Although a wealth of obesity-related genes have been described, how much difference do they make?
In the United States, more than one third of adults are obese.
The estimated medical cost of obesity in the United States was $147 billion in 2008.
In the interest of stemming this tide, much research has been plowed into methods of reducing this burden.
As genetic profiling has grown in speed and accuracy, our knowledge of the influence of genes on our bodies has increased in line.
Recent research into the genetics of obesity has uncovered a range of gene loci associated with body mass index (BMI) and the distribution of body fat. In fact, no less than 97 loci have been shown to account for 2.7 percent of variation in BMI.
The obesity-associated FTO gene, MC4R, and TMEM18 have shown the greatest association. And, of those top three, the FTO gene has been found to explain the largest amount of genetic variance in obesity traits.
Individuals with two copies of the FTO minor allele weigh an average of 3 kilograms more and have a 1.7-fold increased chance of being obese, compared with those who have two copies of the lower risk allele.
A number of studies have investigated how carriers of the FTO minor alleles respond to weight loss interventions; however, to date, findings have been contradictory. Because the question carries a great deal of importance for public health, it deserves further study.
Reopening the obesity gene debate
An international team of investigators set out to examine the interaction of the FTO gene with weight loss interventions by reviewing currently available data. In total, the team analyzed almost 10,000 participants who took part in eight randomized control trials.
At the start of the trials, on average, FTO carriers were heavier than their non-FTO counterparts by 0.89 kilograms. The team took note of the participant’s body weight, waist circumference, and BMI. These metrics were measured against the type of weight loss intervention, its duration, and the participants’ ethnicity, gender, age, and baseline BMI.
By the end of the trials, the researchers found no relationship between the FTO carriers and a reduced ability to lose weight.
The authors conclude that “people who carry obesity risk FTO genotypes respond equally well to weight loss treatment.”
Although the authors acknowledge certain limitations of the research, for instance, they only looked at the effects of the FTO gene, they believe that this is “an important finding for the development of effective weight loss interventions in the context of the global epidemic of obesity.”
The future of weight loss
The team hopes that the results will increase the “focus on improving lifestyle behaviors, principally eating patterns and physical activity, since these will be effective in achieving sustained weight loss irrespective of FTO genotype.”
The research, published this week, is accompanied by an editorial, written by Dr. Alison Tedstone, chief nutritionist at Public Health England. In the article – “Obesity treatment – are personalized approaches missing the point?” – she reminds us that the causes and solutions of obesity are varied and complex, but that the influence of gene profiles does not currently have the backing of evidence.
“Was it ever plausible that the FTO gene would have a noticeable influence on energy imbalance, and hence weight gain, compared with the influence of environmental factors such as food price, availability, and marketing?”
Dr. Alison Tedstone
Dr. Tedstone says that “a rebalancing of research towards whole systems approaches including environmental drivers may be of greater benefit to the population in the long term.”
The results can be considered as positive for those who carry the obese genes; weight loss is still very much achievable. Genes certainly do appear to play a part in body shape and weight, but exercise and good diet should still be the primary concern when attempting to lose weight.
Dr. Tedstone rounds off her editorial by noting: “The solutions to the obesity crisis must be societal, as well as individual.”