The United States has the reputation of the being the fattest country in the world. Obesity is at epidemic levels, as is diabetes and cardiovascular disease. A study, published in the American Journal of Medicine, shows how weed users are much less likely than non-smokers to succumb to metabolic syndrome, which is the primary risk factor for heart disease, type II diabetes, and obesity.
This study, conducted by researchers at the University of Miami in Florida, analyzed the relationship between marijuana consumption and each of the individual symptoms of metabolic syndrome, such as unhealthy cholesterol levels, increased blood sugar, higher abdominal fat, and high blood pressure. The study used survey data provided by nearly 8,500 people between the ages of 20-years and 59-years old.
Scientists separated participants into three groups: Those using marijuana currently, those who used it previously, and those who had never tried it. Despite metabolic syndrome afflicting 22 percent of all adults living in the United States today, less than 14 percent of those currently using cannabis in this study had metabolic syndrome.
Marijuana consumers are 54 percent less likely to develop metabolic syndrome than non-users are, at least among young adults. Past use of cannabis is associated with reduced risk of metabolic syndrome among adults in their middle age, and seniors using marijuana are typically less insulin-resistant and slimmer than those who do not consume weed at all.
What about the munchies?
The study, entitled “Metabolic Syndrome among Marijuana Users in the United States,” may have counterintuitive results. Everyone who has ever used weed has firsthand experience of its most famous side effect – the munchies. Marijuana is a notorious appetite stimulant and it makes food much tastier too. This is because THC activates CB1 receptors in the brain, which heighten smell and increase hunger.
The munchies phenomenon has scientific evidence to back it up. THC acts as an “agonist” on CB1 cannabinoid receptors. This means that it turns the appetite receptor on and causes it to claim hunger. An “antagonist” blocks receptors and prevents them from signaling. THCV, or tetrahydrocannabivarin, is a small but important component of the marijuana plant, and it is a neutral CB1 receptor antagonist.
Scientists are also synthesizing “inverse agonists.” These activate cannabinoid receptors and cause them to transmit a different signal to what it normally does. Inverse agonists of the CB1 receptor will reduce appetite and curb food consumption by binding to CB1 receptors. On the other hand, by binding to CB1 alone, THC increases appetite and boosts food intake.
Given what we already know about munchies, it may be reasonable to assume that increasing marijuana use may result in eating more calories, with consequent metabolic reactions, such as obesity and diabetes. However, this study and many other reports suggest that this is not the case at all. In fact, the opposite is becoming increasingly apparent.
Besides highlighting the potential health benefits of using marijuana, these findings also underscore the discrepancy between research linking cannabis use to reduced rates of obesity and preclinical studies using synthetic isolates to block the munchies receptor. It is clear that inversing the CB1 antagonist, or flipping the hunger switch, actually prevents obesity.
How can it be that cannabis consumption, which activates CB1, prevents obesity in human beings, yet using a synthetic single-molecule compound to reverse or block the CB1 receptor results in both animals and people losing weight? Is there an explanation for such a contradiction? Yes, it has to do with the complementary, yet contradictory, functions of two different types of cannabinoid receptors.
What about CB2 receptors?
Recently, scientists in Australia examined the CB2 cannabinoid receptor and its role “in modulating energy homeostasis and obesity-associated metabolic pathologies.” The body houses most CB2 receptors in immune cells, metabolically active tissues, and the peripheral nervous system. The Australian researchers made an interesting discovery.
Using JWH-015, a “selective CB2 receptor agonist,” to activate CB2 receptors, prevents the buildup of body fat in mice and reduces their food intake. THC, which is a plant-derived, non-selective agonist, binds to both CB1 and CB2 receptors. Because THC, THCV, and other cannabinoids in marijuana plants activate signaling of CB2 receptors, fewer consumers develop metabolic syndrome than abstainers do.
Metabolic syndrome is a low-grade, generalized inflammatory condition. CB2 receptors, which are very sensitive to THC, regulate both inflammation and immune function. Activating CB2 receptors, through marijuana use and eating healthily, may be a smarter way to prevent and treat metabolic syndrome than the misguided attempts of pharmaceutical companies to market and sell their drugs.
One in particular, Sanofi-Aventis, a French pharmaceutical giant, marketed Rimonabant as a synthetic CB1 inverse agonist able to suppress appetite. Back in 2006, Rimonabant was enjoying blockbuster promotion as a diet drug, but because of its severe side effects, Europe soon recalled it from the market, citing neurological imbalances, depression and suicide.
No pill to prevent munchies has ever been available for approved use in the United States. Despite Big Pharma’s desire to see us all on chemical drugs, when it comes to mitigating or even preventing metabolic syndrome, it is obvious that synthetic isolates are significantly less effective than cannabis, with its whole plant, synergistic medicinal properties that balance and enhance each other’s effects.