Endocannabinoids and Eating Disorders: How the Body’s Levels of Anandamide and 2-AG Are Implicated in Anorexia and Binge Eating

If you’re aware of the phenomenon of getting “the munchies” from weed, you already know that cannabis awakens something in the human body that initiates food-seeking behavior. It does this via cannabinoids, which occur naturally in the cannabis plant, but also in our bodies. In the plant, they’re phytocannabinoids; in us, they’re endocannabinoids.

Studies dating back to the 1990s, supplemented by clinical trials with results published as recently as August 2025, show that there is correlation and perhaps causation between the endocannabinoid anandamide and two eating disorders: anorexia and binge eating disorder. Head Magazine performed an extensive literature review of research done in this area to learn what that correlation is, as well as what it could mean for treating disordered eating.

Terminology

The following uncommonly used terms in this article merit a stand-alone glossary:

• 2-arachidonoylglycerol (2-AG): endogenous moderate-to-low-affinity, full agonist of CB1 and CB2
• agonist: substance that binds to a receptor inside a cell or on its surface and causes the same action as the substance that normally binds to the receptor
• anorexia nervosa (anorexia): eating disorder characterized by the loss of appetite; associated with an excessive fear of becoming overweight, body image disturbances, significant weight loss, refusal to maintain minimal normal weight, excessive exercise, and amenorrhea
• antagonist: a substance that stops the action or effect of another substance
• arachidonoylethanolamide (anandamide): endogenous high-affinity, partial agonist of CB1 and negligible agonist of CB2
• binge eating disorder: eating disorder characterized by repetitive periods of excessive food intake (i.e., eating beyond satiety) and loss of control, without increased energy expenditure and/or compensatory behaviors; associated with three or more of the following occurring at least two days a week on average for six months: eating until feeling uncomfortably full, eating large amounts of food when not physically hungry, eating much more rapidly than normal, eating alone due to embarrassment, and experiencing feelings of disgust, depression or guilt after overeating
• bulimia nervosa (bulimia): eating beyond satiety and engaging in compensatory behaviors (fasting, excessive physical exercise, vomiting and/or laxative/diuretic use) intended to control weight
• cannabinoid: natural chemical that binds to or stimulates the cannabinoid receptors found in the brain and throughout the body
• cannabinoid receptors (CB): G-protein-coupled receptors, found on the surface of our cells, that interact with cells to communicate with our body and change nerve activity 
  • CB1: widely distributed in neurons and nonneuronal cells in the brain and peripheral organs; when activated, alters the release of neurotransmitters (e.g., dopamine) from nerve endings
  • CB2: commonly found in cells and tissues of the immune system, where it plays a role in the regulation of inflammation
• eating disorder: syndrome characterized by persistent aberrant patterns of feeding behavior and weight regulation, as well as abnormal attitudes toward, and perceptions of, one’s body shape/image
• endocannabinoid system (ECS): intercellular communication structure with a role in regulating multiple neuro-physiological processes (appetite, pain sensation, mood, learning and memory, emotion and motivation, addictive behaviors, etc.), with the aim to balance metabolic processes and optimize the body’s day-to-day functions; composed of endogenous ligands (i.e., endocannabinoids), cannabinoid receptors and the enzymatic machinery in charge of the synthesis and degradation of the endocannabinoids 
• endogenous cannabinoid (endocannabinoid): neuromodulating molecules that bind to cannabinoid receptors; produced as needed to act on/stimulate cannabinoid receptors to influence sensory and motor responsiveness (movement), heart rate, emotional reactions, appetite and nausea/vomiting, sensitivity to pain, learning and memory, and high-level decision-making
• hedonic feeding/eating: consumption of food just for gustatory rewarding properties, not to maintain energy homeostasis; characterized by the ingestion of pleasurable foods that are rich in fat, sugar and/or salt content
• homeostatic feeding/eating: eating in response to the body’s natural hunger cues to maintain energy balance

The endocannabinoid anandamide was discovered by Dr. Raphael Mechoulam, as we recount in “Listen to Your Father – 3 Things the ‘Father of Cannabis Research’ Taught Us.”

How the ECS Instigates and Steers Food-Seeking Behavior

The endocannabinoid system (ECS) is strategically located in all the key points involved in food intake and energy expenditure, at both the central and peripheral levels. It has been proven countless times to regulate energy homeostasis, food intake, food-related reward processing and metabolism. 

It is present along the entire gut-brain axis, so it plays both central and peripheral roles in eating by acting via central (brain) and peripheral (gut, liver, muscle and fat) mechanisms. This axis seems to modulate central homeostatic and hedonic feeding pathways through the signaling of several peripheral endocrine factors, including the ECS. More specifically, as reported in “Translational Psychiatry”: 

“[E]ndocannabinoids not only regulate the expression and release of hypothalamic orexigenic and anorexigenic signals, but also modulate activity in mesolimbic dopaminergic incentive pathways and opioidergic hedonic circuits, hence facilitating appetitive motivation as well as the pleasure of food during ingestion.”

That reinforced a finding from 2014 in the “American Journal of Clinical Nutrition,” which reported that endocannabinoids and endocannabinoid-related compounds are involved in food-related reward and suggest a dysregulation of their physiology in eating disorders. 

By acting on our gut-brain axis, our endocannabinoid system pushes us not only to crave foods with high fat, sugar and salt content, but also to enjoy these foods more while we eat them. Photo by Cheng/pexels.com

Overall, increasing evidence points toward disturbed endocannabinoid signaling in eating disorders, demonstrating an undeniable correlation. At the more detailed level, it concerns cannabinoid receptors (CB). As reported in 2022 in the journal of the research institute Universitat Autònoma de Barcelona:  

“The CB1 receptor (widely expressed in brain regions that control food intake, reward and energy balance) is considered the main responsible for most of the central and peripheral effects of cannabinoids on the eating behavior. CB1 receptor agonists possess orexigenic effects enhancing appetite and increasing the rewarding value of food. Conversely, CB1 antagonists have been shown to inhibit the intake of food.”

The endocannabinoid anandamide binds more strongly to the CB1 receptors found in the brain and spinal cord (central nervous system) than to CB2 receptors. By binding to CB1 receptors and altering nerve activity in various brain circuits, anandamide can affect appetite and feelings of pleasure, among other things. As Dr. Haran Sivapalan, who holds degrees in cognitive science and experimental psychology, explains:

• Anandamide may enhance smell and taste perception.
• Anandamide activity in the gut drives a preference for high-fat foods.
• Anandamide stimulates brain circuits that promote appetite and food intake.
• Anandamide enhances the rewarding and pleasurable aspects of food.

Accordingly, high anandamide levels are markers of ECS overactivity. This applies to the endocannabinoid 2arachidonoylglycerol (2-AG) too. Like anandamide, 2-AG has an impact on food intake, insulin resistance, visceral fat accumulation and metabolic disturbances when present in elevated levels.

The endocannabinoids that our body produces naturally can reach unhealthy levels, at which point eating disorders and other such disturbances manifest. Image by Green Valley Nutrition via Creative Commoms/ CC BY-NC 4.0

How the ECS is Linked to Eating Disorders

As a signaling system, the ECS is a key modulatory element in the activity in the brain area associated with eating disorders. An authoritative declaration of the correlation can be found in the 2025 edition of the Handbook of the Biology and Pathology of Mental Disorders, in the chapter titled “Eating Disorders and the Endocannabinoid System”: 

“More and more evidence suggest that the endocannabinoid system (ECS) participates in the regulation of food intake and metabolism both at central and peripheral levels, indicating it may have an important role in the development and maintainment of ED [eating disorders].”

One of the key things bridging the ECS to eating disorders is the integral role the ECS plays in the mind’s interpretation and sensation of reward, explained thoroughly in a 2011 article in “Frontiers in Behavioral Neuroscience.” A shorter explanation is provided in a 2021 article in “European Psychiatry,” which concludes that within the ECS, anandamide and 2-AG in particular play a pivotal role in food intake and reward aspects of feeding. 

Gary Wenk, author of “Your Brain on Food: How Chemicals Control Your Thoughts and Feelings,” narrows this down by specifying that anandamide and 2-AG play important roles in regulating our pleasure of eating, and that aberrant eating behavior might be due to dysfunctional reward processing in the brain’s pleasure center. Also, a study conducted in 2020 revealed that anandamide’s main deactivating enzyme can increase the biological susceptibility of eating disorders, while also inducing appetite modulation.

Although it’s helpful to treat yourself occasionally, the concept of treating yourself with food is amplified unrealistically by imbalances in our body’s endocannabinoids, practically convincing us that unhealthful foods are good for us. Photo by Lina Kivaka/ pexels.com

The first study to link the ECS to disordered eating, conducted in 2005, found higher levels of anandamide only in test subjects with anorexia and binge eating disorder (BED), not in those with bulimia. Given that eating disorders can develop as reward-dependent syndromes, this makes sense. Individuals with anorexia perceive eating less food as rewarding, and individuals with BED perceive consuming large amounts of food as rewarding (until they stop eating). By contrast, individuals with bulimia binge and purge to avoid negative emotional states, not to feel rewarded.

Over the past 20 years, however, the reverse has been observed in anandamide and 2-AG levels. Unlike the 2005 findings, lower – not higher – levels of anandamide have been more consistently correlated to disordered eating. This is likely because anandamide levels correlate to better emotional regulation, which ties into another factor: impulse control. Impulsivity is both central to BED and something in which the ECS is involved. Unsurprisingly, in like manner, it’s understandable that individuals with eating disorders frequently have substance abuse disorders as well.

Impulse inhibition can result in substance abuse, such as alcoholism. In the case of binge eating disorder, the substance being abused is food. When anandamide levels are low, impulse control is commensurately low, manifesting as substance abuse. Photo by Conttonbro Studio/pexels.com. Photo for illustrative purposes only.

In a 2023 study, poor emotional regulation also correlated to higher levels of 2-AG, which had basically been a statistically insignificant endocannabinoid in the 2005 study. Also, higher emotional dysregulation predicted greater impulsivity. This supported a finding from 10 years before, published in a 2013 “PLOS ONE” study: 

“AEA [anandamide] and 2-AG have a relevant and opposite role on the executive functioning in humans. … [E]levated levels of AEA are associated with improvement on decision making and cognitive flexibility performance, while elevated levels of 2-AG are associated with disruption of the cognitive flexibility and inhibition response capacities. These results demonstrate, in humans, the association between the endocannabinoid system and prefrontaldepended cognitive functions … probably through mechanisms involving dopaminergic, cholinergic, GABAergic, and glutamatergic systems.”

This is particularly critical, given that deregulation of the ECS has been associated with psychopathological conditions that compromise emotional and cognitive function. 

Research indicates that when your anandamide levels are low, you have less control over yourself, and when your 2-AG levels are low, you have more control over yourself. Photo by Gustavo Fring/pexels.com. Photo for illustrative purposes only.

Interestingly, ECS and eating dysregulation are reciprocal. The 2021 study “Binge sucrose-induced neuroadaptations: A focus on the endocannabinoid system” explains how maladaptive eating patterns involving excessive sucrose intake disrupt the ECS. Additionally, a 2020 study at the Tabriz University of Medical Sciences found that some appetite regulators (leptin, insulin, orexin A, etc.) are involved in the synthesis and release of endocannabinoids, and that changes in their levels can lead to overeating. Back in 2006, a study published in the “International Journal of Obesity” (London) shared similar findings:

“Endocannabinoid biosynthetic and inactivating pathways are under the regulation of neuropeptides and hormones involved in energy homeostasis, and endocannabinoid levels are directly affected by the diet. Endocannabinoids, in turn, regulate the expression and action of mediators involved in nutrient intake and processing. These cross-talks are at the basis of the proposed role of endocannabinoid signalling [sic] in the control of food intake, from invertebrates to lower vertebrates and mammals, and their perturbation appears to contribute to the development of eating disorders.”

Thus, the connection between the ECS and disordered eating can sometimes venture beyond correlation, into causation.

Just as ECS disturbances correlate to disordered eating, disordered eating correlates to ECS disturbances; the direction of the causation varies across decades of research.

In addition to endocannabinoids, cannabinoid receptors establish a link between the ECS and disordered eating. A 2016 study found that the cereb ral homeostatic CB1 system is inextricably linked to a person’s Body Mass Index (BMI), with additional involvement of reward areas under conditions of fluctuating bodyweight. The CB1 receptor is tied to appetite, and greater density in the brain of CB1 receptors correlate to anorexia when the body is fighting to convince the person to eat, and correlate to BED when the body is conditioned to sustaining a large appetite.

Potential for Treating Anorexia and BED via ECS Regulation

If imbalances in anandamide and 2-AG levels perpetuate – if not cause – eating disorders, then the obvious solution is to intervene and restore balance. Unfortunately, attempts thus far to do that (namely, the ill-fated, now-discontinued drug Rimonabant) have wreaked havoc on the central nervous system, making the cure (one not guaranteed, at that) worse than the disease. Blocking CB1 receptors to control anandamide and 2-AG levels did reduce food intake and bodyweight, but most of the people who underwent that treatment developed severe psychological issues, leading U.S. and European regulators to revoke drug approvals. 

Accordingly, scientists are now trying different approaches to blocking CB1 (i.e., using CBI antagonists), such as the peripherally restricted CB1 antagonists described in a 2024 study. As a study conducted in 2023 explains, the peripheral ECS is supported by “bottom-up” cannabinoid signaling, which could minimize side effects. The hope is that peripheral pharmacological targets will prove to be safer and yield more consistent results. 

Tampering with the ECS is a high-risk, high-reward approach to treating eating disorders. Test subjects whose CB1 receptors were blocked managed to refrain from bingeing, but ended up with dangerous mental illnesses as a result of the medicine that blocked the receptors. Photo by cottonbro studio/pexels.com , Photo for illustrative use only.

Another avenue is the use of cannabis itself – specifically, the plant’s two best-known cannabinoids: cannabidiol (CBD) and tetrahydrocannabinol (THC), although the latter has to be a manmade imitation of the plant for legal reasons. NW Pharmatec shared this strategy in a detailed LinkedIn post in April 2025. The claim is that anorexia and BED could be treated with CBD and dronabinol (synthetic THC). The post explains that dronabinol is a full agonist at the CB1 receptor, exhibiting high affinity for presynaptic cannabinoid receptors within the hypothalamus and mesolimbic reward system.

Alarmingly, NW Pharmatec then goes on to buffer that optimism with: “However, chronic CB1 receptor activation via THC analogues is associated with psychiatric adverse effects, including anxiogenesis, cognitive impairment, and exacerbation of psychotic symptoms, limiting its utility in vulnerable populations. Moreover, tachyphylaxis and dysphoria during withdrawal raise concerns about long-term use in psychiatric contexts (Hillard, 2015).” (One can only wonder whether organic THC would be anywhere near as dangerous as pseudo-THC cooked in a lab.) The other half of the approach though, the CBD, is presented in a fully positive light.

Creating THC from chemicals instead of extracting THC molecules from a cannabis plant is a legal loophole commonly used in an attempt to get the benefits of THC without being fined or imprisoned. In our feature “Is Delta-8 Bootlegged THC?”, we examine the social, political and economic impacts of this practice. Image credit: fokusiert/123rf.com

Conclusion

Decades of research have provided ample evidence that the deregulation of the ECS underlies eating disorders. Debate remains as to whether the ECS’s imbalanced endocannabinoids cause disordered eating, or whether disordered eating – caused by external factors – causes the ECS imbalance. Thus far, indications are that the former is the case, given that abnormal levels of anandamide and/or 2-AG affect every single factor that goes into when we eat, why we eat, and what we eat. Regrettably, experiments with tampering with the ECS to alleviate disordered eating have been more harmful than helpful as of yet. However, an increased understanding of this powerful system has introduced hope not provided elsewhere for people afflicted by eating disorders; at least it’s a start.

The information in this article and any included images are for educational purposes only. This information is neither a substitute for, nor does it replace, professional legal advice or medical advice, diagnosis or treatment. If you have any concerns or questions about laws, regulations or your health, you should always consult an attorney, physician or other licensed professional.

Kathleen Hearons is a writer, editor, linguist and voice over actor from Los Angeles. She specializes in creative writing and research-intensive analysis and reporting.

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