We also hope to inspire research into such a spatial foundation of mind, use of perceived massive spaces for therapy, and the integration of biofeedback into virtual therapies.
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Human body systems Representation of planetary system boundaries Representation of human system boundaries Representation of the set of human lifestyle diseases Towards a method for identifying remedial correspondences Patterns essential to individual and global health? (Annex A) Lifestyle diseases as metaphors Global and planetary problems as metaphors Cognitive entanglement Interrelating planetary and human systems through disease metaphors Preoccupations of individual and global 'self-healing' Towards a University of Earth? (Annex B)
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