By Ferris Jabr

Matthew Brien has struggled with overeating for the past 20 years. At age 24, he stood at 5′10′′ and weighed a trim 135 pounds. Today the licensed massage therapist tips the scales at 230 pounds and finds it particularly difficult to resist bread, pasta, soda, cookies and ice cream—especially those dense pints stuffed with almonds and chocolate chunks. He has tried various weight-loss programs that limit food portions, but he can never keep it up for long. “It’s almost subconscious,” he says. “Dinner is done? Okay, I am going to have dessert. Maybe someone else can have just two scoops of ice cream, but I am going to have the whole damn [container]. I can’t shut those feelings down.”

Eating for the sake of pleasure, rather than survival, is nothing new. But only in the past several years have researchers come to understand deeply how certain foods—particularly fats and sweets—actually change brain chemistry in a way that drives some people to overconsume.

Scientists have a relatively new name for such cravings: hedonic hunger, a powerful desire for food in the absence of any need for it; the yearning we experience when our stomach is full but our brain is still ravenous. And a growing number of experts now argue that hedonic hunger is one of the primary contributors to surging obesity rates in developed countries worldwide, particularly in the U.S., where scrumptious desserts and mouthwatering junk foods are cheap and plentiful.

“Shifting the focus to pleasure” is a new approach to understanding hunger and weight gain, says Michael Lowe, a clinical psychologist at Drexel University who coined the term “hedonic hunger” in 2007. “A lot of overeating, maybe all of the eating people do beyond their energy needs, is based on consuming some of our most palatable foods. And I think this approach has already had an influence on obesity treatment.” Determining whether an individual’s obesity arises primarily from emotional cravings as opposed to an innate flaw in the body’s ability to burn up calories, Lowe says, helps doctors choose the most appropriate medications and behavioral interventions for treatment.

ANATOMY OF APPETITE

Traditionally researchers concerned with hunger and weight regulation have focused on so-called metabolic or homeostatic hunger, which is driven by physiological necessity and is most commonly identified with the rumblings of an empty stomach. When we start dipping into our stores of energy in the course of 24 hours or when we drop below our typical body weight, a complex network of hormones and neural pathways in the brain ramps up our feelings of hunger. When we eat our fill or put on excess pounds, the same hormonal system and brain circuits tend to stifle our appetite.

By the 1980s scientists had worked out the major hormones and neural connections responsible for metabolic hunger. They discovered that it is largely regulated by the hypothalamus, a region of the brain that contains nerve cells that both trigger the production of and are exquisitely sensitive to a suite of disparate hormones.

As with so many biological mechanisms, these chemical signals form an interlocking web of checks and balances. Whenever people eat more calories than they immediately need, some of the excess is stored in fat cells found throughout the body. Once these cells begin to grow in size, they start churning out higher levels of a hormone called leptin, which travels through the blood to the brain, telling the hypothalamus to send out yet another flurry of hormones that reduce appetite and increase cellular activity to burn off the extra calories—bringing everything back into balance.

Similarly, whenever cells in the stomach and intestine detect the presence of food, they secrete various hormones, such as cholecystokinin and peptide YY, which work to suppress hunger either by journeying to the hypothalamus or by acting directly on the vagus nerve, a long, meandering bundle of nerve cells that link the brain, heart and gut. In contrast, ghrelin, a hormone released from the stomach when it is empty and blood glucose (sugar) levels are low, has the opposite effect on the hypothalamus, stimulating hunger.

By the late 1990s, however, brain-imaging studies and experiments with rodents began to reveal a second biological pathway—one that underlies the process of eating for pleasure. Many of the same hormones that operate in metabolic hunger appear to be involved in this second pathway, but the end result is activation of a completely different brain region, known as the reward circuit. This intricate web of neural ribbons has mostly been studied in the context of addictive drugs and, more recently, compulsive behaviors such as pathological gambling.

It turns out that extremely sweet or fatty foods captivate the brain’s reward circuit in much the same way that cocaine and gambling do. For much of our evolutionary past, such calorie-dense foods were rare treats that would have provided much needed sustenance, especially in dire times. Back then, gorging on sweets and fats whenever they were available was a matter of survival. In contemporary society—replete with inexpensive, high-calorie grub—this instinct works against us. “For most of our history the challenge for human beings was getting enough to eat to avoid starvation,” Lowe says, “but for many of us the modern world has replaced that with a very different challenge: avoiding eating more than we need so we don’t gain weight.”

Research has shown that the brain begins responding to fatty and sugary foods even before they enter our mouth. Merely seeing a desirable item excites the reward circuit. As soon as such a dish touches the tongue, taste buds send signals to various regions of the brain, which in turn responds by spewing the neurochemical dopamine. The result is an intense feeling of pleasure. Frequently overeating highly palatable foods saturates the brain with so much dopamine that it eventually adapts by desensitizing itself, reducing the number of cellular receptors that recognize and respond to the neurochemical. Consequently, the brains of overeaters demand a lot more sugar and fat to reach the same threshold of pleasure as they once experienced with smaller amounts of the foods. These people may, in fact, continue to overeat as a way of recapturing or even maintaining a sense of well-being.

Emerging evidence indicates that some hunger hormones that usually act on the hypothalamus also influence the reward circuit. In a series of studies between 2007 and 2011, researchers at the University of Gothenburg in Sweden demonstrated that the release of ghrelin (the hunger hormone) by the stomach directly increases the release of dopamine in the brain’s reward circuit. The researchers also found that drugs that prevent ghrelin from binding to neurons in the first place curtail overeating in people who are obese.

Under normal conditions, leptin and insulin (which become abundant once extra calories are consumed) suppress the release of dopamine and reduce the sense of pleasure as a meal continues. But recent rodent studies suggest that the brain stops responding to these hormones as the amount of fatty tissue in the body increases. Thus, continued eating keeps the brain awash in dopamine even as the threshold for pleasure keeps going up.

CURBING CRAVINGS

A kind of surgery that some obese people already undergo to manage their weight underscores ghrelin’s importance in weight control and has provided some of the biological insights into why many of us eat far beyond our physiological needs. Known as bariatric surgery, it is a last-resort treatment that dramatically shrinks the stomach, either by removing tissue or by squeezing the organ so tightly with a band that it cannot accommodate more than a couple of ounces of food at a time.

Within a month after such surgery, patients are typically less hungry overall and are no longer as attracted to foods high in sugar and fat—possibly because of changes in the amount of hormones that their much smaller stomach can now produce. Recent brain-scanning studies reveal that these reduced cravings mirror changes in neural circuitry: postsurgery, the brain’s reward circuit responds much more weakly to the images and spoken names of tempting foods, such as chocolate brownies, and becomes resensitized to smaller amounts of dopamine.

“The idea is that by changing the anatomy of the gut we are changing levels of gut hormones that eventually get to the brain,” says Kimberley Steele, a surgeon at the Johns Hopkins University School of Medicine. A few studies have documented lower levels of hunger-stimulating ghrelin and increased levels of appetite-suppressing peptide YY following bariatric surgery. As recent experiments suggest, these hormones act not only on the hypothalamus but also on the reward circuit. “In the long term, we can probably mimic the effects of bariatric surgery with drugs,” says Bernd Schultes of the eSwiss Medical & Surgical Center in St. Gallen, Switzerland. “That is the great dream.”

In the meantime, several clinicians are using recent revelations about hedonic hunger to help people like Brien. Yi-Hao Yu, one of Brien’s doctors at Greenwich Hospital in Connecticut, proposes that obesity takes at least two distinct but sometimes overlapping forms: metabolic and hedonic. Because he believes Brien struggles primarily with hedonic obesity, Yu recently prescribed the drug Victoza, which is known to reduce pleasure-driven eating. In contrast, drugs that typically target the hypothalamus would work better if a patient’s underlying problem was a flaw in the body’s ability to maintain a steady weight.

Drexel’s Lowe, for his part, has focused on new approaches to behavior modification. “The traditional idea is that we can teach overweight people to improve their self-control,” Lowe says. “The new idea is that the foods themselves are more the problem.” For some people, palatable foods invoke such a strong response in the brain’s reward circuit—and so dramatically alter their biology—that willpower will rarely, if ever, be sufficient to resist eating those foods once they are around. Instead, Lowe says, “we have to reengineer the food environment.” In practical terms, that means never bringing fatty, supersweet foods into the house in the first place and avoiding venues that offer them whenever possible.

Elizabeth O’Donnell has put these lessons into practice. A 53-year-old store owner who lives in Wallingford, Pa., O’Donnell learned to modify her personal food environment at home and on the road after participating in one of Lowe’s weight-loss studies. She says she is particularly helpless before sweets and pastries and so has committed to keeping them out of her home and to avoiding restaurants with all-you-can-eat dessert tables—which in the past led her to consume “an excess of 3,000 or 4,000 calories.” On a recent visit to Walt Disney World, for example, she bypassed the park’s many buffet-style restaurants in favor of a smaller, counter-service eatery, where she bought a salad. That’s exactly the kind of simple change that can make a huge difference in the struggle to maintain a healthy weight.