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A Nonadaptive Scenario Explaining the Genetic Predisposition to Obesity: The “Predation Release” Hypothesis
Open accessAbstract
The "thrifty gene hypothesis" suggests we evolved genes for efficient food collection and fat deposition to survive periods of famine and that now that food is continuously available, these genes are disadvantageous because they make us obese in preparation for a famine that never comes. However, famines are relatively infrequent modern phenomena that involve insufficient mortality for thrifty genes to propagate. I suggest here that early hominids would have been subjected to stabilizing selection for body fatness, with obesity selected against by the risk of predation. Around two million years ago predation was removed as a significant factor by the development of social behavior, weapons, and fire. The absence of predation led to a change in the population distribution of body fatness due to random mutations and drift. Because this novel hypothesis involves random drift, rather than directed selection, it explains why, even in Western society, most people are not obese.
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“While there is an active debate surrounding the mechanisms underlying this process 8,9, most agree that the human body is designed to defend against a lower bound of fat content.”
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“Therefore, redundant systems are in place to overcome any one pathway to appetite suppression, suggesting that a drug acting by one principal mechanism may be unlikely to have long-term efficacy.”
From Cellular bioenergetics as a target for obesity therapy (2010) · cites this paper as [9]
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“First, mammals are designed to guard against starvation.”
From Cellular bioenergetics as a target for obesity therapy (2010) · cites this paper as [9]
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“Now these systems are simply overwhelmed with an abundance of food and food cues that are no longer contested by predators and interrupted by famines”
From Food reward, hyperphagia, and obesity (2011) · cites this paper as [168]
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Casazza, K., Hanks, L. J., Beasley, T. M., & Fernández, J. R. (2011) · American Journal of Physical Anthropology · doi:10.1002/ajpa.21483 · Cited by 18
Simončič, M., Horvat, S., Stevenson, P. L., Bünger, L., Holmes, M. C., Kenyon, C. J., Speakman, J. R., & Morton, N. M. (2008) · Behavior Genetics · doi:10.1007/s10519-008-9199-y · Cited by 24
Self-citation
Metadata
- Authors
- Speakman, J. R.
- Affiliations
- University of Aberdeen (GB)
- Corresponding author
- Speakman, John R.
- ORCID
- Speakman, John R.
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2007-07
- Volume
- 6
- Issue
- 1
- Pages
- 5-12
- ISSN
- 1550-4131 (ISSN-L)
- OpenAlex
- W2071368584
- Cited by
- 242
- References
- 65
- Citations by year
- 2026: 4 · 2025: 10 · 2024: 12 · 2023: 7 · 2022: 10 · 2021: 11 · 2020: 10 · 2019: 8 · 2018: 10 · 2017: 8 · 2016: 15 · 2015: 14 · 2014: 20 · 2013: 8 · 2012: 16
- FWCI
- 3.03
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Obesity, Physical Activity, Diet
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Evolutionary Psychology and Human Behavior
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Evolution and Genetic Dynamics
- Keywords
- genetic predisposition to obesity, thrifty gene hypothesis, adiposity, predation risk, stabilizing selection, genetic drift, hominid evolution, fat deposition
- MeSH terms
- Adipose Tissue, Animals, Humans, Obesity, Predatory Behavior, Selection, Genetic, Starvation, Body Mass Index, Genetic Predisposition to Disease, Metabolic Syndrome
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