Gene environment interactions and the origin of the modern obesity epidemic

A novel "nonadaptive drift" scenario

John R. Speakman*

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapter

2 Citations (Scopus)

Abstract

An epidemic of obesity has been witnessed by the Western societies over the past 50 years. The World Health Organization (WHO) has recognized obesity as the greatest health threat facing the Western world. Twin and genetic-mapping studies reveal that obesity has a strong genetic component, yet the rapidity of its increase cannot be a consequence of population genetic changes. The most accepted model is that modern obesity occurs because of a gene-environment interaction. There is a genetic predisposition to deposit fat that is strongly expressed in the modern environment. There is a consensus that over evolutionary time, exposure to regular periods of famine led to fatter individuals having lower mortality. This chapter discusses some fundamental difficulties with the "famine hypothesis." Famines do not provide sufficient selective advantage and have occurred over an insufficient time period for thrifty genes to spread in the population. It also discusses a novel alternative model for the evolutionary background of the epidemic. In the novel model, it is argued that ancient man like other animals would have been subjected to stabilizing selection for body weight/fatness-constrained at the lower end by the risks of disease, and possibly starvation, and at the upper end by the risk of predation. This selection results in a set point around which body weight and fatness is regulated.

Original languageEnglish
Title of host publicationAppetite and Body Weight
Subtitle of host publicationIntegrative Systems and the Development of Anti-Obesity Drugs
EditorsTim C. Kirkham, Steven J. Cooper
PublisherElsevier Inc.
Pages301-322
Number of pages22
ISBN (Print)9780123706331
DOIs
Publication statusPublished - 1 Dec 2007

Fingerprint

Gene-Environment Interaction
genotype-environment interaction
Starvation
famine
obesity
Obesity
Fats
Body Weight
Western World
body weight
Population Genetics
World Health Organization
Genetic Predisposition to Disease
lipids
chromosome mapping
exposure duration
starvation
population genetics
predation
Mortality

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)

Cite this

Speakman, J. R. (2007). Gene environment interactions and the origin of the modern obesity epidemic: A novel "nonadaptive drift" scenario. In T. C. Kirkham, & S. J. Cooper (Eds.), Appetite and Body Weight: Integrative Systems and the Development of Anti-Obesity Drugs (pp. 301-322). Elsevier Inc.. https://doi.org/10.1016/B978-012370633-1/50012-8

Gene environment interactions and the origin of the modern obesity epidemic : A novel "nonadaptive drift" scenario. / Speakman, John R.

Appetite and Body Weight: Integrative Systems and the Development of Anti-Obesity Drugs. ed. / Tim C. Kirkham; Steven J. Cooper. Elsevier Inc., 2007. p. 301-322.

Research output: Chapter in Book/Report/Conference proceedingChapter

Speakman, JR 2007, Gene environment interactions and the origin of the modern obesity epidemic: A novel "nonadaptive drift" scenario. in TC Kirkham & SJ Cooper (eds), Appetite and Body Weight: Integrative Systems and the Development of Anti-Obesity Drugs. Elsevier Inc., pp. 301-322. https://doi.org/10.1016/B978-012370633-1/50012-8
Speakman JR. Gene environment interactions and the origin of the modern obesity epidemic: A novel "nonadaptive drift" scenario. In Kirkham TC, Cooper SJ, editors, Appetite and Body Weight: Integrative Systems and the Development of Anti-Obesity Drugs. Elsevier Inc. 2007. p. 301-322 https://doi.org/10.1016/B978-012370633-1/50012-8
Speakman, John R. / Gene environment interactions and the origin of the modern obesity epidemic : A novel "nonadaptive drift" scenario. Appetite and Body Weight: Integrative Systems and the Development of Anti-Obesity Drugs. editor / Tim C. Kirkham ; Steven J. Cooper. Elsevier Inc., 2007. pp. 301-322
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