Eating disorders · Opioid system

Opioid and endocannabinoid system appears to play a role in eating disorders

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The opioid and endocannabinoid system appears to play a role in eating disorders and food addiction, new studies show. The endocannabinoid system is the body’s own cannabis-like system. Brain PET scans found fewer mu-opioid receptors in people who overeat. The cannabis-like system acts on hunger in more mixed ways. Both work with dopamine to drive overeating.

Summary: Some people get more pleasure from food than others. So they are more likely to eat too much. Dopamine is tied to addiction and to how we lock in memories. But food addiction is more than dopamine. New studies show that two linked systems play a big role: the opioid and endocannabinoid systems. Brain PET scans show fewer MOR receptors in people who overeat. The cannabis-like system acts on appetite in more mixed ways. So researchers say the opioid system could be one way to treat eating disorders.

Eating too much leads to obesity. Eating disorders also raise the risk of many other diseases. Obesity and the diseases that come with it have a lot to do with how people control the urge to eat. People with obesity often eat more. Hormones and quirks of the brain and nerves make them hungrier.

Dopamine has long been known to drive addiction and the hunt for pleasure. So researchers think dopamine also plays a role in food addiction. Eating too much food leads to a bigger dopamine hit. Dopamine also helps lock in the memory of that reward. So people with eating disorders are more likely to chase that hit by eating more food1.

How do the opioid and endocannabinoid systems affect eating?

Figure 1: Activity of opioid system in various brain centers associated with eating disorders

Targeting dopamine may help, but not in every case. So it became clear that other paths must be at work, too. Researchers turned to two linked systems: the opioid and endocannabinoid systems.

Early studies and real-world use show that cannabinoids may act on hunger in a complex way. For example, cannabis extracts can change hunger a lot. Some cannabinoids boost hunger, while others shut it down2.

Researchers have also found odd levels of the body’s own opioids, like endorphins, in people with eating disorders. These changes look like those in people hooked on drugs3. And like cannabinoids, opioid use can also change hunger and the way people eat.

 

New scans now let us see how active each pathway is in a living brain. In the new study, researchers measured μ-opioid receptors (MOR) and cannabinoid CB1 receptors (CB1) in many brain areas of healthy people. They also tracked how people ate with the Dutch Eating Behavior Questionnaire (DEBQ). The team was at the University of Turku in Finland4.

To measure MOR receptors in each brain area, the team used carfentanil PET scans from 92 healthy people. To measure CB1 receptors, they used FMPEP-d2 scans from 35 adults.

The study showed that people with fewer MOR receptors were more likely to eat more. Changes in CB1 receptors were tied to more mixed eating problems.

So the study confirmed that both the opioid and cannabis-like pathways play a vital role in eating habits. They also play a key role in the food reward pathway. The two pathways overlap a great deal. Still, each one plays its own part in how people eat.

So one new way to treat eating disorders could be to target opioid receptors in the brain. Researchers are less sure about targeting CB1 receptors.

This shows how complex the brain’s reward system is. The same system is at work in opioid addiction treatment. There, we often target these same receptors to calm cravings and bring the brain back into balance.

Frequently asked questions

What in the brain controls food cravings?

Three reward systems play a part. Dopamine rewards overeating and helps lock in the memory of it. The opioid system works through mu-opioid (MOR) receptors. The cannabis-like system works through CB1 receptors. Both help steer eating habits and the food reward pathway. The two overlap, but each plays its own role in how people eat.

Why is my brain constantly thinking about food?

Some people get more pleasure from food than others, so they are more likely to overeat. Eating sets off a dopamine hit. Dopamine locks in the memory, which keeps pulling people back for more. Hormones and the brain itself also drive hunger. Brain scans link low MOR receptor levels to eating more.

Is food addiction like drug addiction?

In the brain, yes. The same dopamine pathways that drive the hunt for pleasure drive food addiction. People with eating disorders also show odd levels of endorphins, the body’s own opioids. These changes look like those in people addicted to drugs. Opioid use itself can change appetite and the way people eat.

Can food addiction be treated by targeting the opioid system?

The research points that way. Brain scans showed that people with fewer opioid (MOR) receptors ate more. So targeting opioid receptors in the brain could be a new way to treat eating disorders. The CB1 cannabinoid receptors are a less clear target, because their effect on appetite is more mixed.

Related reading

Drug-seeking habits play a vital role in drug addiction · Serotonin and Cocaine Addiction · High Sugar Diet Dulls Sweet Taste

References

1. Botticelli L, Micioni Di Bonaventura E, Del Bello F, et al. Underlying Susceptibility to Eating Disorders and Drug Abuse: Genetic and Pharmacological Aspects of Dopamine D4 Receptors. Nutrients. 2020;12(8):2288. doi:10.3390/nu12082288

2. Marco EM, Romero-Zerbo SY, Viveros MP, Bermudez-Silva FJ. The role of the endocannabinoid system in eating disorders: pharmacological implications. Behavioural Pharmacology. 2012;23(5 and 6):526-536. doi:10.1097/FBP.0b013e328356c3c9

3. Lienard Y, Vamecq J. [The auto-addictive hypothesis of pathological eating disorders]. Presse Med. 2004;33(18 Suppl):33-40. doi:10.1016/s0755-4982(04)72380-5

4. Kantonen T, Karjalainen T, Pekkarinen L, et al. Cerebral μ-opioid and CB1 receptor systems have distinct roles in human feeding behavior. Transl Psychiatry. 2021;11(1):1-9. doi:10.1038/s41398-021-01559-5