Today on the podcast, we’ve got some of the latest research on the effects of marijuana. First up – we look at a strange phenomenon involving a temporary quintupling of heart attack risk associated with cannabis smoking. Here’s the story.
Does the so-called “dark side of cannabis” include stroke––here said to be associated with non-synthetic marijuana––by which I assume they mean, uh: marijuana?
There have been case reports of artery damage due to the vasoconstrictor effect of cannabis, something that’s been well documented.
One study found cannabis users had 100 times greater odds of suffering from something called multifocal intracranial stenosis, where the arteries inside your brain clamp down at multiple points, but that’s a rare condition. What about strokes?
“The [lack] of high-level evidence regarding the adverse effects of marijuana usage on [brain artery] health has [led to this] notion that recreational marijuana [may not be a problem].” So, they decided to put it to the test. You want high-level evidence, they said. Well, how about a study of literally millions of pot smokers? Okay, then. And they found that recreational marijuana use did seem to be associated with an increased risk of being hospitalized with an acute ischemic stroke––but this may just be among those who smoke regularly, at least once a week.
The reason we think it’s cause-and-effect is that “the majority of [recorded strokes were] during or shortly after marijuana exposure.” And there are even cases in which strokes recurred after marijuana re-exposure. So, put all that together, and it makes a convincing case––though you’d really have to like randomize people to smoke pot or placebo pot to be sure. It’s like the heart disease story.
A similar “temporal” relationship has been found between marijuana use and the development of heart attacks and sudden cardiac death––meaning the heart attacks seemed to happen while they were using or right afterwards. However, this is complicated by the fact that cannabis is often used in combination with other drugs, such as alcohol or cocaine. So, you can’t just ask heart attack victims if they were smoking pot at the time, and make the connection without asking about other substance use. Within an hour of snorting cocaine, for example, the risk of having a heart attack goes up more than 20-fold.
That’s about five times more than after smoking pot. The hour after you smoke marijuana, your heart attack risk does appear to nearly quintuple, but only for that hour; then, your risk drops down to normal. Okay, but what does that mean? Even though heart disease is our #1 killer, the risk of having a heart attack every hour is only like one in a million in any particular hour. So, even if you then light up a joint, that may quintuple your risk, but that would only bump it to like 1 in 150,000 risk in that hour. But it’s just for that one hour. So, even if you smoked every day, your annual risk might just go up a few percent. But why the increased risk at all?
Well, we’ve known since the 70s that within an hour of smoking a joint, pulse rate goes up about 35 percent. Smoking a single joint increases blood pressure too, as well as carbon monoxide levels in the blood of angina patients, and cuts their ability to exercise nearly in half. Now, is that just because of breathing smoke––any kind of smoke? No, smoking a placebo joint, a joint with marijuana from which the THC has been removed, only cuts down exercise capacity like 9 percent, compared to cutting the time they could exercise before the chest pain started by 48 percent with the cannabis. So, it does seem to be a specific drug effect. Now, whether that’s as bad as tobacco. we’d never know…until a year later.
Smoking a marijuana cigarette decreased the exercise time until angina more than smoking a tobacco cigarette, which only cut exercise capacity 23 percent, compared to 50 percent after the joint. This may be because marijuana puts more demand on the heart. So, no surprise then that it was worse than tobacco.
It may also be the carbon monoxide. Smoking marijuana leads to nearly five times more carbon monoxide in your bloodstream than smoking tobacco. This is because pot smokers inhale deeper and then hold the smoke in, allowing more carbon monoxide into your system. So, between that and the “cardioacceleration” (the increased heart rate and pressure), that could account for the accelerated chest pain in heart disease patients.
Does it have any chronic effects on the arteries? Cannabis users do seem to have relatively stiffer arteries for their age, suggesting an acceleration of the aging process. And we are only as old as our arteries.
Even second-hand marijuana smoke may be harmful, according to this recent study in the Journal of the American Heart Association entitled “One minute of marijuana secondhand smoke impairs vascular endothelial function,” meaning artery function; and so, there was a call to protect vulnerable populations, including the elderly and disabled, and residents of multi-unit housing, pregnant women, and children. Even just one minute of exposure to marijuana second-hand smoke in rats; so, it’s not clear how applicable this is, outside of perhaps not smoking around your pets.
Next up – we share some research on the effects of marijuana smoking on car accidents.
Is cannabis-impaired driving a public health and safety concern? Well, the number of tickets went up for cannabis-impaired driving in Washington State after legalization, and the proportion of drivers in fatal car crashes in Colorado who tested positive went up. But in both cases, this may simply reflect the general increase in marijuana use overall. It doesn’t mean the cannabis is causing the crashes.
Yeah, there’s lots of evidence correlating marijuana use with car accidents. But you have to ask yourself who uses marijuana? Mostly young people and males. And guess who has higher crash risk regardless of what they smoke? Young people and males. But taking that into account, it does seem that roughly 20 to 30 percent of traffic crashes involving cannabis use occur because of the cannabis use. To put that in perspective, though, that number is more like 85 percent when it comes to alcohol.
Yeah, but are the cannabis crashes just low-velocity fender-bender bumps from some wasted driver going like five miles an hour? After a systematic review of the literature, this compilation of studies examining acute cannabis consumption and motor vehicle collisions “found a near doubling of risk of a driver being involved in a motor vehicle collision resulting in serious injury or death.” So, that’s pretty serious; though again, alcohol is even worse. Yes, cannabis may double or triple the risk of car crashes, but alcohol may multiply the risk like 6- to 15-fold. The combo may be even worse, though; 25 times the odds of fatal car crash involvement testing positive for both.
The safety consequence of cannabis intoxication when driving is listed as a primary concern about cannabis legalization. Okay, well what happened in the states where marijuana was legalized. How much did traffic fatalities go up? They didn’t. In fact, they went down. What? Why does legalizing pot reduce traffic fatalities? Because of reduced alcohol consumption. They found that legalization of weed was associated with reduced alcohol consumption; so yes, more drugged driving, but less drunk driving—and that’s so much worse, that overall, fatalities went down.
So, perhaps we’d also see less liver disease, less alcohol-induced brain damage, as pot substitutes for some of the alcohol use. Cannabis is unlikely to produce as much harm as alcohol because, unlike alcohol, cannabis does not cause liver or gastrointestinal diseases, is not fatal in overdoses, and does not appear to be as neurotoxic as alcohol. And, it’s not as potent a cause of car crashes as alcohol, either.
The health problems of cannabis dependence, like bronchitis and memory impairment, are much less serious, on average, than those suffering from alcohol dependence. But this does not mean that cannabis dependence is a minor problem––but public health authorities can be criticized for bringing that up. It’s like in the 40s and 50s after the repeal of Prohibition, you still need to warn people about the problems of heavy drinking, liver cirrhosis, and alcoholism. But you’d just get dismissed as some temperance propagandist. And now, we see a similar thing, where the public health profession wants to educate people about the adverse health effects of cannabis, but are dismissed as reefer madness hysterics.
Still, it’s important to put these adverse health effects in perspective. How does the safety of cannabis stack up against alcohol and tobacco? According to the CDC, alcohol is linked to approximately 88,000 deaths per year, whereas the deaths due to cannabis are from things like car accidents, and they go down when more people smoke pot, because alcohol is so much worse. With hindsight, we can clearly see the enormous problems that have been caused by the legal drugs—tobacco and alcohol.
If asked to decide today which psychoactive drugs should be legal, cannabis might well be much higher on the list.
Finally, today we look at the adverse effects of heavy cannabis use on bone density.
There’s been a recognition that cigarette smoking can have a major effect on bone health for decades––increasing the lifetime risk of hip fracture by about half. It also appears to impair bone healing––so much so that surgeons ask if they should be discriminating against smokers, because the bone and wound healing complication rates are so high. But what about smoking marijuana?
There is accumulating evidence to suggest that cannabis compounds play important roles regulating bone mass and bone loss. Yeah, but are they friend or foe? “Results from research on [cannabis compounds] and bone mineral density in rodent models have been inconsistent. Some studies show increased bone formation, others [show increased] bone loss, and…others [show] no association” at all. This variation in results may be due in part to differences in the mouse strain used. But if you can’t even extrapolate from one mouse to another, how can you extrapolate to human beings?
So, what if you just measure cannabis use and bone mineral density in people? Thousands of adults were tested and asked about their cannabis use, and there did not appear to be any link between the two; that’s a relief. Though in this study, “heavy” cannabis use was defined as just five days or more of use in the last month. They didn’t ask beyond that. So, theoretically, someone who’s just smoked five joints in their entire life could be categorized as a “heavy user.”
How about cannabis use on five thousand separate occasions over a lifetime? Now that’s a heavy user, decades of regular use. And in that case, heavy use was associated with both low bone mineral density and an increased risk of bone fractures. About double the fracture rate––presumably due to lower bone density in the hip and spine, though heavy cannabis users were also skinnier on average, and skinnier people have lighter bones.
Hip fracture risk goes down as your weight goes up; nearly half of underweight women have osteoporosis. But less than 1% of obese women do, which makes total sense. Being obese forces your body to make your bones stronger to carry around all that extra weight. That’s why weight-bearing exercise is so important to constantly put stress on your skeleton: it’s use it or lose it. That’s why astronauts can lose a percent of their bone mass every month. Their bodies aren’t stupid; why waste all that energy making a strong skeleton if you’re not going to put any weight on it?
So, maybe that’s the only reason heavy cannabis users have frailer bones–– because they tend to be about 15 pounds lighter? Wait a second, users are slimmer? What about the munchies? The lower BMI of heavy cannabis users may seem counterintuitive, given the appetite stimulation, but this isn’t the first time this has been noted.
Pop culture “depicts marijuana users as a sluggish, lethargic,…unproductive subculture of compulsive snackers.” And it’s true that marijuana has been found to increase food intake; a single hit can increase appetite. And so, you’d expect obesity rates to rise in states that legalized it. But, if anything, the rise in obesity appeared to slow after medical marijuana laws were passed, whereas it appeared to just keep rising in other states.
The reason pot smokers may be slimmer is because of the effect of smoked marijuana on metabolism. We’ve known for nearly 40 years that within 15 minutes of lighting up, your metabolic rate goes up by about 25%, and stays there for at least an hour. So, that may be playing a role.
So, is that why heavy cannabis use is associated with lower bone mineral density and increased risk of fractures? They’re just not as overweight? No. Even taking BMI into account, heavy cannabis use appears to be an independent predictor of weaker bones.