Snps Genotyping And The Diets To Lose-Weight

April 12, 2010

SNPs Genotyping and the diets to lose-weight

Mindy Dopler Nelson and Christopher Gardner from the Stanford Prevention Research Center, and other researchers of Interleukin Genetics Inc. performed a very interesting Clinical Trial entitled: Genetic Phenotypes Predict Weight Loss Success: The Right Diet Does Matter, presented at the Joint Conference -50th CardiovascularDisease Epidemiology and Prevention- and -Nutrition, Physical Activity, and Metabolism 2010, scheduled March 3, 2010, San Francisco, California.

This trial demonstrated that individuals following diets matched to their genotype, its showed statistically significant greater weight loss and other benefits at all time points (2 months, 6 months and 12 months) when compared to individuals on diets notmatched to their genotype. They studied overweight/obese premenopausal women, in a one-year weight loss study comparing four weight loss diets: very low carbohydrate, low carbohydrate/high protein, low fat and very low fat.

Beginning in 2008, participants who completed the trial were invited by e-mail and postal mail to provide DNA samples by a simple cheek swab. They genotyped 101 Caucasianparticipants, who were categorized using a genetic panel with SNPs, into three pre-determined composite genotype patterns of individuals who are more likely to respond to calorie reduction diets that are: low fat (Ornish diet), low carbohydrate (Atkins diet), or balanced in macronutrients (Zone diet). The primary endpoint analysis compared weight loss for women who were on a diet that was consistentwith their genotype category to those individuals on diets not suitable for their genetic pattern.

They concluded that individuals on a diet identified as appropriate to their genotype by lost an average of over 2.5 times more weight than individuals on diets that were not appropriate (p less of 0.013), and, they showed a waist size reduction of 2.6 inches or 6.6 cm (p less of 0.01). Those areamazing results. However, I have to say that we need to be cautious with those results mainly by four important considerations:
1. The sample size is too small (possible bias?) and it comprised only an specific group
2. The obesity epidemic is an environmental and social problem mostly, even when the genes have shown predisposition
3. The genotypic and allelic frequencies studied arestill unknown in the most ethnic groups
4. It will be necessary further studies that focus in a strict following, at median and long term.
The Human Obesity Gene Map reviewed, screened the evidence for all genetic variations that were associated with body weight, body mass index, or body fat and identified those that had been replicated in at least three clinical studies. Five variationsin four genes were included in this study, those variants include:
1. Fatty acid binding protein 2 (FABP2) Ala54Thr
2. Peroxisome proliferator-activated receptor-gamma (PPARG or γ) Pro12Ala
3. Beta-2 adrenergic receptor (ADRB2) Arg16Gly and Gln27Glu
4. Beta-3 adrenergic receptor (ADRB3) Arg64Trp
FABP2 Ala54Thr (A54T) Polymorphism
The FABP2 gene encodes the intestinal form offatty acid binding protein2 (FABP2). FABP2 protein is found in small intestine epithelial cells where it strongly influences fat absorption. Variations in DNA or polymorphisms in the gene result in greater binding of the fatty acids (released in the intestine from dietary fat consumption) which in turn results in higher absorption of fat. One such polymorphism, Ala54Thr, has been found to beassociated with obesity. Multiple clinical research studies have indicated that individuals with the Thr54 form of the protein show increased absorption and/or processing of dietary fatty acids by the intestine. The Thr54 variant has been associated with elevated BMI and body fat, increased abdominal fat, and obesity and higher LEPTIN levels. Homozygotes for 54Thr/Thr variant show increased levels of...