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Can my genetics stop me from losing weight?

There are genetic factors that predispose (increase the risk of) some individuals to being overweight or obese and the same genetic factors may make it more difficult to lose weight and keep it off.

It’s a common misconception that people with ‘bad genetics’ can’t lose weight and is often a reason why some people don’t want to try losing weight, because they think their genetics will stop them and thus they will fail. Reframe it and think of these genetic contributions as a reason why some people may find it harder to lose weight and why they may have been struggling their entire lives jumping between different fad diets that don’t work for them in the long term.

What are genes?

Our genetic make-up (our DNA) impacts every single one of our traits from visible features to things that are not so visible such as our predisposition to experiencing various diseases. Consider genes to be like a set of written instructions in our DNA; genes come in pairs, one from our mother and the other from our father. Sometimes the pair of genes are identical and other times they are written differently to each other. For some traits to occur we actually only need one out of the pair of genes to have the instruction whereas for other traits we need the instruction to be the same from our mother and father. You might have heard these described as dominant and recessive genes. 

The FTO Gene

We currently know of the FTO gene (fat-mass and obesity-associated gene) which is linked to an increased risk of being overweight. Everyone has this gene in their DNA but some people have a variant that impacts their physiology by increasing one’s drive to eat and decreasing drive to move.

How does this happen?

This occurs by affecting the production of the hunger hormones ghrelin and leptin at a higher than expected body fat percentage. There is an increase in ghrelin production and a decrease in leptin production which, in turn, causes an increased appetite (drive to eat) and decreased desire to move. 

Now the thing here is that the increased desire to eat and decreased desire to move alone won’t cause weight gain (more specifically fat gain) and that’s because the individual has to actually act on these desires, thus behaviours are impacted and are ultimately what cause overeating and insufficient movement. We know that eating more and moving less will alter the energy balance equation and eventually find us in a calorie surplus, thus increasing body weight through fat storage.

This isn’t to say that people who are overweight or obese lack the willpower, motivation or dedication to lose weight and they certainly are not lazy. It does explain why these people may struggle more with fat loss, have to try harder and have more support than people who don’t have this FTO gene variant. 

Hang on…

How would we actually know whether we have this gene variant? Simply put, without doing a DNA test we literally have no idea whether we have this FTO gene variant that predisposes us to weight gain.

In my opinion, there is no point in dwelling on whether or not we have this gene variant and we shouldn’t let it stop us trying to lose weight (if that’s something we want to do to become healthier). There is also no point in going out and getting an expensive DNA test to inform us. What is the value in knowing? Whether or not you have it and you want to lose weight, it won’t make an iota of difference. Make sure you work to the basic weight loss principles of eating less and moving more (shifting the energy balance equation in the right direction) and be sure to have the right support in your corner if you’re struggling. 

Interesting tangent

Interestingly, the FTO gene variant that we’ve been talking about would only be considered disadvantageous in today’s obesogenic environment and not tens of thousands of years ago when we were hunter gatherers and food was scarce. In fact, the gene variant would have been extremely useful in its impact on behaviours, so when food was abundant (e.g. after the hunt or after foraging) the drive to eat would have been high and so would calorie intake, ultimately impacting fat (energy) stores on our caveman/woman bodies. Then the drive to move would have been lower thus reducing loss of these energy stores. And because we wouldn’t know when we were going to eat next, that equals survival many thousands of years ago. 

Today however, those in a position of privilege only have to walk to the shop around the corner to have their pick of as much highly caloric food as they want. Plus, we generally move around less (not only because of lockdown) but also because of all the conveniences in our lives like cars and working from a computer. I’m sure that if our caveperson versions of ourselves had all these luxuries they too would be at a higher risk of obesity. 

It’s mind blowing to think that the majority of the population never truly reach their genetic potential. What I mean by this is those with advantageous genetics that would assist them in being the strongest, the fastest, the most efficient among us maybe won’t ever know they have this potential to unlock. We are not all athletes and neither do we all want to be. 

Knowing we have an advantageous gene isn’t a reason to act on being the best athlete. Likewise, having disadvantageous genes doesn’t necessarily have to be a reason to stop you from losing weight, it just might make things a little more challenging along the way.

Magnitude of effect

When we look at causal effects in health and fitness we often overlook the extent to which that thing has an effect. The effect can sometimes be huge and other times be minimal to the point that it’s not even significant or worth worrying about. In this instance, when looking at the FTO gene variant, it’s important to consider the relative magnitude of effect when looked at in isolation:

• Those with one copy of the gene variant (e.g. from one parent) weigh on average 1.5kg more than those without it. 

• Those with two copies of the gene variant (e.g. from both parents) weigh on average 3kg more than those without it. 

You can probably already see that this is NOT the difference between being a healthy weight and being obese. I shall repeat - it’s a reason why some people find it more difficult to lose weight. 

It’s not all bad news and it certainly doesn’t mean that people with this gene variant can’t lose body fat, or that people who struggle to lose body fat have this gene variant. It might mean more support is needed (and it’s unlikely you’ll know you have this gene variant anyway).

What’s even better is that physical activity has been shown to override the influence of the FTO variant on obesity risk! So even if you do have the FTO variant, being more physically active can negate that!

Exercise really is amazing and so are our genetics!

If you think you might need some more support and want to work with a coach, let’s have a chat.

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- Catherine

References: Benedict et al., 2014 - Fat mass and obesity - associated gene (FTO) is linked to higher plasma levels of the hunger hormone chrelin and lower serum levels of the satiety hormone leptin in older adults; Chueng & Yeo 2011 - FTO biology and obesity: why do a billion of us weigh 3kg more?; Kipelainen et al., 2011 - Physical activity attenduates the influence of FTO variants on obesity risk: a meta-analysis of 218,166 adults and 19,268 children; Turnwald et al, 2019 - Learning one’s genetic risk changes physiology independant of actual genetic risk.