D ietary therapy should always be the first approach to treating hypertriglyceridemia. Dietary factors (caloric content, type of fat, and carbohydrate and alcohol intake) influence serum triglyceride levels through several mechanisms.‘s2 Hypercaloric diets have been shown to stimulate the formation of triglycerides in the liver, promoting the secretion of VLDL particles. In addition, obesity frequently causes secondary hypertriglyceridemia, a condition usually corrected by reducing the caloric intake. Thus, a primary objective of dietary treatment for hypertriglyceridemia is an adequate supply of daily calories in order to achieve and/or maintain the ideal body weight. Regular aerobic physical exercise may be useful both in reducing body weight and in correcting hyperinsulinemia, which is frequently associated with hypertriglyceridemia.3-5 Amounts and types of fats are important in the dietary treatment of hypertriglyceridemia. In familial lipoprotein lipase and apo C-II deficiency (type I), hypertriglyceridemia is aggravated by dietary fat and is best treated by stringent reduction (less than 1520% of daily energy) of fat intake to reduce chylomicron input. An optimal fat intake should be identified for each type I patient, and for most, the diet must be a restricted one.5 Medium chain triglycerides, which are absorbed by the portal vein and do not generate chylomicrons, can be used in cooking or as salad dressing as a supplement to normal dietary long-chain fatty acids once the optimal fat intake has been identified. A transient increase in very-low-density lipoprotein (VLDL) triglyceride may be induced by the high carbohydrate content of very-low-fat diets, but in long-term management, this is of little significance.2 A substantial protein intake (1517% of energy) permits a lower carbohydrate intake.5 Saturated fat intake, in some patients, may increase triglyceride levels, possibly by effecting VLDL metabolism.’ A reduction in the number of hepatic low-density lipoprotein (LDL) receptors has been proposed, and this may also reduce liver uptake of VLDL remnants. Therefore, saturated fatty acids intake should be reduced to less than 10% of daily energy in the dietary management of hypertriglyceridemia. The dietary content of polyunsaturated fatty acids is particularly significant in the hypertriglyceridemic subject. When diets rich in fatty acids of the n-6 series (linoleic acid, c18:2,n-6, present in corn oil) are given to hypertriglyceridemic patients, there is frequently an increase in the fecal excretion of cholesterol and bile acids; a well-known reduction in serum cholesterol also occurs.’ Linoleic acid feeding also lowers triglycerides, although this is not a universal response. In any case, the substitution of linoleic acid for saturated fatty acids is recommended for the dietary treatment of hypertriglyceridemia. Monounsaturated fatty acids will probably serve the same purpose, and they do not have several of the potential disadvantages of high intakes of linoleic acid. Polyunsaturated fatty acids of the n-3 series (fish oils) have been shown to reduce significantly hypertriglyceridemia in hyperlipidemic phenotypes IIb, III, IV and V. Their hypotriglyceridemic action is dose dependent and is explained by a marked reduction of the hepatic synthesis of VLDLtriglycerides.‘j Thus, consumption of fish, which contain high amounts of n-3 long-chain fatty acids, may have a therapeutic benefit in patients with hypertriglyceridemia and is recommended as a source of fat in their diet. In severe hypertriglyceridemias (i.e., type V hyperlipidemia), the use of fish oil capsules has been successfully employed for reducing excess levels of chylomicrons. The optimal dosage, however, remains unknown7 In some diabetic patients with hypertriglyceridemia, the administration of fish oil capsules has impaired diabetic control and increased LDL and