High Carbohydrate Diets Induce Hypertriglyceridemia
Abstract & Commentary
Synopsis: High carbohydrate diets may have a number of metabolic effects that may run counter to expectations.
Source: McLaughlin FA, et al. J Clin Endocrinol Metab 2000;85:3085-3088.
Reaven and associates demonstrated the relationship between carbohydrate intake and triglyceride elevations more than 30 years ago.1 Are we closer to understanding why?
The association between the hyperinsulinemia and hypertriglyceridemia was later extended to include correlations between: 1) insulin resistance and compensatory hyperinsulinemia; 2) hyperinsulinemia and hepatic very-low density lipoprotein (VLDL)- triglyceride (TG) synthesis and secretion; and 3) hepatic VLDL-TG secretion rate and plasma TG concentrations.
McLaughlin and colleagues point out that as a result of acute studies done by other investigators, an opposing view has emerged. Thus, it has been proposed that insulin inhibits hepatic VLDL and TG secretion. "As a consequence, it is argued that hypertriglyceridemia occurs in association with insulin resistance due to a loss in insulin’s ability to inhibit VLDL-TG secretion in resistant individuals."
This study was initiated to test the hypothesis that endogenous hypertriglyceridemia results from a defect in the ability of insulin to inhibit the release of VLDL-TG from the liver. To accomplish this goal, plasma glucose, insulin, free fatty acid (FFA), and TG concentrations were compared in 12 healthy volunteers in response to eucaloric diets consumed for 14 days, containing either 40% or 60% of total calories as carbohydrate (CHO). All subjects consumed both diets with a two-week washout period between each diet. The protein content of the two diets was similar (15% of calories), and the fat content varied inversely with the amount of CHO (45% or 25%). The ratio of saturated, polyunsaturated, and monounsaturated fat was the same for each diet.
On the last day of the diet, hourly blood samples were drawn fasting, and then hourly beginning one hour after the first study meal, for glucose, insulin, FFA, and TG concentrations. There was no effect on blood glucose concentrations from either diet. The 60% CHO diet, however, resulted in higher day-long insulin (P = 0.01) and TG (P = 0.001) concentrations, and lower FFA responses (P = 0.001).
If the role of insulin is to inhibit hepatic TG secretion, the fasting day-long higher insulin levels on the 60% CHO diet should have resulted in a decrease, not an increase, in plasma TG concentrations.
Comment by Ralph R. Hall, MD, FACP
There are important clinical implications of this study. A high CHO, low-fat diet often results in hypertriglyceridemia and a lowering of the high-density lipoprotein cholesterol. There is also a tendency for the low-density lipoprotein cholesterol, to become smaller and more dense, thus more atherogenic.2 However, as McLaughlin et al point out, if weight loss in overweight individuals occurs, with ad libitum high CHO diets, hypertriglyceridemia does not develop.
Unless physicians use weight loss in addition to a low-fat diet, it will be more effective to prescribe a diet with reduced saturated fat and instead of increasing carbohydrates, add polyunsaturated and monounsaturated fats—a Mediterranean diet, if you will.
References
1. Reaven GR, et al. J Clin Invest 1967;46:1756-1767.
2. Knopp, et al. JAMA 1997;278:1509-1515.
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