CHICAGO (Reuters Health) - Genetic differences may explain why some people see their cholesterol levels plummet while on low-fat, high-carbohydrate diets and some people do not.

In fact, in the future doctors may ``steer people toward or away from these diets based on their genetic profiles,'' said researcher Dr. Ronald M. Krauss of the University of California, Berkeley. He presented his findings here Tuesday at the annual meeting of the American Chemical Society.

Krauss spoke to delegates during a symposium on the emerging science of nutrigenomics, which focuses on the way diet interacts with genetics to influence health.

Millions of people around the world have high blood levels of ``bad'' LDL cholesterol, which can stick to artery walls and raise risks of heart attack or stroke.

But according to Krauss, not all LDL cholesterol is created equal.

In fact, our genes seem to divide us into two main groups when it comes to the dangerous blood fat. In group ``A'' types, larger, more buoyant LDL particles predominate, while in group ''B'' types, LDL is smaller in diameter but denser and heavier.

Krauss said that of the two, small LDL is the more lethal due to the fact that ``it is more likely to stick to the artery wall.''

However, there is some good news for type B's. When placed on standard low-fat, high-carbohydrate cholesterol-lowering diets, members of this genetic subgroup typically see their levels of LDL (both large and small) fall dramatically.

In contrast, type A individuals generally chart a decrease in less harmful large-size LDL cholesterol, while experiencing an overall increase in blood levels of more dangerous small-size LDL--hardly the effect they were seeking.

The bottom line? ``Individuals who are genetically predisposed to pattern B are the ones who do better on low-fat diets,'' according to Krauss. And some type A people may want to avoid low-fat diets--especially very extreme ones (less than 10% of calories from fat)--altogether.

Pinpointing who is type A or B requires quick identification of the responsible genes, however, and at this point in time scientists are still searching for the culprits. Right now, Krauss's team is studying dietary and cholesterol patterns within families to hone in on five candidate genes, with the most promising located on chromosome 19p.

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