In the latest revelation about the human genome, researchers say individuals with a certain genetic mutation that predispose them to diabetes may be able to rely on beta carotene to reduce their symptoms.
Scientists from Stanford University report in the journal Human Genetics on an unique study in which they matched genetic variants linked to type 2 diabetes, in which people fail to make enough insulin to process glucose in the diet, against lifestyle risk factors associated with the disease, including diet and behaviors such as smoking and physical activity. Genetic analysis alone, in which scientists compare the genomes of those with diabetes against those without the disease, has previously identified 90 potential genetic changes that can increase the risk of diabetes, but none were especially strong contributors to the disease, and it wasn’t clear which combination of these DNA changes posed the greatest risk. Similarly, lifestyle factors such as diet or exposure to pollutants, which can be measured in blood or urine, couldn’t fully explain risk for the disease either. But by knitting the two databases together, the Stanford researchers say they may have identified some gene-environment match-ups that not only increase risk for diabetes, but may also help to protect against it as well.
“Over the past seven to nine years, [researchers] have been finding genetic risk factors. Some of them are pretty potent and have a lot of effects, but a lot is still relative. We are not really finding the smoking guns of the genome that we were expecting, that would really tell us why diseases like Type 2 diabetes have some genetic basis,” says study author Dr. Atul Butte, an associate professor of systems medicine in pediatrics at Stanford.
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Using data from the National Health and Nutrition Examination Survey, he and his colleagues found five major environmental factors associated with diabetes; all five, including levels of beta-carotene (a precursor to vitamin A), and a form of vitamin E, could be measured in the blood or urine. They then studied the levels of these five factors in people with different combinations of 18 of the major genetic variants linked to diabetes to see if certain DNA patterns were connected to specific nutrient levels. “We realized that maybe some of the reason why these genetic markers aren’t really that potent or haven’t been that potent in other people’s studies, is that the genes themselves may not cause diseases. It’s the genes with the environment that cause disease.”
In other words, having a genetic mutation isn’t enough; that genetic mutation, in the presence of high or low levels of certain nutrients, might prime the body to process glucose less effectively. That may be the case with people who harbor the gene variant SLC30A4, which codes for a protein that is involved in helping beta cells in the pancreas make insulin, which is critical for breaking down glucose in the diet. Both beta carotene, which is commonly found in carrots, and gamma tocopherol, a form of vitamin D, which is found in vegetable fats like canola oils and margarine, interact with the gene and influence risk for Type 2 diabetes, but in opposite ways. Higher beta carotene levels appears to protect against diabetes, and presumably improve the gene’s efficiency in producing insulin, while elevated gamma tocopherol may increase a person’s risk for the disease.
“What the findings suggest is that if you have a genetic marker now or a predisposition for Type 2 diabetes, all you really need to do is increase the number of carrots you eat to increase your beta carotene, and maybe you can compensate for having that spot in your genome,” says Butte.
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If only it were that easy. Butte’s work is still preliminary, and further studies would be needed to confirm that increases beta carotene levels in the diet would be sufficient to offset the effect of the diabetes-causing genetic variants. But, says Butte, the results are promising, especially when previous studies have identified other healthy behaviors that can reduce the risk of type 2 diabetes, such as eating less sugar and exercising daily. His findings, however, suggest more specific changes that could protect against the disease. “It’s not easy to lose weight and to change your appetite and what we eat, but it’s a whole lot easier than changing our DNA,” he says. “It’s not destiny when you have something written in your DNA, but here’s one way to potentially change risk by searching out for certain environmental factors that we can change and do something about our genetics.”