Hello and welcome to Nutrition Facts. I’m your host, Dr. Michael Greger. Today, we’re going to explore smart nutrition choices based, naturally, on facts. Whenever there’s a new drug or surgical procedure, you can be assured that you and your doctor will probably hear about it because there’s a corporate budget driving its promotion; but, what about advances in the field of nutrition? That’s what this podcast is all about.
On today’s show we take a close look at coconut oil, the fat in coconut milk. Should we eat it? Should we avoid it? What does the science say?
Our first study compares the effects of coconut oil to butter and tallow, or beef fat. Even if virgin coconut oil and other products high in saturated fats raise LDL “bad” cholesterol, isn’t that countered by the increase in HDL “good” cholesterol? Let’s find out:
We’ve known for nearly a half century, according to “200 of the country’s leading experts in cardiovascular diseases,” in a report representing 29 “national medical organizations,” including the American Heart Association and the American College of Cardiology, that “coconut oil is one of the most potent agents” for elevating the level of cholesterol in the blood. Studies showing coconut oil elevates cholesterol date back to 1955, when it was first shown experimentally that switching someone from coconut oil to something like soybean oil could drop cholesterol from like 200 down to 150.
Coconut oil can significantly raise cholesterol levels within hours of consumption: a significantly increased blood cholesterol within hours of eating a slice of cake made from coconut oil—or from cod liver oil for that matter—mmm!—but not from the same cake made from flax seed oil.
Coconut oil may even be worse than tallow, or beef fat, but not as bad as butter. The latest interventional trial was published in March of 2017, a month-long randomized, controlled, crossover study looking at “the impact of [two tablespoons a day of] virgin coconut oil,” and it elevated cholesterol about 14% over control—consistent with the other seven interventional trials published to date in this 2016 review.
But wait; saturated fats can make so-called good cholesterol—HDL—go up. So, what’s the problem? The problem is that doesn’t seem to help. Having a high blood HDL level “is…no longer regarded as protective.” What? But, wait a second. Higher HDL is clearly associated with lower risk of heart disease. In fact, “HDL…levels are among the most consistent and robust predictors of [cardiovascular disease] risk.” Ah, but see, there are two types of risk factors: causal and non-causal. Association does not mean causation—meaning that just because two things are tightly linked, doesn’t mean one causes the other.
Let me give you an example. I bet that the number of ashtrays someone owns is an excellent predictor of lung cancer risk. I bet study after study would show that link, but that doesn’t mean that if you intervene and lower the number of ashtrays, their lung cancer risk would drop, because it’s not the ashtrays that were causing the cancer, it was the smoking. The ashtrays were just a marker of smoking, an indicator of smoking, as opposed to playing a causal role in the disease. So, just like having a high number of running shoes and gym shorts might predict a lower risk of heart attack, having a high HDL predicts a lower risk of heart attack. But, raising HDL, just like raising the number of gym shorts, wouldn’t necessarily affect disease risk.
How do you differentiate between causal and non-causal risk factors? You put it to the test. The reason we know LDL cholesterol really is bad is because people who were just born with genetically low LDL end up having a low risk of heart disease. And if you intervene and actively lower people’s LDL through diet or drugs, their heart disease risk drops. Not so with HDL.
People who live their whole lives with high HDL levels don’t appear to have a lower risk of heart attack, and if you give people a drug that increases their HDL, it doesn’t work. That’s why we used to give people high-dose niacin—to raise their HDL. But, it’s time to face the facts. “The lack of benefit of raising…HDL…seriously undermine[s] the [concept of] HDL [being] a causal risk factor.” In simple terms: “High HDL may not protect the heart.” We should “[c]oncentrate on lowering LDL.”
And so, specifically, as this relates to coconut oil: “The increase in HDL…is of uncertain clinical [significance], but the increase in LDL [cholesterol you get from eating coconut oil] would be expected to have an adverse effect on [atherosclerotic cardiovascular disease] risk.”
But, what about the MCTs? Proponents of coconut oil, who lament that this whole “coconut oil causes heart disease” thing “has created this bad image” for their national exports, assert that the medium chain triglycerides, the shorter saturated fats found in coconut oil, aren’t as bad as the longer chain saturated fats in meat and dairy. And, what about that study that purported to show low rates of heart disease among Pacific Islanders who ate tons of coconuts? I’ll cover both these topics, next.
Here’s something to wrap your brain around. Do the medium-chain triglycerides in coconut oil, and the fiber in flaked coconut; counteract the negative effects on cholesterol and artery function? Let’s take a look.
Studies of populations who eat a lot of coconuts are “frequently cited” by those who sell coconut oil “as evidence” that it does not have harmful effects. For example, there was an apparent absence of stroke and heart disease on the island of Kativa. What were they eating? Well, their diets centered around tubers, like sweet potatoes, with fruits, greens, nuts, corn, and beans. Yes, they ate fish a few times a week, but they were eating largely whole food plant-based diets. So, no wonder they may have had such low rates of artery disease, and one of those whole foods was coconut, not coconut oil.
Now, if you go to Pukapuka, they eat even more coconuts. And, there’s even an island where that’s most of what they eat—and they get high cholesterol. What’s a population eating 87% plant-based—red meat, chicken, and eggs only eaten seldomly, no dairy—doing with cholesterol levels over 200? Well, they’re eating all these coconuts every day. What are their disease rates like? We don’t know. There’s no clinical surveys, no epidemiological data, no autopsies. They did do some EKGs, which can sometimes pick up evidence of past heart attacks, and found few abnormalities, but the sample was too small to be a definitive study. And, even if they did have low disease rates, they weren’t eating coconut oil; they were eating coconuts. Coconut oil proponents pointing to these studies is like the high-fructose corn syrup lobby pointing to studies of healthy populations who eat corn on the cob or the sugar industry pointing to studies on fruit consumption, and saying see, eat all the refined sugar you want. But, fruit has fiber—and so do coconuts. Just like adding psyllium fiber—Metamucil—to coconut oil can help blunt the adverse effects on cholesterol, fiber derived from defatted coconut itself can reduce cholesterol levels as much as oat bran. And, the plant protein in coconut—also missing from the oil—may also help explain why whole coconut may not have the same effects on cholesterol.
Although coconut fat in the form of powdered coconut milk may not have the same effects on cholesterol as coconut oil, frequent consumption—defined as three or more times a week—has been associated with increased risk of vascular disease, stroke, and heart attack. And no wonder, as coconut milk may acutely impair artery function—as badly as a sausage-and-egg McMuffin. They tested three meals, three different meals: a Western high-fat meal, comprised of an egg McMuffin, a sausage McMuffin, and two hash browns, versus a local high-fat meal (this was done in Singapore; so, the more traditional high-fat meal was rice cooked with coconut milk, though there were also anchovies and an egg), vs. the same amount of calories in an unhealthy low-fat meal, comprised of Frosted Flakes, skim milk, and juice.
So, whether mostly meat-and-oil fat, or coconut milk fat, the arteries similarly clamped down, whereas that horrible sugary breakfast had no effect, no bad effect, on artery function, because, as terrible as it was, it had no saturated fat at all—though it also didn’t have any egg, which may have also helped.
Coconut oil proponents also try to argue that coconut oil has MCTs—medium chain triglycerides—shorter-chain saturated fats that aren’t as bad as the longer-chain saturated fats in meat and dairy. But you can’t apply the MCT research to coconut oil. Why? MCT oil is composed of MCTs, the medium-chain fats, caprylic and capric acid, about 50% of each, whereas those MCTs make up only like 10% of the coconut oil. Most of coconut oil is the cholesterol-raising longer-chain saturated fats, lauric and myristic. “It is therefore inaccurate to consider coconut oil to contain…predominantly [MCTs].” So, you can’t extrapolate from MCT studies to coconut oil.
That’s actually quite a common misconception, that the saturated fat in coconut oil is mainly MCTs. Actually, coconut oil is mainly lauric and myristic, which have potent LDL (bad cholesterol)-raising effects. “Coconut oil should therefore not be advised for people who should or want to reduce their risk of” the #1 killer of U.S. men and women—heart disease.
It’s like how the beef industry loves to argue that beef fat contains stearic acid, a type of saturated fat that doesn’t raise cholesterol. Yeah, but it also has palmitic and myristic that, like lauric, does raise cholesterol. If you compare the effects of different saturated fats, yes, stearic has a neutral effect on LDL, but palmitic, myristic, and lauric shoot it up. And, frankly, so may MCT oil itself, bumping up LDL like 15% compared to control. So, this “[p]opular belief,” spread by the coconut oil industry, that “coconut oil is healthy” is “not supported by [science].”
So, basically “coconut oil should be [treated no] differently than [animal] sources of dietary saturated fat.” The latest review, published in March 2017 in the Journal of the American College of Cardiology, put it even more simply in their recommendations for patients: “Avoid.”
Though there have been more than a thousand papers published on coconut oil in medical journals, there is little evidence it helps with Alzheimer’s disease. Here’s why.
Those that tend to profit from coconut oil claim it has miraculous powers—curing everything from cancer to jock itch. Perhaps the boldest claim may be as a potential cure for Alzheimer’s, based on a series of anecdotes, and one study. “Study of the ketogenic agent AC-1202.” You can certainly make money selling 20-pound buckets of coconut oil, but even more, selling some kind of patented supplement, which is what this is—a concentrated form of the medium-chain fatty acids in coconut oil, purported to be the active ingredient.
At first, it looked like it was working. But, by the end of the study, any effect it had had disappeared—though there was one genetic subgroup where it appeared to be working better. But, when that group was properly randomized, even that effect disappeared. So, the only such study ever done on concentrated coconut oil components found little effect.
And, no studies have ever been done whatsoever on Alzheimer’s and coconut oil itself. As the Alzheimer’s Association put it, “there is no scientific evidence that coconut oil helps with Alzheimer’s.” And hey, you know, “The coconut oil promise has been around for more than three years. If the administration of coconut oil was, indeed, beneficial, it would presumably be shouted from every mountaintop.” And, not just the mountains that sell coconut oil.
And that’s all we know so far. Why don’t we know more? There have been over a thousand articles published on coconut oil in the medical literature. The problem is, they’re studies like this. Did you know “Coconut Oil Enhances Tomato Carotenoid Tissue Accumulation Compared to Safflower Oil in the Mongolian Gerbil?” It includes nuggets like this: “The testes of the coconut oil-fed animals…weighed significantly less than those of the safflower oil-fed animals.” Who says coconut oil isn’t effective? How else are you going to shrink the testicles of Mongolian gerbils?
To see any graphs, charts, graphics, images, or studies mentioned here, please go to the Nutrition Facts podcast landing page. There, you’ll find all the detailed information you need plus links to all the sources we cite for each of these topics.
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Thanks for listening to Nutrition Facts. I’m Dr. Michael Greger.
This is just an approximation of the audio content, contributed by Allyson Burnett.