This Commentary explores the possibility that the tuberculosis epidemic during previous centuries generated selective pressures that intensified the metabolic syndrome and the inflammatory processes now associated with obesity. These proinflammatory defenses (with immune systems that are especially robust and more easily triggered) in partnership with the metabolic syndrome (insulin resistance, dyslipidemias, and hypertension),1 may have provided an advantage during the tuberculosis pandemic when food availability was limited and average life span was short. Currently, in developed countries, tuberculosis is relatively uncommon, food is abundant, and life expectancy beyond the reproductive years is substantial; the evolutionarily enhanced immune and metabolic elements now act possibly to intensify the pathological consequences of obesity.
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