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Jesse Roth, MD

JAMA. 2009;301(24):2586-2588.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

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.

Thrifty Genes and the Metabolic Syndrome

One hypothesis for the obesity pandemic posits that thrifty genes, mutations incorporated into the genome during millennia of lean times to protect against starvation, produce obesity in times of plenty.² If the evolutionary goal is to store . . . [Full Text of this Article]

Author Affiliation: Albert Einstein College of Medicine of Yeshiva University, Feinstein Institute for Medical Research, North Shore-Long Island Jewish Health System, Manhasset, New York.

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RELATED LETTER

Tuberculosis and the Inflammatory Processes of Obesity in Human Evolution
Giamila Fantuzzi
JAMA. 2009;302(16):1754.
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THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Tuberculosis and the Inflammatory Processes of Obesity in Human Evolution
Fantuzzi
JAMA 2009;302:1754-1754.
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