Maybe people who eat fatty foods without negative health consequences really haven’t sold their souls to the devil. They may just have good genes. The link between dietary fat intake and heart disease is hardwired into our genes, according to research reported in today’s rapid access issue of Circulation: Journal of the American Heart Association.
The fat risk is greatest for people who have a specific genetic mutation in the hepatic lipase (LIPC) gene that is involved in the way high-density lipoprotein (HDL) – “good cholesterol” – is metabolized. The mutation is called –514 (C/T) LIPC, and occurs in the promoter (or expression) region of the LIPC gene encoding the –514 T allele.
“This genetic mutation helps explain why some people are able to adapt to a Western high-fat diet, while others are not able to,” says lead author Jose M. Ordovas, Ph.D. Ordovas is professor of nutrition and genetics at the Nutrition and Genomics Laboratory, Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University in Boston.
Exercise, moderate alcohol and diets high in saturated fatty acids increase the levels of HDL in the blood. But saturated fats also increase the level of low-density lipoprotein (LDL), called “bad cholesterol” because it’s associated with heart disease. Generally, LDL increases much more than HDL with saturated fat intake. Because the net effect of saturated fat is detrimental, scientists suggest limited intake.
But the body doesn’t always respond to cholesterol this way and earlier studies showed a wide variation in response to dietary fat, specifically animal fat, Ordovas says. He and colleagues investigated a genetic link that could explain the differences.
They studied 1,020 men and 1,110 women (average age 55) participating in the Framingham Offspring Study. The researchers collected blood samples for DNA testing as well as cholesterol tests and the participants provided detailed information about dietary intake. HDL concentrations were lowest among subjects with two copies of the “T” allele (TT genotype) whose fat intake represented 30 percent or more of their diets, Ordovas says. Their average HDL was 1.15 millimoles per liter (mmol/L) [44 milligrams per deciliter]. People with the TT genotype and whose total fat intake was less than 30 percent of their total calories had average HDL of 1.35 mmol/L [52 mg/dL], which represents a 16 percent increase in HDL.
“When TT individuals consumed a low-fat diet, HDL concentrations increased. But there was a dose response to fat – the more fat consumed, the lower the HDL,” Ordovas says.
Conversely, people who had no copy of the “T” allele seemed to have the good genes. Their HDL level increased even as fat consumption increased and their HDL decreased when they ate a low-fat diet.
“The effect was seen only for animal fats. Consumption of fat from oils, polyunsaturated fatty acids, did not influence the relationship between the “T” allele and HDL,” he says.
“This is another piece in the puzzle that helps us explain why some people will react to a dietary change while others do not. Our goal is to use this information to help us formulate dietary recommendations that are specifically tailored to different populations. For example, people with the TT genotype would greatly benefit from a severe restriction in animal fats.”
But Ordovas cautioned that it’s too soon to recommend widespread genetic testing to determine hepatic lipase gene type.
Co-authors are Dolores Corella, Ph.D.; Serkalem Demissie, Ph.D.; L. Adrienne Cupples, Ph.D.; Patrick Couture, M.D.; Oscar Coltell, M.Sc; Peter W.F. Wilson, M.D.; Ernst J. Schaefer, M.D.; and Katherine L. Tucker, Ph.D.