Hunger and Eating: Learn It 1—Metabolism

  • Describe how hunger and eating are regulated
  • Understand the link between metabolism, obesity, and health
  • Describe anorexia and bulimia nervosa and their negative impacts

Eating is essential for survival, and it’s no surprise that powerful drives exist to ensure we seek out sustenance. While this section focuses primarily on the physiological mechanisms that regulate hunger and eating, social, cultural, and economic influences also play important roles in food consumption. We’ll explore how hunger is regulated, how the body manages weight, and the consequences of disordered eating.

Physiological Mechanisms

Hunger Signals

An outline of the top half of a human body contains illustrations of the brain and the stomach in their relative locations. A line extends from the location of the hypothalamus in the brain illustration, out to the left, past the outline, where it meets a box labeled “Hunger.” Down-facing arrows connect that box to a box labeled “Food,” and the box labeled “Food” to a box labeled “Satiety.” A line extends out to the right from the box labeled “Satiety,” and meets with the illustration of the stomach.
Figure 1. Hunger and eating are regulated by a complex interplay of hunger and satiety signals that are integrated in the brain.

Multiple physiological mechanisms trigger hunger:

  • Stomach contractions of an empty stomach send chemical messages signaling the need to eat
  • Glucose levels — When blood glucose drops, the pancreas and liver generate chemical signals that induce hunger (Konturek et al., 2003)
  • Ghrelin — Often called the “hunger hormone,” ghrelin is released by the stomach when it’s empty and stimulates appetite

Satiety Signals

Satiation—the feeling of fullness and satisfaction after eating—is also regulated by physiological mechanisms:

  • Glucose increases signal the pancreas and liver to shut off hunger (Drazen & Woods, 2003)
  • Gastrointestinal signals — Food passing through the digestive tract provides important satiety signals to the brain (Woods, 2004)
  • Leptin — This hormone, produced by adipose (fat) tissue, signals fullness to the brain. Higher fat stores lead to more leptin, which typically reduces appetite

The Brain’s Role

The various hunger and satiety signals are integrated in the brain, particularly in the hypothalamus and hindbrain (Ahima & Antwi, 2008; Woods & D’Alessio, 2008). The hypothalamus contains distinct populations of neurons:

  • Orexigenic neurons (appetite-stimulating) — including NPY and AgRP neurons
  • Anorexigenic neurons (appetite-suppressing) — including POMC and CART neurons

The balance of activity between these neural populations ultimately determines whether we feel hungry or full.

New Insights: GLP-1 and Appetite Regulation

Recent advances in obesity treatment have deepened our understanding of hunger regulation. Glucagon-like peptide-1 (GLP-1) is a hormone released by intestinal cells when nutrients are detected. GLP-1 plays a crucial role in signaling satiety to the brain.

How GLP-1 Works

GLP-1 acts on receptors throughout the brain, particularly in:

  • The hypothalamus, where it activates satiety-promoting neurons and inhibits hunger-promoting neurons
  • The brainstem (area postrema and nucleus of the solitary tract), which lacks a blood-brain barrier and serves as a key entry point for appetite-regulating signals

GLP-1 also slows gastric emptying, meaning food stays in the stomach longer, prolonging feelings of fullness.

GLP-1 Medications

Medications that mimic GLP-1 (such as semaglutide, marketed as Ozempic and Wegovy) have transformed obesity treatment. These drugs bind to GLP-1 receptors in the brain, reducing hunger signals and increasing satiety. Clinical trials show average weight loss of 15-20% of body weight—far exceeding previous medications.

The success of these medications confirms what researchers long suspected: hunger and satiety are not simply matters of willpower but are powerfully regulated by hormonal and neural systems. Understanding these biological mechanisms helps explain why weight loss can be so challenging and why pharmacological interventions can be effective for some individuals.

Metabolism and Body Weight

Body weight is affected by multiple factors, including genetics, environment, and the balance between calories consumed and calories burned. When caloric intake exceeds use, the body stores excess energy as fat. When we consume fewer calories than we burn, stored fat is converted to energy.

metabolic rate

Metabolic rate is the amount of energy expended in a given period. There is tremendous individual variability in metabolic rates—people with higher rates burn calories more easily than those with lower rates. Metabolic rate is influenced by:

  • Body size and composition (muscle burns more calories than fat)
  • Age (metabolism tends to slow with age)
  • Sex (males typically have higher metabolic rates)
  • Genetics
  • Physical activity level
  • Hormones (including thyroid hormones)

Theories of Weight Regulation

Most people’s weight fluctuates within a relatively narrow range over time, even without conscious effort. This observation led researchers to propose theories about how body weight is regulated.

set point theory

Set-point theory proposes that each person’s body establishes and attempts to maintain a stable body weight that is partly genetically predetermined. According to this view, efforts to move weight significantly from the set point are resisted by compensatory changes in hunger, satiety, and energy expenditure (Speakman et al., 2011).

However, set-point theory has limitations:

  • It struggles to explain why obesity rates have risen dramatically in recent decades if we all have fixed set points
  • Some predictions of the theory haven’t been supported—for example, studies found no lasting changes in metabolic rate between people who had lost significant weight and control groups (Weinsier et al., 2000)
  • The theory underemphasizes social and environmental factors in weight regulation

Settling-Point Theory

Contemporary researchers increasingly favor settling-point theory, which proposes that rather than defending a single fixed weight, the body can stabilize at different “settling points” depending on the interaction between biology and environment.

In this model, body weight settles at a point where energy intake and expenditure reach equilibrium—but that equilibrium point can shift based on:

  • Food environment (availability of high-calorie foods)
  • Physical activity patterns
  • Stress and sleep
  • Social and economic factors

This helps explain why the same person might maintain a stable weight of 150 pounds in one environment but settle at 180 pounds in an environment with abundant high-calorie food and limited physical activity.

The Dual Intervention Point Model

A more recent model proposes that rather than a single set point, there may be upper and lower intervention points—boundaries beyond which the body actively defends against further weight change. Within this range, weight may drift based on environmental factors, but pushing beyond these boundaries triggers stronger physiological resistance.

This model helps explain why:

  • The body strongly resists weight loss below a certain point (defending against starvation)
  • Some individuals can gain significant weight before physiological “brakes” engage
  • Weight regain after dieting is so common

Review the information presented above in the following exercise: