Dr Sam Decombel is the chief science officer of genetic research and development company MuscleGenes and has a PhD in Genetics from the University of Birmingham. She is based in Oxfordshire.
Have you ever struggled to shed body fat after bulking up? Do you find it seemingly impossible to lose those last few final pounds? We often think that diet and lifestyle are the main causes of weight gain, and undeniably these two factors have a significant impact. But can you also inherit a predisposition towards being fat? If your parents are overweight are you destined to be overweight too? Can you really blame your genes for your inability to cut down to size?
The first evidence that genetics might play a role in how easily we gain weight came from twin studies in the 1980s. In these type of studies, researchers look at the differences between identical and non-identical twins to determine how much of a characteristic is genetic, and how much is due to a shared environment.
As identical twins share both their genetic code and home environment, comparing them to non-identical twins – who do not share the same genetic code but do share the same environment – provides us with an estimate of how much of a contribution the genetic element makes. They found that identical twins are much more likely to share a similar waistline than non-identical twins, suggesting that genetics does indeed play a significant role in our predisposition towards carrying excess fat.
However, we had to wait 20 more years for the first firm evidence of a gene link to weight gain. It came in 2007, when a team of British researchers announced that they had identified a number of genetic variants within a gene called FTO (fat mass and obesity-associated protein). On average, people with one particular set of these variants weighed 1.6kg more than people with none, and those with two sets – including one in six Europeans – weighed 3kg more.
So what was going on? What was making those carrying the FTO risk variants gain the extra weight? Was it a slower metabolism, or less efficient fat burning? Interestingly enough, the answer turned out to be much simpler than that: they ate more food. But more than that, they tended to reach for higher fat foods more often than the non-risk carriers.
So do FTO risk gene carriers have less willpower than those without? Perhaps, but with good reason it seems. FTO is highly expressed in the hypothalamus, a region in the brain involved in regulation of food uptake and energy expenditure. While the effect these FTO gene variants are having does not appear to be metabolic in nature (so the effect of food consumed is likely to be no different between risk and non-risk carriers), they do seem to have a role in appetite regulation, through changes in the levels of certain chemical messages that tell our bodies how hungry or full we feel.
Biologically, hunger can be attributed to the fluctuating levels of many hormones, one of which includes ghrelin, informally known as the ‘hunger hormone’, because it increases appetite. Research has suggested that ghrelin levels play a large role in determining how quickly hunger comes back after we eat. The quicker your ghrelin levels rise, after a meal, the sooner you feel hungry again.
While the precise mechanism is still to be determined, we know that ghrelin levels in FTO gene risk carriers are not suppressed as strongly following a meal as those with the non-risk version. If you carry the FTO risk variant then, it’s likely you will not fill up as quickly after a meal, and therefore consume more food than non-carriers. In short, you are genetically programmed to eat more food.
There is a good biological explanation for why we might have evolved this way. Genes that make us desire food and eat as much as possible are obviously an advantage historically in environments with sporadic or limited access to sufficient nutrients.
We have evolved to actively search out food and eat as much as possible when it is available. Now, for the first time in our history, many of us live in an environment where there is an excess of food available around the clock, and it takes extra effort to overcome this very basic instinct to eat.
Is carrying a copy or two of the FTO risk variant an excuse for being fat? A survey of over 10,000 people by the BBC suggested that more than 70% of us think not, and I would tend to agree with them. Apart from the fact that this is only one gene among over 75 found, so far, to be linked to weight gain, at MuscleGenes we see plenty of customers who carry two copies of the FTO risk gene and nonetheless manage to control their fat levels extremely well. What are these guys doing differently to everyone else then?
Clearly you can’t change your genes, but with a bit of effort you don’t need to be dictated by them.
It’s not rocket science and it won’t come as a surprise to you but, according to the research, if you are a carrier of the FTO risk variants then the first and foremost thing you can do to aid weight loss is exercise.
A recent meta-study of over 235,000 people indicated that physical activity is a significant modifier of FTO, with those FTO risk carriers with an active lifestyle reducing their odds of obesity by 27%. It’s believed that part of this impact is due to the effect that exercise has on appetite. Exercise is known to alter levels of ‘hunger hormones’, such as ghrelin, and a growing body of evidence indicates that a short bout of exercise can curb appetite for up to two to ten hours post-exercise.
In terms of what exercise is likely to work best, the majority of studies at present lean towards higher intensity interval training being the most beneficial in terms of appetite suppression.
Avoid high-fat foods
Are there any dietary interventions to control our ‘hunger hormones’ and rein in appetite? Avoiding high-fat foods could be the place to start. A study looking at the effect the FTO risk variant had on body composition in response to different diets found that carriers were significantly less likely to complete a 10-week calorie-restricted dietary intervention on a high-fat and low-carb diet than those on a low-fat and high-carb diet, possibly because they were less responsive to the filling effects of fat.
The type of fat consumed also seems to matter: those FTO risk carriers consuming more than 12.6% of their total energy intake as saturated fatty acids (SFA) further increased their obesity risk. So what can you eat? By contrast, high-protein diets are known to drive weight loss because protein makes you feel fuller. It could be that certain amino acids contribute more towards that full feeling we get after a high-protein meal, and by careful adjustment of levels we can achieve that feeling of fullness sooner.
The amino acid L-cysteine in particular appears to be associated with regulation of food intake with recent research showing that it reduced hunger and ghrelin levels in humans in a dose-dependent manner. The temptation to increase the levels of L-cysteine in your diet artificially should be approached with caution however, as at least one study has also linked high dosages of L-cysteine to oxidative stress.
Watch what you eat
The real key for us to avoid overconsumption of course is to pay attention to what we are eating. It’s very easy to mindlessly eat due to routine or boredom when we are not actually hungry, or eat too much of the wrong types of food. Developing good eating habits, like preparing your meals for the week in advance and taking more time to eat, can be practical ways of reducing your chances of giving in to those cravings.