Book contents
- Frontmatter
- Contents
- List of contributors
- Preface
- Part I Theory and Methods
- Part II Phenotypic and Genotypic Variation
- Part III Reproduction
- Part IV Growth and Development
- Part V Health and Disease
- 27 Evolutionary Medicine, Immunity, and Infectious Disease
- 28 Complex Chronic Diseases in Evolutionary Perspective
- 29 Evolutionary Medicine and the Causes of Chronic Disease
- 30 Beyond Feast–Famine: Brain Evolution, Human Life History, and the Metabolic Syndrome
- 31 Human Longevity and Senescence
- 32 Evolutionary Psychiatry: Mental Disorders and Behavioral Evolution
- 33 Industrial Pollutants and Human Evolution
- 34 Acculturation and Health
- Index
- References
30 - Beyond Feast–Famine: Brain Evolution, Human Life History, and the Metabolic Syndrome
Published online by Cambridge University Press: 05 August 2012
Book contents
- Frontmatter
- Contents
- List of contributors
- Preface
- Part I Theory and Methods
- Part II Phenotypic and Genotypic Variation
- Part III Reproduction
- Part IV Growth and Development
- Part V Health and Disease
- 27 Evolutionary Medicine, Immunity, and Infectious Disease
- 28 Complex Chronic Diseases in Evolutionary Perspective
- 29 Evolutionary Medicine and the Causes of Chronic Disease
- 30 Beyond Feast–Famine: Brain Evolution, Human Life History, and the Metabolic Syndrome
- 31 Human Longevity and Senescence
- 32 Evolutionary Psychiatry: Mental Disorders and Behavioral Evolution
- 33 Industrial Pollutants and Human Evolution
- 34 Acculturation and Health
- Index
- References
Summary
EXPLAINING THE MODERN METABOLIC DISEASE EPIDEMIC: THE THRIFTY GENOTYPE HYPOTHESIS AND ITS LIMITATIONS
Today, more than 1 billion people are overweight or obese, and the related condition of cardiovascular disease (CVD) accounts for more deaths than any other cause (Mackay et al.,2004). Why this epidemic of metabolic disease has emerged so rapidly in recent history is a classic problem for anthropologists concerned with the role of culture change in disease transition (Ulijaszek and Lofink, 2006). In 1962, the geneticist James Neel proposed an explanation for this phenomenon that looked for clues in the “feast–famine” conditions that he believed our nomadic, foraging ancestors faced in the past. Given the unpredictability of food resources in natural ecologies, Neel suggested that a “thrifty” metabolism capable of efficiently storing excess dietary energy as body fat when food was abundant would have provided a survival advantage during later periods of shortage. In the wake of the rapid dietary and lifestyle change in recent generations, and the comparatively slow pace of genetic change, these foraging-adapted genes would now be “rendered detrimental by progress” (Neel, 1962), leading to obesity and diabetes.
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- Information
- Human Evolutionary Biology , pp. 518 - 527Publisher: Cambridge University PressPrint publication year: 2010
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