Fatty acids and cardiovascular risk clinical epidemiology

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Abdominal obesity is linked to increased non-esterified fatty acid (NEFA) concentrations and turnover that are resistant to suppression by insulin (1,2). Similarly, physical activity and maximal oxygen consumption, a marker of physical fitness, are inversely associated with plasma NEFA concentrations measured as the area under-the-curve during a standard 2-h oral glucose tolerance test (3). Familial combined hyperlipidemia, a relatively common autosomal dominant trait, is associated with high plasma NEFAs as well as greater and more prolonged elevation of NEFAs following a fat load (4). Obesity, sedentary lifestyles, and familial combined hyperlipidemia are associated with high blood pressure, abnormal glucose and lipid metabolism, and more cardiovascular events including sudden death (5-7).

NEFAs may be a common denominator linking diverse entities such as central obesity, physical inactivity, and familial combined hyperlipidemia to elevated blood pressures and greater cardiovascular risk. In the Paris Prospective Study, e.g., elevated fasting NEFA concentrations were independently predictive of the development of hypertension and sudden death (8,9). In the same study, hypertensive men had higher fasting NEFA concentrations than normotensive men with the greatest differences evident in leaner than more obese subjects (10). Moreover, in 50-yr-old Swedish men, higher serum levels

From: Contemporary Endocrinology: Hypertension and Hormone Mechanisms Edited by: R. M. Carey © Humana Press Inc., Totowa, NJ

of saturated fatty acids and oleic acid were independently predictive of left ventricular hypertrophy assessed at age 70 (11). Collectively, these data suggest that abnormalities of NEFA metabolism characterized by relatively high plasma concentrations that do not suppress normally in response to insulin may participate in increasing metabolic and hemodynamic risk factors for cardiovascular disease and events. Clinical physiologial evidence supporting the notion that abnormalities of NEFAs contribute to metabolic and hemodynamic risk will now be examined (Fig. 1).

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