[Lipid metabolism and aging]

Abstract

Lipids have important biochemical functions, but their excess in plasma is a risk factor for atherosclerotic disease. After puberty, the plasma total and low-density lipoprotein (LDL) cholesterol concentrations increase with age as a consequence of an increase in production and a decrease in catabolism mediated by LDL receptors. On the other hand, the plasma high-density lipoprotein (HDL) cholesterol concentrations remain constant. The correlation between serum cholesterol and coronary risk becomes weak with age but also exists in the elderly, while low levels of HDL cholesterol remain to be a risk. The rise in serum triglycerides with age results mainly from the increase in body weight and the decrease in physical activity. Dietary polyunsaturated fatty acids (PUFAs) such as linoleic acid protect against progression of atherosclerosis in part by their hypocholesterolemic effect. The proportion of linoleic acid in serum phospholipids decreases with age. This change also is a separate risk factor for cardiac and cerebral infarction. Among many prostanoids, prostaglandin I2 has antiaggregatory and vasodilatory effects and thromboxane A2 has the opposite effects. Lipid peroxides which are produced inevitably from PUFAs may damage biomembranes and might accelerate cellular aging. The questions of whether dietary manipulation can reduce the age-related changes in lipid metabolism and can improve cellular functions are of major importance.