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:

Arsenic in Infant Rice Cereal

When it comes to rice and rice-based products, pediatric nutrition authorities have recommended that arsenic intake should be as low as possible.

“The US Food and Drug Administration (FDA) has been monitoring the arsenic content in foods” for decades, yet despite the “well-established science describing the health risks associated with arsenic exposure, no standards have been set limiting the amount of arsenic allowable in foods” in the United States. In 2001, the EPA “adopted a new stricter standard for arsenic in drinking water,” and in 2013, the FDA proposed a legal limit for apple juice. “There are still no standards for arsenic in food products despite the fact that food sources are our main source of exposure.”

Unlike the United States, China has standards. As of 2014, China set a maximum threshold of inorganic arsenic at 150 parts per billion, stricter than the World Health Organization’s limit of 200 ppb. In the United States, a 200 ppb limit wouldn’t change the cancer risk much. If we had China’s safety limits of 150 ppb, though, cancer risk would be reduced up to 23 percent and a maximum threshold of 100 ppb would lower cancer risk up to 47 percent—but that could seriously affect the rice industry. In other words, U.S. rice is so contaminated with arsenic that if a safety standard that really cut down on cancer risk were set, it “would wipe out the U.S. rice market.” However, with no limits, what’s the incentive for the rice industry to change its practices? Setting arsenic limits would not only directly protect consumers but also encourage the industry to stop planting rice paddies on arsenic-contaminated land.

Those cancer estimates are based on arsenic-contaminated water studies. Might the arsenic in rice somehow have a different effect? You don’t know…until you put it to the test. We know rice has a lot of toxic arsenic that urine studies have shown we absorb into our body, but there hadn’t been any studies demonstrating “deleterious health impacts” specific to rice arsenic—until now. Since arsenic causes bladder cancer, the researchers figured they would see what kind of DNA mutations the urine of rice eaters can have on human bladder cells growing in a petri dish. And, indeed, they clearly demonstrated that eating a lot of arsenic-contaminated rice every day can “give rise to significant amounts of genetic damage,” the kind that‘s associated with cancer. Yes, but the study used pretty contaminated rice. However, only about 10 percent of the rice in certain parts of Asia might ever reach those levels of contamination, though a quarter of rice in parts of Europe might and more half in the United States, making for considerable public health implications.

So, “there remains little mystery surrounding the health risks associated with arsenic levels in rice. The remaining mystery is why long-overdue standards for arsenic levels in rice have not been set by the FDA” in the United States, but that may be changing. In 2016, the FDA proposed setting a limit on toxic arsenic—at least in infant rice cereal, which I discuss in my video Arsenic in Infant Rice Cereal.

As you can see at 3:24 in my video, infants and children under four years of age average the highest rice intake, in part because they eat about three times the amount of food in relation to their body size, so there’s an especially “urgent need for regulatory limits” on toxic arsenic in baby food.

Pediatric nutrition authorities have recommended that when it comes to rice and rice-based products, “arsenic intake should be as low as possible,” but how about as early as possible? Approximately 90 percent of pregnant women eat rice, which may end up having “adverse health effects” on the baby.

You can estimate how much rice the mother ate while pregnant by analyzing arsenic levels in the infant’s toenail clippings. “Specifically, an increase of 1/4 cup of rice per day was associated with a 16.9% increase in infants toenail [arsenic] concentration,” which indicates that arsenic in rice can be passed along to the fetus. What might that arsenic do? A quarter cup of rice worth of arsenic has been associated with low birth weight, increased respiratory infections, and, above that, a 5- to 6-point reduction in IQ, among other issues. So, “based on the FDA’s findings, it would be prudent for pregnant women to consume a variety of foods, including varied grains (such as wheat, oats, and barley),” which is code for cut down on rice. Saying eat less of anything, after all, is bad for business.

Once the baby is weaning, “what’s a parent to do?” Asks Consumer Reports, “To reduce arsenic risks, we recommend that babies eat no more than 1 serving of infant rice cereal per day on average. And their diets should include cereals made of wheat, oatmeal, or corn grits, which contain significantly lower levels of arsenic”—that is, rely on other grains, which are much less contaminated than rice. As the American Academy of Pediatrics has emphasized, “there is no demonstrated benefit of rice cereal over those made with other grains such as oat, barley, and multigrain cereals, all of which have lower arsenic levels than rice cereal.” As you can see at 5:28 in my video, reducing consumption of infant rice cereal to just two servings per week could have an even more dramatic effect on reducing risk.

 The proposed limit on toxic arsenic in infant rice cereals would end up removing about half of the products off the shelves. The FDA analyzed more than 500 infant and toddler foods, and the highest levels of toxic arsenic were found in organic brown rice cereals and “Toddler Puffs.” Based on the wording in the report, these puffs appear to be from the Happy Baby brand. Not-so-happy baby if they suffer brain damage or grow up to get cancer. A single serving could expose infants to twice the tolerable arsenic intake set by the EPA for water. I contacted the Happy Baby company and was told they “are not able to provide any comments” on the FDA’s results.

“Eliminating all rice and rice products from the diets of infants and small children up to 6 years old could reduce the lifetime cancer risk from inorganic arsenic in rice and rice products by 6% and 23% respectively.” That is, there would be a 6 percent lower chance of developing lung or bladder cancer later in life if infants stopped, and a 23 percent lower chance if young kids stopped. However, switching to other grains is a move described as “drastic and dramatic,” creating “a huge crisis”—for the rice industry, presumably—and therefore “not feasible at all.”

I was hoping Happy Baby, upon learning of the concerning FDA arsenic toddler puffs data (regardless of whether the data were about its brand or not) would have kicked its own testing and potential remediation into high gear like Lundberg did (see Which Brands and Sources of Rice Have the Least Arsenic?). But, unfortunately, in my email correspondence with the company, I got no sense that it did.


For more videos on this topic, see:

And here are five more:

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:

The Role of Meat and Dairy Viruses in Cancer

“Nearly 20% of cancer cases arising worldwide can be linked to infectious agents, including viruses.” Seven viruses are now conclusively tied to human cancers, and, as new viruses enter into human populations, the incidence and causes of cancer will likely change accordingly.

The foundation of modern tumor virology was laid more than a century ago with the discovery of a cancer-causing chicken virus, for which a Nobel Prize was awarded. Another Nobel Prize went to the “medical doctor-turned-virologist” who discovered that the HPV virus was causing cervical cancer. In his acceptance speech, he mused that there may be a bovine polyoma virus—a multiple tumor virus in cattle—that could be playing a role in human colon cancer, lung cancer, and breast cancer, but no polyoma virus had ever been discovered in meat…until now.

As I discuss in my video The Role of Burger Viruses in Cancer, polyomaviruses are a particular concern—not only because they are known to be carcinogenic, but also because they can survive cooking temperatures. Since a single burger these days can contain meat from “many dozens of animals,” researchers felt “this could present an ideal situation for virus-hunting…” Researchers from the National Cancer Institute purchased meat samples from three separate supermarkets and found three different polyomaviruses in ground beef, as you can see at 1:52 in my video. Now, just because three types of “polyomavirus species are commonly detectable in food-grade ground beef” doesn’t necessarily mean they are causing human disease. What made this Nobel laureate suspect them? Well, for one thing, some people got cancer right where they had been vaccinated for smallpox—a whole bunch of different cancers, in fact. The vaccine had been harvested from the skin of calves, so “it is possible” there could have been some cancer-causing cow virus.

“Many people are exposed to potentially virus-contaminated meat and dairy products” through their diets, but those in the industry, “such as farm workers, butchers, veterinarians, and employees in dairies,” would be even more exposed. Do these groups have higher cancer incidence? Indeed, it now appears to be clear “that workers in the meat industry are at increased risk of developing and dying from cancer.”

Another reason to suspect the involvement of some kind of bovine infectious factor in colorectal cancer is the fact that there appear to be relatively low rates of colorectal cancer in countries where not a lot of beef is eaten. And, when meat consumption suddenly increases, rates shoot up, as you can see at 3:15 in my video. “The only exception is Mongolia where they have low rates of colon cancer and eat a lot of red meat, but there they eat yak.” Maybe yaks don’t harbor the same viruses.

Can’t you just avoid steak tartare? Even steak cooked “medium” may not reach internal temperatures above 70° Celsius, and it takes temperatures higher than that to inactivate some of these viruses, so we would expect viruses to survive both cooking and pasteurization. In fact, researchers followed up with a paper suggesting the consumption of dairy products may “represent one of the main risk factors for the development of breast cancer” in humans. The recent discovery of a larger number of presumably new viruses in the blood, meat, and milk of dairy cows should be investigated, since one might speculate that infectious “agents present in dairy products possess a higher affinity to mammary [breast] cells,” since they came from breast cells. The fact that people with lactose intolerance, who tend to avoid milk and dairy throughout their lives, have lower rates of breast and other cancers could be seen as supporting this concept. Though, there are certainly other reasons dairy may increase cancer risk, such as increasing levels of the cancer-promoting growth hormone IGF-1 or adversely affecting our gut microbiome. Or, for that matter, maybe the plant-based milks they’re drinking instead could be protective. That’s the problem with population studies: You can’t tease out cause and effect. It doesn’t matter how many viruses are found in retail beef, pork, and chicken, as you can see at 5:16 in my video, if we can’t connect the dots.  

Can’t we just look for the presence of these viruses within human tumors? Researchers have tried and did find some, but even if you don’t find any, that doesn’t necessarily mean viruses didn’t play a role. There’s a “viral hit-and-run” theory of cancer development that suggests that certain viruses can slip in and out of our DNA to initiate the cancer, but be long gone by the time the tumor matures.

There’s still a lot of work to be done. But, if the link between bovine polyomaviruses and human disease pans out, the National Cancer Institute researchers envision the development of a high potency vaccine. So, just like the HPV vaccine may prevent cervical cancer from unsafe sex, perhaps one day, vaccines may prevent breast and colon cancer from unsafe sirloin.


This reminds me of the story of bovine leukemia virus and breast cancer. For more on that, see:

What about chicken? Check out The Role of Poultry Viruses in Human Cancers and Poultry and Penis Cancer.

One of the problems with eating other animals is that we put ourselves at risk of their diseases. Not once have I diagnosed anyone with Dutch Elm Disease or a really bad case of aphids. See Eating Outside Our Kingdom for more on this concept.

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: