Abstract

In this issue of the journal, Brima et al. report thought-provoking research providing a potential evolutionary rationale whereby natural selection might have preserved genes that predispose to metabolic syndrome. When CD-1 mice were fed a high fat diet, this induced metabolic changes characteristic of metabolic syndrome. In addition, the high fat diet provided substantial protection from lethality due to infection with Trypanosoma cruzi. The authors hypothesize that the same genes predispose to both metabolic syndrome and protection against infectious disease. Thus, the selective advantage of not dying from infectious disease implicitly provides selective pressure predisposing to metabolic syndrome. This hypothesis follows a similar line of reasoning that has provided explanations for the survival of the HbS mutation for sickle cell disease and renal disease-associated genetic variants in apolipoprotein L1. Variants in these two genes provide protection from malaria and Trypanosoma brucei rhodesiense, respectively.

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