You’ve just devoured a massive meal. There is not an inch of space left in your stomach. But you’re still hungry — for sweets. This is not an altogether unfamiliar situation. Researchers have now discovered that what is commonly known as “dessert stomach” is in fact a product of what happens in the brain. Here’s how. Maximising calories “Dessert stomach is actually an evolutionary holdover,” wrote University of Camridge geneticist Dr Giles Yeo, whose research focuses on food intake, genetics, and obesity, wrote. “It’s there to make sure that even when full, you are still craving the right types of foods to ensure you are able to maximise your caloric intake at every meal,” he wrote in an article in BBC’s Science Focus magazine. For much of history, most humans have never had a guarantee of when their next meal would come. In the days before settled agriculture, no human had this guarantee. This is why we have evolved to specifically crave calorically dense food. As have many other species. Salmon-devouring North American grizzly bears, for instance, eat the whole fish, down to the bone, when they start fishing. But as they get more full, bears switch to eating only the skin and the thin layer of fat that lies underneath. “Why? Because this is the most calorically dense part of the fish,” Dr Yeo wrote. The proliferation of sugar in diets across the world is very much a colonial and post-colonial development. But the reason why we are hooked to desserts today, is the product of evolution. After all, desserts, with their free sugar and fat, are some of the most calorie-dense foods out there. All in mice brains The latest study, published on February 12 in the journal Science, provides the biological mechanism by which sugar cravings take place. Researchers from the Max Planck Institute for Biology of Ageing, in Köln, Germany fed a bunch of mice to a point where they should be full. Then they gave the mice sugar, which the rodents nonetheless devoured. While seemingly satiated mice kept on eating sweet treats, the researchers studied their brains. They found that the so-called pro-opiomelanocortin (POMC) neurons, located in the mice’s hypothalamus and brain stem, were activated the moment they were given access to sugar. POMC neurons are responsible for regulating our food intake. In most cases, when activated they trigger the release of α-melanocyte which makes us feel satiated. But “unlike most other POMC neuron projections” consumption of sugar does not trigger the release of this chemical. “Rather [POMC neurons] produce the appetite-stimulating opioid β-endorphin”, the study said. ß-endorphin is basically one of the body’s own opiates. Among other things, it triggers a feeling of “reward” — stimulating mice’s appetite for sugar even when they were otherwise full. Notably, “this opioid pathway in the brain was specifically activated when the mice ate additional sugar, but not when they ate normal or fatty food,” a report in Science News said. And when researchers blocked this opioid pathway, the mice stopped eating sugar. Why this matters The same process also works in humans. The researchers in fact verified their findings by studying the brains of volunteers who received a sugar solution through a tube. “The cell types which are extremely well-known for driving satiety, also release signals that cause the appetite for sugar, and they do so particularly in the state of satiety,” head of the study Henning Fenselau, of the Max Planck Institute for Metabolism Research, told New Scientist. “This would explain why animals — humans — over-consume sugar when they’re actually full,” he said. Fenselau added that “from an evolutionary perspective, this makes sense [since] sugar is rare in nature, but provides quick energy. The brain is programmed to control the intake of sugar whenever it is available”. Understanding the mechanism behind “dessert stomach”, researchers believe, may help in coming up with better solutions to fight it. While most weight-loss medication today focusses on suppressing appetite, scientists may want to revisit drugs blocking opiate-receptors in the brain. As Fenselau put it, while opiate-receptor-blockers may be less effective than appetite suppressants, “a combination [of both drugs] could be very useful.”
