Atherosclerosis is the build-up of cholesterol-rich plaques in artery walls. It is the leading cause of heart attacks and strokes.
LDL (“bad” cholesterol) particles appear to be the primary source of the cholesterol in these plaques. Lowering LDL by diet and/or drugs has been shown to slow and sometimes even reverse (regress) the build-up of atherosclerotic plaques.
Potent statin drugs appear to cut the risk of a heart attack or stroke by no more than one third. Used alone, these drugs rarely produce regression of cholesterol-rich plaque or get rid of angina – a symptom of severely clogged coronary arteries.
By contrast, a very low fat, near vegetarian (VLFNV) diet has been shown to regress atherosclerosis, reduce or eliminate angina, and reduce total mortality.
Despite the demonstrated safety and effectiveness of VLFNV diets for treating and preventing atherosclerotic disease, the American Heart Association has warned Americans to avoid diets with less than 15% of calories from fat. Why? They believe the drop in HDL may promote atherosclerosis. They also site data from studies showing increased fasting triglyceride levels and a shift toward smaller more dense LDL particles on very-low-fat diets.
However, the studies showing presumably adverse changes in blood lipids from very low fat diets have some flaws. First these diets get most of their carbohydrate from refined sugars and grains. No one who advocates a VLFNV diet to treat atherosclerosis recommends mostly refined carbohydrate.
Secondly, these studies require subjects to consume the same calorie level on the high-carbohydrate diet as they consumed willingly on an American Heart Association-style or even on a high fat diet. When fed ad libitum, people generally eat fewer calories on low fat diets than higher fat diets. This is especially true if the low-fat diet is high in fiber-rich fruits, vegetables, whole grains, and beans. Lower calorie consumption is one of the most important benefits of consuming a low-fat diet!
It is hard to rectify the belief of the American Heart Association that diets very low in fat promote pro-atherogenic changes in blood lipids with data demonstrating people following VLFNV diets usually see dramatic improvements for angina, regression of atherosclerosis and reduced coronary artery disease and total mortality.
Physicians are trained to assess the risk of atherosclerotic-related heart attacks and strokes by looking at the ratio of “bad” LDL or total cholesterol to “good” HDL in the blood. Because lower HDL have been associated with an increased risk of atherosclerosis it is assumed when HDL drops on a VLFNV diet this may promote atherosclerosis.
However, Pfizer recently withdrew a drug that markedly elevates HDL levels (and lowers (LDL too) because this drug was shown in a clinical trial to increase total mortality by 49%. Clearly atherosclerosis is far more complicated than simply looking at fasting levels of blood lipids.
UCLA researchers reported the impact on blood lipids and other coronary artery disease risk factors in 22 overweight and obese men, most of whom had several risk factors for the metabolic syndrome. Subjects adopted a VLFNV diet and exercised for 3 weeks. The diet was fed ad libitum with the only limitation on animal products.
Not surprisingly, HDL dropped 10% on average. However, the HDL removed from their blood and tested in vitro was found to be pro-inflammatory before the intervention but became anti-inflammatory when measured again after 3 weeks.
The authors conclude their “data indicate that intensive lifestyle modification improves the function of HDL even in the face of reduced levels.”1
It seems unlikely that a drop in HDL, as a result of adopting a VLFNV diet, is dangerous. Claims that very-low-fat diets promote atherosclerosis simply because they lower HDL is without scientific merit. On the contrary, very low fat diets have been shown to reverse atherosclerosis. They also help individuals control their weight and blood sugar for diabetes. And there is much evidence that this diet will reduce the risk for certain cancers as well.
By James J. Kenney, PhD, RD, FACN
1. J Appl Physiol. 2006;101:1727-32
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.