Published on Healthier Talk (http://www.healthiertalk.com)
By Dr. Al Sears
Created 07/29/2010 - 6:00am
Turn Off Your Obesity Gene
Bad genetics doesn’t have to catch up with you. You can change your genes simply by making a few adjustments to your diet.(1)
When you eat certain foods, nutrients release hormones that switch your genes on and off. And the nutrients in low-glycemic foods turn off genes that lead to weight gain and diseases that may follow.
We found this out when we studied the response to the glycemic index (GI) in people who have metabolic syndrome.
The glycemic index measures how fast your food breaks down to sugar in your bloodstream. Metabolic syndrome is a medical term for overweight people whose cholesterol, triglycerides, and blood sugar levels are high. It puts them at risk for diabetes, heart attack, and stroke.
In the study, one group ate foods with a low GI rating of 40-60. The other group ate foods with a high GI rating of about 80-100.
In just 12 weeks, the high GI diet increased the activity of 62 genes that lead to disease. These genes activate your stress response. It puts your body in a constant “fight or flight” mode. This lowers your immunity and causes damage to your cells.
But the low GI diet decreased the activity of 71 disease-causing genes, including hormone-sensitive lipase (HSL).(2)
High HSL is what causes fat to settle around your middle.(3) But when scientists studied animals bred to have little HSL, they found the animals became resistant to obesity, whether it was hereditary or from diet.(4)
I suggest you eat a wide variety of low GI foods. Follow the example handed down by our primal ancestors. Choose foods you could have gotten either by hunting or gathering:
Eat fresh, low-glycemic foods. Look for grass-fed beef. Fish. Beans. Plenty of above-ground and green, leafy vegetables. Onions and garlic. Berries, nuts, and seeds. Fresh fruits.
Avoid high-glycemic foods. These include white potatoes, most grains such as rice, corn, and wheat, cereals, cereal bars, and low-fiber or sweetened foods.
Shun pre-packaged items and fast food. These products contain high-glycemic ingredients and artificial chemicals. Avoid sweetened foods. Diet foods. Foods like these turn on the genes responsible for weight gain and disease.(5)
For more information on the glycemic index, click here .
Finally, if you have a family history of disease, you may want to supplement with additional nutrients:
- Pick up a multi-vitamin and mineral supplement that contains high levels of B vitamins such as B12 and folate. These two vitamins directly contribute to DNA health. I recommend at least 100 mcg per day of vitamin B12 and 800 mcg of folate.
- MSM is a great detoxifier known to keep your DNA healthy. You can take 900 mg up to 3 times a day.
- SAMe is a nutrient you won’t find in food, but you can buy supplements at your local vitamin shop. This is one of the best-known for DNA protection. Take 200-1,600 mg daily.
1. D Ornish, MJ Magbanua and G Weidner et al., “Changes in prostate gene expression in men undergoing anintensive nutrition and lifestyle intervention.” Proc Nat Acad Sci USA 2008;105 8369–8374.
2. Kallio P, Kolehmainen M, Laaksonen DE, et al. “Dietary carbohydrate modification induces alterations in gene expression in abdominal subcutaneous adipose tissue in persons with the metabolic syndrome: the FUNGENUT Study.” Am J Clin Nutr 2007;85:1417–27.
3. Carlsson, E. et al. “The hormone-sensitive lipase C–60G promoter polymorphism is associated with increased waist circumference in normal-weight subjects Hormone-sensitive lipase and obesity.” International Journal of Obesity 2006, Sept;30: 1442-1448.
4. Sekiya M, Osuga JL, Okazaki H, et al. “Absence of hormone-sensitive lipase inhibits obesity and adipogenesis in Lep ob/ob mice.” J Biol Chem 2004;279:15084–90.
5. Salsberg SL, Ludwig DS. “Putting your genes on a diet: the molecular effects of carbohydrate.” Am J Clin Nutr 2007 May;85(5):1169-70.
6. Paolo Raggi, et al. “Coronary Artery Calcium to Predict All-Cause Mortality in Elderly Men and Women.” J Am Coll Cardiol 2008 52: 17-23.
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