Background information on presentation by Ronald M. Krauss, M.D., Lawrence Berkeley National Laboratory, Berkeley, Ca., at AAAS symposium on "Gene-Diet Interactions in Coronary Heart Disease"
Saturated fat and cholesterol are two of the strongest dietary determinants of blood cholesterol levels, particularly the low-density lipoprotein (LDL) or "bad cholesterol" fraction. The LDL response to reduced saturated fat and cholesterol intake, however, can vary widely among individuals. Recent evidence indicates that genetic factors can contribute to these differences in dietary response.
The most well defined genetic trait affecting LDL response to diet is the apoE4 variant of apoprotein E, a protein that has a number of important functions in both the cardiovascular and nervous systems. ApoE4 is due to a single DNA change in the gene for apoprotein E and has a prevalence of approximately one in seven in the population. Compared with individuals who have the normal form of apoprotein E, designated apoE3, those with apoE4 have a tendency for higher blood cholesterol levels, increased heart disease risk, and as discussed elsewhere, increased risk of Alzheimer's disease. Most studies have found that LDL reductions on low-fat, low-cholesterol diets are greater in subjects with apoE4 than in those with apoE3.
Other less common lipoprotein gene variants also have been shown to influence the LDL response to diet. One, designated apoAIV-2, appears to prevent the rise in LDL induced by increased intake of dietary cholesterol.
A much more common genetically influenced condition that can influence
the blood cholesterol response to a low fat diet is that responsible for the
"small, dense" subtype of LDL, also called LDL subclass pattern B. This trait,
which can be detected by specialized analytic tests, is found in about one in
three adult men and one in 5 to 6 postmenopausal women. It is not so common in
Contact: Cathy Yarbrough
American Heart Association