An Introduction to the Regulation of Hunger and Appetite

Table of Contents


In this series of articles I am going to discuss how the human body regulates hunger and appetite. My goal is to not only provide this information for educational purposes but also to provide interesting and useful insights that can help people who are attempting, while potentially struggling, to eat in a healthier manner and obtain a healthier body composition. There are 6 parts in this series:

This is an incredibly complex topic and we are far from having a full understanding of all of the important variables. We actually do not (yet) have the technology needed to determine specifically how various aspects of the brain function together to generate appetite and related sensations. Additionally, much of the research is done in rodents, cell culture, or other research avenues as opposed to in the human brain itself. Nonetheless, it is interesting and informative to consider what has been determined and how this differs between people with and without obesity. I will present much of the research here, and at the end I will discuss how I believe all of this basic knowledge can be translated into practical advice.

Note: Unlike other portions of this website where I generally cite things as they are stated, for this article series I will simply list the majority of the relevant citations at the end of the series. This is because I have gone through many reviews and research articles and have tried to compile all the various components into a cohesive overview; most of the various topics are covered in several of the citations and trying to disentangle which portion of each sentence or paragraph came from which citation would be difficult to follow.

I will, however, cite images appropriately to ensure full credit is given for them. Additionally, in the few instances where I state something published in one specific reference I will cite that reference specifically.

Introduction to energy regulation

The primary purpose of consuming food is to provide energy for the body. While I will not discuss all aspects of energy regulation in detail, I do want to make it clear that this involves the entire body to some degree. All active cells in the body contribute to energy expenditure, generally measured in calories, with certain organs such as the brain, heart, liver, and kidneys being more metabolically active than others. All of the organs are connected by the bloodstream, and there is a nerve supply that connects many different organs as well. Thus, all of the organs can at least potentially communicate with each other from a metabolic standpoint, with signals traveling to the brain to indicate the body’s total energy state (ie, a caloric surplus, maintenance, or deficit). The brain can then incorporate all of these signals, plus any additional thoughts/desires for specific food items (ie, cravings) to influence hunger and appetite.

The following image demonstrates some of the various aspects involved in energy regulation and thus body weight control. This is not exhaustive but should demonstrate that many different components work together. PYY, GLP-1, and CCK are all satiety-promoting hormones produced by the gastrointestinal tract and discussed later, UCP1 is an uncoupling protein that allows heat dissipation (and thus energy expenditure) in lieu of ATP production from mitochondria, and BMR = basal metabolic rate.

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Now I will discuss some of the more relevant terminology for hunger and appetite.

Basic definitions

Hunger itself is generally described as a drive to eat; it is a sensation that does not necessarily have a specific underlying mechanism but rather relates a feeling of low energy balance with the desire to remedy this with food consumption. This can be acute or chronic and may include weakness and a sensation of an empty stomach. After alleviating hunger by eating, most people will stop eating when they begin to feel full; this is considered the point of satiation, which is the process that brings consumption to an end. After people finish consuming a meal there is some period of time before feelings of hunger return; this period of time is considered satiety.

The word appetite can be used in different ways. Some use it to entail all of the various aspects of desired food intake (somewhat similar to “hunger”), while some use it to describe more specifically the qualitative aspects targeting specific food items with the expectation of some type of reward (ie, eating ice cream because it will make you feel good). I will use it in this latter manner. This brings us to the concept of homeostatic vs hedonic drive to eat. Homeostatic refers to energy balance considerations (short and long-term) while hedonic refers to desires for specific food items that will lead to positive sensations. For example, you may be hungry for dinner and be willing to eat almost any food due to a homeostatic drive to eat, and then after eating dinner when you no longer feel hungry you may still want dessert due to hedonic drive. Within the hedonic drive to eat are additional considerations such as liking (the pleasantness experienced when eating specific foods) and wanting (the desire to actually ingest a specific food, typically for some type of reward).

Many of these definitions may not seem very precise and that is because different bodies of literature use them in different ways.(Blundell, 2010) This imprecision also applies to various anatomic terms used to describe various hunger and appetite control regions in the brain, which generally reflects the incomplete body of research we have evaluating these topics. Nonetheless, I will mostly use the terms as described above, and I will make it clear if I am using them in a different way for any specific reason. Most importantly, I will generally use “hunger” to refer to the homeostatic aspects of eating and “appetite” to refer to the hedonic aspects of eating, though as you will see there is overlap between the two.

Tip: Appetite ratings generally do not predict energy intake as there is a distinction between emotional and behavioral aspects of appetite and feeding behavior.(Dhillon, 2016; Holt, 2017) This is a useful concept to consider when making any dietary modifications because if you can make choices to minimize appetite signals for specific food items you may find it easier to let natural hunger levels guide you to an appropriate quantity of food intake.

Additionally, many genes associated with obesity are expressed in the central nervous system, and in particular in the brain areas involved in homeostatic and hedonic signaling for food intake regulation. Thus, understanding the relevant physiology to then help discern how to dampen the strength of some of these signals that encourage excess food intake should allow people to more easily combat obesity. This is the primary purpose of this article.

The big picture of hunger and appetite control

Before delving into more detail, I want to provide a brief overview of the main aspects of hunger and appetite regulation.

At any given time, there are several peripheral signals that your brain is assimilating that influence homeostatic energy regulation. These come from:

  • hormones that move throughout the bloodstream (such as leptin, ghrelin, insulin, CCK, etc)
  • other molecules that move throughout the bloodstream such as glucose or FGF21
  • nerve signals that transmit input from your various senses
  • nerve input primarily from the GI tract transmitted directly through the vagus and spinal sensory nerves

These peripheral signals reach the brain in several ways, such as by either directly interacting with various aspects of the hypothalamus (after permeating the blood-brain barrier) or by sending signals through the vagus nerve to reach the medulla of the brainstem. These initial brain centers then interact with each other and several other intermediary centers as well, allowing various influences from your current emotional state, stress level, state of health, etc, to coalescence and influence your overall level of hunger. At the same time, other intermediary brain regions involved in hedonic food intake may be active and generate their own subconscious influences while also directly impacting the brain areas involved in homeostatic energy regulation. These collective signals are then transferred to the conscious decision-making regions of your brain, thus ultimately driving your desire and subsequent choices to seek out and/or eat various food items.

You can look at the following figure, starting from the bottom and moving upward, that highlights these features.

Reproduced from: Campos A, Port JD, Acosta A. Integrative Hedonic and Homeostatic Food Intake Regulation by the Central Nervous System: Insights from Neuroimaging. Brain Sci. 2022 Mar 24;12(4):431. doi: 10.3390/brainsci12040431. PMID: 35447963; PMCID: PMC9032173.

You can see in the following diagram that both the brain stem and the hypothalamus are near the inferior surface of the brain and thus are in a good position to receive signals from the rest of the body. They are able to assimilate various peripheral signals and then send projections elsewhere in the brain.

As the hypothalamus itself is a primary regulator of homeostatic energy regulation, I will discuss this in detail in the next article.

Click here to proceed to article 2 of this series, or jump around with the drop-down menu below.


  1. Blundell J, de Graaf C, Hulshof T, Jebb S, Livingstone B, Lluch A, Mela D, Salah S, Schuring E, van der Knaap H, Westerterp M. Appetite control: methodological aspects of the evaluation of foods. Obes Rev. 2010 Mar;11(3):251-70. doi: 10.1111/j.1467-789X.2010.00714.x. Epub 2010 Jan 29. PMID: 20122136; PMCID: PMC3609405.
  2. Dhillon, J., Running, C. A., Tucker, R. M., & Mattes, R. D. Effects of food form on appetite and energy balance. Food Quality and Preference. 2016;48(Part B), 368–375. doi:10.1016/j.foodqual.2015.03.009
  3. Holt GM, Owen LJ, Till S, Cheng Y, Grant VA, Harden CJ, Corfe BM. Systematic literature review shows that appetite rating does not predict energy intake. Crit Rev Food Sci Nutr. 2017 Nov 2;57(16):3577-3582. doi: 10.1080/10408398.2016.1246414. PMID: 27736161.
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