Milner believes that this new science could lead to the “nutritional preemption” of some forms of cancer—and also of cardiovascular disease, diabetes, Alzheimer’s, arthritis, and other chronic illnesses. In time, this knowledge will help turn supermarkets into a kind of nutritional pharmacy.

“You don’t just ‘get’ a disease,” says Ruth DeBusk. “You ultimately trigger the susceptibility you have within your genes by the diet and lifestyle choices you make on a day-by-day basis.”

Driving the new science of nutritional genomics is the 2003 completion of the Human Genome Project, which sequenced all human genes. This event thrust genetics onto center stage in the science of medicine, and it could establish nutritional genomics as a cornerstone of preventive medicine.

The first issue of the Journal of Nutrigenetics and Nutrigenomics was published in 2007, and in October 2009 the National Institutes of Health held the Third Congress of the International Society of Nutrigenetics/Nutrigenomics at NIH’s Bethesda campus.

The field is growing rapidly, but understanding the complex interplay between genes and diet will take time: Humans have about 25,000 genes, and the food supply contains some 25,000 bioactive components. Multiple genes are involved in chronic diseases, and bioactive food components interact with one another in ways not yet fully understood.

In a broad sense, the primary function of genes—which are segments of DNA—is to instruct our cells to make proteins. Through a process still being studied, diet influences our genes’ behavior, causing some of them to be overexpressed and others to be underexpressed, much like the brightening and dimming of a light bulb. How a gene behaves and how nutrients influence that behavior determine the impact on human health.

Seen through the lens of nurture versus nature, diet’s influence on genetic behavior can be as consequential as inheriting genes known to cause a disease. The study of this environmentally influenced genetic behavior is called epigenetics. By showing how diet can prompt the activation or deactivation of genes, epigenetics is proving that genes are not destiny, that we have more influence on our own well-being than previously realized.

“We know from mice studies that there are food items that will modify a specific gene called HER2,” says Milner. “Mice bear a remarkable genetic similarity to humans, HER2 is present in both mice and humans, and we know it is involved in human breast cancer. If the HER2 gene is overexpressed, you have an increased risk of breast cancer. If it is suppressed, the risk is diminished. But if you take mice that also overexpress this gene and you give them corn oil [omega-6], they develop tumors faster. If you then give them fish oil high in omega-3, their tumor development is slowed. Is the fish oil maintaining a normal cell, preventing it from becoming cancerous, or influencing the cancer? It may be doing all three.”

Milner also notes that when these mice are given Herceptin—an expensive medication used in treating some human breast cancers—the gene is suppressed and the mice live longer and have fewer tumors. He says when the results from the studies with fish oil and Herceptin were compared, the diet of fish oil was seen to be as effective as Herceptin in slowing tumor development.

“There may be incredible implications for this,” he says, “but the studies have only been done in mice, not humans.”

Genetic testing is available for HER2 overexpression—meaning a person has extra copies of the gene—and women who suspect they may have it because of family history might consider genetic testing. If the test reveals that the gene is overexpressed and they have no evidence of disease, they might consider a diet rich in omega-3, including oily fish such as salmon, mackerel, and sardines, as well as walnuts and some dairy products. Omega-3 is also available as a supplement in capsule form.

Another example of diet’s influence on genes came out of animal experiments by a team of Duke University researchers who studied the offspring of genetically identical yellow Agouti mice. These mice normally give birth to mostly yellow-coated litters of mice pups as well as some that have coats in varying shades of brown.

With funding from the National Institute of Environmental Health Sciences, Dana Dolinoy and her colleagues fed one group of female mice a normal diet before and during pregnancy. They fed the same to a second group of females, except that they added genistein, a nutritional component of soy.

At birth, the offspring of the two sets of mouse pups appeared different. The mothers that were fed a regular diet predictably gave birth to mostly yellow-colored pups. The genistein-fed female mice produced a few yellow pups, but most had brown-colored coats. Because genistein was the only variable, researchers knew it to be responsible for the shift in the coat colors.

The study revealed something more significant. Genistein apparently turned off a genetic switch that muted the bad effects of the so-called Agouti gene. The brown pups born to mothers that consumed genistein were leaner and healthier and lived nearly twice as long as the yellow pups born to mothers not fed genistein. The yellow pups also grew to be twice as heavy as their brown counterparts and were more susceptible to cancer and diabetes. The study was published in Environmental Health Perspectives in 2006.

Dana Dolinoy, the study’s lead researcher, says one reason soy was selected for the experiment is that Asians who consume a high soy diet have lower incidences of many cancers, including breast and prostate.

“We wanted to see if soy’s impact on the Agouti gene might be what kept these cancers in check for Asians,” she says. Humans also have an Agouti gene, but Dolinoy says it doesn’t act the same way it does in mice. “People should not go out and eat a lot of soy or take genistein supplements to protect themselves from getting fat or to help them live longer,” she says. “We’re not there yet.”

Dolinoy—who is now with the University of Michigan School of Public Health—next carried out a kind of reverse experiment, again on genetically identical yellow Agouti mice. This time, she fed one group of female mice a normal diet. She fed another set of females the same diet but added a moderate amount of bisphenol A—or BPA—a chemical used in hundreds of everyday products, including the lining of canned goods and the manufacture of hard-plastic water bottles.

Recent studies at Harvard found that BPA leaches into the bottle’s contents and winds up in the people who drink it. It also leaches into canned soups lined with plastic containing BPA. The chemical is suspected of causing birth defects and perhaps diabetes, heart disease, and cancer. According to a 2007 survey by the Centers for Disease Control and Prevention, 93 percent of Americans over age six who were tested had evidence of BPA in their systems. There are as yet no federal regulations banning or limiting the use of BPA in food products.

When the two groups of female mice gave birth, those given BPA had many more yellow mouse pups than in normal litters, and these mice suffered more obesity and shorter lives than the mothers not fed BPA.

“The BPA had the exact opposite effect on the mice pups as genistein,” she says. “With genistein, the mice went toward brown, lean, and better health, and with BPA they shifted toward yellow, fatter, and shortened lives.”

In a third experiment, Duke researchers fed pregnant female mice both BPA and genistein. Because genistein was able to offset the harm from BPA, it has led to speculation that genistein might counteract potential damage from BPA exposure in human pregnancies.