Coconut Oil and the Boost in HDL “Good” Cholesterol

The effects of coconut oil were compared to butter and tallow. Even if virgin coconut oil and other saturated fats raise LDL “bad” cholesterol, isn’t that countered by the increase in HDL “good” cholesterol?

According to “the experience and wisdom of 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, we’ve known for nearly half a century that “coconut oil is one of the most potent agents for elevating [blood] serum cholesterol level.” As I discuss in my video Coconut Oil and the Boost in HDL “Good” Cholesterol, studies showing coconut oil elevates cholesterol date back to 1955, when it was first shown experimentally that switching someone from coconut oil to soybean oil could drop cholesterol from around 200 down to 150, as you can see at 0:39 in my video.

Coconut oil can significantly raise cholesterol levels within hours of consumption. In fact, a significant increase in blood cholesterol was found within hours of eating a slice of cake made from either coconut oil (or cod liver oil for that matter), but not from the same cake made from flaxseed oil.

As you can see at 1:10 in my video, coconut oil may even be worse than tallow, or beef fat, but it is not as bad as butter. An interventional trial was published in March 2017: a month-long randomized, controlled, crossover study looking at the impact of two tablespoons per day of virgin coconut oil. The result? Coconut oil elevated cholesterol about 14 percent over the control, which was consistent with seven other interventional trials published to date in a 2016 review.

Hold on. Saturated fats can make HDL, the so-called good cholesterol, go up, so what’s the problem? The problem is that it doesn’t seem to help. Having a high blood HDL level is “no longer regarded as protective.” What? Wait a second. Higher HDL levels are clearly associated with lower risk of heart disease, as you can see at 2:01 in my video. In fact, HDL levels “are among the most consistent and robust predictors of CVD [cardiovascular disease] risk.” Ah, but there are two types of risk factors: causal and non-causal. Association does not mean causation—that is, just because two things are tightly linked, it doesn’t mean one causes the other.

Let me give you an example, which you can see at 2:30 in my video. I bet that the number of ashtrays someone owns is an excellent predictor of lung cancer risk and that study after study would show that link. But, that does not mean that if you intervene and lower the number of ashtrays someone has, their lung cancer risk will drop, because it’s not the ashtrays that are causing the cancer, but the smoking. The ashtrays are 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 also 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 them to the test. The reason we know LDL cholesterol truly is bad is because people who were just born with genetically low LDL cholesterol 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—but 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 help. That’s why we used to give people high-dose niacin—to raise their HDL. But, it’s “time to face facts.” The “lack of benefit of raising the HDL cholesterol level with the use of niacin…seriously undermine[s] the hypothesis that HDL cholesterol is a causal risk factor.” In simple terms: “High HDL may not protect the heart.” We should concentrate on lowering LDL. So, specifically, as this relates to coconut oil, the increase in HDL “is of uncertain clinical relevance,” but the increase in LDL you get from eating coconut oil “would be expected to have an adverse effect” on atherosclerotic cardiovascular disease risk.

But, what about the MCTs, the medium-chain triglycerides? Proponents of coconut oil, who lament “that ‘coconut oil causes heart disease’ has created this bad image of [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 large amounts of coconuts? I cover both of those topics in my video What About Coconuts, Coconut Milk, and Coconut Oil MCTs?.

I love topics that give me an excuse to talk about scientific concepts more generally, like various study designs in my video Prostate Cancer and Organic Milk vs. Almond Milk or my discussion of direct versus indirect risk factors in this one.

How do we know LDL is bad? Check out How Do We Know That Cholesterol Causes Heart Disease?.

But, wait. Isn’t the whole saturated fat thing bunk? No. See:

In health,

Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live presentations:

What About Coconuts, Coconut Milk, and Coconut Oil MCTs?

Do the medium-chain triglycerides in coconut oil and the fiber in flaked coconut counteract the negative effects on cholesterol and artery function?

Studies of populations who eat a lot of coconuts are “frequently cited” by those who sell coconut oil “as evidence that coconut oil does not have negative effects on cardiovascular health.” For example, there was an apparent absence of stroke and heart disease on the island of Kativa in Papua New Guinea. What were they eating? Their diets centered around tubers, like sweet potatoes, with fruits, greens, nuts, corn, and beans. Although they ate fish a few times a week, they were eating a largely whole food plant-based diet. It’s no wonder they may have had such low rates of artery disease. And, one of the whole foods they were eating was coconut, not coconut oil.

Now, if you go to Pukapuka, even more coconuts are eaten. In fact, as you can see at 0:51 in my video What About Coconuts, Coconut Milk, and Coconut Oil MCTs?, there’s even an island where coconuts make up most of what people eat—and they do get high cholesterol. How can a population eating 87 percent plant-based, with no dairy and only rare consumption of red meat, chicken, and eggs, have cholesterol levels over 200? Well, they’re eating all those coconuts every day. What are their disease rates like? We don’t know. There are no clinical surveys, no epidemiological death data, and no autopsies. Some EKGs were taken, which can sometimes pick up evidence of past heart attacks, but they found few abnormalities. The sample was too small to be a definitive study, though. And, even if they did have low disease rates, they weren’t eating coconut oil—they were eating coconut in its whole form.

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 you can eat all the refined sugar you want. But fruit has fiber and so do coconuts. Just as 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. What’s more, the plant protein in coconuts, which is also missing from the oil, may help explain why whole coconuts 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 disease. And, no wonder, as coconut milk may acutely impair artery function as badly as a sausage and egg McMuffin.

Researchers tested three different meals including a Western high-fat meal that “consisted of an Egg McMuffin®, Sausage McMuffin®, 2 hash brown patties and a non-caffeinated beverage (McDonald’s Corporation)” a local high-fat meal, and an “isocaloric low-fat meal.” The study was conducted in Singapore, so the more traditional local high-fat meal was rice cooked in coconut milk and served with anchovies and an egg. These two different high-fat meals were put up against the same amount of calories in an unhealthy low-fat meal of Frosted Flakes, skim milk, and juice. At 3:21 in my video, you can see the artery function—that is, its ability to relax normally—before and after eating each of the three meals. Researchers found that artery function is significantly crippled within hours of consuming the McMuffins and also the local high-fat meal with coconut milk. So, whether the fat is mostly from meat and oil or from coconut milk, the arteries clamped down similarly, whereas that horrible sugary breakfast had no bad effect on artery function. Why? Because as terrible as the Frosted Flakes meal was, it had no saturated fat at all. (It also didn’t have contain any eggs, so that might have helped, too.)

Coconut oil proponents also try to argue that coconut oil has MCTs, medium-chain triglycerides, which are shorter-chain saturated fats that aren’t as bad as the longer-chain saturated fats in meat and dairy. You can’t apply the MCT research to coconut oil, though. Why not? Well, MCT oil is composed of MCTs—about 50 percent of the medium-chain fat caprylic acid and the other 50 percent of the MCT capric acid—whereas those MCTs make up only about 10 percent of 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 either predominantly medium-chain fatty acids or predominantly medium-chain triglycerides. Thus, the evidence on medium-chain triglycerides cannot be extrapolated to coconut oil.”

It’s actually quite “a common misconception” that the saturated fat in coconut oil is comprised of mainly MCTs. Actually, as we discussed, coconut oil is mainly lauric and myristic, both of which have potent bad LDL cholesterol-raising effects. “Coconut oil should therefore not be advised for people who should or want to reduce their risk of CHD,” coronary heart disease, which is the number-one killer of U.S. men and women. The beef industry, for example, loves to argue that beef fat contains stearic acid, a type of saturated fat that doesn’t raise cholesterol. Yes, but it also has palmitic and myristic acids that, like lauric acid, do raise cholesterol, as you can see at 5:12 in my video.

If you compare the effects of different saturated fats, as you can see at 5:29 in my video, stearic acid does have a neutral effect on LDL, but palmitic, myristic, and lauric acids shoot it up—and, frankly, so may MCT oil itself, as it bumps up LDL 15 percent compared to control. Bottom line? “Popular belief”—spread by the coconut oil industry—“holds that coconut oil is healthy, a notion not supported by scientific data.” The science just doesn’t support it.

So, basically, “coconut oil should be viewed no differently” from animal sources of dietary saturated fat. A recent review published in the Journal of the American College of Cardiology put it even more simply in its recommendations for patients. When it comes to coconut oil, “avoid.”

Okay, but doesn’t saturated fat boost HDL, the so-called good cholesterol? Check out Coconut Oil and the Boost in HDL “Good” Cholesterol.

Isn’t coconut oil supposed to be good for Alzheimer’s, though? See my video Does Coconut Oil Cure Alzheimer’s?

If you want to learn more about the original McMuffin artery studies, see The Leaky Gut Theory of Why Animal Products Cause Inflammation.

You may also be interested in Flashback Friday: Coconut Oil and Abdominal Fat.

In health,

Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live presentations:

What White Blood Cell Count Should We Shoot for?

At the start of my video What Does a Low White Blood Cell Count Mean?, you can see what it looks like when you take a drop of blood, smear it between two pieces of glass, and view at it under a microscope: a whole bunch of little, round, red blood cells and a few big, white blood cells. Red blood cells carry oxygen, while white blood cells are our immune system’s foot soldiers. We may churn out 50 billion new white blood cells a day. In response to inflammation or infection, that number can shoot up to a 100 billion or more. In fact, pus is largely composed of: millions and millions of white blood cells.

Testing to find out how many white blood cells we have at any given time is one of the most common laboratory tests doctors order. It’s ordered it hundreds of millions of times a year. If, for example, you end up in the emergency room with abdominal pain, having a white blood cell count above about 10 billion per quart of blood may be a sign you have appendicitis. Most Americans fall between 4.5 and 10, but most Americans are unhealthy. Just because 4.5 to 10 is typical doesn’t mean it’s ideal. It’s like having a “normal” cholesterol level in a society where it’s normal to die of heart disease, our number-one killer. The average American is overweight, so if your weight is “normal,” that’s actually a bad thing.

In fact, having excess fat itself causes inflammation within the body, so it’s no surprise that those who are obese walk around with two billion more white cells per quart of blood. Given that, perhaps obese individuals should have their own “normal” values. As you can see at 2:06 in my video, if someone with a 47-inch waist walks into the ER with a white blood cell count of 12, 13, or even 14, they may not have appendicitis or an infection. That may just be their normal baseline level, given all the inflammation they have in their body from the excess fat. So, normal levels are not necessarily healthy levels.

It’s like smoking. As you can see at 2:31 in my video, if you test identical twins and one smokes but the other doesn’t, the smoker is going to end up with a significantly higher white cell count. In Japan, for example, as smoking rates have steadily dropped, so has the normal white count range. In fact, it’s dropped such that about 8 percent of men who have never smoked would now be flagged as having abnormally low white counts if you used a cut-off of 4. But, when that cut-off of 4 was set, most people were smoking. So, maybe 3 would be a better lower limit. The inflammation caused by smoking may actually be one of the reasons cigarettes increase the risk of heart attacks, strokes, and other inflammatory diseases. So, do people who have lower white counts have less heart disease, cancer, and overall mortality? Yes, yes, and yes. People with lower white blood cell counts live longer. Even within the normal range, every one point drop may be associated with a 20 percent drop in the risk of premature death.

As you can see at 3:39 in my video, there is an exponential increase in risk in men as white count goes up, even within the so-called normal range, and the same is found for women. The white blood cell count is a “stable, well-standardized, widely available and inexpensive measure of systemic inflammation.” In one study, half of the women around 85 years of age who had started out with white counts under 5.6 were still alive, whereas 80 percent of those who started out over 7 were dead, as you can see at 4:05 in my video—and white blood cell counts of 7, 8, 9, or even 10 would be considered normal. Being at the high end of the normal range may place one at three times the risk of dying from heart disease compared to being at the lower end.

The same link has been found for African-American men and women, found for those in middle age, found at age 75, found at age 85, and found even in our 20s and 30s: a 17 percent increase in coronary artery disease incidence for each single point higher.

As you can see at 5:00 in my video, the higher your white count, the worse your arterial function may be and the stiffer your arteries may be, so it’s no wonder white blood cell count is a useful predictor of high blood pressure and artery disease in your heart, brain, legs, and neck. Even diabetes? Yes, even diabetes, based on a compilation of 20 different studies. In fact, it may be associated with everything from fatty liver disease to having an enlarged prostate. And, having a higher white blood cell count is also associated with an increased risk of dying from cancer. So, what would the ideal range be? I cover that in my video What Is the Ideal White Blood Cell Count?.

A higher white blood cell count may be an important predictor for cardiovascular disease incidence and mortality, decline in lung function, cancer mortality, all-cause mortality, heart attacks, strokes, and premature death in general. This is no surprise, as the number of white blood cells we have circulating in our bloodstreams are a marker of systemic inflammation. Our bodies produce more white blood cells day to day in response to inflammatory insults.

We’ve known about this link between higher white counts and heart attacks since the 1970s, when we found that higher heart attack risk was associated with higher white blood cell counts, higher cholesterol levels, and higher blood pressures, as you can see at 0:53 in my video What Is the Ideal White Blood Cell Count?. This has been found in nearly every study done since then. There are decades of studies involving hundreds of thousands of patients showing dramatically higher mortality rates in those with higher white counts. But why? Why does white blood cell count predict mortality? It may be because it’s a marker of inflammation and oxidation in the body. In fact, it may even be a biomarker for how fast we are aging. It may be more than just an indicator of inflammation—it may also be an active player, contributing directly to disease via a variety of mechanisms, including the actual obstruction of blood flow.

The average diameter of a white blood cell is about seven and a half micrometers, whereas our tiniest vessels are only about five micrometers wide, so the white blood cell has to squish down into a sausage shape in order to squeeze through. When there’s inflammation present, these cells can get sticky. As you can see at 2:20 in my video, a white blood cell may plug up a vessel as it exits a small artery and tries to squeeze into a capillary, slowing down or even momentarily stopping blood flow. And, if it gets stuck there, it can end up releasing all of its internal weaponry, which is normally reserved for microbial invaders, and damage our blood vessels. This may be why in the days leading up to a stroke or heart attack, you may find a spike in the white cell count.

Whether white count is just a marker of inflammation or an active participant, it’s better to be on the low side. How can we reduce the level of inflammation in our body? Staying away from even second-hand smoke can help drop your white count about half of a point. Those who exercise also appear to have an advantage, but you don’t know if it’s cause and effect unless you put it to the test. In one study, two months of Zumba classes—just one or two hours a week—led to about a point and a half drop in white count. In fact, that may be one of the reasons exercise is so protective. But is that just because they lost weight?

Fitness and fatness both appear to play a role. More than half of obese persons with low fitness—51.5 percent—have white counts above 6.6, but those who are more fit or who have less fat are less likely to have counts that high, as you can see at 3:47 in my video. Of course, that could just be because exercisers and leaner individuals are eating healthier, less inflammatory diets. How do we know excess body fat itself increases inflammation, increases the white count? You’d have to find some way to get people to lose weight without changing their diet or exercise habit. How’s that possible? Liposuction. If you suck about a quart of fat out of people, you can significantly drop their white count by about a point. Perhaps this should get us to rethink the so-called normal reference range for white blood cell counts. Indeed, maybe we should revise it downward, like we’ve done for cholesterol and triglycerides.

Until now, we’ve based normal values on people who might be harboring significant background inflammatory disease. But, if we restrict it to those with normal C-reactive protein, another indicator of inflammation, then instead of “normal” being 4.5 to 10, perhaps we should revise it closer to 3 to 9.

Where do the healthiest populations fall, those not suffering from the ravages of chronic inflammatory diseases, like heart disease and common cancers? Populations eating diets centered around whole plant foods average about 5, whereas it was closer to 7 or 8 in the United States at the time. How do we know it isn’t just genetic? As you can see at 5:38 in my video, if you take those living on traditional rural African diets, who have white blood cell counts down around 4 or 5, and move them to Britain, they end up closer to 6, 7, or even 8. Ironically, the researchers thought this was a good thing, referring to the lower white counts on the “uncivilized” diet as neutropenic, meaning having too few white blood cells. They noted that during an infection or pregnancy, when more white cells are needed, the white count came right up to wherever was necessary. So, the bone marrow of those eating traditional plant-based diets had the capacity to create as many white cells as needed but “suffers from understimulation.”

As you can see at 6:26 in my video, similar findings were reported in Western plant eaters, with an apparent stepwise drop in white count as diets got more and more plant based, but could there be non-dietary factors, such as lower smoking rates, in those eating more healthfully? What we need is an interventional trial to put it to the test, and we got one: Just 21 days of removing meat, eggs, dairy, alcohol, and junk affected a significant drop in white count, even in people who started out down at 5.7.

What about patients with rheumatoid arthritis who started out even higher, up around 7? As you can see at 7:03 in my video, there was no change in the control group who didn’t change their diet, but there was a 1.5 point drop within one month on whole food plant-based nutrition. That’s a 20 percent drop. That’s more than the drop-in inflammation one might get quitting a 28-year pack-a-day smoking habit. The most extraordinary drop I’ve seen was in a study of 35 asthmatics. After four months of a whole food plant-based diet, their average white count dropped nearly 60 percent, from around 12 down to 5, though there was no control group nor enough patients to achieve statistical significance.

If white blood cell count is such a clear predictor of mortality and is so inexpensive, reliable, and available, why isn’t it used more often for diagnosis and prognosis? Maybe it’s a little too inexpensive. The industry seems more interested in fancy new risk factors it can bill for.

I touch on the health of the rural Africans I discussed in How Not to Die from Heart Disease.

For more on fighting inflammation, see:

In health,

Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live presentations: