The Science Behind Feeling Full

Millions of years have honed the mechanisms that compel us to eat. Unfortunately, when it’s time to stop eating, evolution has given us far fewer tools.

It is once again time to celebrate a uniquely American holiday in uniquely American fashion: by ingesting record-breaking, dining room table-straining quantities of glorious food. After all, you’re just doing exactly what evolution tells you to do: taking advantage of a plentiful moment before winter sets in and you’re confined to your cave. You’re striking while the stuffing is hot.

But while evolution has spent the last several million years honing the mechanisms that compel us to eat, it’s been comparatively lax on the mechanisms that cause us to stop eating, which are much less important for survival, unless you’re in the fashion industry. Over millenia, from one gene pool to the next, the impulse to stock up on nutrients whenever they’re available has been so reinforced that we now have more biological systems than we actually need to ensure that we regularly appear at the dinner table. A depleted glucose supply sends both the brain and the liver into high-alert mode, and an empty stomach rushes a hormone called ghrelin to the brain, inscribed with simple yet urgent instructions: feed me.

It seems that cocaine and crème brulee present a similar challenge to the practice of moderation.

But if our evolutionary drive says eat, eat, eat – but never stop, stop, stop – why don’t we just stuff ourselves till we burst? Where does the “I feel full” sensation come from?

The feeling of fullness is described by scientists as “satiety signals,” and they come from several different sources, which researchers in the field divide between two categories: short and long-term signals.

Short-term signals of satiety arise directly from the meal you just consumed. They include memory of the taste and smell of the food, the sensation of your stomach stretching, and several different hormones released from your digestive tract in proportion to the nutrients you ingested. Basically, one big physical reminder from your body to your brain: Hey, fatso, you just ate.

Long-term signals of satiety are less is fully understood, and refer to chemical messages that the body sends to the brain, which modulate how full a particular meal will make us feel. Perhaps the best known and most publicized example is a hormone called leptin, which stems from the Greek word for “thin.” Leptin is produced by the body’s fat cells in direct proportion to how much fat that body has. In other words, the heavier you are, the more leptin you have, and the more quickly your brain realizes you’ve had enough to eat. This is the brain’s way of attempting to keep you from becoming fat&mdsh;for overweight people, it takes less food to satiate their appetite. Up to a point.

When leptin was first discovered in 1994, nutritional researchers pounced, believing that a leptin deficiency might be the explanation for obesity. As it turned out, this is true only for a tiny minority of overweight people. In general, the obese have no shortage of leptin (given that leptin is produced by fat cells, if anything they tend to have more). The problem is that overweight people’s leptin is no longer able to do its job, because their levels of the leptin hormone are so chronically high, their brains have become desensitized to it.

As for the thin and thinning, leptin remains an important consideration. The thinner you become, the lower your leptin levels droop, and the more food it takes to satisfy your appetite. This is precisely why you should never believe anyone who tells you that your diet will get easier the longer you do it. It won’t. As Diana Williams, a professor of psychology and neuroscience at Florida State University explains, losing weight means that “now you eat the same meal you might have had the other day, and it’s not as satisfying. You actually need to eat more in order to feel that same sense of fullness.” She says this is part of the reason it’s easier to cut down your portions earlier in your diet than later. “When a person diets and loses some weight, it’s harder and harder to maintain that low level of food intake that you need to maintain in order to keep that weight off.” A grim prognosis for the post-Thanksgiving dieter.

So we eat when certain hormones float up to our brain and tell us we’re hungry, and we stop eating when a different set of signaling systems convey to our brain that we’re full. But there’s an obvious problem with this model: food tastes great. “We enjoy eating,” says Ms. Williams, “You can feel full, you can have a stomach full of food, and then dessert comes out, and we eat more. So these mechanisms of hunger and satiety sort of go out the window in the face of really rewarding food.”

Given the well-documented power of pecan pie, it’s no surprise that the mechanisms that cause hunger and fullness don’t tell the whole story. Scientists are still trying to unravel the complex relationship human’s have with food, and they’ve made some strides.

For instance, recent evidence suggests that good food and addictive drugs trigger many of the same responses in the brain, the neural mechanisms that underlie so-called “reward learning.” It makes sense, evolutionarily speaking, that the brain treats food as a natural reward, releasing neurotransmitters like dopamine when we eat that strengthen our desire to eat again. The fact that food prompts our brain to produce these feel-good chemicals helps to explain why so many of us struggle to stop eating when we’re full. It seems that cocaine and crème brulee present a similar challenge to the practice of moderation.

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So this Thursday, go ahead and eat as much turkey and pumpkin pie as you want. You can always blame it on the dopamine. Bon appétit.