Posted on 05/14/2012 at 04:12:48 PM by Student BloggerBy Larry Istrail
Since the late 1970s, the prevalence of metabolic syndrome has skyrocketed. Associated with the obesity epidemic, metabolic syndrome is conspicuously characterized by high triglycerides, low HDL, and small dense LDL particles(1). This characteristic lipid profile has been termed atherogenic dyslipidemia, and it appears to be mediated by the macronutrient content of the diet.
The American Heart Association (AHA) recently published a report discussing this topic entitled Triglycerides and Cardiovascular Disease(2), chronicling the rising rates of serum triglyceride levels and its role in cardiovascular disease, in order to "update clinicians on the increasingly crucial role of triglycerides in the evaluation and management of CVD risk and highlight approaches aimed at minimizing the adverse public health–related consequences associated with hypertriglyceridemic states."
This report is interesting and important for physicians to be aware of, but the major concepts are absolutely predictable with a basic understanding of serum cholesterol responses to carbohydrates in the diet. Simply stated, when people eat carbohydrates their High-density lipoprotein (HDL) levels go down and their triglycerides go up. This is uncontroversial, and so consistent that researchers use triglycerides and HDL as objective measures of carbohydrate consumption. Dr. Frank Sacks of Harvard Medical School explains in a recent paper on low carbohydrate diets that "HDL is a biomarker for dietary carbohydrate."(3) High triglycerides and low HDL means the subjects are eating lots of carbs. The AHA's report confirms this as well, explaining that "very high intakes of carbohydrate (>60% of calories) is accompanied by a reduction in HDL cholesterol and a rise in triglyceride."
Yet perhaps the most interesting quote in the report comes in the introduction: "It is especially disconcerting that in the United States, mean triglyceride levels have risen since 1976, in concert with the growing epidemic of obesity, insulin resistance, and type 2 diabetes mellitus."
It is quite disconcerting, but it is EXACTLY what should be expected. If it is true that triglycerides increase in response to carbohydrates, then one would expect that at some point circa 1976, there should have been an increase in U.S. carbohydrate consumption. And there was.
It was in response to the first ever Dietary Goals for the United States, issued in 1977 by the U.S. Senate Select Committee on Nutrition and Human Needs(4). Here are the first few recommendations:
• Increase carbohydrate consumption to account for 55 to 60 percent of the energy intake.
• Reduce overall fat consumption from approximately 40 to 30 percent energy intake
• Reduce saturated fat consumption to account for about 10 percent of total energy intake
Interestingly, the recommendation to eat more carbohydrates happened almost precisely at the same time that triglyceride levels began to increase to "disconcerting" levels. Of course the recommendations would not cause hypertriglyceridemia if the general population did not follow them. Yet we did.
As you can see, since about 1976 carbohydrate intake increased and dietary fat intake decreased. Here is another graph of carbohydrate intake over the past 30 years(5):
During this same time period researchers were discovering that the simplified model of “bad and good cholesterol” was more complicated, and not all LDL are created equal. In fact the LDL particles could be further divided into multiple subclasses, ranging from small and dense to large and buoyant(6). Dr. Ronald Krauss, one of the primary researchers involved, came to the dramatic discovery that those patients with a higher percentage of small dense LDL particles circulating in their bloodstream were far more likely to have a myocardial infarction (MI) (7). This phenomenon is likely explained by the enhanced ability with which these dense particles are able to lodge themselves into the intima of blood vessels – infamously in the coronary arteries of the heart - and contribute to the development of an MI.
When Dr. Krauss and other researchers began testing the effects of diet on these LDL particles, he consistently found that the dietary carbohydrates seemed to be changing the density of the LDL particles(8). As the carbohydrate content of the diet increased, along with a concomitant decrease in dietary fat, the LDL particles migrated from their buoyant form to the small, dense, atherogenic form.
These findings surprisingly suggest that carbohydrates have the ability to transform our cholesterol levels into those that characterize metabolic syndrome. As carbohydrate intake increases HDL levels decrease, triglycerides increase, and LDL particles become small and dense.
As explained in the introduction of the AHA report on triglycerides, it will be of value to the Adult Treatment Panel IV of the National Cholesterol Education Program (NCEP), from which evidence-based guidelines will ensue. So what does the NCEP recommend in order to lower our triglycerides?
Why nothing more than the exact same recommendation we received in 1977:
"Very high intakes of carbohydrate (>60% of total calories) are accompanied by a reduction in HDL cholesterol and a rise in triglyceride …. These latter responses are sometimes reduced when carbohydrate is consumed with viscous fiber …; however, it has not been demonstrated convincingly that viscous fiber can fully negate the triglyceride-raising or HDL-lowering actions of very high intakes of carbohydrates...Carbohydrate intake should be limited to 60 percent of total calories."