It’s crazy when you think about all of the different kinds of foods we eat. We just swallow – and hope it all works out for the best. Well – as it turns out there are better ways to think about keeping our bodies humming healthfully along. Welcome to Nutrition Facts – I’m your host Dr. Michael Greger.
It’s time for the Nutrition Facts grab bag, where we look at the latest science on a whole variety of topics. We start with a story on how cannabis smoking may help with IBD symptoms in the short term.
“Medical marijuana: A panacea or scourge?” For 5,000 years, cannabis has been used throughout the world for medicinal purposes, even prescribed by American physicians early on––a fact that’s often used by medical marijuana proponents to justify modern medical applications. But the field of old-timey medicine was fraught with patent medicine snake-oil nonsense, not to mention bloodletting and other questionable and harmful remedies.
Sceptics criticize the medical marijuana movement as the “medical excuse marijuana movement,” insinuating that epileptic children and the terminally ill are just being used as props to Trojan horse in the legalization of recreational use, or to peddle outlandish claims about “miracle cancer cures,” frustrating researchers in the field who just want to get at the science.
For example, what about the therapeutic use of cannabis for inflammatory bowel diseases like Crohn’s disease and ulcerative colitis? Conventional therapies mainly work by suppressing the immune system to try to tamp down the inflammation. Given the limited therapy options and known adverse side effects from these drugs, often people suffering these diseases ended up having to get inflamed sections of their bowels removed surgically. So, you can see why there’s so much interest in alternative approaches.
About one in six IBD patients who use marijuana say it helps with their symptoms; so, researchers decided to put it to the test. Thirteen patients with inflammatory bowel disease were given a third of a pound of marijuana to smoke at their leisure over a period of three months, and they felt significantly better. Now there was no control group; so, you don’t know if they would have gotten better anyway, or what role the placebo effect may have played. It’s like some of the studies of cannabis used for pediatric epilepsy: response rates of over 30 percent, seizure frequency cut in half in a third of the kids. That’s amazing, until you realize you can sometimes get the same kind of amazing response giving kids nothing, giving them a sugar pill placebo. That’s why it’s critical to do randomized, double-blind, placebo-controlled trials. But there weren’t any on cannabis and IBD until 2013.
Twenty-one patients with Crohn’s disease for which nothing seemed to help; so, they randomized them to either smoke 2 joints a day of real pot or a look-alike placebo pot. And, 90 percent of the subjects in the cannabis group got better, compared to only 40 percent in the placebo group. The cannabis group like cut their symptoms in half.
They acknowledge that long-term cannabis use is not without risks, but it may be a cakewalk compared to the potential adverse and even life-threatening side effects of some of the more powerful conventional therapies; so, the study was heralded as offering “High Hope” for digestive disorders.
Now, the study was funded by a medical marijuana advocacy organization––in fact, the main supplier in the country––and so, there may have been expectations placed on the subjects on how much better this stuff is going to make them feel (in other words, a set-up for the placebo effect). But they controlled for that, right? Those getting the real stuff did significantly better than those randomized to get the placebo pot. But wait a second. The whole point of a placebo is to be indistinguishable from the real thing, so the subjects don’t know which group they’re really in. How do you do that with a psychoactive drug? You can’t, which is the problem. They tried to hide which group people were in by recruiting only patients who never tried pot before in hopes that they wouldn’t notice, but of course, most of them did. So, what we’re left with is basically another unblinded study. They asked them a bunch of subjective questions, “How you feelin’?”, and those who mostly knew they were taking the drug said they were feeling better.
There was no change in the objective lab values, like CRP, a sign of inflammation, and so maybe the marijuana is just masking symptoms without actually affecting intestinal inflammation. Another indicator that cannabis may not be affecting the course of the disease itself is how quickly the symptoms rebounded. Two weeks after the study ended, the cannabis group was right back up to where they started. So, no difference in objective inflammatory markers, and given the rapid rebound, it seems more plausible that cannabis ameliorated the symptoms of Crohn’s disease, rather than actually modulating the disease itself. Okay, yeah, but the symptoms are terrible. A reduction in pain is a reduction in pain. From the point of view of the patients, a marked symptomatic improvement and ability to resume normal life is not trivial, whether or not the inflammation persists––unless, of course, cannabis somehow made the disease worse in the long run.
This survey study, published the following year, found that cannabis provided that same immediate symptomatic relief, but was associated with a worse disease prognosis over time. Patients with inflammatory bowel disease reported that cannabis improved their pain, cramping, and diarrhea, but use for more than six months in Crohn’s patients appeared to be a strong predictor of them ending up in surgery––five times the odds of them ending up under the knife.
Now, there’s two possible explanations for this. It’s quite possible that it was the increased severity that led to the cannabis use, and not the other way around. But the alternative explanation is that cannabis use may worsen the prognosis, leading to greater surgeries and hospitalizations.
That’s why we really need prospective clinical trials where we follow people over time to see which came first. But until then, maybe we should consider cannabis use in IBD as potentially harmful. Not just to err on the side of caution, but there was this other study on hepatitis C patients that found that daily cannabis use was associated with nearly seven times the odds of worse liver fibrosis, which is like scar tissue. And so hey, if cannabis really does make fibrosis worse, then that could potentially explain why cannabis users with IBD may be more likely to end up on the operating table.
In our next story – we look at the leading risk factor for death in the United States – the American Diet.
About a decade ago, the American Heart Association expressed concern that their “2020 target of improving cardiovascular health by 20 percent by 2020 [would] not be reached if current trends continue[d].” By 2006, most people were already not smoking, and had nearly achieved their goal for exercise. But when it came to healthy diet score, only about 1 percent got a 4 or 5 out of their 0 to 5 diet quality score, and that’s with so-called “ideal” criteria of like drinking less than four and a half cups of soda a week.
In the last decade, they saw a bump up to like 1 percent of Americans even reaching those kinds of basic criteria. But given their aggressive goal of improving that by 20 percent by 2020, they hoped to turn that 1 percent into about 1.2 percent! Okay, so how’d we do? Let’s look at the 2019 update, and it looks like we’ve slipped down to as low as one in a thousand. And American teens got a big fat zero.
No wonder, perhaps, that “for all mortality-based metrics, the U.S. rank declined…to 27th or 28th among 34 [industrialized] countries.” “Citizens living in countries with a substantially lower [GDP] and health expenditure[s] per capita…have lower mortality rates than those in the United States.” Slovenia beat us by three countries, coming in at 24th in life expectancy to our 27th. And, more recently we seem to have slipped to 43rd, even though we spend trillions on health care—more than anyone else.
What’s the leading risk factor for death in the United States? What we eat. The standard American diet is just to die for—literally. Those trillions in health care spending aren’t addressing the root cause.
“Approximately 80 percent of chronic disease and premature death could be prevented by not smoking, being physically active, and adhering to a healthful dietary pattern.” But what exactly is meant by “healthy diet”? Unfortunately, what we hear about nutrition in the media is often inconsistent and confusing. “There[’s a] pressure within today’s competitive journalism market for sensationalism. There may even be a disincentive to present the facts in…context…” to sell more magazines. In fact, about three-quarters of a century ago, it was noted that unfortunately, “the subject of nutrition seems to have a special appeal to the credulous, the social zealot, and, in the commercial field, the unscrupulous,” a combination “calculated to strike despair in the hearts of the sober, objective scientist.”
“The most important [health care] problem [we face may be] our poor lifestyle choices based on misinformation.” It’s like the climate change deniers; “healthy…dietary advice [is] overshadowed by critics, diet books, [industry interests], and misguided information in the media.” Maybe what we need is like an IPCC (Intergovernmental Panel on Climate Change) of nutrition.
These days “[n]o single expert, regardless of academic stature or reputation, has the prominence to overcome the obstacles created by confusing media messages and [effectively] deliver the fundamental principles of healthy living…to the public.” However, what if there was “a global coalition consisting of a variety of nutrition experts, who collectively represent the views held by the majority of scientists, physicians, and health practitioners…”? It could “serve as the guiding resource of sound nutrition information for improved health and prevention of disease.” And…boom! “The True Health Initiative was conceived for that very purpose.” A nonprofit coalition of hundreds of experts from dozens of countries agreeing to a consensus statement on the fundamentals of healthy living. Check out https://www.truehealthinitiative.org/. Spoiler alert—the healthiest diet is one generally comprised mostly of minimally processed plants.
Finally today – we look at how the incidence of side effects from statins is low in clinical trials but high out in the real world.
There is now overwhelming evidence to support reducing LDL cholesterol—bad cholesterol—to reduce atherosclerotic cardiovascular disease, the number one killer of men and women. So, why is adherence to cholesterol-lowering statin drug therapy such a major challenge? The majority of studies reported at least 40 percent, and as much as 80 percent, of patients did not comply fully with statin treatment recommendations. Three-quarters may flat out stop taking them, or sometimes up to nearly 90 percent discontinue treatment.
When asked why, most former statin users, or discontinuers, cited muscle pain, a side effect, as the primary reason for stopping the pills. By far the most prevalent and important adverse events, up to 72 percent of all statin side effects, are statin-associated muscle symptoms. Taking coenzyme Q10 supplements as a treatment for statin-associated muscle symptoms was a good idea in theory, but they don’t actually appear to help. Normally, side-effect symptoms go away when you stop the drug, but sometimes can linger a year or more. But there is evidently growing evidence that statin intolerance is predominantly psychosocial, not pharmacological. Meaning – wait – maybe it’s mostly just in people’s heads?
Statins have developed a bad reputation with the public, one editorial read, “a phenomenon driven largely by proliferation on the Internet of bizarre and unscientific…criticisms of these drugs.” Maybe it’s Googling that leads to statin intolerance? But come on, people had been going off statins for decades before there even was an Internet. What kind of data have doctors suggesting that patients are falsely misattributing normal aches and pains to be statin side effects?
Well, if you take people who claim to have statin-related muscle pain and randomize them back and forth between statins and an identical-looking placebo in three-week blocks, they can’t actually tell whether they’re getting the real drug or the sugar pill. The problem with that study, though, is that it may take months to not only develop statin-induced muscle pain, but months before it goes away; so, no wonder three-weeks-on and three-weeks-off may not be long enough for the participants to discern which is which.
But these data are more convincing. In the study, 10,000 people were randomized to a statin or sugar pill for a few years. But they had to stop the study early, because so many more people were dying in the sugar pill group. And so, everyone was then offered the statin. What they noted was that there was no excess of reports of muscle-related adverse effects among patients assigned to the statin over those assigned to the placebo; but then, when the placebo phase was over and the people knew they were on a statin, then they reported more muscle side effects than those who knew they weren’t. These results illustrate the so-called nocebo effect––kind of like the opposite of the placebo effect.
Placebo effects are positive consequences falsely attributed to a treatment, whereas nocebo effects are negative consequences falsely attributed to a treatment. There was an excess rate of muscle-related adverse effects reported only when patients and their doctors were aware that statin therapy was being used, and not when its use was concealed. They hope these results will help assure both physicians and patients that most adverse effects associated with statins are not actually caused by the drug and should help counter exaggerated claims about statin-related side effects. It’s these kinds of results from placebo-controlled randomized trials that are said to have shown definitively that almost all of the symptomatic adverse events that are attributed to statin therapy in routine practice are not actually caused by the drug. Now, only a few patients will believe this, that their statin-associated muscle symptoms are of psychogenic origin––meaning all just in their head––but their denial may have deadly consequences. Discontinuing statin treatment may be a life-threatening mistake.
Here’s the mortality of those who stopped their statins after having a possible adverse reaction, compared to those who stuck with them. This translates into about 1 excess death for every 83 patients who discontinued treatment within a four-year period. So, when there are media reports about statin side effects and people stop taking them, this could result in thousands of fatal and disabling heart attacks and strokes, which would otherwise have been avoided. Seldom in the history of modern therapeutics have the substantial proven benefits of a treatment been compromised to such an extent by serious misrepresentations of the evidence for its safety.
But, is it a misrepresentation to suggest statin therapy causes side effects in up to one-fifth of patients? That is actually what you see in clinical practice. Between 10 percent to 25 percent of patients placed on statins complain of muscle problems, but because we don’t see anywhere near those kinds of numbers in controlled trials, patients are accused of being confused. Why in clinical trials is the incidence of side effects from statins so low, but out in the real world appear to be so high?
For example, take this meta-analysis of clinical trials, finding muscle problems not in 1 in 5, but only 1 in 2,000 patients. So hey, maybe everyone over a certain age should be on them. But, of course, every single one of those trials was funded by the statin manufacturers themselves. So, for example, how could the randomized controlled trials miss detecting statin-related adverse side effects such as muscle pain? By not asking. A review of 44 statin trials revealed that only 1 directly asked about muscle-related adverse effects. So, are the vast majority of side effects just being missed in all these trials, or are the vast majority of side effects seen in clinical practice just some figment of patients’ imagination? The bottom line is we don’t know, but there is certainly an urgent need to figure it out.
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