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Appetite is controlled by dopamine levels in the brain's reward center.
If you are experiencing serious medical symptoms, seek emergency treatment immediately.
Dopamine signaling is modified by hormones from the gut, pancreas and fat stores that detect nutritional status and needs. In normal circumstances, this self-regulation maintains a healthy appetite and body weight.
However, in eating disorders such as anorexia, binge eating and obesity, the dopamine pathway is disrupted. As a result, inappropriate cues to eat or starve become as compelling as drug addictions.
Motivation for Food
Appetite is the body's way to balance food intake with energy expenditure to maintain a stable and healthy body weight. The brain receives signals from a number of different hormones that indicate when food is needed or not. These signals converge on dopamine-producing neurons in the hypothalamic region of the brain. This modifies dopamine output to the brain's reward center, which controls motivation for food.
Brain Research illustrates the essential role of dopamine in appetite control with a report on dopamine-deficient laboratory mice 3. These experimental animals die of starvation, completely lacking motivation to feed themselves. When given dopamine supplementation, the mice begin to eat normally.
- Appetite is the body's way to balance food intake with energy expenditure to maintain a stable and healthy body weight.
- When given dopamine supplementation, the mice begin to eat normally.
What Causes Dopamine Depletion?
Many indicators of nutritional status are produced from the gastrointestinal tract in response to food cues. Some hormones signal lack of food and stimulate appetite; others curb food cravings after a meal.
Ghrelin and neuropeptide Y are two hormones that stimulate appetite, as described in Johnson's “Essential Medical Physiology.” Ghrelin is produced primarily by the stomach; neuropeptide Y is secreted from the intestine 1. Both hormones are released during fasting when blood sugar is low, signaling the need for food. In the brain, they stimulate dopamine producing neurons, which increases motivation to eat, reports the journal Trends in Neuroscience 4.
Alternatively, insulin is a hormone that suppresses appetite in response to high blood sugar. When you eat, sugar from the meal goes into your bloodstream.
The pancreas senses the availability of nutrients and releases insulin, which signals to the body to start storing energy. Trends in Neuroscience also reports that insulin travels to the brain, where it inhibits dopamine-producing neurons, thereby decreasing appetite 4.
Leptin also decreases appetite in response to nutrient availability, according to Johnson's text. It is released by fat cells, indicating to the brain how much energy is being stored by the body in fat reserves in case food becomes scarce. When you put on weight, leptin levels increase.
This inhibits dopaminergic neurons and decreases motivation for food because energy stores are sufficient. Conversely, when you lose weight or begin fasting, leptin levels decrease, dopaminergic neurons are activated and appetite increases to restore energy reserves.
- Alternatively, insulin is a hormone that suppresses appetite in response to high blood sugar.
- The pancreas senses the availability of nutrients and releases insulin, which signals to the body to start storing energy.
Eating Disorders and Anorexia
Effects of Alcoholism on Appetite
Most people maintain a stable, healthy body weight as ghrelin, insulin, leptin and other nutrient sensing hormones self-regulates appetite according to their body's needs. However, in case of eating disorders and obesity, the dopamine-regulated system malfunctions.
Anorexia is linked to increases in dopamine receptor levels, resulting in decreased appetite and low motivation for food, explains the journal Genes Brain and Behavior. Dopamine blockers have been shown to improve appetite and are currently under investigation to restore motivation for food in anorexic patients, as reported in the journal European Neuropsychopharmacology.
- Most people maintain a stable, healthy body weight as ghrelin, insulin, leptin and other nutrient sensing hormones self-regulates appetite according to their body's needs.
- Anorexia is linked to increases in dopamine receptor levels, resulting in decreased appetite and low motivation for food, explains the journal Genes Brain and Behavior.
Binge Eating and Obesity
Obesity and binge eating disorders are complicated conditions in which many of the hormones that control appetite become dysregulated, particularly leptin and insulin. This can elevate dopamine levels in the reward center, triggering hunger when it is unnecessary and inappropriate.
Individual genetic differences in dopamine response can also contribute to these disorders. Science magazine reports that obese people tend to have underactive dopamine response to food intake, meaning they must eat more to be satiated 5.
Binge eating also leads to a reduction in dopamine receptor expression, which exacerbates the situation. Ultimately, chronic overeating becomes an addiction, reports Experimental Clinical Psychopharmacology.
Deficits in dopamine signaling result in more food cravings but yield less satisfaction--much like the diminishing returns of alcoholism or cocaine addiction. In fact, binge eating triggers the same dopamine response in the brain's reward center as drugs of abuse such as nicotine, methamphetamine and cocaine. Genetic abnormalities in the dopamine pathway put certain people at risk for developing both substance addictions, as well as obesity.
- Obesity and binge eating disorders are complicated conditions in which many of the hormones that control appetite become dysregulated, particularly leptin and insulin.
Food addiction can be treated by targeting the dopamine pathway, stimulating feelings of satisfaction in the brain's reward center without the food stimulus. Drugs that can accomplish this are not hard to come by. Nicotine, caffeine, methamphatimine and cocaine all suppress appetite due to stimulation of dopamine signaling. Goodman & Gilman's Therapeutics indicates that amphetamines and amphetamine-like drugs have been used for decades as appetite suppressants to treat obesity 2. However, their appetite suppressant effects are linked to high risk of addiction, which are both dependent on elevated dopamine signaling in the brain's reward center. Many of these prescription drugs have been pulled off the market for this reason. Goodman warns that the "wisdom of their use is questionable" as it becomes likely that food addiction will be replaced by an arguably more dangerous, harmful, costly and potentially illegal drug addiction. The Merck Manual instead recommends treating obesity with drugs that do not directly target the dopamine pathway but instead act on serotonin in the brain or nutrient breakdown in the gut.
- Food addiction can be treated by targeting the dopamine pathway, stimulating feelings of satisfaction in the brain's reward center without the food stimulus.
- The Merck Manual instead recommends treating obesity with drugs that do not directly target the dopamine pathway but instead act on serotonin in the brain or nutrient breakdown in the gut.
What Causes Dopamine Depletion?
Effects of Alcoholism on Appetite
After Eating Why Do I Have Severe Hunger Pains?
Does Exercise Release Dopamine?
Signs of Food Addiction Withdrawal
What Triggers Dopamine?
What Are the Effects of Too Much Dopamine?
Allergies and Feeling Hungry
How Does Seroquel Affect the Brain?
Differences Between Fasting and Starving
- "Essential Medical Physiology"; Leonard R Johnson; 2003
- "Therapeutics"; Goodman & Gilman; 2006
- Brain Research
- Trends in Neuroscience
- Science Magazine
- Cohen, B.M. & Carlezon, W.A. (2007). Can't get enough of that dopamine. The American Journal of Psychiatry, 164(4):543-6.
- Friedel, R.O. (2004). Dopamine dysfunction in borderline personality disorder: a hypothesis. Neuropsychopharmacology, 29(6):1029-39.
- Ingenhoven, T.J., & Duivenvoorden, H.J. (2011). Differential effectiveness of antipsychotics in borderline personality disorder: meta-analysis of placebo-controlled, randomized clinical trials on symptomatic outcome domains. Journal of Clinical Psychopharmacology,31(4):489-96.
- Siddiqui S.V., Chatterjee U., Kumar, D., Siddiqui A., & Goval, N. (2008). Neuropsychology of prefrontal cortex. Indian Journal of Psychiatry, 50(3):202-8.
Shannon Weiman started writing in 2009. She is the science-in-the-community correspondent for the website MySDScience and she freelances for Red Funnel Consulting Group and the San Diego Zoo's Institute for Conservation Disease Labs. Weiman received her Bachelor of Arts in molecular and cell biology from Cornell University and a Ph.D. in biomedical sciences from University of California at San Diego.