Tuesday, September 9, 2008

Genes are not destiny - part 2

I've mentioned before that while your genes may lay out an ultimate potential, this is not a determined end point towards which you move. You have some influences on the expression of these genes, whether they are turned on or off to be crude. Diet, environment, exercise, infection, attitude, stress etc will all cause certain genes switch on.

The BBC carried a story yesterday about this.

Exercise 'blunts fat gene effect'



Carrying two copies of the FTO gene significantly increases the chances of becoming obese. However, a study carried out among the US Amish community found an active lifestyle appeared to remove this risk.

Genes are not destiny - you have an influence......

The abstract of the study is below:

Physical Activity and the Association of Common FTO Gene Variants With Body Mass Index and Obesity

Background Common FTO (fat mass and obesity associated) gene variants have recently been associated with body mass index (BMI) and obesity in several large studies. The role of lifestyle factors (such as physical activity) in those with an underlying FTO genetic predisposition is unknown.

Methods To determine if FTO variants are associated with BMI in Old Order Amish (OOA) individuals, and to further determine whether the detrimental associations of FTO gene variants can be lessened by increased physical activity, a total of 704 healthy OOA adults were selected from the Heredity and Phenotype Intervention (HAPI) Heart Study, an investigation of gene x environment interactions in cardiovascular disease, for whom objective quantified physical activity measurements were available and for whom 92 single-nucleotide polymorphisms (SNPs) in FTO were genotyped.

Results Twenty-six FTO SNPs were associated with BMI (P = .04 to <.001), including rs1477196 (P < .001) and rs1861868 (P < .001), 2 SNPs in moderate linkage disequilibrium in the OOA (D' = 0.82; r2 = 0.36). Stratified analyses of rs1861868 revealed its association with BMI to be restricted entirely to those subjects with low sex- and age-adjusted physical activity scores (P < .001); in contrast, the SNP had no effect on those with above-average physical activity scores (P = .29), with the genotype x physical activity interaction achieving statistical significance (P = .01). Similar evidence for interaction was also obtained for rs1477196.

Conclusions Our results strongly suggest that the increased risk of obesity owing to genetic susceptibility by FTO variants can be blunted through physical activity. These findings emphasize the important role of physical activity in public health efforts to combat obesity, particularly in genetically susceptible individuals.

2 comments:

Anonymous said...

The bbc article gives three or four hours of activity as the amount necessary to "flip the switch" in those genetically susceptible to obesity. I'm assuming that's per day? The article didn't say. William Banting claimed to have tried rowing vigorously every evening for several hours, and it only ending in increased hunger, and no weight loss. Maybe he was an hour or two short?
The only weight loss program I can think of offhand that advocates more than two hours a day of any kind of exercise is The Biggest Loser.
No wonder Taubes couldn't find evidence that exercise is effective for weightloss. How many controlled studies could there be involving this much exercise?
Fred Hahn's not gonna like this one.

Anonymous said...

I'm currently reading The Agile Gene, by Matt Ridley. It's a fascinating look at gene expression & the nature vs. nurture debate. There (can be) a huge difference between one's genotype and the expression of such as influenced by and through the environment, or the ultimate phenotype. Interesting stuff.