If you’re anything like me, you’ve had days where you can’t escape a craving for sugar. You feel compelled to drive to your local Vons, pick up a pack of Oreos, and gorge. And, while you might not intend on eating two-thirds of the sugary death packets provided, this is invariably what you do.

Curiously, there’s a science behind this unfortunate predilection. It explains everything from our affinity to awful foods to our apparent inability to stop eating them. It also explains why some of us are more drawn to their lure than others.

But this science is more important than just a diagnostic for why we eat (and continue to eat) terrible foods. It’s also a remedy for much of the stigma that currently surrounds the growing obesity epidemic. Understanding the mechanics of terrible foods not only teaches us about ourselves, but also about those with whom many of us have trouble empathizing.


The story of terrible foods starts with hunger: Our brain senses it’s low on energy, sends out signals to other parts of the brain, then coordinates with these regions to make us want food. Most of this happens when the brain realizes it’s low on glucose, its primary food source.

To know when it’s low on glucose, the brain utilizes its various glucose detectors — specialized cells that monitor glucose availability in the brain’s blood vessels. These enable the brain to assess when it has enough to function normally, when it has too much, or when it’s running low and should make us hungry to get more.

Actual sensations of hunger come from a few small clusters of cells in the hypothalamus, an area considered the cosmic overlord of endocrinology. It’s so important it governs the Four Fs of Physiology: fighting, fleeing, feeding, and…sex. The area most implicated in hunger and feeding, though, is the lateral hypothalamus.

The lateral hypothalamus works with other areas of the hypothalamus to coordinate the release of orexigenic hormones. (Orexis means “appetite” in Greek.) These interact with organs like the pancreas, stomach, and small and large intestines to make us hungry. While the list of hormones involved in hunger is long, two are particularly relevant: neuropeptide Y and orexin.

Neuropeptide Y is considered the “most potent” orexigenic hormone. When injected into select parts of the hypothalamus, for instance, rats, mice, and humans will eat insatiably. A similar thing happens with orexin: The more it’s secreted from our hunger centers, the more we eat. Both hormones get secreted from the lateral hypothalamus and elsewhere when the brain needs food.


Unlike hunger, feelings of satiation often come from the periphery: Either fat cells, specialized cells in the pancreas, or other similar sources tell us we’ve eaten and should start to feel full. And, just like with hunger, these feelings are created by hormones. The two that are best known for satiation are leptin and insulin.

Leptin is secreted from fat cells in proportion to the amount of fat we have. Typically, this helps us maintain homeostasis: The more fat we accumulate, the weaker our appetites. Insulin, in contrast, is secreted from pancreatic beta cells when they sense glucose in the surrounding environment. Both get secreted after meals to suppress hunger.

Leptin and insulin exert their effects in a panoply of ways. Leptin, for instance, binds to neurons that express orexin and reduces their firing. Insulin does something similar — it binds to its receptors in the brain’s hunger centers and prevents their orexigenic signals from sending. More surprisingly, though: Both also work on the brain’s so-called “pleasure centers.”

The brain’s pleasure centers operate mostly via dopamine — and they do so in two ways. First, they secrete it when we want something: We start craving Oreos, say, and dopamine flushes through this system. But they also secrete it when we actually get that thing — i.e., when we finally sink our teeth into that terrible treat. Respectively, these are called the “wanting” and “liking” responses.

As we evolved as partially starved scavengers of the African savannah, foods high in fat and sugar were difficult to come by. When we found them, it made sense to eat as much as possible.

When leptin and insulin bind to our pleasure centers, they inhibit their dopaminergic signaling. What this means is that they lessen both our physical desire for food and the pleasure we’d get from eating it. The more we ingest, the more we grow numb to the pleasurable effects of eating. This is when we start to feel full.

Terrible Foods

Terrible foods work their magic by manipulating these hunger and satiety systems; they trigger the release of hunger hormones while simultaneously weakening satiety signals. The result — as our plight with Oreos, ice cream, fast food, and the like shows — is that we eat well beyond what we should.

The reason these foods trigger such a response is thought to be our evolutionary past. As we evolved as partially starved scavengers of the African savannah, foods high in fat and sugar were difficult to come by. When we found them, it made sense to eat as much as possible. Our brains evolved mechanisms like these to ensure we’d do exactly that.

The first way terrible foods implement such manipulation is by inducing the release of hunger hormones. Orexin, for instance, gets secreted when we eat highly palatable foods. This causes our hunger to linger. But such hormones also trick our pleasure centers into overactivity, amplifying our cravings. The area of the brain most responsible for this shift is the ventral tegmental area.

The ventral tegmental area is a cluster of cells that starts our wanting and liking pathways. It, along with another little cluster, is the primary arbiter behind our impulse to drive to the store, buy terrible foods, and enjoy the feeling of eating them.

When excited by foods high in fat and sugar, the ventral tegmental area gets kicked into overdrive. In response, it sends signals to the lateral hypothalamus that deplete its ability to respond to leptin and insulin. Without these satiety signals, we’ll want to keep eating. This is why we can have two columns of Oreos without feeling like we’ve ingested a whole day’s worth of calories: Terrible foods manipulate us such that we don’t become full.

Individual Differences

There are several ways that one person can respond to terrible foods differently from another. You could, for instance, have receptors for leptin or insulin that don’t work as well as intended. Such idiosyncrasies would stifle the ability to feel full as quickly after meals. But variation like this applies to most meals — not just terrible foods.

The science of metabolism suggests that, despite some widely held opinions, obesity is not some choice made by imprudent consumers of modern day terrible foods.

Another possible explanation is early exposure. When rats and mice are given high-fat foods at a young age, for instance, they show an increased affinity for those foods in adulthood over all their little rat and mice friends. This change persists throughout the lifetime.

Differences can also come from our pleasure centers. Our proclivities to gamble, get addicted to drugs, and engage in other risky behaviors, for instance, are tied to deficiencies in dopaminergic signaling. The less dopamine, the reasoning goes, the more we try to fill this gap with risk, a dopamine-inducing behavior. The same could be true of terrible foods.

Any way you spin it, the science of metabolism suggests that, despite some widely held opinions, obesity is not some choice made by imprudent consumers of modern day terrible foods. Instead, it’s a physiological disposition built from individual differences in a world of western diets. And whatever its precise origins, blaming those affected doesn’t really make sense.

The story of terrible foods, then, is one of hijacking: Our normal systems of hunger and satiation get manipulated by sugary and fatty foods that resemble something our bodies think is advantageous. As a result, our metabolisms push us to eat more of them than we should. Maybe understanding this will help us choose carrots next time instead.

Especially Fun Papers

  1. This paper describes a few of the ways in which our brains recognize and respond to glucose fluctuations in the body.
  2. These two papers (here and here) provide a thorough background on many of the constituents of our hunger and satiety systems.
  3. These three papers (here, here, and here) will tell you all you need to know about the different dopaminergic pathways.
  4. These three papers (here, here, and here) discuss the interactions between dopaminergic circuitry and our hunger and satiety systems.
  5. These two papers (here and here) cover obesity from a neurobiological standpoint.