Orignally published on 2022-01-14 17:00:14 by slate.com
Fikadu Tafesse wasn’t expecting to wake up on Wednesday to a text in which his former mentor blamed him for his children’s new interest in weed. Earlier this week, Tafesse, a professor of molecular microbiology and immunology at Oregon Health & Science University, published evidence that some compounds found in cannabis plants could prevent the coronavirus from infecting cells. The internet latched onto the idea that weed might protect them from COVID: Twitter users made memes about the bong resin supposedly shielding their lungs from infection, Tafesse’s mentor’s children got wind of the miraculous healing powers of weed, and late-night hosts reveled in the incongruous simplicity of marijuana perhaps succeeding where hotly debated, ever-changing public health measures had failed.
And it would be simple, wouldn’t it? These days, CBD stores invade abandoned storefronts like an opportunistic mold; THC, the psychoactive compound in marijuana that makes users feel high, is now legal in 18 states. Little matter that the cannabinoid compounds tested in the study were CBDA and CBGA, not the more familiar CBD and THC—they all come from cannabis plants, in the end. Raw cannabis flower does contain CBDA and CBGA, as do CBD oils, albeit in small amounts.
But frequent users of cannabis products shouldn’t consider themselves immune, no matter how thick a layer of bong resin might coat their lungs. “That’s a complete misinterpretation,” Tafesse says. “This is just a lab study. We didn’t do any sort of clinical trial, or even [use] an animal model.”
What the researchers actually did was test whether CBDA and CBGA could, when mixed with cells in a dish, protect them from coronavirus infection. They had a good reason for doing so: They’d previously observed that these cannabinoids bind to the coronavirus spike protein, which the virus uses to latch onto and enter cells. Monoclonal antibodies also bind to this protein, and that’s how they protect people from COVID: With another molecule attached to it in the right way, the spike protein is effectively useless. With enough CBDA or CBGA mixed into cultured cells, Tafesse found, these compounds, too, could stop infection.
“It’s an interesting first observation,” says Nevan Krogan, director of the Quantitative Biosciences Institute at the University of California, San Francisco. “But much more work is required to say that there’s any value here.”
After all, working in a petri dish is a relatively low bar for a drug to clear. The conventional wisdom in pharmaceutical sciences holds that, of every 10,000 drugs that shows potential effectiveness, only one will make it to market. Dish experiments need to be followed up with animal studies, and then comes the rigorous gauntlet of human trials. And between cells and humans, there’s a lot that can go wrong. In a dish, scientists can deliver a drug precisely to where it is needed, but it’s difficult to know ahead of time how drugs will move through a body and whether they will reach their intended targets, such as the lungs and the upper respiratory tract. At this stage, it’s impossible to know how CBDA and CBGA will fare, but the odds aren’t fantastic.
Other drugs that showed similar early promise for treating COVID have since failed spectacularly, harming users and sowing political discord in the process. Ivermectin, azithromycin, and hydroxychloroquine all fought coronavirus infection in cells, but we now know that they do nothing to prevent or treat COVID in humans. But at least cannabinoids are largely safe; humans have been guinea pigs in their Phase 1 trial for millennia. Richard van Breemen, professor of medicinal chemistry at Oregon State University and the paper’s lead author, hopes that their known safety will help him and his team get the compounds into human trials sooner.
Even if the cannabinoids perform better than anyone might have imagined in those trials, there still will be no reason to smoke more joints or eat more weed brownies, at least when it comes to COVID. CBDA and CBGA are in some sense the “raw” form of the more familiar CBD and CBG (THCA plays the same role for THC). When users smoke cannabis or bake it into sweets, they heat up the CBDA, CBGA, and THCA, transforming them into their shorter-named counterparts. If you want to get high, this is good news, since THCA doesn’t have any psychological effects. If CBDA and CBGA are your goal, however, you’re going to have to look for another method of administration. Contra Twitter, bong resin doesn’t contain any CBDA or CBGA at all—and smoking weed, like all types of smoking, could increase the risk of COVID complications.
It’s not impossible to get a hold of CBDA. Some boutique online outlets sell it in a tincture form, although it seems recently to have gone on back order in some places, and you could always eat a cannabis plant if you’re really desperate. If the idea of consuming unpleasant-tasting oils with unknown health benefits appeals, they are unlikely to cause any harm, although van Breemen cautions that “the recommended dosages are there for a reason.”
But based on how much cannabinoid scientists had to administer to protect the cells, Joshua Brown, professor of pharmaceutical outcomes and policy at the University of Florida, thinks those recommended dosages are extremely unlikely to have an effect. And for an oil that probably does nothing, CBDA is expensive—about $2 to $4 per recommended dose. To have even a chance of protecting yourself, Brown estimates, you’d have to spend upward of $60 a day—and the safety of such large doses is unknown, as van Breemen pointed out.
“It’s probably not going to hurt [users] in any way, except financially,” Brown says. But at this stage, he adds, there’s also very little evidence that it will help. “The primary benefit we could get from cannabis right now,” he says, “is just relaxation.”