Understanding Hunger Hormones: The Missing Link in Cravings, Energy, and Metabolism
Most people are familiar with hunger as a feeling—an emptiness in the stomach, a craving, a dip in energy. But few understand that hunger is actually a highly coordinated hormonal conversation happening throughout the brain, gut, fat tissue, pancreas, and nervous system.
In clinic, I meet people across the full spectrum of this conversation:
People with no appetite.
People who struggle with “food noise” all day.
People who get full extremely quickly.
People who cannot lose weight despite doing everything “right.”
People who swing between intense cravings and complete disinterest in food.
I experience it too. Some days I have no appetite. Sometimes I can’t feel the sensation of hunger. Some days I am starving, and other days, cravings feel louder than logic. These experiences are incredibly common—and they all point to the same truth:
There are many factors that impact hunger, fullness, cravings, energy, and metabolism. Few people discuss the role of hunger hormones and how they shape the messages our bodies send us.
When you understand the science of hunger, you can begin to understand yourself—your energy, your appetite, your cravings, your plateaus, your metabolism—and what’s actually happening beneath the surface.
What Are Hunger Hormones?
Hormones are chemical messengers produced by endocrine glands. Gastrointestinal hormones—produced by endocrine cells throughout the gut—are released in response to food intake, nutrient availability, digestion, stress, sleep, and metabolic health.
These hormones regulate far more than appetite; they influence satiety, energy expenditure, mood, reward pathways, digestion, nutrient absorption, fat storage, body composition, and long-term metabolic health.
Below is a full overview of the primary hunger and satiety hormones, what they do, and how they shape the way we experience hunger on a daily basis.
Ghrelin is released primarily from the stomach and rises before meals to promote the physical sensation of hunger. It activates the hypothalamus and stimulates neurons that drive appetite. Elevated ghrelin increases the desire for food—especially high-calorie, high-reward foods—and contributes to increased body weight when chronically elevated. Ghrelin also influences lipid metabolism through activation of AMP-activated protein kinase (AMPK), a key regulator of energy homeostasis. It affects the dopaminergic reward system and corticotropin-releasing factor system, which explains why hunger, stress, and emotional eating are so tightly connected. Ghrelin not only stimulates hunger; it enhances the pleasure response to food.
Leptin is produced by adipocytes (fat cells) and communicates the status of energy stores to the hypothalamus. When functioning properly, leptin reduces appetite, increases energy expenditure, and promotes fat breakdown and glucose metabolism. However, in many cases of obesity or chronic metabolic dysfunction, individuals develop leptin resistance—a reduced ability of leptin to suppress appetite or regulate weight. Despite high circulating leptin levels, the brain does not “hear” the signal, leading to persistent hunger, weight retention, and impaired metabolism. Leptin resistance is strongly associated with inflammation, elevated triglycerides, chronic stress, and excess adiposity.
Insulin is produced by pancreatic beta cells in response to rising blood glucose after eating. It facilitates glucose uptake into muscle, fat, and liver cells and supports protein synthesis and lipogenesis. Insulin also plays a role in appetite and satiety. Stable insulin signaling helps regulate appetite by promoting fullness and reducing both physiological and reward-driven food intake. In insulin resistance, cells no longer respond effectively, causing elevated blood sugar, increased glucose production by the liver, impaired lipid metabolism, and dysregulated hunger and cravings. This can lead to overeating, energy crashes, and weight gain.
Adiponectin is another hormone produced by adipose tissue and is crucial for metabolic health. It enhances insulin sensitivity, regulates glucose and lipid metabolism, reduces inflammation, and provides cardiovascular protection. Higher adiponectin levels are associated with metabolic health, while lower levels are seen in obesity, insulin resistance, PCOS, and metabolic syndrome. Lifestyle interventions—such as maintaining a healthy body weight, consuming plant-centered diets, prioritizing omega-3s and monounsaturated fats, and engaging in regular exercise—significantly increase adiponectin levels.
Peptide Hormones That Regulate Satiety and Appetite
Peptide-YY is produced by L-cells in the ileum and colon and is a potent satiety hormone. It slows gastric emptying, signals nutrient status to the brain, and helps reduce hunger after meals. PYY is particularly responsive to protein and fat intake. Low levels or reduced sensitivity are associated with higher BMI, insulin resistance, and metabolic syndrome.
Glucagon-like peptide-1 is secreted by enteroendocrine L-cells after eating and plays a major role in blood sugar regulation and appetite control. It:
stimulates insulin release in a glucose-dependent manner
decreases hepatic glucose production
slows gastric emptying
promotes satiety
This is the same pathway leveraged by GLP-1 medications (like semaglutide), but your body naturally produces GLP-1—especially in response to protein, fat, fiber, and certain fatty acids.
Cholecystokinin (CCK) is released from the upper small intestine in response to fats and proteins. It stimulates gallbladder contraction and bile release, promotes digestive enzyme secretion, slows gastric emptying, reduces stomach acid production, communicates with the brain via the vagus nerve to reduce meal size, and works with insulin to support metabolic regulation. CCK is heavily influenced by the composition of meals.
What Disrupts Hunger Hormones? Communication between hunger hormones becomes imbalanced when:
Meals are irregular or skipped
Diets are high in sugar or processed foods
Protein/fat intake is too low
Chronic stress is high
Sleep is insufficient
Insulin resistance develops
Inflammation is elevated
Emotional eating becomes habitual
Nutrient deficiencies accumulate
This creates a hormonal environment where hunger cues feel unpredictable, cravings intensify, energy crashes become common, and metabolism becomes less efficient.
How to Promote Balance + Restore Hunger Hormone Communication
As a nutritionist, my goal is to help you reconnect with your body’s cues—to feel empowered, not confused; in control, not chaotic; nourished, not frustrated.
Here are seven science-backed strategies to optimize hunger hormone balance:
1. Meet Your Protein Needs
Many satiety hormones—including GLP-1, PYY, and CCK—are activated by adequate protein intake. Aim for: 1.6–2.2g protein/kg ideal body weight per day and 30–40g per meal (roughly a 5-oz chicken breast)
Protein is essential for:
maintaining lean muscle mass
improving insulin sensitivity
supporting bone health
preventing sarcopenia (age-related muscle loss)
2. Prioritize Healthy Fat Intake
Fatty acids—especially omega-3s like alpha-linolenic acid—stimulate GLP-1 secretion and support satiety. Healthy fats also stabilize blood sugar and support cognitive function.
Emphasize:
extra-virgin olive oil
avocados and avocado oil
nuts and seeds
fatty fish rich in omega-3s
3. Increase Fiber + Complex Carbohydrates
Fiber fermentation in the gut produces short-chain fatty acids (SCFAs) that stimulate GLP-1 and PYY and decrease ghrelin. Fiber also slows gastric emptying, improves digestion, and stabilizes blood sugar.
4. Get Adequate Sleep
Sleep is one of the most powerful hormonal regulators. Sleep restriction decreases leptin (fullness) and increases ghrelin (hunger), while also worsening insulin resistance and raising fasting insulin levels.
Even one night of poor sleep impacts appetite the next day.
5. Reduce and Regulate Stress
Stress is one of the most disruptive forces on hunger hormones. Acute and chronic stress increase ghrelin, decrease leptin, impair insulin sensitivity, and make cravings for sugar and salt more intense.
Stress also interferes with digestion, sleep, nutrient absorption, blood sugar stability, and inflammation—creating a full-body metabolic ripple effect.
6. Choose Whole, Real Foods
Whole foods support natural hormone rhythms. Processed foods—especially those high in sugar, additives, and refined carbohydrates—overstimulate insulin, reduce satiety hormone responses, and hijack reward pathways.
7. Eat Consistent, Balanced Meals
Your hunger hormones thrive on predictability. Regular meals that contain adequate protein, fat, fiber, and complex carbohydrates help recalibrate appetite and reduce extremes of hunger and cravings.
Your hunger is not random. Your cravings are not failures. Your appetite is not a lack of willpower. Hunger is a complex hormonal dialogue influenced by stress, sleep, digestion, nutrient intake, metabolic health, inflammation, and emotional state.
When you understand the role of hunger hormones, you can finally make sense of your body’s messages—and support them with nourishment, not judgment.
If you saw yourself in these patterns—low appetite, food noise, quick fullness, intense cravings—you don’t have to navigate this alone. Work with me, and let’s rebuild your hunger cues, metabolism, and relationship with food from the inside out.
Written by: Kristen Carlson, LDN, CNS. MS, NBC-HWC
Resoures:
May AA, DiMaggio CJ, Smith Y, et al. CCK increases the transport of insulin into the brain. J Neuroendocrinol.2016;28(10). doi:10.1111/jne.12422. PMCID: PMC5028313.
Davis EM. Glucagon-like Peptide-1: Actions and Influence on Pancreatic and CNS Function. Physiol Rev.2020;100(1):1-33. doi:10.1152/physrev.00026.2020. PMCID: PMC9190119.
Diz-Chaves Y. Ghrelin, Appetite Regulation, and Food Reward: Interaction with Chronic Stress. Int J Pept.2011;2011:898450. doi:10.1155/2011/898450. PMCID: PMC3178114.
Zhou Y, Rui L. Leptin signaling and leptin resistance. Front Med. 2013;7(2):207-222. doi:10.1007/s11684-013-0263-4. PMCID: PMC4069066.
Saltiel AR. Insulin signaling in health and disease. J Clin Invest. 2021;131(1):e142241. doi:10.1172/JCI142241. PMCID: PMC7773347.
Yang Q, Graham TE, Mody N, et al. Metabolites as regulators of insulin sensitivity and metabolism. Nat Rev Mol Cell Biol. 2018;19(10):654-672. doi:10.1038/s41580-018-0030-2. PMCID: PMC6380503.
Woods SC, Lutz TA, Geary N, Langhans W. Pancreatic signals controlling food intake; insulin, glucagon and more. Proc R Soc B. 2006;273(1581):1193-1204. doi:10.1098/rstb.2006.1858. PMCID: PMC1642707.
Lee B, Shao J. Adiponectin and energy homeostasis. Rev Endocr Metab Disord. 2014;15(2):149-156. doi:10.1007/s11154-013-9283-3. PMCID: PMC4006341.
Janiszewska J, Ostrowska J, Szostak-Węgierek D. The influence of nutrition on adiponectin—A narrative review. Nutrients. 2021;13(5):1394. doi:10.3390/nu13051394. PMCID: PMC8143119.
Chao AM, Jastreboff AM, White MA, et al. Stress, cortisol, and other appetite-related hormones: Prospective prediction of 6-month changes in food cravings and weight. Obesity (Silver Spring). 2017;25(4):713-720. doi:10.1002/oby.21776. PMCID: PMC5373497.
Sinha R, Gu P, Hart R, Guarnaccia JB. Food craving, cortisol and ghrelin responses in modeling highly palatable snack intake in the laboratory. Physiol Behav. 2019;208:112563. doi:10.1016/j.physbeh.2019.112563. PMCID: PMC6620125.
Lyon MR, Kacinik V. Is there a place for dietary fiber supplements in weight management? Nutr Metab (Lond).2012;9:76. doi:10.1186/1743-7075-9-76. PMCID: PMC3342503.