The publication below landed in my mailbox last week. I've watched a video lecture or two by Dr. Friedman, who discovered leptin, but did not know he was an RPI alum!
|Rensselaer Alumni Magazine - Fall 2011 (pgs. 18-25)|
There's nothing groundbreaking about the article, but I thought I'd share it here. It does make a few things about leptin clear.
Friedman's work has been latched on to by the Healthy At Every Size, HAES crowd, (and he seems to have embraced this movement as well) and is cited in almost every anti-CICO rant by a certain prolific internet (multiple) personality. Listening to Friedman he, unfortunately, seems locked in the obesity = genetics mode. But the article seems to tell a slightly different story.
... obesity isn't really an "epidemic", as it is popularly described, because it doesn't spread from person to person like an infection. What is happening is more likely the consequence of a long legacy of calorie conservation playing out against a present-day environment of plenty, at least in some parts of the world.
"Very powerful evolutionary forces shape the weight of a species. If too thin, a person can't survive a famine, and if too fat, can't outrun a predator," explains Friedman.
Populations that, over time, have preferentially passed on gene variantes enabling people to survive famine are the ones whose descendants today, given a high-calorie "western" diet, become obese and have the highest diabetes rates in the world. "It's hard to lose weight with a biological system that resists weight change," Friedman says.
Clearly this guy never read Good Calories, Bad Calories and someone ought to get him a copy stat! Has he never heard of the Pima? C'mon man! But I digress.
The article discusses the role of leptin in energy homeostasis, and the appetite suppression. And then there on p. 21 ... just before the excerpts above, we find that *reward* word!
Leptin also binds cells in a brain area called the nucleus accumbens, which is a "reward center." The discovery of leptin, a long-sought factor regulating appetite and the first hormone found in adipose tissue, has gone a long way toward explaining why reducing one's weight is not as simple as "deciding" to eat less and exercise more.
At around the 32 minute mark of the talk linked earlier, Friedman discusses leptin resistance and lays out a means by which obesity results. The term is not used in the article. But there's one rather prolific blog comment contributor ItsTheWoo who posts lengthy treatises about leptin deficiency being the issue. The genetic mutant ob/ob mouse is, after all, leptin devoid. This article puts that notion to rest for the population at large:
If something seems too good to be true, it usually is, and that was the case for leptin. Once Friedman had discovered a hormone that controls weight and identified its gene in humans, researchers began looking for leptin deficiency in people. But the same hormone deficiency that causes obesity in the mutant mice soon proved to be extremely rare in people.
Perhaps this woman is one of those extremely rare, but that particular genetic underpinning simply cannot explain the obesity epidemic. Perhaps all who become obese in childhood should have their leptin levels checked. I imagine it would be life changing for those rare genetic-obese. I sense her frustration that obesity research seems to have been hijacked in a sense, to trying to solve environmental obesity -- that is far more within our control -- while neglecting to distinguish those who are genetically obese. But that is what it is, and it is also unfortunate that much of the research is looking for that magic pill that will excuse us from the environment we've created.
Friedman likes to downplay the epidemic itself in his lectures (and the linked video is no exception), but those of us of a certain age need only look around and we don't need science and theories and studies to notice that there are a whole lot more morbidly obese Americans than there used to be.
Even if leptin isn't the weight-loss wonder that the media first envisioned, its discovery may have a more profound effect -- lifting the stigma of obesity. Body weight is a trait, like height or blood pressure, that varies among individuals, with input from heredity and the environment. Friedman has become an advocate for those with obesity, attesting in frequent talks and articles to the scientific fact that this condition is part of human variation and not a personality flaw.
The bolded statement, however, is all too commonly truncated after "heredity". And somehow "environment" is all about carbohydrates for some, despite innumerable examples of carb-eating lean cultures (including the traditional Pima!) existing for millenia to the contrary. Clearly there is an environment factor -- a huge one -- in the SAD that disrupts leptin signalling in some way. Wheat belly says it's wheat, except when it's oats or any other carb. Lustig says it's fructose. Rosedale says it's those leptin-spiking carbs. Kruse says it's some epigenetic switch that flipped off your leptin receptors or something about quantum levees and puffy afghans. Taubes says it's really all about the insulin. Stephan Guyenet says food reward is a dominant factor. I find that last one closest of all to explaining the SAD-provoked obesity epidemic.
When one looks at the so-called "cafeteria rat" study and relate it to the diets consumed by those who become obese, we notice that why we get fat is, in the end, actually due to overeating after all. And how do we get rats to overeat? Feed them foods that in most cases are engineered to be highly palatable, and are also energy dense. Throw in a whole host of factors separating food intake from true hunger in us human types (celebrations, eating disorders, "comfort foods", guilt over starving kids in Ethopia, fitting in, body image, moral considerations, etc., etc.) and it's no wonder modern day humans become obese so easily. Friedman seems to imply that given our environment, we are at the behest of our genes to become obese.
The answer is remarkably simple if this is the case. Change the environment. Not so easy to do ... But not impossible.