Why we get hungry

Science by Dr. Ben Bikman

Why we get hungry

Hunger and satiety are in a never-ending rotation—we’re hungry, we eat until satisfied, then we’re hungry again, etc. Because the prevailing paradigm on weight loss is centered exclusively (and erroneously) on calorie number and calorie restriction, the ability of resisting hunger is of paramount importance. But when it comes to resisting the temptation to eat when you’re hungry, it’s forcing you to push back against fundamental physiological drives. However, hunger isn’t as simple as most people think. In fact, it’s wildly complex—an orchestra of dozens of hormones and countless receptors in the body. But it’s also understood at its simplest levels, which involves a minor cause and a major cause.

“Gastric Hunger”

The minor cause, which is temporary and fairly subtle, is the one that receives all the attention. This one is largely a function of a lack of swallowing food and an empty stomach after it’s been stretched. In other words, this is hunger as a result of not eating recently. We could refer to this as “gastric hunger”—if your stomach is full, you’re satisfied; if it’s empty, you’re hungry [1]. But again, this isn’t a long-term or overly powerful hunger signal.

However, simply filling the stomach isn’t the whole story even with “gastric hunger”, as artificially placing nutrients into the intestines past the stomach (in a part of the small intestine) [1, 2] reduces hunger despite not filling the stomach at all. In fact, people who have had a complete gastrectomy (the surgical removal of the stomach) report that hunger is “just the same” as it was with a stomach [3]. Clearly, something beyond stretching the stomach is at work—“gastric hunger” only takes us so far.

Imagine if hunger was completely driven by “gastric hunger” and you were a patient receiving all your nutrition via intravenous (IV) infusion—you’d be constantly complaining of hunger! But this doesn’t happen. By providing nutrition directly into the blood, a person experiences little or no hunger. In fact, the person reports being most satisfied if the infusion includes fat as opposed to carbohydrates alone [4]. There is no question that dietary fat provides a strong satiety signal that reduces hunger [5].

“Cellular Hunger”

The major form of hunger is impossible to ignore—it will drive a person to extreme lengths—it’s not subtle at all. However, its causes are subtler. This major source of hunger is driven by the degree to which the cells of the body sense nutrients and the energy they provide; if there’s too little, the cells induce myriad signals to the brain in order to drive hunger. Let’s call this “cellular hunger”.

In its most obvious manifestation, cellular hunger is starvation—a chronic lack of sufficient calories to meet the body’s needs. In this state, the body is genuinely running out of fuel—glucose and fat. At this point, the body begins stripping down the muscle, bones and more, in an effort turn those proteins into glucose (a process the liver can do quite well).

The Rebound and the Brain

Thankfully, starvation is an exceedingly rare situation (certainly for those reading this post). But interestingly, a small version of this appears in everyday life in some people following a sugary/starchy snack or meal. This fascinating metabolic roller coaster is caused by a large spike in blood glucose levels, with, in some people, a commensurate large insulin release from the pancreas. Ultimately, insulin “overshoots” the glucose levels, resulting in a rapid blood glucose drop that drops below the starting glucose levels. This is referred to as “reactive hypoglycemia” [6]. This contributes to a unique situation where the brain starts to “run low” on energy.

The brain relies on two fuels to meet its high energy needs: glucose and ketones. Insulin lowers both of them. While an increase in insulin lowers blood glucose by pushing the glucose into muscle cells (and a few others), it lowers ketones by stopping the production of ketones from the liver. Thus, the exaggerated insulin spike deprives the brain of its two fuels: removing too much glucose from the blood and stopping the production of ketones.

This short-term state where both glucose and ketones are relatively lower than normal, and the subsequent relative “low energy” state of the brain, likely contributes to the hunger that happens soon after eating an insulin-spiking starchy/sugary snack or meal [7]. What is so important to fully understand this situation, is that the “brain hunger” occurs despite the intestines still being full of food!

Take-away Thoughts

Controlling hunger is critical to controlling metabolic health. Thus, the smartest strategy is to nourish the body with foods that: 1. Don’t leave you feeling uncomfortably full; 2. Prevent a rapid and significant increase in insulin. If you eat until you’re “stuffed”, you simply increase the likelihood of feeling “empty” shortly after the food is digested, prompting you to eat again. And if you spike insulin, you run the risk of getting low on glucose and ketones, the brain’s two fuels.


1 Geliebter, A. (1988) Gastric distension and gastric capacity in relation to food intake in humans. Physiology & behavior. 44, 665-668
2 Welch, I., Saunders, K. and Read, N. W. (1985) Effect of ileal and intravenous infusions of fat emulsions on feeding and satiety in human volunteers. Gastroenterology. 89, 1293-1297
3 Carlson, A. J. (1993) Contributions to the physiology of the stomach.–II. The relation between the contractions of the empty stomach and the sensation of hunger. 1912. Obesity research. 1, 501-509
4 McCutcheon, N. B. and Tennissen, A. M. (1989) Hunger and appetitive factors during total parenteral nutrition. Appetite. 13, 129-141
5 Kirchner, H., Gutierrez, J. A., Solenberg, P. J., Pfluger, P. T., Czyzyk, T. A., Willency, J. A., Schurmann, A., Joost, H. G., Jandacek, R. J., Hale, J. E., Heiman, M. L. and Tschop, M. H. (2009) GOAT links dietary lipids with the endocrine control of energy balance. Nature medicine. 15, 741-745
6 Luyckx, A. S. and Lefebvre, P. J. (1971) Plasma insulin in reactive hypoglycemia. Diabetes. 20, 435-442
7 Roslin, M., Damani, T., Oren, J., Andrews, R., Yatco, E. and Shah, P. (2011) Abnormal glucose tolerance testing following gastric bypass demonstrates reactive hypoglycemia. Surgical endoscopy. 25, 1926-1932


This article is for informational and educational purposes only. It is not, nor is it intended to be substitute for professional medical advice, diagnosis, or treatment and should never be relied upon for specific medical advice.