Socially, the stigma of obesity has been associated with an individual being stereotyped, perhaps wrongly, as lazy and greedy. However, research has discovered that a lack of will power may not be the only cause of weight gain; you can start blaming your genes. Yes, it is true, “I have bad genes” can be added to the frequently used excuses of “I’m big boned” or “It’s just water retention”, however fortunately this one has much scientific backing. Here HCX explores recent research into the newly discovered fat gene: the FTO gene.
What is obesity?
The measure of obesity is based on our body mass index (BMI) scores; a number between 25 and 29 relates to the overweight category and over 30 equates to obesity. The higher a BMI score the higher the chance of an individual developing obesity related diseases which contribute to thousands of deaths every year. Amongst this doom and gloom however, there is hope: it can be reversed.
We are constantly bombarded with the message that losing weight is as simple as “eating less and moving more”, yet, thousands of people embark on diet and exercise changes that achieve minor, and ultimately disheartening, results compared to their skinny minnie friends. But HCX is here to tell you that the relatively small results are not necessarily due to lack of effort, but due to your genes. Yes, some people may have the form of the FTO gene that means they find it easier to gain weight and find it harder to shift it – as unfair as it seems!
Do genetic factors play a role in obesity?
Although met with scepticism, the general consensus since the 1980s is that yes, your genes play a role. Twin and adoption studies have been used to substantiate this claim; two related individuals have a higher correlation of BMI scores than those who are not related.
It is speculated that up to 40- 70% variation in common obesity is due to genetic factors. However, without hard scientific evidence of particular genes or the role they play, it is not surprising that the public scoffed at the idea, lumbering it as another lousy excuse.
The “fat gene”: FTO
Since then research has started to uncover the “fat genes”. Research in 2007 first identified the FTO (fat mass and obesity-associated) gene. FTO variants that are associated with obesity-related traits such as body weight, BMI score and fat mass are called “risk alleles”, the most studied of which is called allele “A”.
Homozygous individuals (those with two copies of allele A) make up 16% of the population of European descent and are unlucky enough to be 70% more likely to become obese. 62% are predicted to have one copy of the risk allele and have a 30% chance.
So now we know it exists, how exactly does FTO increase the chances of someone becoming obese?
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In 2013 some light was shed on exactly how allele A influences an individual’s chance of becoming obese. The three reasons discovered were:
1) FTO regulates ghrelin production
Ghrelin is a hunger hormone and high levels enhance appetite, therefore the more ghrelin present in your blood system the hungrier you feel. Allele A is associated with increased FTO expression, which in turn increases ghrelin production. In other words, FTO makes you fat by keeping you hungry.
2) Increases overeating
Individuals with two A alleles showed increased food intake, particularly of high fat foods that are notoriously (and regrettably) linked to weight gain, compared to those with two low risk alleles. In addition, the brain’s cues to food were impaired, with high calorie foods being more appealing.
3) Effecting your metabolism
Brand new research published in 2014 found that variants of FTO are functionally connected with the gene 1RX3. This is significant as IRX3 is thought to play a role in metabolism regulation. Perhaps the old age excuse “I have a slow metabolism” has some scientific backing after all – who knew?
What does all this mean?
The answer to the question “Does obesity run in the family?” is not as straight forward as a simple yes and no. If 63 % of people are thought to carry at least one risk allele and a further 16% have two copies, it begs the question: how come everyone is not obese? Indeed, you can inherit high risk alleles that increase your chances of becoming obese but these do not inherently make you so.
The bottom line: Having these high risk alleles does not mean you can’t be slim and healthy, nor does having low risk alleles make you immune to becoming obese. “Fat genes” don’t change your body to such an extent that all attempts to lose weight are futile. A healthy diet and exercise still works, in fact research has shown that exercise serves to suppress the risk alleles.
To read more about the facts on obesity visit the World Health Organisation website.
References:
The research articles on the link between obesity, genetics and the FTO gene:
1. O’Rahilly, S. and Farooqi, I. S. (2006). Genetics of obesity. Philos Trans R Soc Lond B Biol Sci. 361 (1471), 1095–1105.
2. Frayling, T.M. et al (2007) A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity. Science 316, 889–894.
3. Karra, E. et al. (2013). A link between FTO, ghrelin, and impaired brain food-cue responsivity. J Clin Invest. 123 (8), 3539–3551.
4. Gerken, T. et al. (2007). The Obesity-Associated FTO Gene Encodes a 2-Oxoglutarate–Dependent Nucleic Acid Demethylase. Science. 318 (5855), 1469-1472.
5. Smemo, S. et al. (2014). Obesity-associated variants within FTO form long-range functional connections with IRX3. Nature. 507 (7492), 371-5. doi: 10.1038/nature13138
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