Obesity Gene

Obesity overweightToday’s claims in the media about the recently discovered obesity gene are at best overwrought and at worst downright dangerous. A vast study involving more than twenty research centres across the UK has allegedly demonstrated that almost one fifth of us carry a variant of the gene known as FTO that predisposes us to obesity or overweight.

According to the researchers, “Obesity is a serious international health problem that increases the risk of several common diseases.” Fair comment. They add that, “The genetic factors predisposing to obesity are poorly understood.” Another fair comment.

They then report that while carrying out a genome-wide search for type 2 diabetes susceptibility genes among 13 groups of almost 40000 participants they have identified a common variant in the FTO gene that predisposes to diabetes through an effect on body mass index (BMI).

Additionally, the team reports that there is a cumulative, or additive, association of the variant with BMI. They found that 16% of the adults with the risky genetics weighed about 3 kilograms more than the others and were almost twice as likely to be obese, when compared to people without the risk allele. Moreover, the team says that they observe this genetic risk factor in individuals age 7 years and older and say that it reflects a specific increase in fat mass.

But, all this talk of obesity being down to genes will provide many individuals with an excuse along the lines of “it’s my glands”, which has become something of a serious cliche for some people who simply refuse to reduce the calorie intake and to add serious amounts of exercise to their daily routine.

The politics of obesity aside, I contacted metabolic expert Jeremy Nicholson of Imperial College London who recently discovered that calorie restriction in dogs extends life, reduces the risk of diabetes and metabolic disorders, and could be due to a change in the behaviour of microbes in the gut. He is less than impressed with the response of the media to the Science paper on FTO. “Basically, no amount of genetics can explain how humans have got fat so fast,” he told me. I would have to agree, genetics has long-term effects one usually does not see major changes in body function and form happening across a single generation.

So, might there be an alternative explanation for the apparent obesity epidemic in the developed world? Nicholson thinks so. “Changes in the gut microbes and caloric bioavailability probably could be the explanation,” he says. If we are suffering severe disturbances in the profile of gut bacteria – either they have changed behaviour or the species have changed – then those heading for overweight or who are already obese could be absorbing far more calories even from the same amount of food because of it.

Liposuction, like Vaser, Smartlipo and laser liposuction is one option, but could a dose of live yogurt or an antibiotic regimen be the solution to obesity? We are only just starting the hors d’heuvre when it comes to understanding the interplay between our bodies and microbes. Much more work into metabolism and the role of the guy microflora needs to be done before we can cast aside obesity as yet another genetic construct and so abandon sufferers to the realm of the untreatable.

Nicholson explains that the microflora in our gut are laid down in infancy and there is not a lot we can do about that. However, he says, “The real secret is eating a lot of beans and pulses (lentils etc) – lots of them every day, they keep the lower gut microbes very happy and the products of their
breakdown (catabolism) do not cause diabetes.” Nicholson laments that the windy side-effects of such a diet are far less malign than the problems associated with a diet deficient in beans and pulses.

Genetics, microbes, and beans aside, Nicholson has what I think has to be the final word on the debate: “Even genes and bugs added together still fade into insignificance if you sit on your butt all day eating pork rinds – you will get fat but its not genetic!”

19 thoughts on “Obesity Gene”

  1. @Ronald You cannot “speed up” the thyroid gland. You can treat a thyroxin deficiency but that has the disadvantage to causing the thyroid gland to atrophy in the end, which means thyroxin is for life. I am not sure that there is much evidence that treating hypothyroidism leads to a reduction in obesity despite its effects on metabolic rate. It seems that reducing calorie intake and increasing calorie use through exercise remains the most promising treatment for obesity.

  2. Dear sirs has anyone considered speedin ing up the thyroid gland as most have noticed low thyroid counts go hand and hand with normal obesity

  3. people should do something about it. there is a lot of things people could do about it but no one is taking charge.

  4. David Bradley says: Numbers like 1 in 100 and 1 in 200 are worth considering in the context of genetic disposition, i agree with you. But if those were the numbers that we were talking about, it certainly wouldn’t be in a conversation about the epidemic in the United Sates. So yes, genetic disposition may account for “hard losers,” who are a fraction of the obese population in the US. And since we can safely assume that the genetic disposition in the US is not multiples of the rest of the world, perhaps we should consider the cultural habits of Americans that make us so much fatter than every other first world country.

  5. Well, anonymous, I hope your reference to bombing Burger King is as flippant as mentioning Ethiopia in this context. Weight loss is not rocket science, for the vast majority, sure. Ingest fewer calories than you use and you will lose weight. However, there are perhaps individuals who are the opposite of what body builders call “hard gainers”, people who for whatever reason accumulate more calories from their diet than others. If the vast majority are fine, then what percentage may be “hard losers”? 1 in 100, 1 in 200. Those are still significant numbers in a population of several hundred million people, surely?

  6. Funny how there seem to be so many more people with this genetic problem and faulty gut flora etc in the US and UK compared to, say, Ethiopia. If all the money spent on this research was channeled instead into bombing all the burger kings perhaps the problem would be solved. Just a thought. Maintaining a healthy weight (in the VAST majority of people) is not rocket science. Why try to turn it into it?

  7. Good point, most Brits will know only too well how awful overboiled Brussels sprouts with their Sunday roast can be, delicately steamed they’re almost a delicacy (the sprouts, that is, not the Brits)

  8. You know, it’s a matter of getting over the psychological hump that has developed from a lifetime exposure to vegetables in the form of creamed corn and boiled carrots that make us think that vegetarian meals are boring and tasteless.

    I still consider myself a meat-eater, but since my teenage daughter became a vegetarian about a year ago and started doing a lot of the cooking I would never have known just how good and satisfying a veggie meal could be. In other words: it’s the preparation more than the content that’s central to good food. Our problem is as a culture we know more about how to make pork rinds tasty than doing the same for pulses.

    And it is just the preparation – boil a steak and see how much you like it.

  9. Michael, it is indeed a perennial problem – how to switch from porkrinds to pulses? But, what makes the obesity issue so odd is that given our society’s infatuation with life extension and age deferral (which simply boils down to a fear of death) individuals don’t recognize the life-threatening effects of being overweight, eating sh*t, smoking, and avoiding exercise. Invert those habits and most people would get instant life extension without all the expensive health supplements, plastic surgery, liposuction, and stomach stapling.

    Of course, if it’s “in my genes”, then they have a perfect excuse not to bother. By the way, make mine a veggie cheeseburger on rye, with a side order of dahl, thanks, and hold the mayo.

  10. If only there was a magic solution to the obesity epidemic. I agree that a genetic argument could not explain the dramatic rise in obesity; the population’s genes simply haven’t shifted that quickly. However, a study of genetic components of obesity may improve medical care(again, not looking for a miracle pill, but medical therapies are desperately needed given the negative impact of obesity).

    The question for me is, how do we get more people eating pulses instead of pork rinds? What changes in the broader system could we make to encourage this behavior?
    In case you are interested in these types of questions, researchers at the Yale Rudd Center for Food Policy & Obesity talk about them regularly at: http://www.ruddsoundbites.com

  11. It’s almost like medical science is looking for excuses for excess calorie intake and a failure to exercise.

  12. Obesity may be linked to middle ear effusions in children
    “Childhood obesity may be associated with a condition known as otitis media with effusion, which consists of fluid build-up in the middle ear space without symptoms of acute ear infection, according to a report in the April issue of Archives of Otolaryngology–Head & Neck Surgery, one of the JAMA/Archives journals.

    Otitis media with effusion, a condition in which fluid is retained in the middle ear space, but without earache, fever or other symptoms, has become increasingly frequent in children, according to background information in the article. Obesity has also become more prevalent in children, but the relationship between these two conditions has not been explored.”

    From here: http://www.eurekalert.org/pub_releases/2007-04/jaaj-omb041207.php

  13. Reader Julie Wood just emailed to ask what are the “pulses” to which I refer in this post. Well, I’ve edited in a quick example. More specifically, a pulse is a generic term for the seeds of leguminous plants. Beans themselves are therefore pulses by definition, so it is a little tautological to talk of beans and pulses. Nevertheless, that is common parlance.

    Examples of pulses are lentils, beans, peas, although in agricultural circles, the term is usually reserved from dried leguminous seeds and grains, which means strictly speaking green beans and peas, soybeans, oilseed grains (used for oil), and peanuts are excluded.

    However, in terms of health, we need not be so strict, peas, peanuts (unless you’re severely allergic) kidney beans, green beans, yellow beans, lentils (of all kinds), should be a good part of your daily diet, regardless of the adverse wind forecasts from initial ingestion.

  14. We certainly can’t, but it could be that modified fats and starches actually underlie the changes in the way our gut microflora behave. If processed glucose syrup, for instance, which is present in so many “modern” foods, alters the distribution of non-diabetegenic bacteria detrimentally, then it’s perhaps not surprise that we are facing a diabetes epidemic.

  15. We can’t rule out the influence of preprepared food with and the suite of modified fats and sugars that they contain.

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