BOSTON -- The relative amount of protein, carbohydrate, and fat that people choose to eat may be influenced by genetics, according to new research. Jose Ordovas, PhD, director of the Nutrition and Genomics Laboratory at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University (USDA HNRCA), and colleagues found that the apolipoprotein A-II gene (APOA2) is associated with proportions of fat, carbohydrate, and protein in the diet, along with total calories and, therefore, with body-mass-index (BMI). These results, published in Clinical Chemistry, are the first to show that the APOA2 gene is linked to food preferences that shape dietary patterns, particularly preferences for dietary fat.
Ordovas, corresponding author, and colleagues analyzed genetic alleles, or variants, in the APOA2 promoter, a region that controls expression, or behavior, of the APOA2 gene. The alleles of the APOA2 promoter, T and C, form combinations; TT, TC, and CC, which indicate genotype. Of more than 1,000 study participants, approximately 85 percent had the common TT and TC genotypes, whereas 15 percent of participants had the CC genotype. “Both men and women with the CC genotype had a statistically significant higher intake of fat than people with the TT and TC genotypes,” says Ordovas. “People with the CC genotype also consumed an average of 200 more calories per day and were nearly two times more likely to be obese, as compared to those with the two more common alleles.”
In addition to preference for dietary fat, the researchers found evidence that the APOA2 gene influences preferences for protein and carbohydrate. People with the CC genotype consumed higher absolute amounts of protein and lower absolute amounts of carbohydrate than those with the TT and TC genotypes. “People with the CC genotype also exhibited dietary patterns with a lower amount of carbohydrate relative to fat and protein than people with the TT and TC genotypes,” says Ordovas, “despite their caloric intake or BMI.”
Study participants, who were part of the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) Study, funded by the National Institutes of Health, were asked to fill out dietary and lifestyle questionnaires. Researchers measured participants’ weight, height, and waist and hip circumference, along with blood lipid levels both before and after a high-fat meal.
The researchers did not find an association between any alleles of APOA2 and blood lipid levels, including triglycerides, total cholesterol, or LDL or HDL cholesterol. People with the CC genotype, however, did have greater amounts of small HDL cholesterol particles, as compared to larger HDL cholesterol particles, in their blood after eating the high-fat meal than did people with at least one T allele. Small HDL cholesterol particles are more of a risk factor for cardiovascular disease than are larger HDL particles.
“This study adds to our understanding of the relationship among nutrition, genetics, and obesity,” says Ordovas, who is also a professor at the Friedman School of Nutrition Science and Policy at Tufts. “Nutrients from the foods we eat activate proteins in our body, which in turn bind to promoter regions, like the APOA2 promoter. These promoters then tell our genes how to behave,” he explains. “Understanding these relationships may help to shape future recommendations for prevention of undesirable health outcomes, especially in populations that may be genetically vulnerable to certain dietary patterns or specific nutrients. More studies are needed in diverse populations to determine if APOA2 might play a role not only in food preferences, but also in satiety signaling.”
This work was supported by a grant from the National Heart, Lung, and Blood Institute, part of the National Institutes of Health. It was also supported by the U.S. Department of Agriculture Agricultural Research Service, the chief scientific research agency of the USDA; Ministerio de Educacion, Spain; and Centro de Investigación Biomédica en Red (CIBER) from the Instituto de Salud Carlos III (ISCIII), Spain.
In an earlier study investigating the link between genes and diet, Ordovas found that, for most adults in the Framingham Heart Study, fat intake was associated with BMI. However, for 13 percent of the study population with a specific allele of the apolipoprotein A5 gene (APOA5), higher dietary fat was not related to a greater BMI. For more information on APOA5 and Ordovas’ research at the USDA HNRCA, please see “Study Finds Dietary Fat Interacts with Genes” [http://nutrition.tufts.edu/news/notes/2007-03.html] in the March-April 2007 issue of Friedman Nutrition Notes and “Genes and Diet Linked to Risk Factors for Heart Disease” [http://nutrition.tufts.edu/news/notes/2006-09.html] in the September-October 2006 issue of Friedman Nutrition Notes.
Corella D, Arnett DK, Tsai MY, Kabagambe EK, Peacock JM, Hixson JE, Straka RJ, Province M, Lai C-Q, Parnell LD, Borecki I, Ordovas JM. Clinical Chemistry. 2007 (June);53(6):1144 – 1152. “The -256T>C Polymorphism in the Apolipoprotein A-II Gene Promoter Is Associated with Body Mass Index and Food Intake in the Genetics of Lipid Lowering Drugs and Diet Network Study.”
The Gerald J. and Dorothy R. Friedman School of Nutrition Science and Policy at Tufts University is the only independent school of nutrition in the United States. The school’s eight centers, which focus on questions relating to famine, hunger, poverty, and communications, are renowned for the application of scientific research to national and international policy. For two decades, the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University has studied the relationship between good nutrition and good health in aging populations. Tufts research scientists work with federal agencies to establish the USDA Dietary Guidelines, the Dietary Reference Intakes, and other significant public policies.
If you are a member of the media interested in learning more about this topic, or speaking with a faculty member at the Friedman School of Nutrition Science and Policy at Tufts University, or another Tufts health sciences researcher, please contact Siobhan Gallagher at 617-636-6586 or Christine Fennelly at 617-636-3707.