A meta-analysis study, led by Katherine M Livingstone and Professor John Mathers of Human Nutrition Research Centre, Institute of Cellular Medicine at Newcastle University, has heated up the debate surrounding the association between obesity and individual genome –FTO — does not and should not necessarily make you fat.
After evaluating the data collected from eight studies that recruited 9,563 participants, this latest study concludes that carrying FTO minor alleles showed no significant association with the change in adiposity, following weight loss interventions.
Although, it is true that the carriers of FTO gene are on an average 3kg heavier than those without this gene which puts these people at a 70% higher risk to become obese, no evidence is found which can make weight loss difficult for the carriers of this gene. These significant findings were also published by the British Journal of Medicine (BMJ) on 20th September.
The data for this study was collected from Ovid Medline, Embase, Chochrane and Scopus till November 2015. As the results found that for all intervention types, duration, ethnicity, baseline body mass index, sex and age, it was found that FTO genotype had no effects on the differential change in body mass index, waist circumference and body weight.
Professor John Mathers reflected on this established finding, saying, “You can no longer blame your genes. Our study shows that improving your diet and being more physically active will help you lose weight, regardless of your genetic makeup.”
Obesity and its association with individual lifestyle has been a debate for long. However, in recent years, a relationship between obesity and genome has led many people to believe that personalized interventions are required for weight loss. With this finding, however, all the claims about tailor-made dietary interventions for the carriers of genes associated with weight gain seem pointless all at once.
Although personalized interventions and tracing back into the genetic makeup of an individual have helped understand many health conditions and in bringing novel preventive, diagnostic and therapeutic interventions to practice, the disease burden cannot always be tagged to one’s genetic predisposition. This very notion has emerged in all its glory in this study.
An editorial piece by Alison E Tedstone, Chief Nutritionist at the Public Health England (PHE), based on these findings and published in BMJ, slammed at the credibility of businesses that are selling the idea of personalized diet plans to the consumers based on the individual genome. She says that although the association of genetic makeup and risk of obesity cannot be nullified, genetic predisposition to obesity simply does not outweigh one’s lifestyle and environmental factors which are the major contributors towards an individual’s obesity. Similarly, the notion which relates the presence of obesity associated genes with difference in the outcomes of weight loss interventions seems to lose its ground.
She added that the epidemic of obesity is complex in nature and restricting it to gene profiles is unlikely to yield desired results, at least as a short term goal. She emphasized that rebalancing the research towards whole system approach to study the obesity drivers will help populations fight out obesity in the long run.
What Is The Fuss About FTO Gene?
Estimates show that over 2.1 billion adults are overweight or obese, while in the UK alone 25% adults are obese. Obesity isn’t as simple as it sounds. It is a trigger to numerous serious ailments, out of which cardiovascular diseases are most prevalent at present.
The genomic medicine set out to delve into the dilemma of this increasing global health problem and identified as many as 97 regions which are associated with the increased risk of obesity, higher body mass index and body fat distribution (adiposity). What is known to us till know suggests that these genetic factors account for about 2.7% variation in the body mass index.
Out of these many genes, the most common genes identified to have a link with obesity include FTO, MC4R and TMEM18 genes. But the FTO (also known as fat mass and obesity associated) gene got most of the attention from researchers and its effects on obesity and weight loss were observed in detail.
FTO is an alpha-ketoglutarate dependent dioxygenase whose enzymatic activity has an association with body mass index, obesity risk and type 2 diabetes. People who are homozygous (two copies of FTO genes) are more likely to store fat and gain body mass because these people are biologically programmed to eat more. These people have higher levels of hunger hormone “ghrelin” in their blood which makes them hungry after shorter time intervals. These people are also prone to consuming foods with higher calorie count because the fMRI scans suggest that their brain pictures food differently, subsequently making them prefer fatty foods. These factors join together and put them at a higher risk of becoming obese.
Can You Blame Your Genes For Your Lack Of Interest In Following A Diet Plan? Not, You Can’t
The situation isn’t bleak after all, studies have shown that the effects of FTO gene variations can be counteracted by exercising and eating foods which are high in protein, which is further linked with reducing the ghrelin levels which in turn reduces the hunger and discourages unhealthy eating habits.
Supported by another study recruiting 742 obese adults, the interaction between FTO genotype and lifestyle changes on adiposity was found. The study ran for two years and it was found that people with FTO minor allele showed an average weight loss of 1.5kg as compared to the control group that was on a protein-rich diet. These changes in body mass were significantly found to have modified fat-free mass, whole body total percentage of fat mass, superficial adipose tissue mass, visceral adipose tissue mass and total adipose tissue mass. On the contrary, diet which was low in protein showed opposite effects on the weight loss outcomes.
Similarly, a six-month study of moderate exercise recruiting 105 obese women showed twofold greater weight loss in people with FTO gene variation as compared to their counterparts.
At another instance, another study including 3548 adults showed that the FTO phenotype had no significant effect on the weight loss of people. In additional to this, it was also concluded that the weight loss interventions worked equally well for people with and without FTO gene variant.
This meta-analysis has shown that the weight loss interventions including diet, physical activity or drug based interventions are similar for all, regardless of the FTO gene variations. It has been found that genetic risk of obesity does not hinder the weight loss intervention outcomes. As Professor John Mathers says: “For public health professionals, it means that the adverse effects of the FTO genotype on weight gain are not an impediment to weight loss interventions.”