Appetite vs Cravings: GLP‑1s, Amylin and Satiety

Appetite vs Cravings: GLP‑1s, Amylin and Satiety

Appetite

Appetite vs Cravings: GLP‑1s, Amylin and Satiety

Learn the difference between appetite and cravings, how GLP-1s and amylin analogs affect satiety, and why fullness feels different from food reward.

5 min read

October 2, 2025

Oct 2, 2025

Appetite vs Cravings: GLP-1s plus Amylin Analogs. Why Satiety Feels Different from Reward

Appetite and cravings are often used interchangeably, but biologically they are very different. Appetite is the homeostatic drive to eat when the body needs energy. Cravings are hedonic - the brain’s reward system assigning value to certain foods even when energy needs are met.

This distinction explains why you can feel “full” after dinner but still want dessert. It also explains why new classes of medications, including GLP-1 receptor agonists and amylin analogs, target different parts of the eating experience. GLP-1s extend satiety and reduce background appetite, while amylin analogs deliver a strong meal-ending signal. Understanding why satiety feels different from reward helps make sense of how these treatments work - and why combining them is so compelling.

Appetite vs Cravings: The Biological Split

Appetite: The Energy Regulator

Appetite is regulated primarily in the hypothalamus, where signals from the gut, pancreas, and fat tissue inform the brain about energy needs. Hormones like GLP-1, PYY, insulin, and leptin tell the body when to eat and when to stop. Appetite is fundamentally about survival - ensuring enough calories are consumed to maintain function.

Cravings: The Reward Drive

Cravings arise from the mesolimbic dopamine system, the same circuits that process pleasure, novelty, and reinforcement. Cravings are not about energy balance. Instead, they are about the wanting of a specific sensory experience - often sweet, salty, or highly processed foods. This is why cravings persist even in the absence of hunger.

Why They Feel Different

Satiety is a “quieting” signal: a sense of fullness, calm, and lack of drive to eat more. Cravings are a “pull”: a motivated urge toward a specific reward. They operate in parallel, which is why fullness does not always eliminate desire.

GLP-1s: Extending Satiety and Reducing Drive

GLP-1 receptor agonists such as semaglutide and tirzepatide mimic incretin hormones released after meals. Their main actions include:

  • Slowing gastric emptying, so food stays in the stomach longer

  • Enhancing satiety signaling in the hypothalamus and brainstem

  • Reducing reward valuation of highly palatable foods

Patients often describe the effect as “I get full faster, stay full longer, and food feels less urgent.” GLP-1s primarily calm appetite and background drive, but cravings can still occur in some cases.

Amylin Analogs: The Meal-Ending Signal

Amylin is secreted with insulin after meals and signals the brain that a meal is complete. Synthetic analogs such as pramlintide (FDA-approved for diabetes) and investigational compounds like cagrilintide extend this effect.

Amylin acts in the area postrema of the brainstem, providing a potent “stop eating” signal. It reduces meal size and frequency, and also modestly slows gastric emptying. Patients often describe it as “I just can’t keep eating - my body tells me to stop.”

Why Combine GLP-1s and Amylin Analogs?

GLP-1s and amylin analogs target different aspects of appetite regulation:

  • GLP-1s: Increase satiety, reduce hunger between meals, dampen reward.

  • Amylin analogs: Deliver a sharp signal to end meals, reducing portion size.

Clinical studies of cagrilintide + semaglutide show additive effects on weight loss and metabolic improvement. By addressing both appetite and satiation, plus reducing cravings through reward modulation, the combination creates a more comprehensive approach to weight management.

Why Satiety Feels Different from Reward

Satiety arises from physiological signals of energy sufficiency - a sense of calm and absence of hunger. Reward comes from dopamine-driven circuits that chase pleasure.

  • Satiety is about “enough.”

  • Reward is about “wanting more.”

This is why fullness after a balanced meal doesn’t always prevent reaching for dessert. GLP-1s help quiet appetite, amylin helps end meals, but cravings involve the reward system - which requires both pharmacology and behavioral strategies (environment, stress, sleep) to fully address.

FAQs on Appetite, Cravings, GLP-1s, and Amylin

What is the difference between appetite and cravings?
Appetite is the physiological drive to eat for energy. Cravings are hedonic urges for specific foods, often independent of hunger.

Do GLP-1s stop cravings?
GLP-1s mainly reduce appetite and satiety signaling. Some patients report fewer cravings, but results vary.

What do amylin analogs add?
Amylin analogs send a powerful meal-ending signal, reducing portion size and frequency of eating.

Why use both GLP-1s and amylin analogs?
Together, they address both background hunger and meal termination, creating stronger overall appetite control.

Are amylin analogs available now?
Pramlintide is FDA-approved for diabetes. Longer-acting amylin analogs like cagrilintide are still in trials.

Why do cravings feel stronger than hunger sometimes?
Because cravings are tied to dopamine reward circuits, which can override satiety signals in environments with highly palatable foods.

Conclusion

Appetite and cravings are different - one keeps us alive, the other makes food rewarding. GLP-1s enhance satiety and lower hunger, while amylin analogs end meals decisively. Together, they reshape both appetite and cravings, offering a more complete strategy for weight and metabolic management.

But satiety will never feel quite the same as craving satisfaction, because they come from separate circuits. Understanding this split helps clinicians, patients, and longevity enthusiasts see why modern pharmacology - paired with lifestyle changes - works best when it targets both sides.

Research References

  1. Cassidy RM, Tong Q. Hunger and satiety gauge reward sensitivity. Nature Rev Neurosci. 2017.

  2. Drucker DJ. Mechanisms of GLP-1 receptor agonists in metabolic disease. Cell Metab. 2018.

  3. Lutz TA. Amylin and meal termination. Physiol Behav. 2010.

  4. Garvey WT, et al. Cagrilintide and semaglutide in obesity management. NEJM. 2025.

  5. Morales I, Berridge KC. Liking vs wanting in food reward. Curr Opin Behav Sci. 2020.

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Picture of Jake Reynolds

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