A Potential Hidden Factor in Why People Have So Much Trouble Losing Weight

The American conventional wisdom about weight loss is simple: A calorie deficit is all that’s required to drop excess pounds, and moderating future calorie consumption is all that’s required to maintain it. To the idea’s adherents, the infinite complexity of human biology acts as one big nutritional piggy bank. Anyone who gains too much weight or loses weight and gains it back has simply failed to balance the caloric checkbook, which can be corrected by forswearing fatty food or carbs.

Endocrinologists have known for decades that the science of weight is far more complicated than calorie deficits and energy expenditures. And in 2016, the fickle complexity of weight came to broad national attention. In a study of former contestants on a season of the weight-loss reality show The Biggest Loser, scientists found that years later, the contestants not only had gained back much or all of the weight they’d lost on the show, but also had far weaker metabolisms than most people their size. The contestants’ bodies had fought for years to regain the weight, contrary to the contestants’ efforts and wishes. No one was sure why.

Along with a team of researchers, Ann Marie Schmidt, an endocrinologist at the New York University School of Medicine, has been unraveling the mystery. In a new study published today, Schmidt and her team have unlocked a molecular mechanism controlling weight gain and loss in mice: a protein that shuts down the animals’ ability to burn fat in times of bodily stress, including when dieting or overeating. This discovery might hold the key to understanding why it’s so hard for humans to lose weight, and even harder to keep it off.

In 1992, Schmidt was studying the complications of diabetes when she and her team made what she calls a startling discovery: Humans and other mammals have a protein on the surface of fat cells called the receptor for advanced glycation end products, or RAGE, which appeared to play previously unobserved roles in a host of the body’s metabolic and inflammatory responses. Eventually, it became clear that the protein was also present in nondiabetic tissues, which suggested RAGE had consequences far beyond just a few chronic diseases.

Over the course of millennia, mammals might have developed things like RAGE to contend with their often-challenging surroundings. For humans, whose life spans have lengthened significantly in the space of only a few generations, that might be both a blessing and a curse. To meet the contemporary needs of people whose circumstances have changed at rates far quicker than evolution’s ability to keep up, findings like Schmidt’s are leading scientists toward ways to hasten the process.

For those advances to have the best chance of improving people’s lives, Schmidt cautions against the tendency to gloss over human complexity in favor of too-simple cultural beliefs, such as the idea that weight loss is just calorie deficits and willpower. “Weight loss is very, very difficult,” she says. “Only by studying the good things, the bad things, and how sometimes things that were meant to be good can go awry can we figure out the big picture and how to safely make people’s lives healthier and better.”

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