Beyond Feast–Famine: Brain Evolution, Human Life History, and the Metabolic Syndrome
Abstract
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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Peripheral insulin resistance is effective at shunting scarce glucose to high-demand tissues or organs, such as to the fetus during the mild diabetes of pregnancy or to the brain during stress-induced insulin resistance.
“Although an important precursor to type 2 diabetes, peripheral insulin resistance is also effective at shunting scarce glucose to high-demand tissues or organs, such as to the fetus during the mild diabetes of pregnancy (58), or to the brain during the insulin-resistance triggered by stress (59).”
From Metabolic costs and evolutionary implications of human brain development (2014) · cites this paper as [59]
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- Authors
- Kuzawa, C. W.
- Corresponding author
- Kuzawa, Christopher W.
- Venue
- Human Evolutionary Biology
- Publisher
- Cambridge University Press
- Published
- 2010-07-29
- Pages
- 518-527
- OpenAlex
- W2284010517
- Cited by
- 39
- References
- 80
- Citations by year
- 2026: 1 · 2024: 1 · 2023: 1 · 2022: 2 · 2021: 3 · 2020: 3 · 2019: 3 · 2018: 2 · 2017: 3 · 2016: 2 · 2015: 1 · 2014: 8 · 2013: 3 · 2012: 2
- FWCI
- 16.18
- Type
- book chapter
- Language
- en
- Open access
- closed
- Locations
- Cambridge University Press eBooks (publishedVersion)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Nutrition, Genetics, and Disease
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Obesity, Physical Activity, Diet
- Keywords
- thrifty genotype hypothesis, metabolic syndrome, obesity, diabetes mellitus, brain evolution, human life history, energy storage, cardiovascular disease
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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