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Although it’s a well-known effect, for a long time scientists haven’t been able to explain why smoking weed drives you to finish off a multipack of crisps before going on to scoff down a McDonald’s—that is, why it gives you the munchies.
A new study published in Nature Neuroscience offers an answer: THC, marijuana’s active ingredient, acts on certain receptors in the brain related to your sense of smell. It essentially makes you smell food more, which increases your appetite, and leads you to eat more. That's what seems to happen in fasted mice, at least.
“Hunger arouses sensory perception, eventually leading to an increase in food intake, but the underlying mechanisms remain poorly understood,” the researchers wrote in their paper. “We found that cannabinoid type-1 (CB1) receptors promote food intake in fasted mice by increasing odor detection.”
The researchers experimented on the mice by observing how sensitive they were to the scent of banana and almond oils, and how much chow they ate when under the influence. They found that a dose of THC “decreased the threshold of odor detection and this effect was clearly correlated with successive food intake.”
That, it seems, is because THC fits into a cannabinoid receptor in an area of the brain known as the “olfactory bulb.” When the researchers genetically engineered mice not to have this receptor, the THC didn’t affect their appetite. The Smithsonian blog has a good explainer on the paper and points out that, separate from giving them THC, when the genetically engineered mice were denied food for a while, they still didn’t show an increased appetite. That, they said, “indicates that both THC and the natural cannabinoids that result from starvation are acting on the same neural pathway to allow us to smell and taste with greater sensitivity, and thus eat more.”
The findings don’t just offer an explanation for the munchies, but also give rise to potential clinical applications. Knowing how to increase sense of smell or appetite could be a useful tool in treating illnesses where these are deficient.
Lead author Edgar Soria, of the University of Bordeaux in France, told me in an email that their study was just the first step in this field of research and that more work was needed, but suggested it could one day have medical uses. “It is widely known that several neuropsychiatric diseases like Alzheimer’s or depression are characterized by a deficit in olfactory perception,” he wrote. “Interestingly, the endocannabinoid system (ECS) seems to be also implicated in such disorders. Thus, we can think that by manipulating the ECS in the olfactory system we could ameliorate such pathological conditions in human subjects.”
He emphasised that for now this was fantasy, but suggested something like a nasal spray containing cannabinoid compounds could be used to this effect. And, he continued, a way to block the effect caused by the same cannabinoid receptor could be desirable in treating conditions where the opposite scenario is the case, and you want to decrease sense of smell or appetite. “For example, in the case of metabolic disorders such as obesity, we expect (but we still do not know) that there is an hyperactivation of the olfactory ECS,” he said. “So, in this particular case, it would be useful to block cannabinoid transmission in the olfactory bulb.”
For now, the research is limited to mice and remains in early stages. Soria warned against moving too quickly into therapeutic solutions, as happened with the cannabinoid-blocking drug Rimonabant, which was sold as an anti-obesity treatment only to be withdrawn when serious side effects were discovered. But the potential could be there, and he concluded, “a better knowledge of the basic mechanisms involved in a particular function will lead to a better (and safer) therapeutic approach.”