(Circulation. 2002;105:2.)
© 2002 American Heart Association, Inc.
Editorials |
On Evolutionary Biology, Inflammation, Infection, and the Causes of Atherosclerosis
From the Center for Cardiovascular Disease Prevention and the Leducq Center for Cardiovascular Research, Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass.
Correspondence to Dr Paul Ridker, Center for Cardiovascular Disease Prevention, Brigham and Women’s Hospital, 900 Commonwealth Ave East, Boston, MA 02214. E-mail pridker@partners.org
"Often there is no assignable cause for the attack, that is, for the coronary thrombosis itself."— —J.B. Herrick
For most of human history, the primary causes of death have included infection and famine. It is thus not surprising that large portions of the human genome are dedicated to 2 interrelated problems: innate immunity and the inflammatory response (how to ward off infection and survive trauma) and cellular metabolism in times of crisis (how to sustain gluconeogenesis during prolonged periods of malnutrition).
See p 15
From an evolutionary biology standpoint, these interrelated pressures might be expected to select for individuals with relatively enhanced inflammatory function, as well as mild to moderate insulin resistance.1 However, our ancestors, who lived a demanding hunter-gatherer lifestyle characterized by extended periods of physical activity and a high-protein diet, were also largely free of atherosclerosis and diabetes. Thus, for many investigators interested in the underlying causes of these disorders, a key evolutionary question is now openly being asked: is it possible that the adaptive pattern of an earlier time has resulted in a maladaptive response in our modern environment dominated by increasingly sedentary habits, an abundance of high-carbohydrate foods, and a reduced risk of mortality due to common infections?1,2 If so, is our current epidemic of atherosclerosis and diabetes predictable on the basis of evolutionary biological principles?
Clinical data supporting this position come from several disparate sources. For one, atherosclerosis is now recognized as a disorder characterized by a chronic alteration of inflammatory function,3
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