Psilocybin, the primary psychoactive compound found in certain species of mushrooms, is well-known for its profound effects on perception, mood, and thought. As the compound is ingested and metabolized, the body undergoes a series of temporary physiological and psychological changes. Among the more commonly reported side effects of this experience are distinct alterations in the normal patterns of hunger and satiety. Understanding how this substance interacts with the body’s digestive and signaling systems can clarify why appetite is affected during and after the acute experience.
Appetite During the Acute Experience
The majority of people who consume psilocybin mushrooms report noticeable appetite suppression during the acute experience. This lack of interest in food is often compounded by mild to moderate nausea, a notorious side effect of ingestion. Physical discomfort ranges from slight stomach unease to pronounced gastrointestinal distress, making solid food unappealing or difficult.
Clinical trials report that transient nausea occurs in a significant percentage of participants, ranging from 22% to nearly 50% depending on the study and dose. The mushrooms contain chitin, a polysaccharide found in their cell walls that is generally indigestible by humans, contributing to stomach burden. Even when synthetic psilocybin is used, nausea remains a frequent complaint, indicating a mechanism beyond difficulty in digesting the fungal matter.
Practical advice suggests consuming a light meal several hours before the experience or preparing the mushrooms to minimize stomach upset. Methods like the “Lemon Tek,” where ground mushrooms are soaked in an acidic liquid, help pre-digest chitin and jumpstart the conversion of psilocybin to its active form, psilocin. During peak effects, the altered state of consciousness shifts focus away from basic physiological needs, contributing to disinterest in food.
The Neurochemical Explanation for Appetite Suppression
Changes in appetite and nausea are directly linked to how psilocybin interacts with the body’s complex serotonin system. Once ingested, psilocybin is rapidly converted into the active compound, psilocin, which functions as an agonist for various serotonin (5-HT) receptors. The psychedelic effects are largely mediated by activating the 5-HT2A receptor in the brain.
Psilocin also binds to other serotonin receptor subtypes that regulate feeding behavior. The 5-HT2C receptor, in particular, promotes satiety, or the feeling of being full. Activation of this receptor by psilocin mimics the body’s natural signals of fullness, chemically dampening the desire to eat.
Gastrointestinal side effects, specifically nausea, are primarily mediated by the 5-HT3 receptor. This receptor is abundant in the enteric nervous system, the network of neurons governing the digestive tract. Excessive activation of 5-HT3 receptors in the gut triggers excitatory effects, activating vagal afferent nerves that signal the brainstem’s vomiting center. This biological action contributes to the physical feeling of sickness, diminishing appetite.
Post-Experience Appetite Changes
Once the acute effects of psilocybin subside and the body returns to its baseline physiological state, a distinct shift in appetite occurs. After the compound is metabolized and serotonin receptor activity lessens, physical discomfort and psychological disinterest in food dissipate. This is frequently followed by a period of intense hunger, often called a “rebound appetite.”
This compensatory hunger is a natural response to the body’s lack of caloric intake and sustained metabolic activity during the experience. Homeostatic mechanisms, temporarily overridden by the drug’s action on the 5-HT system, begin to reassert themselves, prompting the individual to seek nourishment. Many people report desiring comforting and easily digestible foods during this phase as the gastrointestinal system recovers.
While psilocybin does not operate as a traditional appetite suppressant drug, its influence on the serotonergic system and resulting behavioral changes can indirectly affect eating patterns. Some reports suggest that profound shifts in perspective may lead to long-term changes in a person’s relationship with food, such as reduced emotional eating or unhealthy cravings. These changes are likely due to psychological processing enabled by the experience, rather than a direct, lasting metabolic effect.