Do Bad Genes Cause Big Jeans?

Do these jeans make my ass look bigIn the area of childhood obesity, does genetic research lead to a light at the end of the tunnel, or a dead end? Is the whole genetic thing just a cop-out for people who are in denial about their food addiction?

A couple of years ago, Maggie Fox of Reuters reported on the activities of obesity researchers at Boston’s Harvard Medical School. A special team, headed by Joel Hirschhorn, was titled GIANT, which stands for Genetic Investigation of Anthropometric Traits. Its task was to screen 15 different studies, and it has found six previously undiscovered gene mutations “strongly associated with a height-to-weight ratio known as body mass index or BMI.” Fox quotes Dr. Kari Stefansson, who said,

One of the most notable aspects of these discoveries is that most of these new risk factors are near genes that regulate processes in the brain.

Genetic factors that appeared linked to obesity had been found before, of course, leading scientists to theorize that in some cases, the way our bodies regulate weight is programmed into us. For instance, the “thrifty gene” theory proposed that a built-in mechanism urges us to eat as much as possible when food is available, because there might be famine in the future. It was later disproved by Dr. James Neel, the same person who suggested it in the first place. In Overweight: What Kids Say, Dr. Pretlow dismisses the “thrifty gene” theory as illogical. He says,

Pacific Islanders, who have a very high rate of obesity, have always lived on tropical islands, which had plentiful fruit and vegetation all year round and were surrounded by lukewarm waters full of fish. There were never any famines and thus no reason that Pacific Islanders with a thrifty gene would have survived better to pass on the gene. Moreover, if a thrifty gene drives us to consume as many calories as possible, then we would eat pure sugar or pure fat, which doesn’t happen. It is pleasurable taste that drives us to eat, not a thrifty gene.

But what is it that makes some people helpless against the lure of pleasurable taste, and unable to control the impulse to overeat? The problem is food addiction, obviously, as many current and recovering food addicts freely admit. But what makes some people addiction-prone? Could that be genetic? The possible genetic basis for addiction is still an open question.

Meanwhile, another “obesity gene” has been found, Tim Utton of the Daily Mail tells us, by scientists at London’s Imperial College. This gene is called GAD2, and apparently it speeds up production of the brain chemical GABA, which combines with yet another type of molecule to create an appetite-enhancing cocktail of brain chemicals. The theory is, these chemicals have the effect of making a person have little or no resistance to hunger. The lead researcher here was Professor Philippe Froguel, who is quoted as saying,

The discovery that this one gene plays a role in determining whether someone is likely to overeat could be crucial in understanding the continued rise in obesity rates around the world… Genetic factors alone can not explain the rapid rise in obesity rates, but they may provide clues to preventative and therapeutic approaches that will ease the health burden associated with obesity.


When our cells store fat, a hormone called leptin is released into the bloodstream. Leptin is part of the body’s hunger control system. A scarcity of leptin in the blood signals the brain to tell the body it’s hungry, it needs to eat. But it doesn’t work the other way around. An abundance of leptin won’t tell the brain and body they are not hungry. So having a lot of it doesn’t necessarily lead to weight loss. This fact has crushed the hopes of those who were optimistic that simple hormone replacement therapy would help obese patients.

Elena Conis reported for the Los Angeles Times on the disappointing fact that, in obese humans, the action of leptin is very iffy, depending on all kinds of poorly-understood variables. She said,

The countless pathways and still-unclear mechanisms through which leptin works in the body have frustrated many researchers’ hopes that the hormone would lead to an anti-obesity wonder drug… Leptin was discovered by happenstance in the mid-1990s, when researchers noted that mice with a mutation in the gene that carries instructions for making the hormone became rapidly obese.

So, we’re back to genetics again. Or maybe not. Conis goes on to say that, in most obese individuals, the leptin genes are intact. But the hormone just doesn’t do what it’s supposed to do any longer, because somehow the body has become resistant. And leptin also affects serotonin, one of the brain chemicals that tells us whether we’re having a good time. So leptin does not simply signal a full tummy, but gets all involved with the pleasure and reward systems of the brain. Which means,

The findings were further evidence that the emotional and physiological aspects of why we eat are tightly intertwined…

Nevertheless, in the presentation, “Why Are Children Overweight?” (Slide 40), Dr. Pretlow talks about how comfort eating and stress eating, which may become an addiction, overrides the normal satisfied or fullness feeling which stops kids from overeating.  Such addictive comfort and stress eating might also override the the leptin control system and be the reason that elevated leptin levels in obese individuals doesn’t cause weight loss. Which brings us back, once more, to addiction.

Your responses and feedback are welcome!

Source: “Study finds six new gene mutations linked to obesity,” Reuters, 12/14/08
Source: “Found: The Obesity Gene,”, 01/12/11
Source: “Why Are Children Overweight?,”
Source: “The waning promise of leptin in the obesity fight,” LA Times, 08/09/10
Image by Crystal, used under its Creative Commons license.


  1. Two resources I’ve come across recently that I find very compelling re overriding of normal appetite controls are:

    1) Brain Development & Addiction with Gabor Mate (

    2) New Directions in Understanding Obesity ( or

    I’m a lay person, but I find both explanations make sense in the context of our current food environment full of refined wheat, added fructose, and excess omega 6s via veggie oils.

    Re the latter, I’ve only begun to look into this, but it’s very curious to me that so far, all the research in the endocannabinoid system wrt obesity has involved antagonist action via pharmaceuticals. I’ve not yet seen whether anyone has considered whether or not all of the omega 6s we now eat may be driving the ECS via arichidonic acid synthesis.

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