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.
|Title of host publication||Appetite and Body Weight|
|Subtitle of host publication||Integrative Systems and the Development of Anti-Obesity Drugs|
|Editors||Tim C. Kirkham, Steven J. Cooper|
|Number of pages||22|
|Publication status||Published - 1 Dec 2007|