Obesity from a Biocultural Perspective (original) (raw)
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Obesity in biocultural perspective
Annu. Rev. Anthropol., 2006
Obesity is new in human evolutionary history, having become possible at the population level with increased food security. Across the past 60 years, social, economic, and technological changes have altered patterns of life almost everywhere on Earth. In tandem, changes in diet and physical activity patterns have been central to the emergence of obesity among many of the world's populations, including the developing world. Increasing global rates of obesity are broadly attributed to environments that are obesogenic, against an evolutionary heritage that is maladaptive in these new contexts. Obesity has been studied using genetic, physiological, psychological, behavioral, cultural, environmental, and economic frameworks. Although most obesity research is firmly embedded within disciplinary boundaries, some convergence between genetics, physiology, and eating behavior has taken place recently. This chapter reviews changing patterns and understandings of obesity from these diverse perspectives. 337 Annu. Rev. Anthropol. 2006.35:337-360. Downloaded from arjournals.annualreviews.org by Appalachian State University on 08/13/08. For personal use only. 338 Ulijaszek · Lofink Annu. Rev. Anthropol. 2006.35:337-360. Downloaded from arjournals.annualreviews.org by Appalachian State University on 08/13/08. For personal use only. www.annualreviews.org • Obesity in Biocultural Perspective 339 Annu. Rev. Anthropol. 2006.35:337-360. Downloaded from arjournals.annualreviews.org by Appalachian State University on 08/13/08. For personal use only.
Obesity - a natural consequence of human evolution
Anthropological Review, 2000
Obesity is considered a major epidemic of the 21st century. In developed countries, about 1/3 of adults are obese and another 1/3 overweight according to the oversimplified measure -the Body Mass Index. More precise indicators of adiposity: waist circumference, skinfolds, underwater weighing and absorptiometry indicate similar levels of fatness. Obesity per se does not necessarily lead to pathological states, nor to premature mortality. Recent results of large sample studies indicate that more than 1/3 of people classified as obese by fatness indices are physiologically normal. Others, however, suffer from a number of pathological conditions, common among them being the metabolic syndrome and cardiovascular disease. The classical explanation for increasing obesity is the positive energy balance -too much food intake and too little exercise. It seems, however, that this explanation is too simplistic. In societies, and in families, exposed to overeating and lazy lifestyles, about 1/3 of individuals have normal body mass and low levels of fatness, while others become obese. There is, therefore, individual variation in propensity for obesity. We have identified two specific variables differentiating fatness. People who have large lean trunk frames -large volumes of abdominal cavities and thus large gastrointestinal tracts -put on more subcutaneous fat than those with smaller trunk frames (Henneberg and Ulijaszek 2010). This may be a result of larger volumes of food required for antral extension to release ghrelin, or larger surface area of small intestines for food absorption. The second variable is concentrations of Alanine Transaminase, an enzyme responsible for conversion of an amino acid to a carbon skeleton that can be used in fat synthesis. Our study of 46000 young Swiss males (Henneberg, Rühli, Gruber and Woitek 2011) found consistent correlation between levels of Alanine Transaminase and body weight in groups of normal body mass individuals, overweight individuals and moderately obese individuals. Coupling this finding with the fact that among vegetarians, even those living in North America with overabundance of food and low levels of exercise, obesity and overweight are much less common than among non-vegetarians, we have now hypothesized that the increased obesity of modern affluent societies is a result of consumption of animal protein when energy needs are already covered by carbohydrates and fat consumed concurrently. Until the advent of agriculture, humans relied on consumption of a variety of terrestrial and aquatic animals supplemented by relatively small amounts of plant foods. In this situation our bodies became adapted to use proteins as a source of energy, and became efficient at storing occasional surpluses of amino acids by their deamination and conversion to fats. In the modern diets carbohydrates are abundant and provide, together with fats, energy required by human bodies, proteins after deamination are efficiently converted to fats. When new types of crops are introduced to mass production of cheap foods our bodies may not be able to react correctly to all their contents and some of the ingredients may cause additional fatness. An example of widespread recent introduction of industrially processed soybean products that correlates with prevalence of obesity across countries of the world is discussed.
Genetic predisposition to obesity presents a paradox: how do genetic variants with a detrimental impact on human health persist through evolutionary time? Numerous hypotheses, such as the thrifty genotype hypothesis, attempt to explain this phenomenon yet fail to provide a justification for the modern obesity epidemic. In this critical review, we appraise existing theories explaining the evolutionary origins of obesity and explore novel biological and sociocultural agents of evolutionary change to help explain the modern-day distribution of obesity-predisposing variants. Genetic drift, acting as a form of 'blind justice,' may randomly affect allele frequencies across generations while gene pleiotropy and adaptations to diverse environments may explain the rise and subsequent selection of obesity risk alleles. As an adaptive response, epigenetic regulation of gene expression may impact the manifestation of genetic predisposition to obesity. Finally, exposure to malnutrition and disease epidemics in the wake of oppressive social systems, culturally mediated notions of attractiveness and desirability, and diverse mating systems may play a role in shaping the human genome. As an important first step towards the identification of important drivers of obesity gene evolution, this review may inform empirical research focused on testing evolutionary theories by way of population genetics and mathematical modelling.
The evolution of human fatness and susceptibility to obesity: an ethological approach
Biological Reviews, 2006
Human susceptibility to obesity is an unusual phenomenon amongst animals. An evolutionary analysis, identifying factors favouring the capacity for fat deposition, may aid in the development of preventive public health strategies. This article considers the proximate causes, ontogeny, fitness value and evolutionary history of human fat deposition. Proximate causes include diet composition, physical activity level, feeding behaviour, endocrine and genetic factors, psychological traits, and exposure to broader environmental factors. Fat deposition peaks during late gestation and early infancy, and again during adolescence in females. As in other species, human fat stores not only buffer malnutrition, but also regulate reproduction and immune function, and are subject to sexual selection. Nevertheless, our characteristic ontogenetic pattern of fat deposition, along with relatively high fatness in adulthood, contrasts with the phenotype of other mammals occupying the tropical savannah environment in which hominids evolved. The increased value of energy stores in our species can be attributed to factors increasing either uncertainty in energy availability, or vulnerability to that uncertainty. Early hominid evolution was characterised by adaptation to a more seasonal environment, when selection would have favoured general thriftiness. The evolution of the large expensive brain in the genus Homo then favoured increased energy stores in the reproducing female, and in the offspring in early life. More recently, the introduction of agriculture has had three significant effects : exposure to regular famine ; adaptation to a variety of local niches favouring population-specific adaptations; and the development of social hierarchies which predispose to differential exposure to environmental pressures. Thus, humans have persistently encountered greater energy stress than that experienced by their closest living relatives during recent evolution. The capacity to accumulate fat has therefore been a major adaptive feature of our species, but is now increasingly maladaptive in the modern environment where fluctuations in energy supply have been minimised, and productivity is dependent on mechanisation rather than physical effort. Alterations to the obesogenic environment are predicted to play a key role in reducing the prevalence of obesity.
On the Evolutionary Origins of Obesity: A New Hypothesis
Obesity is an escalating threat of pandemic proportions, currently affecting billions of people worldwide and exerting a devastating socioeconomic influence in industrialized countries. Despite intensive efforts to curtail obesity, results have proved disappointing. Although it is well recognized that obesity is a result of gene-environment interactions and that predisposition to obesity lies predominantly in our evolutionary past, there is much debate as to the precise nature of how our evolutionary past contributed to obesity. The "thrifty genotype" hypothesis suggests that obesity in industrialized countries is a throwback to our ancestors having undergone positive selection for genes that favored energy storage as a consequence of the cyclical episodes of famine and surplus after the advent of farming 10 000 years ago. Conversely, the "drifty genotype" hypothesis contends that the prevalence of thrifty genes is not a result of positive selection for energy-storage genes but attributable to genetic drift resulting from the removal of predative selection pressures. Both theories, however, assume that selection pressures the ancestors of modern humans living in western societies faced were the same. Moreover, neither theory adequately explains the impact of globalization and changing population demographics on the genetic basis for obesity in developed countries, despite clear evidence for ethnic variation in obesity susceptibility and related metabolic disorders. In this article, we propose that the modern obesity pandemic in industrialized countries is a result of the differential exposure of the ancestors of modern humans to environmental factors that began when modern humans left Africa around 70 000 years ago and migrated through the globe, reaching the Americas around 20 000 years ago. This article serves to elucidate how an understanding of ethnic differences in genetic susceptibility to obesity and the metabolic syndrome, in the context of historic human population redistribution, could be used in the treatment of obesity in industrialized countries.