Researchers may have unmasked mystery of cannabis 'munchies'
"Cannabis 'munchies' explained by new study," The Guardian reports. "Munchies" is widely used slang for a common effect of cannabis: sudden hunger pangs, even if a user has just eaten. A new study set out to find why cannabis causes increased appetite.
Previous studies have shown certain pathways of nerve cells in the hypothalamus of the brain (called pro-opiomelanocortin, or POMC) have a role in regulating our appetite.
This latest study found that when mice were given a chemical to stimulate cannabinoid receptors (the parts of the brain that respond to cannabis), this caused increased feeding.
A series of subsequent tests confirmed this feeding response was being driven by the activation of POMC nerve cells. This caused a release of beta-endorphins (opioid-like proteins that can have various feel-good effects).
The findings further our understanding of why cannabis may cause the "munchies".
The hope is that this effect could be harnessed for a more serious use, such as stimulating the appetite of people who have a reduced appetite due to illness.
Whether this could be possible is too early to say, based on this animal research.
While similar biological pathways may be involved, the processes may not be identical in humans, so it is currently uncertain whether a "munchie drug" could be created.
Where did the story come from?
The study was carried out by researchers from the Yale University School of Medicine and other institutions in the US, Germany and Australia.
It was funded by the US National Institutes of Health, the American Diabetes Association, The Klarmann Family Foundation, the Helmholtz Society (ICEMED), and the Deutsche Forschungsgemeinschaft (a German research institute).
The study was published in the peer-reviewed journal Nature.
The UK media accurately presents the general findings of this research, but none of the sources make it immediately apparent that this research was in mice.
Extrapolations of the findings, such as claiming this could help people who lose their appetite as the result of illness, while interesting, are not supported by this early-stage research.
What kind of research was this?
This was research in mice that aimed to see how cannabis affects our appetite.
The hypothalamus is a region of the brain that plays a role in regulating many of our bodily processes, such as hunger, sleep and body temperature. Hypothalamic POMC nerve cells are reported to be responsible for causing a feeling of fullness.
However, substances that we take into our body can disrupt our normal body rhythms.
One such substance is cannabinoids, which are chemicals that act on cannabinoid receptors in the body, the most notable being the compound found in cannabis. This often triggers hunger, even though a person is full.
Previous research has shown that activation of the cannabinoid receptor 1 (CB1R) can cause animals to eat excessively, despite being full.
This study aimed to see whether the reason for this could be because activation of CB1R is associated with decreased activity of POMC nerve cells, thereby turning off the signals that tell us we are full.
What did the research involve?
The researchers carried out a range of feeding experiments in mice to see how the stimulation of the cannabinoid receptor influenced feeding responses, and how this was being driven by the activation of POMC nerve cells.
They first carried out experiments to see what happened when they injected mice with a chemical that stimulates the cannabinoid receptor.
In the next experiment, they injected the mice with a different chemical that blocks the cannabinoid receptor.
They then demonstrated how the subsequent activation of POMC nerve cells drove feeding response, by injecting the mice with chemicals that either stimulate or block POMC cells.
What were the basic results?
The researchers found that stimulation of the cannabinoid receptor increases feeding in mice. When mice were injected with a chemical to stimulate the cannabinoid receptor (ACEA), this increased feeding response. Subsequent injection of a chemical to block the cannabinoid receptor (RIMO) reduced food intake.
The researchers then showed that the increased feeding associated with stimulation of the cannabinoid receptor was being driven by the activation of POMC nerve cells.
When mice who had been given ACEA where given a chemical that blocks POMC cells, this gradually diminished feeding over the course of a few hours. But when they were given a chemical to activate the POMC cells, this caused increased feeding.
The POMC gene is reported to code for two chemicals: alpha-melanocyte-stimulating hormone and beta-endorphin.
The researchers' subsequent experiments showed that the activation of the cannabinoid receptor selectively causes the release of beta-endorphin from the hypothalamus, and this causes increased feeding.
When mice were given a chemical to block the receptors for beta-endorphins, this blocked the cannabinoid receptor-induced feeding response.
How did the researchers interpret the results?
The researchers concluded that, "These results uncover a previously unsuspected role of POMC [nerve cells] in the promotion of feeding by cannabinoids."
Conclusion
This research in mice demonstrates how cannabis may cause increased appetite. The findings show that when mice were given a chemical to stimulate cannabinoid receptors, this caused increased feeding.
A series of subsequent tests showed how this feeding response was being driven by the activation of POMC nerve cells in the hypothalamus.
Giving chemicals to block POMC activation led to gradual suppression of feeding, while giving a chemical to increase POMC activation caused enhanced feeding. This increased feeding response seemed to be because POMC activation was causing the release of beta-endorphin from the hypothalamus.
The findings further our understanding of why cannabis may cause the "munchies", but the results are only from experiments on mice.
Studies such as this can give a good indication of the effect that different chemicals can have upon animals and the biological pathways that may be involved.
However, the nerve cell stimulation and feeding response when humans take cannabis may not be identical to these tests, where mice were injected with chemicals to stimulate the cannabinoid receptors.
These findings currently have limited implications. Though the media suggests that the findings could be used to help people who have lost their appetite as the result of illness – presumably through using drugs to stimulate the cannabinoid receptors, rather than suggesting people smoke cannabis – this is pure speculation.
Regardless of how cannabis may trigger increased appetite, cannabis is a class B drug that is illegal to possess or supply to others, and can have very uncertain effects on our brain function.
