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Are You Really What You Eat?
Scientists are discovering more about the relationship among genes, diet, and health.
Editor's note: Genetic tests are about to become much more accessible: Walgreen's has announced that it will begin selling genetic test kits at its 7,500 drugstores across the country. This article, from the April Washingtonian, focuses on how genetic tests might be used to lose weight and improve your health.
Dr. Melik: This morning for breakfast he requested something called wheat germ, organic honey, and tiger’s milk.
Dr. Aragon: Oh, yes. Those are the charmed substances that some years ago were thought to contain life-preserving properties.
Dr. Melik: You mean there was no deep fat? No steak or cream pies or hot fudge?
Dr. Aragon: Those were thought to be unhealthy—precisely the opposite of what we now know to be true.
—From the 1973 Woody Allen comedy “Sleeper.” The doctors are discussing the eating habits of Allen’s character, who awakens in the 22nd century after a slumber of 200 years.
If you’ve wondered whether the green tea you’re drinking is really good for you or whether having a glass of red wine will help you live longer—as it seems to do for the French—or whether passing up a juicy steak for a plate of steamed vegetables will keep you healthier, answers are on the way. But they may not be the ones you expect.
An emerging science called nutritional genomics is illuminating how the food we eat influences our genes and our health.
This new knowledge won’t be as fanciful as Sleeper, but in time it will revolutionize our understanding of the relationship between diet and health. We’ll learn why certain foods might be lifesaving for some but, because of genetic variations, might bring no benefit—or could even be harmful—to others.
We’re seeing a similar phenomenon with therapeutic drugs. A drug that may save one person’s life might jeopardize another’s and for a third have no effect. This is why genetic testing has emerged as an important part of cancer treatment, guiding physicians’ selections of drugs to treat individual patients.
Similarly, nutritional genomics—or nutrigenomics, as it’s also known—will let us individualize healthy dietary choices in ways that go well beyond what we can learn from family history. Scientific evidence suggests that dietary habits are related to a third of all cancers, and diet plays a powerful role in cardiovascular disease, obesity, diabetes, and other chronic infirmities.
Individualized genetic tests already exist to help predict the most effective diet for losing weight and delaying or preventing some forms of cardiovascular disease, and more tests are emerging. But consumers beware: Some commercial labs market genetic tests over the Internet purporting to guide dietary choices, but experts say they offer incomplete and often worthless information.
“The power of nutritional genomics is enormous,” says Ruth DeBusk, a geneticist and dietician and the author of Genetics: The Nutrition Connection, “because it will allow us to prevent disease, especially chronic disease, by manipulating our diet. But the big challenge right now is not to oversell it before the science is ready.”
Nutritional genomics will alter but not completely overturn conventional dietary advice.
“There will always be population-based recommendations for diet to address the basic needs of biology,” says Sharon Ross, program director of the Nutritional Science Research Group in the Division of Cancer Prevention at the National Cancer Institute in Bethesda. “But nutritional genomics could give us the ability to make recommendations to clusters of individuals who have genetic differences that might require them to consume more or less of a specific nutrient to reduce their risk of disease.”
Although the field of nutrigenomics is new, its antecedents reach back to the 1960s, when the first newborn screening programs for phenylketonuria—or PKU—were mandated in all 50 states. PKU is a genetic metabolic disorder in which the body can’t break down an amino acid called phenylalanine. Untreated, PKU can lead to mental retardation, but a low-phenylalanine diet can prevent it. The PKU experience demonstrated that the interplay between nutrients and genes can be powerful.
“The work with PKU makes it clear that the way we handle food is different for different people,” says Artemis P. Simopoulos, past president of the International Society of Nutrigenetics/Nutrigenomics and formerly an NIH researcher and director of the newborn nursery at George Washington University Hospital. “If you took ten people and gave them four eggs a day, five of them would not show any change in their cholesterol, but the other five would—and that’s because of their genetic makeup. We also know that 50 percent of heart attacks for men under 50 occur in only 5 percent of families. Nutritional genomics not only will help identify who is at risk but also will help establish nutritional guidelines.”
Consider the “lower your fat intake” mantra for people with high cholesterol levels.
“We know of a subgroup of society who have what is called a Type 4 hyperlipoproteinemia,” says John Milner, chief of the Nutritional Science Research Group in the National Cancer Institute’s Division of Cancer Prevention. “They have elevated cholesterol, and Type 4 means it is carbohydrate-induced. They account for about 15 percent of the population. The classic recommendation we have today for people with elevated cholesterol is to lower fat intake, and when people lower fat intake, they usually increase their intake of carbohydrates such as vegetables and grains. When this doesn’t work, they’re given a statin drug to lower their cholesterol. But for that 15 percent, switching to more carbohydrates and less fat actually increases their cholesterol level, so with these people we are making an error—they don’t need the drug, and they don’t need to lower their fat intake.”
Milner says that a test for this genetic variation would make it possible to identify people with this form of high cholesterol in order to prevent them from taking unneeded medication and eating the wrong diet.
It’s widely known that moderate alcohol consumption can help lower the risk of heart disease for many, but less well known is that perhaps 20 percent of people have a variation on a gene called Apo E that reverses the protective effect of alcohol.
Similar variations are seen with regard to cancer. Milner says some people have a genetic variant that makes them “highly susceptible” to colorectal cancer if they eat meat regularly, especially red meat. For most of these people, substituting fish for meat will reduce this risk. But Milner adds that because of genetic variations, a high-fish diet may increase disease risk for some.
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.
“If we can identify genetic biomarkers influenced by dietary factors or environmental toxins that are involved in the fetal origins of adult disease,” says Dolinoy, “then we might be able to nutritionally supplement mothers to change their child’s genetic fate and prevent diseases that occur when their child reaches adulthood.”
To Milner, these studies provided “proof of principle” that diet, in addition to maternal exposure to an environmental factor such as genistein or BPA, had altered how one or more genes functioned.
Research suggests that many foods have health and anti-cancer benefits. These include spinach, green and black tea, broccoli, soybeans, garlic, berries, and grains such as oats. Simopoulos of the International Society of Nutrigenetics/Nurigenomics is a believer in the protective power of omega-3 fatty acids and has written several books about it. As beneficial as omega-3 appears to be, might some people be harmed by it? Simopoulos says no, but given the genetic variability present in the population, Milner—while recognizing omega-3’s benefits—considers it a possibility.
A new focus for Milner is curcumin, the main component of the spice turmeric, which is an ingredient in curry powder. He believes curcumin may possess anti-cancer properties because the substance damps down several genes known to promote inflammation linked to heart disease, some cancers, and Alzheimer’s disease. There is speculation that the wide use of curcumin in Indian food might be why India appears to have one of the world’s lowest incidences of some cancers and Alzheimer’s. Research from UCLA published in the July 2009 issue of the Journal of Alzheimer’s Disease found that curcumin in combination with vitamin D3 might combine to offer protection against Alzheimer’s.
There also is evidence that tomatoes might offer cancer protection for some people. “It’s more than just the lycopene in tomatoes,” Milner says. “We have pre-clinical evidence that you’re better off eating the tomato than taking lycopene supplements.” He says that if lycopene is consumed with some fats, it’s absorbed better.
“This is all very encouraging,” Milner says, “but on the flip side, there may be small subgroups of people who could be placed at risk by eating some of these foods. That’s why we need to arrive at a point where we can offer a personalized approach to diet to reduce disease risk.
“The human genome will allow us to do that, and it will have many implications—not only in the foods we eat but in the drugs we take. But it’s going to take more research.”
Just as some foods confer benefits, Simopoulos believes we already have enough information to implicate foods that jeopardize human health. She singles out soft drinks because of their contribution to obesity and diabetes. She also is concerned about the consumption of omega-6 fatty acid—or linoleic acid—which is plentiful in many commercial vegetable oils, including corn, sunflower, soybean, and safflower.
“We know from animal studies that linoleic acid increases tumor and metastatic development in breast, prostate, and colon cancers and perhaps others as well,” she says. “That’s why I’m strongly opposed to the recent recommendations of the American Heart Association that it’s okay to consume up to 10 percent of calories in linoleic acid.”
The American Heart Association says its recommendations were based on studies indicating that linoleic acid in the diet, along with omega-3, can help reduce the risk of heart disease.
Simopoulos contends that a segment of the female population has specific genetic variants that make those women more vulnerable to breast cancer when they consume the amount of linoleic acid allowed in the AHA guidelines.
“So when the AHA says we can increase our linoleic acid to 10 percent of our diet, it means women who consume 2,000 calories a day could consume 22 grams of linoleic acid a day. This is far too high and means we are putting the women with these genetic variants at increased risk of breast cancer.”
Simopoulos doesn’t think eating corn or sunflower seeds entails risks, only consuming the oils from them, because they’re “so concentrated.”
According to Simopoulos, our genes have remained the same for the past 50,000 years or so, but out diet has undergone a big change, not just over millennia but in the past few decades; vegetable oils are one example.
“We have very good evidence that if you compare the composition of foods in the 1930s to food in 1980 and beyond,” she says, “one-third of the vitamins and minerals are lost because our fruits and vegetables are manipulated to be bigger or have a longer shelf life.”
Some people try to overcome this nutritional shortfall by taking vitamin supplements. More than 100 million Americans spend about $10 billion annually on supplements. But just as the impact of food on our genes can differ from one person to another, so can the impact of vitamin supplements.
“We have some good examples where certain genetic variants can influence the requirement for a vitamin,” says Paul Coates, director of the NIH Office of Dietary Supplements. “There’s a polymorphism [genetic variant] in the folate pathway where people with one form of the genetic variant may not be getting enough folate [folic acid] from the diet compared to people without that genetic variant.”
Folic acid is a B vitamin found in spinach and many other vegetables. When folic-acid supplements are consumed by expectant mothers before and during pregnancy, it reduces the risk of neural-tube defects, including spina bifida, for newborns. The evidence of benefit is so compelling that the flour in breads, muffins, and other supermarket grain products is fortified with folic acid.
But at the same time that there has been a reduction in neural-tube defects, there is evidence that folic-acid supplements might be giving rise to an increase in the cancer rate for others.
In 2009, a three-year study of heart patients in Norway—where foods are not enriched with folic acid—found that patients were more likely to die of cancer if they took folic acid and vitamin B12 supplements. The Norwegian researchers also reported a higher death rate overall among patients who took folic-acid supplements as well as a 25-percent higher rate of lung cancer.
Milner suggests that the results of the folic-acid study might reflect a vulnerable population and may be related to the “existence of a tumor which is being promoted by additional folic acid.” He says other studies from Canada and Chile support the Norwegian findings of higher cancer risk, including colon cancer, and point to the fact that folic-acid supplementation may be protective early in life but harmful, at least to some, in later life.
“Folic acid has reduced the number of neural-tube defects,” adds Dolinoy, “but when you give it to the whole population, it is beneficial for some women of childbearing age, but it may not be good for a 50-, 60-, or 70-year-old man or for a four-year-old child. A lot of people are beginning to argue that it isn’t good for everyone.”
Vitamin E also came under suspicion in 2004 when a Johns Hopkins team did a medical-literature review of 19 vitamin E supplementation studies involving 135,967 patients. It revealed that the supplement might actually increase death from all causes.
“We need to learn how normal genetic variation can influence vitamin supplementation,” says Coates, a geneticist. “It’s the same principle that applies to food. If we get better information, it might enable us to make recommendations for one person’s vitamin requirements that are different from someone else’s.”
There may come a time when you send in a cotton-swab sample of your saliva to a lab and in return receive your genetic profile encoded on a chip that provides a readout of the foods you should eat and the supplements you should take. It may tell you to avoid red meat and folic acid but to eat broccoli and salmon and take vitamin C supplements. It might tell you what supplements and food additives to avoid. It could also guide you to the best foods to eat for losing weight—not just to avoid obvious ones such as high-sugar foods—and for delaying or preventing Alzheimer’s disease.
More than 1,000 genetic tests are available from commercial genetics labs. Although most tests are either for rare genetic disorders or issues unrelated to nutritional genomics, more and more labs are offering genetic tests for nutritional guidance. For fees ranging from $150 to more than $1,000, labs offer gene tests for every risk from heart attack to Alzheimer’s disease to baldness.
Many US-based genetics labs—such as 23andMe, SeqWright, deCODEme, Navigenics, and Genelex—offer their services over the Internet. Two foreign companies, Synergenz BioScience of New Zealand and deCode Genetics of Iceland, offer similar services online. Synergenz BioScience conducts gene testing for smokers to determine lung-cancer risk.
Basically, the companies work like this: You send in a saliva swab and your genetic information is “decoded” and sent back to you, alerting you to certain disease susceptibilities and offering dietary recommendations to reduce your risk.
Are the test results reliable? According to some, they may be doing more harm than good. Milner contends that most of the commercial companies are looking at perhaps 18 or 20 genes out of some 25,000. And they look at only a handful of genetic variations, whereas there may be thousands.
A study of four genetics labs conducted by the Government Accountability Office concurred.
“The results from all the tests GAO purchased misled consumers by making predictions that are medically unproven and so ambiguous that they do not provide meaningful information to consumers,” the GAO study said. It added that in many cases the information provided was so general that it could be widely applied, and in other cases the same recommendations for supplements were made to people “at risk” for very different diseases. This kind of genetic testing has been called “recreational genomics.”
As of now, there is scant federal regulation of genetic labs and genetic testing. Food and Drug Administration approval is not required for genetic test marketing. Two states, New York and California, strictly regulate testing. In 2008, both issued cease-and-desist orders to three dozen direct-to-consumer genetics labs in their jurisdictions, including Navigenics and 23andMe. California maintained that the genetic tests could be ordered only with the patient’s physician involved.
While geneticist Ruth DeBusk concedes that there are “absolutely legitimate issues of concern” about nutritional genetic testing and many genetics labs, she calls the GAO report “irresponsible.”
“It’s clear the GAO investigators did not understand what nutritional genomics was all about,” DeBusk says. She says that some genetic-testing labs are doing solid research and offering legitimate genetic tests. She specifically cites Interleukin Genetics of Waltham, Massachusetts.
Kenneth Kornman is president and chief scientific officer of Interleukin Genetics. A former professor at the University of Texas Health Science Center in San Antonio, Kornman says his company has focused on scientifically based gene tests with high clinical utility. The two major tests available now, for weight management and inflammation control—which he says took years to develop—are, in Kornman’s words, “anchored in science.”
Genetic variations present at birth lead to production of excess levels of inflammatory mediators, the best-known being C-reactive protein (CRP). The percentage of people with high CRP levels varies by ethnicity. About 48 percent of Caucasians have gene variations linked to high inflammation, while African-Americans test lower and Asians lower still.
Elevated CRP levels can be detected by blood tests ordered by physicians during regular checkups. CRP is important because elevated levels have been linked to an increased risk of cardiovascular disease and may also underlie other diseases including diabetes, high blood pressure, and possibly Alzheimer’s.
CRP blood-test results, Kornman says, can be helpful but may also be imperfect because levels fluctuate so much. CRP goes up if you are stressed, eat high-fat foods, don’t get enough sleep, or exercise heavily. The genetic test—which requires a cheek swab—doesn’t fluctuate, and it positively identifies people at risk for elevated inflammation levels.
More important, Kornman says, it detects specific genetic patterns that put a subgroup of healthy people at “significantly greater risk” for developing inflammation-related heart disease. The test further identifies a genetic pattern associated with excess inflammation but not with elevated CRP levels. Both findings have been validated in two studies, including one by the Mayo Clinic.
Kornman says drugs are available to control inflammation, but he looked into a nutritional therapy by joining with Nutrilite, a dietary-supplement company based in Buena Park, California, to devise an anti-inflammatory formulation. He says Nutrilite tested 200 botanical extracts for anti-inflammatory properties and chose three to combine in one supplement: rose hips, a blueberry-and-blackberry extract, and a grapevine extract very high in resveratrol, a component of grapes and red wine thought to decrease disease risk.
Scientists conducted a 12-week, placebo-controlled study of young adults with elevated CRP levels caused by genetic variations identified by Kornman’s lab. Kornman says the adults who received the specially formulated supplement experienced reduced expression of the suspect genes and significantly decreased their inflammation levels. The study was published in the journal Nutrition in 2007.
He says other studies show that high-quality omega-3 oils available in a couple of capsules a day can help reduce inflammation, as does exercise—as long as the levels aren’t measured right after exercise. Antioxidants such as green tea and dark chocolate also can be effective, as can curcumin. Fatty foods are known to increase inflammation levels.
Kornman says he’s excited by the results of research into genetic variations linked to overweight and obesity undertaken by his lab more than three years ago. The research began with a question: Do we know enough today about gene variations to guide effective weight loss in healthy individuals?
It took a year and a half of research in consultation with Louis Pérusse of Laval University in Quebec, one of the developers of the Obesity Gene Map, to create tests to identify genetic variations that in Kornman’s words “place people into different buckets” regarding weight management.
In a clinical study conducted by Interleukin Genetics in collaboration with Stanford University and presented March 3 at an American Heart Association meeting, 101 otherwise healthy, premenopausal Caucasian women who ranged from overweight to mildly obese were randomized into four groups. All were on calorie-restricted diets, but one group followed a low-carbohydrate regimen, another a low-fat regimen, and the third and fourth groups diets with varying fat and carbohydrate levels. The women had been genetically tested and were monitored over 12 months.
“We found that the women on the ‘right’ diet, based on their genetic test, had lost 2½ to 3 times more weight than the woman on the ‘wrong’ diet based on those tests,” Kornman says.
In effect, the study found that women on genetically appropriate diets lost weight most effectively not because of how much or how little they ate but because of the type of foods they ate. The study showed that one size does not fit all and runs contrary to the current dogma that calorie reduction is the only proven way to lose weight.
According to Christopher Gardner, director of nutrition studies at the Stanford Prevention Research Center, the genetically matched diet “represents an approach to weight loss that has not been previously reported in the literature.”
Kornman’s company charges $149 for each of these tests. The inflammation test has been approved by New York state, currently the country’s strongest watchdog for genetic testing; the weight-management test is pending approval. Kornman says the low cost is possible because his lab has the high-speed technology to locate the variation efficiently.
While the tests offered by Interleukin Genetics can be useful, they are limited. More research is needed if nutritional genomics is to reach a point that will allow health-care professions with genetic training to prescribe individualized diets to prevent or delay diseases.
“Early on I think we will be able to apply this new knowledge to specific vulnerable groups, and as we refine it more it will be used for individuals,” DeBusk says. “A major shortcoming is that we’ve never invested enough in nutrition research the way the pharmaceutical industry did for drugs. That’s why the field of pharmacogenomics is ready to run with this as soon as the genetic information becomes available, but nutritional genomics will lag behind.”
Nutrition research accounts for about $1 billion a year—or about one-thirtieth of the NIH budget—one reason our understanding of the full implications of diet on health may lag even as we better understand gene function.
DeBusk suspects that there might be some discomfort on the part of the medical profession because most physicians are not knowledgeable about genetics or nutrition.
There’s concern that nutritional genomics could become an “elitist” science because only the well-to-do will pay for genetic tests for nutritional guidance. The counterargument says that genetic technology and entrepreneurial competition will continually lower the price for tests and that the new science will be cost-effective because preventing disease is far less expensive than treating it.
Another issue is privacy. Who will control your genetic information? Can insurance companies or employers gain access to it? And if so, could potentially damaging genetic information be used against you—to deny health insurance or a job?
Two years ago, Congress passed the Genetic Information Nondiscrimination Act to protect Americans from being treated unfairly because of differences in their DNA that may affect their health. The new law prevents discrimination from health insurers and employers. President Bush signed the act on May 21, 2008. Whether it can do the job remains uncertain.
What is certain is that nutritional genomics is coming fast. It will arrive piece by piece until it can be assembled into what will likely be the most powerful weapon in the arsenal of preventive medicine, a road map that can help us live longer and healthier lives.