Imagine you’re reviewing applications from aspiring graduate students to decide who will and will not be admitted entrance to your exclusive program. Would you automatically exclude overweight applicants, using the following rationale?
“Dear obese PhD applicants: if you don’t have enough willpower to stop eating carbs, you won’t have the willpower to do a dissertation #truth“.
The above quote is an actual tweet from Dr. Geoffrey Miller, professor of Psychology at the University of New Mexico and visiting scholar at New York University. As Elaina Plott of the New York Observer puts it, Dr. Miller believes the likelihood of academic success is inversely proportional to eating carbs.
As indiscreet as Dr. Miller’s comment was, it succinctly captures a prevailing belief concerning obesity, namely, that obesity is caused by gluttony, laziness, and lack of self-control. It was perhaps acceptable to subscribe to Dr. Miller’s belief in days gone by. But now, in the 21st century, we know far more about the complexity of biological processes underlying the development of obesity. And this kind of bigotry can no longer be excused.
One of the best summaries of what we now know can be found in the book Rethinking Thin, by New York Times writer Gina Kolata. Here is a summary of what we’ve discovered about obesity. And, sorry to say, Dr. Miller, it has little to do with will power.
For many of us, obesity just isn’t an issue. When the scale starts to creep up, we cut down on the chow and up our exercise regimen. That does the trick—the weight comes off. If it starts to come back again, we know we’ve been slacking off. But what we fail to realize is that this simple solution doesn’t work for everyone. It particularly doesn’t seem to work for people living in America. I have known many a foreign student who lamented the rapidity with which he or she gained weight upon coming to America, even when the American diet was rigidly avoided.
The real truth of the matter is that anyone who has followed an obese person in his or her quest to lose weight could hardly accuse them of a lack of discipline. Kolata expresses it best:
“No one could have been more determined than the dieters in the Penn study. They committed themselves to a two-year program. They kept food diaries. They exercised. They worked on avoiding thoughts and feelings and situations that tempted them to eat. And yet, as happens to dieters time and time again, most ended up gaining back almost every pound so painfully lost.” (p.187)
“I told a skinny acquaintance about the Penn dieters I had been following and the sad, but predictable, outcome of their attempts to lose weight. ‘Did they really, really try?’, he asked. I drew in my breath. It was like a slap. ‘Yes, of course they really, really tried,” I said. Of course, of course. How could they have tried any harder? It thought of Jerry Gordon, playing cards with his friends who were laughing and snorting, saying he felt like the librarian because he turned down the drinks, turned down the food. I thought of Carmen Pirollo, taking his Atkins snacks when he went to the movies with his friend, telling himself that the smell of popcorn was not even tempting. I thought of Graziella Mann, hiring a personal trainer, going to the gym at 6:00 am…Of course, they had really, really tried.” (p. 219)
Here is what several decades of obesity research has taught us:
The relationship between food intake and energy expenditure is far more complex than the simple “calories eaten, calories burned” equation that our doctors or our personal trainers would have us believe. A myriad of mechanisms have been selected and honed over the course of millions of years of evolution to guard against starvation and unpredictable food supplies. When challenged—particularly by stress, these mechanisms err on the side of hording energy rather than expending it. Some of us have thrifty genetic makeups that make putting on weight remarkably easy and losing it extraordinarily difficult.
Rather than a simple equation with two variables (diet and exercise), obesity is a multi-factorial disorder in which environmental and genetic factors interact to yield a disorder of energy balance.
More than 250 genes have been implicated in human obesity. Specific genes govern food intake, energy expenditure, fat metabolism, glucose metabolism, and adipose tissue development.
A study reported in the New England Journal of Medicine required 12 pairs of twins (all thin, young men) to spend 120 days in a separated section of a dormitory. They were all fed 1,000 calories more than what they needed to maintain their original body weight. If weight gain were simply a matter of eating too much and exercising too little, we would expect that all of the men would have gained significant weight during this study. In fact, this is what happened: The amount of weight gained varied greatly, with some gaining as little as 9.5 pounds while others gained 29 pounds. The distribution of weight also varied, with some gaining in the midsection while others gained in the buttocks and thighs. Most importantly, each brother gained the same amount of weight and in the same body area as his twin. The researchers concluded, “genetic factors are involved in adaptations to overfeeding, variations in weight gain, fat distribution, tendency to store energy as fat or lean tissue and the various determinants of how energy is metabolized”.
Another study examined obesity rates among 540 Danish adoptees. There was a strong relationship between the weight of the subjects and their biological parents, but no such relationship with their adopted parents.
The results of studies using transgenic mice are even more intriguing. Agouti mice carry gene variants that make them bright yellow, extremely obese, and prone to cancer and diabetes. Researchers Randy Jirtle and Robert Waterland fed a test group of pregnant mice a diet rich in methyl donors. These molecules are found in certain foods, and they can attach to a gene and turn it off. The results were astonishing. These mice gave birth to brown, slender mice who did not display their parents’ susceptibility to cancer and diabetes. In other words, the negative effects of the “obesity” gene these mice inherited were turned off by the kind of diet their mothers ate during pregnancy. As Jirtle puts it, you are not just what you eat, you are what your mother and your grandmother ate as well. You can see these mice in this fascinating video clip (from minute 3:00 to 7:20).
In studies of a different type of obesity gene, mice who inherit mutated copies of the “ob” gene from both parents were found to be grossly obese and to have voracious appetites. They are also heavier than normal mice even when fed a controlled diet. The reason they overeat is that these gene variants alter the receptors for leptin, a hormone that suppresses appetite. These mice are leptin-deficient and therefore do not experience the same feelings of satiety or satisfaction from food. So, like normal mice, they attempt to eat until they are satisfied. But unlike normal mice, they continue to feel hungry even after consuming a normal amount of food. Obese people tend to be leptin resistant, indicating altered function in their leptin receptors.
PYY is released by the intestines after a meal, and overweight people make less of it than thin people. Following bariatric surgery, the amount of PYY released in the intestines greatly increases, and patients report that their appetites are greatly reduced. This means that the feedback between intestines and the brain’s satiety circuitry is altered in overweight people, and correcting the feedback normalizes appetite, satiety, and weight.
So does this mean that your genes control your destiny and there is nothing you can do to lose weight? No. But it does mean that you need to know how your own individual body responds to specific foods and to different types of exercise. There is no one-plan-fits-all diet and exercise regimen, and something that worked for your friend may not work for you. There are several firms that specialize in providing clients with weight loss regimens based on analysis of their genetic profile. It also means that some of us will need serious medical intervention if our genes predispose us to obesity. For weight loss gurus and family physicians, this means that if simple diet and exercise are not working for a patient, don’t assume they are lying or cheating. Alternatives must be developed to assist weight-loss resistant patients to achieve reasonable goals.
But most of all, it means that those of us who have never struggled with weight loss should think twice about attributing laziness, gluttony, lack of will power, or any other kind of moral turpitude to the obese.
Denise Cummins, PhD, is the author of Good Thinking: Seven Powerful Ideas That Influence the Way We Think (Cambridge, 2012).
Copyright Denise Cummins, June 4, 2013