Even those largely unfamiliar with cannabis know at least one thing about smoking pot: It gives you the munchies. That night-time itch, the distant grumble of your stomach when you know you’ve just eaten a full box of mac and cheese but you still also need an Entenmann’s mini donut (or five). The plain facts of smoking might make you assume that it causes weight increase—after all, one of its first legal modern American medical uses was to increase appetite in patients suffering from wasting illnesses and cancers. But, as it turns out, this is far from the case.
A number of studies analyzed by researchers at Indiana University South Bend for the recently released paper “Theoretical Explanation for Reduced Body Mass Index and Obesity Rates in Cannabis Users” revealed that the BMIs of cannabis consumers are actually lower across the board than those of non-smokers. Scientific and anecdotal evidence has begun to pile up: Obese lab rats stopped gaining weight as quickly when exposed to cannabis, the researchers say, and rates of obesity in states that legalized cannabis rapidly dropped after the changes in policy.
The weight loss isn’t for a lack of trying: Despite these lowered BMIs and rates of obesity, cannabis consumers eat an average of 834 kcal/day more than non-consumers. Some researchers tried to argue that the weight discrepancy might be the result of differing physical activity levels, but there is no evidence anecdotal or otherwise to support the idea that people who smoke are more active than those who don’t. The IUSB researchers wanted to know how such a paradox could be possible, and they think they found their answer in tetrahydrocannabinol (THC) and how the human body processes it.
It’s important to note that this IUSB study is not peer-reviewed, meaning that its methodology hasn’t been looked over by experts in the field. As such, the research is exactly what its title suggests, “theoretical.” But theoretical though it may be, the IUSB researchers actually make a pretty compelling case for why THC might hold the key to disrupting American obesity statistics.
Western diet habits are dire. Even though the past three decades demonstrate a drop in the amount of fat (saturated and otherwise) that we eat relative to our total calorie consumption, obesity rates have kept increasing. Research has shown that the issue lies in the kinds of fats we eat as much as it does the amount. In prehistory, we’re estimated to have been eating an equal level of omega-6 and omega-3 fatty acids, both of which are necessary for healthy bodily functioning. But as we move towards a world of processed foods full of cheap vegetable oils and grains, the amount of omega-6 fatty acids we ingest has grown to the point that the average omega-6 to omega-3 ratio has jumped from the prehistoric 1:1 to a modern Western average of up to 17:1. In addition to obesity, this imbalance can also increase inflammation and lead to arthritis, heart disease, diabetes, Alzheimer’s and many cancers.
So where does cannabis come into all of this? It turns out that those omega-6s and 3s break down into neurotransmitters that plug into the cannabinoid type 1 receptor (CB1R), which is located all across our body’s central nervous system and is also activated by THC. Along with the rest of the endocannabinoid system, this receptor manages an astounding level of human functioning, helping to maintain homeostasis in the body as well as mitigating anxiety-dependent behaviors like avoidance. Too constant a stream of THC, and the CB1R receptor “downregulates,” becoming less sensitive to THC and other cannabinoids including the omega-6-derived inflammatory neurotransmitters AEA and 2-AG. That desensitization to THC is what we know as a (reversible) tolerance to cannabis, the reason why everyone needs to take breaks from smoking now and then. It’s also why cannabis is such a good treatment for hyper-inflammatory diseases.
AEA and 2-AG, known as “strong signaling” neurotransmitters, can overload CB1R like THC can. As with an acute consumption of THC, overloading CB1R with AEA and 2-AG can result in the “excess intake, storage and conservation of energy”—eating too much and not processing enough of it. This can be prevented by balancing your diet and using the enzymes that would usually make AEA and 2-AG to instead break down omega-3s, which produce weak signaling neurotransmitters DHEA and EPEA that don’t overload the receptor.
The IUSB research suggests that, if balancing your diet isn’t your thing, cannabis can do the job in a pinch. It doesn’t take much for CB1R to become downregulated, apparently: One or two uses a week can keep the receptor desensitized for up to three or four weeks. And when it becomes desensitized to THC, it also stops being so likely to uptake AEA and 2-AG, meaning it’s less likely to become overloaded by an imbalance of omega-6s and therefore not going to react by storing an unnecessary amount of energy.
“Weight loss will increase as energy intake and storage remain depressed,” the research explains, “and metabolism stimulated, until CB1R returns to pre-Cannabis use levels.”
Problem solved, right? Why not just make a diet pill that just keeps CB1R depressed all the time? Well, in addition to being able to modulate possibly life-saving inflammation, CB1R also functions as an uptake for a host of other bodily chemicals like the anxiety-mitigating neurotransmitter GABA. This is part of why, researchers explain, obesity cures that downregulate CB1R can cause “severe psychiatric side effects… including depressive disorders, dizziness, nausea and anxiety.”
Downregulation has been pegged as the cause of cannabis withdrawal syndrome (CWS), which a 2017 study explained happens after the “cessation from long-term and regular cannabis use [and] precipitates a specific withdrawal syndrome with mainly mood and behavioral symptoms of light to moderate intensity.” As in the Indiana University study, these researchers say that CB1R sensitivity and functioning is fully back to normal “within four weeks of abstinence” and starts to ease “within the first two days of abstinence,” demonstrating the impressive speed of neuroplasticity in these receptors.
While a couple of weekly sessions of smoking wouldn’t cause CWS, which is the result of long-term chronic intoxication, researchers are also quick to point out that simply maintaining a balanced omega fatty acid ratio would have a similar health benefit to cannabis intake for weight loss. Plus, cannabis can’t block all of the polyunsaturated fatty acids omega-6 creates, as some of them, including arachidonic acid, don’t act on the CB1R receptor, so “it is likely that the overlap is not complete.” Researchers instead suggest that the two tactics be taken together, and that when combined, they “should reduce BMI and cardiometabolic risk factors more than either option alone.”
And that’s no snake oil—it’s fish oil.