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Article by Infofit

Look Good in Your Genes!

Tweaking a gene influences whether your body accumulates or burns fat

Can We Control Our Genes?

We have some control over our genetics. Tweaking a gene that influences whether your  body accumulates or burns up fat may not be such  a  far-fetched  dream  for millions of  overweight and obese  people  around  the  world.  Recent breakthrough genetic research indicates that some genes such as our “fat” and “thin” genes can be influenced by our actions. Within this article we will provide you with insight regarding the latest genetic fat loss research and how to use this information to sculpt your body. Armed with the right information we will show you how to look good in your genes !

First, let’s look at an underlying concept purported by Dr. Neal Barnard (2001). In his work, Dr. Barnard suggests that you can control your shape by first, understanding what your genetics are regarding fat loss and second, match your nutrition and exercise programs accordingly to maximize your fat reduction potential.

In this article we will look at:

1. Appetite and the Leptin gene
2. Fat building genes
3. Fat burning genes
4. Diet and resting metabolic rate

Appetite And The Leptin Gene

Eating traits are not accidental; they are controlled by genes and hormones¹. Researchers have timed the rate at which people eat. Most start a meal at a moderate-to-fast pace, but slow down as they fill-up; others begin quickly and keep this pace until finished². This “racing” behaviour can result in a greater ingestion of food and kilocalories. Leptin is an appetite-reducing hormone secreted by one’s fat cells.

Some people secrete less leptin than others leading to an increase of appetite³. If you lose weight, leptin secretion is reduced and appetite increases (making it harder to stay on a diet). Diets consisting of 1,000 Kcal per day showed a dramatic drop in leptin and a strong increase in appetite4. Losing ten percent of body fat cuts in half the amount of leptin in blood, resulting in a strong increase in appetite5. This increase in hunger makes it harder to stick to your diet. Take Home Message: If you “fall-off” your diet, don’t whip yourself with feelings of guilt, your genes, not your will-power was partly to blame. If you are a “racer” eater, modify your pace. Also, learn to avoid dramatic decreases in leptin (I.E. crash diets) so as to avoid potentially detrimental increases in appetite.

Fat Building Genes   

Chromosome Let’s first address a fat storing gene found on Chromosome 8. About one-third of your ability to shed kilocalories as body heat comes straight from your parents6. It has been reported by German researchers that one in thirty obese people carry a gene that turns other non-fat cells (fibroblasts) into fat cells7. Chromosome 8 holds the gene for a critically important fat-storing enzyme called Lipoprotein Lipase also known as LPL¹. This enzyme wants to drive fat into cells. Depending on what you do or don’t do, will determine whether LPL propels the blood fat into fat cells or exercising muscle cells. Manipulating LPL through diet and exercise is another one of the keys to fat loss.

Take Home Message: Get LPL working for you, decrease the amount of fat in your diet and get the muscles working.

Fat Burning Genes

Genes influence your metabolism. Fat burning is controlled by several factors; one of which is a gene found on Chromosome 11 called Uncoupling Protein 2 (UCP28,9). UCP2 causes the fat you eat to be burned-off instead of stored in your fat cells 8 . People with this gene have higher metabolic rates and less body fat 9 . One in every fourteen people has UCP2, which speeds up the resting metabolic rate (RMR)10; others, such as Pima Indians, have a gene that slows down RMR11. This gene is passed down from one generation to the next¹. That said, it is important to note that genetics still only explain about 30%-40% of the metabolic differences from one person to the next; the main fat burning influences are still diet and exercise.

Take Home Message: Most cases of over-fat reflect (a) a predisposition to store fat, (b) a consumption of the wrong foods and/or too much food and (c) too little physical activity¹.
Diet and Metabolic Rate

Severe decreases in daily caloric intake (less than 600 kilocalories) can cause the RMR to slow an average of 10%-20% over six weeks12,13,14 . Once off this calorie restricted diet, the metabolism remains slow for several more weeks13 making it easier to pack on more weight. Even vigorous exercise does not appear to offset completely the reduced metabolic rate.

Take Home Message: Don’t do crash diets; you deserve to treat yourself better than that. A healthy eating plan does not restrict you from eating the essential nutrients needed for growth, repair and fat burning. Also, learning to eat according to your genetic profile can greatly enhance your fat burning capacity¹.

Happy Training!

Posted by: Andre Noel Potvin, MSc,BCRPA-TFL, ACSM CPT


1. Barnard, N. Turn off the fat genes. The revolutionary guide to taking charge of the genes that control your weight. Harmony Book (2001) NY.
2. Perusse L, Bouchard C. Genetics of energy intake and food preferences. The Genetics of Obesity. CRC Press, Boca Raton, 1994, 125-34.
3. Keim NL, Stern JS and Havel PJ. Relationship between circulating leptin concentrations and appetite during a prolonged, moderate energy deficit in women. Am J Clin Nutr. 794-801, 1998.
4. Wadden TA, Considine RV, Foster GD, Anderson DA, Sarwer DB, Caro JS. Short- and Long-term changes in serum leptin in dieting obese women: Effects of caloric restriction and weight loss. J Clin Endocrin Metabl 83:214-18, 1998.
5. Girard J. “Is leptin the link between obesity and insulin resistance?” Diab Metab 23:16-24, 1997.
6. Bouchard C, Deriaz O, Perusse L, Tremblay A. Genetics of energy expenditure in humans. Genetics of Obesity, 135-45
7. Ristow M, Muller-Weiland D, Pfeiffer A, Krone W, and Kahn CR. Obesity associated with a mutation in a genetic regulator of adipocyte differentiation. N Engl Med 339: 953-59, 1998.
8. Fleury C, Nerverova M, Collins S et al. Uncoupling protein 2: A novel gene linked to obesity and hyperinsulinemia. Nature Genet 15:269-72, 1997.
9. Bouchard C Perusse L, Chagnon YC, Warden C and Ricquier D. Linkage between markers in the vicinity of the uncoupling protein 2 gene and resting metabolicv rate in jumans. Hum Mol Genet 6 6:1887-89.
10. Rice T, Tremblay A, Deriaz O, Perusse L, Rao DC and Bouchard C. A major gene for resting metabolic rate unassociated with body composition: Results from the Quebec Family Study. Obes Res 4:441-49, 1996.
11. Ravussin E , Lillioja S Knowler Wc et al. Reduced rate of energy expenditure as a risk factor for body-weight gain. N Engl J Med 318: 467-72.
12. Jung RT, Shetty PS and James WP. The effect of refeeding after semistarvation on catecholamine and thyroid metabolism. Int J Obes 4:95-100.
13. Wadden TA, Foster GD, Letizia KA and Mullen JL. Long-term effects of dieting on resting metabolic rate in obese outpatients. JAMA 264: 707-11, 1990.
14. Leibel RL, Rosenbaum M, and Hirsch J. Changes in energy expenditure resulting from altered body weight. N Engl J Med 332:621-28., 1995.