There is no doubt that individuals with lower HDL levels who are consuming a high fat, low-fiber “Western-style” diet are at increased risk for coronary artery disease (CAD). Often the people with lower HDL levels have what is called the “metabolic syndrome,” a cluster of factors which include high triglycerides, high blood pressure, high blood sugar, abdominal obesity and low HDL. If you have at least three of these five factors, chances are you have metabolic syndrome. The new National Cholesterol Education Program ATP III guidelines correctly label this metabolic syndrome a risk factor for CAD.
What causes low HDL?
Genetic factors play a major role in determining how much HDL one has in his/her blood. Lifestyle factors are critical, too. HDL levels often fall when people are sedentary and gain weight. This is particularly true if they have a genetic tendency towards this metabolic syndrome. There is currently no way to change these genetic factors. However, genetic factors only predispose people to low HDL levels and the metabolic syndrome. Diet and other environmental factors interact with genetic factors to influence HDL levels.
HDL levels usually drop when less dietary fat is consumed. This is because dietary fat stimulates the production of HDL primarily in the gut. Calorie restriction and/or replacing fat calories with those from carbohydrates do lower dietary fat intake and so often lower HDL levels. Does this mean a higher fat diet is healthier for those with the metabolic syndrome and lower HDL levels as the new ATP III guideline suggests? Not necessarily.
Four Reasons to Question the ATP III New Guideline
First, the initial decline in HDL levels when a very-low fat (VLF) diet is adopted is often transient. This is because reducing dietary fat usually promotes weight loss in the long run. When body weight stabilizes at a lower level, HDL levels almost always rebound.1,2 Even though dietary fat intake is very low, the loss of weight often counterbalances the drop in HDL production by the gut. As a result, HDL levels on a lower fat diet will eventually end up just a little lower or about the same, or even higher than they were when the patients were consuming a higher fat diet but were heavier. 3, 4
Second, lower HDL levels that result from eating less fat do not impair HDL’s prime job, which is to remove excess cholesterol from where it is not needed, like on artery walls, and return it back to the liver -- where it can be disposed of. This has been shown in both human and animal studies.5, 6
Third, lower HDL levels are usually associated with an increase in fat-rich lipoprotein particles in the blood after a high-fat meal has been eaten (called postprandial lipemia). This postprandial lipemia is believed to promote the growth of atherosclerotic plaque (a.k.a. clogged arteries). Each time a high-fat meal is consumed, there is a large increase in these fat-enriched lipoprotein particles in the blood. This postprandial lipemia lasts for several hours and occurs after every fat-rich meal. By contrast, diets with little dietary fat do not increase postprandial lipemia significantly. This may be another reason why a VLF diet is less likely to promote the growth of atherosclerotic plaque than a higher fat diet, even though HDL levels on the lower fat diet can sometimes be lower.
Fourth, the metabolic syndrome is largely the result of excessive body fat stores. There is compelling evidence that increasing dietary fat often promotes weight gain. Replacing high-fat foods with high-carbohydrate foods like whole grains, beans, fruits and vegetables generally leads to a drop in caloric intake, fat intake, and weight loss. With a loss in weight, there would naturally be a loss in body fat stores, and, as a result, a decrease in factors associated with metabolic syndrome.
Indeed, such a VLF near vegetarian (VLFNV) diet has been shown to reverse CAD in most patients who already have developed advanced atherosclerotic lesions. This occurs even though HDL levels may not be any higher or even a little lower than they were when the these patients were consuming a typical high-fat American diet or moderate fat American Heart Association diet.
It is debatable whether people with the metabolic syndrome who are almost always overweight or obese should be told to consume a higher fat diet as the new ATP III guidelines now recommend. This is because the metabolic syndrome itself is largely the result of excessive body fat stores.
High-fat diets have been repeatedly shown to promote excessive calorie intake and body fat stores when compared to diets with less fat and more fiber. Increased body weight, higher postprandial lipemia, and the metabolic syndrome are all known risk factors for CAD. All three can be improved (often dramatically) by adopting a VLFNV. Such a diet has already been shown to reverse atherosclerosis in most research subjects with advanced CAD. This appears to be the case even though HDL levels sometimes may fall, particularly in the short run on a VLFNV diet. In many cases a VLFNV diet may be the best choice for patients with low HDL levels and/or the metabolic syndrome.
By Dr. James J. Kenney, PhD, RD, FACN. Dr. Kenney has just published a new 4 hour CPE course on using the new ATP III guidelines and we will have new educational materials on this topic coming soon. For more information, call 800-462-2352.
1. Dattilo AM, Am J Clin Nutr 1992;56:320-328
2. Zimmerman, J. Arterio-sclerosis 1984;4;115-123
3. Thuesen L, Am J Clin Nutr 1986;44:212-9
4. Ornish D, et al. JAMA 1998;280:2001-7
5. Brinton EA, JL. J Clin Nutr 1999;85:144-51
6. Woolett LA. J Lipid Res 1997;38:2289-302
Stephanie Ronco has been editing for Food and Health Communications since 2011. She graduated from Colorado College magna cum laude with distinction in Comparative Literature. She was elected a member of Phi Beta Kappa in 2008.