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Health & Nutrition

Coconut oil

1. Many claims, little evidence
2. What's special about coconut oil?
3. The studies
4. Nutritional content and fat types
   a. MCTs: a lot less of them than claimed
   b. But it's a moot point for birds anyway
   c. Cholesterol risks for birds
   d. Diarrhea: the hidden "benefit" of MCTs
   e. Evolutionary factors?
5. How healthy are coconut-eating human populations?
   a. Isolated examples
   b. The big picture
6. Metabolism boosting fats
6. Impact on cholesterol levels
7. Antimicrobial indeed: it's 60% pesticide
8. Anti-inflammatory: not in a good way
   a. Acute inflammation
   b. Chronic inflammation
9. Ketones and brain function
10. The bottom line
11. Semi-related topic: red palm oil (RPO)

Many claims, little evidence

In recent years coconut oil has been heavily promoted as a "miracle food" for both humans and their pet birds.  But there is very little that has actually been substantiated, and most of the claims fall apart when you look at them closely. There is no clear evidence that coconut oil is either beneficial or harmful to humans, although our current knowledge suggests that there may be more harm than benefit. The "establishment" health authorities do not approve of it.

The "alternative" health claims tout the curative power of coconut oil for diabetes, cancer, Alzheimers, Parkinsons, autism, kidney and liver problems, digestive problems, immune function, infection prevention, weight loss, as a skin and hair conditioner, and more. Any time you see a long list of claims like this it's a red flag that there's probably a lot of exaggeration going on, and it's likely that the amount of truth in these claims is somewhere between zero and 10%. There's no doubt that coconut oil really does work well as a skin and hair oil.  But all the other claims are based on small short-term studies that found a modest benefit at best. Marketers are making massive assumptions and huge leaps of faith about long term benefits on the basis of a very limited amount of data, and they're not telling you about the studies that found no results or bad results. 

Coconut oil is composed primarily of fats that most birds do not eat in the wild, which means that their evolution may not have equipped them to deal with eating these fats. Although a small amount once in a while isn't likely to do any harm, there is a risk that consistently consuming these fats on a long term basis could be harmful to their health.

In short, it looks like coconut oil doesn't have any significant special properties.  It's really just a cooking oil with an exceptionally high level of saturated fat in it, and an exceptionally high level of marketing behind it. It doesn't provide any nutrients other than fat. It's best to view it the same way you look at other cooking oils and saturated fats in general. That's the quickie summary.  The rest of this article will explore the details and check out some of the health claims.

What's special about coconut oil?

Most of the fuss about coconut oil is related to its content of unusual saturated fats called medium chain triglycerides (MCTs). This is where most of the "magic" in coconut oil is supposed to come from. It's true that MCTs are metabolized differently than other fats, but the results of this are much more modest than what's being claimed.

The only natural foods that are known to contain significant amounts of these fats are coconuts, palm kernels, and milk (which contains much less than the coconut and palm kernels).  A small amount of MCT is presumably beneficial for infant mammals, since it's a minor component of their mother's milk. But the vast majority of birds don't consume MCTs at any time during their lives, and the effect that MCTs might have on them is unknown.

The studies

Websites belonging to representatives of the coconut industry at Coconut Research Center and have long lists of studies that supposedly prove that coconut oil provides special benefits. The lists don't include the studies that don't serve their marketing agenda, and the studies that do support the agenda are a lot shakier than they look.  A number of the links at the first site have no visible relationship to coconut oil at all. The second site is more on topic, but many of the studies listed here were (1) "glass dish" (in vitro) experiments, which are irrelevant because they tell us absolutely nothing about what happens in the body, and/or (2) studies on isolated, manufactured MCTs, not on coconut oil itself.  According to Eyres et al "Research on manufactured medium-chain triglycerides in the [scientific] literature cannot be applied to coconut oil because the triglycerides predominant in coconut oil are different in their structure, absorption, and metabolism." The predominant triglycerides in coconut oil are long chain trigycerides (LCTs), aka ordinary fat.

In addition, many of these studies used MCT in a way that is very different from the way people would consume coconut oil in real life, and it should not be assumed that eating coconut oil will produce the same results as manufactured medical-grade MCT in a laboratory setting.

It looks like the coconut industry's lists are all short-term studies on a small number of subjects, which is a very weak form of evidence.  As NeurologicaBlog explains, preliminary studies of traditional "natural" cures have a strong favorable bias that results in a large number of false positives.  Substances that look promising at first turn out to be ineffective most of the time when the more serious longer-term studies are performed. There don't seem to be any long term studies on MCTs or coconut oil at all, and there isn't enough data to make any assumptions about significant benefits or long term effects.

At present, the best evidence we have on the health value of coconut oil comes from a 2016 review by Eyres et al. They concluded that with regard to heart disease, the scientific studies to date do not show that coconut oil has any special beneficial effects, and its effect on cholesterol is likely to be detrimental.  In general it was found to be better than animal fat like butter, but worse than other types of vegetable oil like corn, soybean, and olive. They stated that

"No convincing evidence that consumption of coconut oil, as opposed to consumption of unsaturated oils, led to improved lipid profiles and a decreased risk of CVD [cardiovascular disease] was discovered during the literature search. Overall, the weight of the evidence to date suggests that replacing coconut oil with cis unsaturated fats would reduce CVD risk. Therefore, this review does not support popular claims purporting that coconut oil is a healthy oil in terms of reducing the risk of CVD. There was no evidence that coconut oil acted consistently different from other saturated fats in terms of its effects on blood lipids and lipoproteins."

"In summary, this review found no evidence that coconut oil should be viewed differently from other sources of dietary saturated fat with regard to dietary recommendations. This is in line with recommendations from the American Heart Association and the US Department of Agriculture’s Dietary Guidelines for Americans, 2010, which suggest that coconut oil is not preferable to other saturated fats."

"it appears that consuming cis unsaturated fat in place of coconut oil is likely to result in substantial reductions in the risk of CVD..."

"Studies suggest that the consumption of coconut products that contain fiber, such as coconut flesh and coconut flour, within a traditional dietary pattern that includes sufficient polyunsaturated fats (omega-3) in the absence of excessive calories from refined carbohydrates does not pose a risk for heart disease. In contrast, the excessive use of coconut oil as the major lipid in the typical Western diet produces effects similar to those of other saturated fats. Despite claims that coconut oil may reduce cardiovascular risk factors, this review found no evidence indicating that coconut oil is preferable to other unsaturated plant oils."

The American Heart Association released a Presidential Advisory in 2017 agreeing that consuming coconut oil doesn't seem like a good idea. Follow the link then click Download PDF to read the section on coconut oil (page 13 of the statement).

It looks like the general response of the pro-coconut oil contingent is to accuse the researchers and/or the AHA of corruption, implying that they are in the pockets of Big Pharma, which wants people to get heart disease so they can sell them drugs to treat it.  It really demonstrates the character of these fanatics that they would rather accuse a charity of cold-blooded slow-motion mass murder for the sake of profit than to admit that just maybe coconut oil might not be as marvelous as they've been told.

I wonder how many of the studies finding something good about coconut oil were funded by the coconut oil industry.  Funding studies for marketing purposes does happen sometimes. For example, POM Wonderful spent $40 million on studies about the benefits of pomegranate juice, then got in trouble with the FDA for overstating the results to the point that it constituted false advertising (Forbes, FDA Law Blog). It would be harder to nail the coconut oil industry this way since it does seem to be industry organizations (which don't sell coconut oil themselves) who are making the claims.  The FDA would have to catch a company that actually sells coconut oil in the act of making false claims, but the companies don't need to do this themselves because there are so many other people already doing it for them.

Side note:  the most-publicized pomegranate study (Seeram et al) found that POM Wonderful had more antioxidants than the fruit juice from apple, acai, black cherry, blueberry, cranberry, Concord grape, and orange, and also had more than red wine and a variety of teas.  What's not on the list?  Tomato juice and carrot juice are obvious omissions, in spite of being loaded with antioxidants and touted as health drinks for decades longer than some of the others.  So if you're looking for a high antioxidant beverage, there's reason to suspect that they might be better than pomegranate juice. You may think they taste better too. Most of the antioxidants in POM Wonderful apparently come from juicing the entire fruit including the peel, which has more antioxidants than the part of the fruit that's actually edible. Pomegranate peels are normally thrown in the trash because they're too disgusting to eat, and many people think that POM Wonderful tastes nasty because of the bitter flavor that the peel imparts.

Back on topic:  Today's Dietitian summarizes the evidence for a variety of coconut oil claims, including weight loss, heart disease, diabetes, and Alzheimer's disease.  The evidence is weak and it appears that any benefits are modest at best. 

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Nutritional Content and Fat Types  

All oils are a processed food. The oil extraction process strips away most of the nutrients in the original seed/nut, leaving you with a product that is essentially 100% pure fat with relatively small amounts of a few other nutrients. The dramatic difference in nutritional content can be seen in the USDA listings for coconut meat and coconut oil. The coconut meat contains protein, carbohydrates, fat, fiber, vitamins, and minerals.  The oil contains fat and a couple of vitamin remnants, nothing else.  It makes more sense to eat coconut meat than coconut oil; the meat has the oil in it plus a lot of nutrients that you don't get with plain oil.  In the real world, obesity and atherosclerosis are major health problems for both humans and pet birds.  Adding more fat to the diet is not going to solve the problem and will most likely make it worse. The claims to the contrary are unsubstantiated marketing hype.    

Four main categories of fats are found in foods, with several types of fatty acids in each category.  Omega 3 and Omega 6 fats are the polyunsaturated fats. They are essential nutrients; they can not be synthesized in the body and must be obtained from the diet. The Omega 9 fats are the monounsaturated fats, and the fourth category is saturated fat, which does not have an Omega number.  Saturated and monounsaturated fats are not essential nutrients because they can be synthesized in the body. Conventional wisdom says that polyunsaturated and monounsaturated fats are good fats and saturated fat is bad because of its role in heart disease, but this simplistic notion is currently being questioned and more research on the issue is needed.

Coconut oil is roughly 85-90% saturated fat; the exact percentage varies according to which source you look at (NutritionData, ChemPro, ChartsBin, Wikipedia), and some go a few points higher or lower than that. That's considerably more than butter, which is about 50% saturated fat (NutritionData) and lard, which is about 40% (NutritionData). Animal fat contains cholesterol and plant fat does not, but for humans at least it's believed that cholesterol in foods has considerably less impact on their blood cholesterol level than the amount of saturated fat in their diet does. The types and amount of carbohydrates in the diet may also have an influence since the body uses them to make cholesterol.

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MCTs: a lot less of them than claimed.  The hype says that coconut oil is 60-65% medium chain triglycerides, which has a grain of truth in it but is inaccurate overall. The real level of MCTs is much less than this.

In general, the hype doesn't make any distinction between a medium chain fatty acid (MCFA) and a medium chain triglyceride (MCT). There is a major difference between them, but it might not matter too much for discussion purposes, so this article will use the terms interchangeably. 

This is how fat digestion works for mammals. Most dietary fats enter the body in the form of triglycerides (3 fatty acid molecules attached to a molecule of glycerol). The small intestine breaks them down into individual fatty acids, and their digestive fate is determined at this stage. In general, a large percentage of the MCFAs enter directly into the liver through the portal vein, while most of the longer chain fatty acids are re-combined into triglycerides and incorporated into structures called chylomicrons, which travel through the lymph system to reach the bloodstream (FAO). Fatty acids don't always follow the typical route for their type however. For a specific fatty acid, a percentage of it will go one way and the rest will go the other way.

The problem comes with the way that the hype is defining an MCFA. Coconut oil's true and undisputed medium chain fatty acids are caprylic and capric acid, which together make up about 13-15% of coconut oil. Lauric acid makes up about half of coconut oil, and if it is counted as a medium chain fatty acid this raises the total MCFAs to the 60-65% level. But it's misleading to classify lauric acid this way for marketing purposes, because it doesn't accurately describe the way this fat works in the body. Lauric acid was designated as an MCFA a long time ago when fatty acids weren't very well understood, and nowadays it's technically acceptable to call it either an MCFA or an LCFA. But most of the time it acts like an ordinary fat, not an MCT, and it's often called a pseudo-MCT for this reason.  According to Eyres et al:

"In terms of digestion and metabolism, however, it [lauric acid] behaves more as a long-chain fatty acid because the majority of it (70%–75%) is absorbed with chylomicrons. In comparison, 95% of medium-chain fatty acids [capyrlic and capric acid] are absorbed directly into the portal vein... 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."

The percentage of lauric acid that's observed going through the portal vein varies considerably from one study to another.  Eyres et al based their statement on the study by Denke and Grundy, which seems to be the most comprehensive as well as one of the few that used human subjects instead of rats. So it's reasonable to use this percentage

If we assume that caprylic and capric acid are 13% of the total and that 30% of the lauric acid behaves like an MCFA, coconut oil is 27% MCT and 73% ordinary fat. Round it off to 25-30% MCT, and that's about as generous as an evidence-based estimate can get.

According to Eyres et al, only 4% of the triglycerides in coconut oil are MCTs. Strictly speaking, this is probably true. Fatty acids do not form triglycerides in an organized way, and a lot of the MCFAs will end up in a triglyceride that also contains LCFAs and does not meet the definition of an MCT. But this seems overly strict if it's correct that absorption occurs when the fatty acids are free and not bound into triglycerides.

Chemical of the Day has information on the process for making manufactured MCTs, which is an efficient way to obtain 100% MCTs instead of the much smaller percentage in coconut oil.  If you're still convinced of the benefits of MCTs at the end of this article, this is a better way to get them than using coconut oil.  Look for an MCT oil that contains only caprylic and capric acid, not lauric acid. And beware of the side effect described in the next section.

But it's a moot point for birds anyway. The previous section described the way that mammals process dietary fat, sending long-chain fatty acids through the lymphatic system in the form of chylomicrons, but sending MCTs directly to the liver via the portal vein. This special processing for MCTs is the entire foundation for the claims about coconut oil's alleged benefits.

Well, the way birds process fat is very different from the way mammals do it, and the discussion in the previous section doesn't apply to them.  Birds send ALL fats directly to the liver via the portal vein. For birds there's nothing special about the way MCTs are processed, so the whole house of cards just collapsed as far as the health claims are concerned.  Here are some relevant (and somewhat repetitive) quotes from the scientific community:

From Beaufrere, in the section of the paper called Peculiarities of Avian Lipoprotein Metabolism:

"as birds do not have a well-developed lymphatic system, triglycerides absorbed from the gastrointestinal system are transported directly to the liver via the liver portal system as portomicrons; chylomicrons are not present."

From the bottom of page 55 of Lipids and Their Metabolism (Stevens):

"With mammalian plasma lipoproteins, it is usual to distinguish the chylomicrons that transport exogenous [dietary] triglyceride from the intestine from the VLDLs that transport endogenous [internally produced] triglyceride from the liver, the former being larger and having a higher lipid content. In avian species, the VLDL class includes lipoproteins containing lipid of both endogenous and exogenous origins. Birds do not have a well-developed lymphatic system, and triglycerides absorbed in the small intestine are transported directly via the portal system to the liver as lipoprotein particles referred to as portomicrons."

From page 156 of Lipid Transport in the Avian Species Part 1 (Kelley & Alaupovic):

"The absorption of exogenous long-chain fatty acids in the avian species occurs exclusively by way of the portal vein. These fatty acids are transported from the intestine into the systemic circulation as triglycerides of VLDL. It has been suggested that, by analogy to mammalian chylomicrons, these avian lipoproteins rich in dietary lipids be named portomicrons."

From Dietary Fats and Performance (lecture notes by Prof. David Swanson of the University of South Dakota):

"Mammals: dietary fats absorbed as chylomicrons = lipoprotein complex of triglycerides, cholesterol, phospholipids, and β–lipoprotein. β–lipoprotein forms part of outer coat of complex. Taken up by lacteals (lymph vessels) that deliver dietary FA to circulatory system, which carries FA throughout the body.

Birds: dietary fats absorbed into hepatic portal vein as portomicrons = lipoprotein complex containing protein, triglycerides, cholesterol and phospholipids, with relatively high fat/protein ratio. Delivered by portal vessels to liver, where they can be metabolized and modified."

From Pearce:

"Lipid transport differs between birds and mammals because in chickens the absorbed lipid enters the portal blood system directly as very-low-density lipoproteins, whereas in mammals it passes into the lymph as chylomicra."

In case anyone hasn't gotten the point yet: the coconut oil health claims made for humans don't apply to birds, because birds process fats differently than humans do.

Cholesterol risks for birds. The fatty acid profile of coconut oil is very similar to that of palm kernel oil (Pantzaris & Ahmad). In a study on African grey parrots,  Bavelaar & Beynen found that a diet high in palm kernel oil significantly raised the birds' cholesterol levels, while a diet high in sunflower oil did not have this effect and neither did a diet that was low in either oil:

"Plasma cholesterol concentrations were found to be significantly higher when the parrots were fed the high-fat diet rich in saturated fatty acids (lauric and myristic acid) in the form of palm kernel oil. No difference in plasma cholesterol was found for the two low-fat diets versus the high-fat diet rich in the polyunsaturated fatty acid linoleic acid (in the form of sunflower oil). It can be concluded that, for low-fat diets, the type of dietary fat has no important influence on plasma cholesterol concentration. However, when a high-fat diet is given, polyunsaturated fatty acids versus saturated fatty acids may lower plasma cholesterol concentrations in parrots. A high-fat diet rich in polyunsaturated fatty acids may lower cholesterol to levels seen for low-fat diets. Thus, both the amount and type of dietary fat should be considered in relation to plasma cholesterol concentrations."

They conclude with "For the time being, it would appear advisable to use diets with up to 10% fat in the dry matter." Tree nuts and oil seeds are roughly 45-75% fat so you can hit that level really fast using those babies, but at least it's polyunsaturated fat. If you insist on feeding a lot of fat, at least have the decency to not do it with coconut oil. You're just begging for your bird to get heart disease if you do.

Diarrhea: the hidden "benefit" of MCTs.  The claims about the amazing benefits of MCTs usually fail to mention that it doesn't take very much MCT oil to give you hours of explosive diarrhea, often accompanied by other symptoms like nausea, vomiting, gas, cramps, and generally feeling like crap. A single tablespoon will do it for a lot of people if they aren't used to it, and less than that will cause problems for some. In general they warn you to work up to this stuff gradually, but even experienced users have problems sometimes. It can disrupt the digestive tract so much that some people report ongoing problems for weeks after they stop using the oil.  Here are some links on MCT diarrhea, chosen because the titles and/or text are hilariously lurid: FixYourGut, Ketogenic Forums, Keto, Bulletproof.

Regular coconut oil can also cause these problems (FussyBody, Mark's Daily Apple), although it might be less severe since the MCTs are a relatively small percentage of coconut oil. There have been some efforts to spin this diarrhea as a "detox" side effect that actually shows how beneficial coconut oil is, but this isn't credible so don't believe it.  The truth is that the body tends to react badly when you eat weird things that it isn't used to. MCTs are weird fats, but some people get used to them and some don't. There are some people who say they "love the whoosh", so if you're one of the few who actually enjoy diarrhea then MCT or coconut oil can be a way to have some fun.

Evolutionary factors? Most cultures in the world don't eat much of these medium chain fatty acids. No one knows how well these people can deal with large amounts of them, but the diarrhea associated with MCTs might be a clue.  Dairy products contain these fats too, but not nearly as much. According to Butter Through the Ages, butter contains 0.8% caprylic acid, 1.6% capric acid, and 5.8% lauric acid, while NutritionData says it's 1.2% caprylic, 2.5% capric, and 2.6% lauric. So butter has 6-8% total content of caprylic, capric, and lauric acid, versus 60-65% in coconut oil.

Different human ethnic groups tend to vary in their ability to tolerate different foods, for example many groups are lactose intolerant while people of European ancestry can usually digest lactose. This is an evolutionary difference based on the need to eat what was available in the local area. People who couldn't survive and reproduce using the available food resources were eliminated from the gene pool. There are many cultures in Southeast Asia and Polynesia whose ancestors have been eating a coconut-heavy diet for centuries. Europeans did not have access to coconut and relied on animal fat instead, or olive oil in the Mediterranean region.  They may be better adapted to the lower or nonexistent MCT levels in the fats their ancestors ate.

What about birds? Most of the fat in seeds and grains is polyunsaturated and monounsaturated.  The saturated fat content is usually less than 20% (often considerably less), and the MCT content is virtually nonexistent (chart). This is the type of food that most parrots are evolved to eat; I haven't looked into the type of fat that insectivorous birds consume. It doesn't seem wise to feed significant amounts of a radically different type of fat than what your birds would eat in the wild. They're probably less adapted to it than humans are.

Some of the larger cockatoos are known to eat young coconut in the wild, but young coconut has much less fat and much more carbohydrates than mature coconut (Coco Jack). So young coconut is really a very different type of food, with a nutrient profile more like a grain than an oil seed. We don't know whether its fatty acid profile is different from mature coconut, but in any case there's a lot less fat.

The oil of some palm kernels (aka palm nuts) has an MCT profile that is fairly similar to that of coconut oil, while other palm species contain much less.  But mature palm nuts are very tough and it appears that the hyacinth macaw is the only parrot that eats a lot of them.  The nuts are so tough that even the mighty hyacinth has to wait for the nuts to pass through the digestive tract of a cow before it's possible to crack them open.  The palm nuts eaten by the hyacinth are primarily from the acuri palm (Attalea phalerata) and the bocaiuva palm (Acromia aculeata). The MCT content of acuri palm nuts is not too different from coconut oil (Ghen page 35), but the bocaiuva palm kernels are primarily oleic acid (Omega 9) fat with only 13% lauric acid (Hiane et al).

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How healthy are coconut-eating human populations?

Isolated examples. The health claims for coconut oil include statements like "populations that eat a LOT of coconut are among the healthiest people on the planet". Does this reflect reality? The populations that are usually cited to support this claim are two obscure Polynesian tribes, the Kitavans (population 2300) and the Tokelauans (population 1500).  The abstracts for the papers indicate that both tribes were living a traditional subsistence lifestyle that is drastically different from the modern Western lifestyle (Prior et al, Lindeberg & Lund), and the only conclusion made about coconut was that it didn't appear to be harmful in the context of a traditional "Paleolithic" island lifestyle. So it's not logical or reasonable to point to one component of one specific item in their diet and give it credit for their apparent health, especially since the researchers didn't do any such thing. For that matter, we can't be sure that these tribes were really as healthy as claimed; the assessment was made based on simple, inadequate tests and anecdotal reports from the local population (Carb-Sane Asylum, Science-Based Medicine).

Even if they really were ridiculously healthy, it proves nothing about coconut oil because neither tribe used processed coconut oil (Eyres et al). They got their coconut fat from coconut meat and coconut cream (aka coconut milk). Extrapolating this to coconut oil is like saying you should consume corn oil because people who eat a lot of whole grains are healthy.

I've already discussed the major nutritional difference between whole coconut and coconut oil. The Eyres review also says,

"It has been hypothesized that the more favorable lipid profiles and lower mortality rates observed in coconut-consuming populations are due to the foods that constitute the rest of their traditional diets... Studies suggest that the consumption of coconut products that contain fiber, such as coconut flesh and coconut flour, within a traditional dietary pattern that includes sufficient polyunsaturated fats (omega-3) in the absence of excessive calories from refined carbohydrates does not pose a risk for heart disease. In contrast, the excessive use of coconut oil as the major lipid in the typical Western diet produces effects similar to those of other saturated fats. Despite claims that coconut oil may reduce cardiovascular risk factors, this review found no evidence indicating that coconut oil is preferable to other unsaturated plant oils."

"The extraction and use of coconut oil in edible applications is a relatively recent phenomenon. Furthermore, when earlier data were collected, coconut products were consumed as part of a traditional diet, which was characterized by a low intake of processed foods. Subsequent to this, a large shift toward the Western diet has occurred among many indigenous populations"

In other words, it's probably the general lifestyle and the other things in the diet that are providing the benefit, not the coconut oil. The paper points out a variety of inherent limitations in studies like this that make it difficult to rely on the results. 

The big picture.  But even if we assume that the studies on these indigenous diets are 100% accurate, why are coconut oil proponents using these tiny tribes as their example? There are hundreds of millions of people in Southeast Asia and Polynesia who use a lot of coconut oil and eat a lot of coconut in other forms. A large population is a more persuasive example than a small one, but when we look at the big picture the results aren't so pretty.   

Check out the World Life Expectancy website to look at a series of "cause of death" charts for every nation in the world, to see how the coconut belt compares to the United States or any other nation/region. Looking at diseases where coconut is said to provide benefits or where saturated fat may play a role, we see the following: the US has a higher rate of Alzheimers and Parkinsons and is generally higher for cancer.  The coconut belt has a higher rate of heart disease, high blood pressure (hypertension), stroke, ulcers, kidney disease, liver disease, and diabetes.

The World Health Organization's obesity chart shows that the US has a much higher obesity rate than the coconut belt, with the exception of some Polynesian islands that also have a high rate. WHO's tobacco use chart shows that some coconut belt nations have a higher smoking rate than the US and others have a lower rate.  Wikipedia's life expectancy map shows that the US life expectancy is 5 to 20 years longer than life expectancy in the coconut belt. World Life Expectancy has a more up-to-date map but it's harder to see the details and tell the colors apart, but it's obvious that there's still a major gap. Alzheimers, Parkinsons and cancer are diseases that are more likely to occur in older people, so our higher rate of these diseases might be due to our longer life expectancy rather than any protective effect of coconut oil. 

The first map at left from the World Health Rankings website shows coronary heart disease mortality rates based on 2011 WHO statistics, with "coconut belt" markings added by me (click on the thumbnails to see a larger image). The second map shows updated rates based on 2014 WHO statistics. The aging population and the obesity epidemic in the US are helping us catch up to the heart disease rates in the coconut belt nations (CNBC, CBS), but there are quite a few coconut-belt nations that are still worse than us.

This map from a 2011 paper by Kim & Johnston shows the "disease burden" rate, which includes the losses from both death and disability. The death rate is expected to be higher in countries where it's hard to get good medical care, so the combined rate in this chart should give a more accurate picture than the death rate alone.  This paper indicates that the disease burden rate usually follows the same pattern as the death rate. The countries that use a lot of coconut oil and/or palm oil tend to have a worse heart disease rate overall than the US or Western Europe.

There are many different factors that affect population health, so we can't assume that public health statistics (whether good or bad) are due to coconut oil consumption. Based on the data available to me, it looks like the poverty rate is probably a bigger factor in heart disease than how much fat you eat, what kind of fat you eat, the proportion of saturated and unsaturated fat, the obesity rate, or the smoking rate. Poor people have a higher risk of malnutrition and they also tend to have more stressful lives than people who are prosperous, and that's not good for your heart or your general health. But the global health statistics certainly don't make it look like coconut oil is protecting anybody from anything, and if there's something miraculous going on it's really hard to see it.

Metabolism boosting fats

The hype says that coconut oil will help you burn more fat and will boost your metabolism for hours after you eat it.  This is true, with a really big BUT.

What they don't tell you is that eating ANY kind of food will temporarily boost your metabolism above the resting rate, because it takes energy to digest food. The metabolic boost ends when digestion is complete, which frequently takes several hours. This is called the thermic effect of food, aka thermogenesis.

This isn't something that's unique to coconut oil, and eating fat is actually the least efficient way to boost your metabolism this way.  Carbohydrates boost it more than any fat (including MCTs), protein boosts it more than carbs, and alcohol boosts it most of all (Westerterp). 

It's meaningless in terms of weight control, because the number of calories in food is always greater than the number of calories that it takes to digest the food. You're adding calories to the body, not taking them away, and fat adds more calories than any other kind of food. See the Calories article for more information.

As for burning more fat: this is also technically true. Dietary fats are usually the last thing to be digested, so they're the nutrient that's most likely to be turned into body fat instead of being burned immediately for energy.  But the unique feature of MCTs is that they are digested ahead of everything else. Some of the fat has moved to the head of the line, so it's possible that you'll end up with leftover carb calories instead of leftover fat calories. These leftover calories will be turned into body fat in either case, so it doesn't make any difference. But technically you will have burned more fat because you changed the order in which calories are used.

I've seen people comparing the metabolism of MCTs to that of alcohol and sugar (Mark's Daily Apple). It's not really true, since the metabolic pathway is different, but it's the same general principle. If you're eating too much, the stuff that metabolizes fastest will be burned for energy, and the stuff that metabolizes slowest will be turned into body fat.  The total number of calories is what really counts, not the source of the calories.

MCTs have just slightly less calories than regular fats (8.3 calories per gram versus 9 calories per gram), and a lot more calories than carbohydrates or protein. This 0.7 calorie difference between MCTs and regular fat is the total amount of the extra metabolism boost from MCTs, because that's how much extra energy it takes to process MCTs compared to regular fats. The MCTs won't help you burn the calories that you get from other foods or the fat that's already stored in your body. They just let you eat empty fat calories that are slightly less fattening than usual. Butter (which is not pure fat like coconut oil) has only 7.2 calories per gram.

Most of the studies on the metabolism-boosting properties of coconut oil were actually conducted on manufactured MCTs, not on coconut oil itself (Clegg et al, Noguchi et al, Kasai et al, Baba et al, Hill et al). The amount of true MCTs in coconut oil is small, so if you consume coconut oil you won't be seeing very much of this slight calorie savings. In some cases, the coconut oil/MCT was more advantageous at first, but this advantage disappeared in two weeks and there was no difference after that (White et al, Papamandjaris et al-1, Papamandjaris et al-2). I wonder how much of this initial difference was due to the MCT oil giving people diarrhea in the beginning.  This does happen a lot, and it would certainly interfere with their ability to absorb calories and nutrients from food.

In general, the human weight loss studies involved overweight or obese subjects who lost a very small amount of weight over a period of several weeks or months, with a coconut oil or MCT group sometimes losing slightly more than the group consuming a different type of fat. Mumme & Stonehouse identified 13 studies lasting at least three weeks where the average weight loss was about a pound, and "commercial bias was detected" in some of them. Healthline summarizes the results for two studies including the duration and total weight lost; see #4 and 5 on their list. In one study, the coconut oil group lost lean mass as well as fat mass, which is not desirable (St-Onge & Bosarge). This was also the study with the greatest weight loss: about five pounds after four months.

Apparently none of these studies were holding their subjects prisoner, so they couldn't control for factors like cheating on the diet or breaking the study's rules in other ways, and not telling the researchers about it. Another study by St-Onge et al that DID more or less hold the subjects prisoner found that MCT increased their metabolism, but this did not lead to a measurable difference in their weight or body fat deposits.

With all these studies, there were no major differences between the groups in the end, so the results are not impressive at all. At best, these studies indicate that coconut oil is not much help if you want to lose a noticeable amount of weight and do it within a reasonably short time period. When it comes to satiety (feeling full for a long time), foods that are high in protein and/or fiber are usually recommended over fats. All these foods take a long time to digest, but high-protein and high-fiber foods are much lower in calories than the fats are, and they're better for you in other ways too.

Side note:  the claims about coconut oil being helpful for diabetes are based primarily on the very dubious assumption that coconut oil helps you lose enough weight to make a difference, and a couple of small, unimpressive rodent studies ( There's no real evidence at all for this claim, so don't take it seriously.

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Impact on cholesterol levels

The hype proudly proclaims that coconut oil increases your "good" HDL cholesterol, and it's true that it really does do this.  There's not as much publicity about the fact that it also increases your "bad" LDL cholesterol, for an overall increase in total cholesterol.  The HDL cholesterol increases proportionately more than the LDL does, but it would be unwise to assume that this change in the balance is beneficial and that the increase in total cholesterol is harmless. The health community is certainly not making that assumption, and this increase in total cholesterol is the reason that Eyres et al took such a dim view of coconut oil.

Calling HDL "good" is an oversimplification because HDL functionality is complicated.  There are several HDL subtypes; some are beneficial, some are neutral, and some have a negative effect. So having more HDL cholesterol isn't necessarily a good thing; a lot depends on the balance of the different HDL types, and higher HDL can actually lead to negative consequences sometimes (Chei et al, Sceptical Nutritionist, URMC, Harvard Health).

The American Heart Association issued an advisory document in 2017 agreeing with the Eyres review (at the website, click the Download PDF button to see the complete document). They summarize the current state of research into dietary fats and cardiovascular disease.  Page 13 discusses coconut oil's effect on cholesterol and rejects the notion that it is a healthy fat.  They conclude with "because coconut oil increases LDL cholesterol, a cause of CVD, and has no known offsetting favorable effects, we advise against the use of coconut oil." The whole thrust of the AHA document is that you should eat less saturated fat and more unsaturated fat. In effect, they have thrown coconut oil into the same bucket as butter or lard, and are telling you not to go crazy with any of them.

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Antimicrobial indeed: it's 60% pesticide

It's "fun fact" time: coconut oil is 60% registered pesticide, but you probably don't need to worry about it.  Most of the claims about coconut oil are a gross exaggeration of very modest preliminary research. But there is one claim about its fatty acids that has been substantiated beyond a reasonable doubt, and that is their antibacterial properties. Coconut oil is 7.1% caprylic acid, 6% capric acid, and 47.1% lauric acid (chart), and these are the same MCTs and pseudo-MCTs that everyone talks about so much. The first two are so effective that they’re registered as antimicrobial pesticides with the United States Environmental Protection Agency. Lauric acid is apparently not quite as strong; it’s registered as a pesticide with the state of California but not with the EPA. (EPA-caprylic, Pesticides Database-caprylic, EPA-capric, Pesticides Database-capric, Pesticides Database-lauric). That's 60% of the total content of coconut oil that is registered as a pesticide with a major government agency.

Caprylic acid is an industrial-strength commercial sanitizer according to Wikipedia:

"Caprylic acid is an antimicrobial pesticide used as a food contact surface sanitizer in commercial food handling establishments on dairy equipment, food processing equipment, breweries, wineries, and beverage processing plants. It is also used as disinfectant in health care facilities, schools/colleges, animal care/veterinary facilities, industrial facilities, office buildings, recreational facilities, retail and wholesale establishments, livestock premises, restaurants, and hotels/motels. In addition, caprylic acid is used as an algaecide, bactericide, and fungicide in nurseries, greenhouses, garden centers, and interiorscapes on ornamentals. Products containing caprylic acid are formulated as soluble concentrate/liquids and ready-to-use liquids."

Several other fats in coconut oil are said to have potential antimicrobial properties. But based on a not-too-thorough investigation, it looks like they are less potent than caprylic, capric, and lauric, and are not registered as pesticides anywhere. 

The antimicrobial effects occur when these fatty acids come into direct contact with microbes.  It hasn't been established whether these fatty acids have the same effect in natural coconut oil that they have when they're in an isolated (and probably manufactured) form. It's also not known whether they have the same effect in the body that they have in a laboratory dish or on a hard surface, which is a very different environment. 

You'd better hope that they don't have the same effect in the body; antimicrobial agents can't tell the difference between good microbes and bad, and if they are effective in the digestive tract they will wipe out the beneficial bacteria in the gut at the same time they're wiping out the bad bacteria. And a negative impact on gut flora actually has been observed with lauric acid (Haghikia et al).

Contact agents like this can only kill the microbes that they can physically touch. The pesticides in coconut oil might help kill microbes in food, in the digestive tract, or on the skin when applied there.  They can't kill microbes located elsewhere in the body, for example the bloodstream or the respiratory system. 

There are other foods with antimicrobial effects, like the capsaicin in chili peppers and the acid in vinegar or lemon juice.  So if you’re looking for a direct-contact antimicrobial without all the fat of coconut oil, you might want to consider one of these.  Keep in mind that all of them do have a downside and are harmful in excess.

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Anti-inflammatory: not in a good way

It is currently accepted that Omega 3 fats have anti-inflammatory effects, and the mechanism behind this effect is known (Calder). Coconut oil is also touted for its anti-inflammatory properties, although this is not generally accepted and its operating mechanism is unknown.  Unfortunately, it looks like coconut oil is more likely to promote inflammation and suppress the immune system than to provide a beneficial anti-inflammatory effect.

There are two main types of inflammation.  Acute inflammation is the body's first response to harmful external forces like injury, irritants, and pathogens. Swelling, redness, pain, and heat/fever are typical signs of acute inflammation. Acute inflammation isn't what people are worried about. It's not pleasant but it's temporary, and it's beneficial because it helps limit the damage caused by external events.  It's part of the body's natural defense system and it's supposed to happen.

The real concern is with chronic inflammation, a long-term condition that comes from having your biochemistry out of whack. The symptoms are generally less dramatic than acute inflammation, and it may be "silent" or show itself in less obvious ways. Chronic inflammation is essentially an immune system malfunction - the body is failing to heal itself or is fighting against itself. This is not supposed to happen. It can lead to various types of permanent damage, and is believed to play a role in serious autoimmune disorders like heart disease and cancer. 

Acute inflammation. The "anti-inflammatory" studies cited by the pro-coconuters deal with acute inflammation, not chronic inflammation. There were several studies where rats and mice were fed some form of coconut oil that was not necessarily natural, and then experienced less acute inflammation when heat or chemicals were used to induce injury and irritation (Zakaria et al, Intahphuak et al, Nair et al, Herrera).

Is this good news?  I wouldn't say so. The studies report the results as a desirable outcome, but why is it good to reduce the body's ability to respond to injury?  It sounds more like immune suppression than anything else. But the reason for the reduced inflammation hasn't been investigated so we can't really say what's happening. 

We frequently do try to reduce the symptoms of acute inflammation, without worrying about whether this is really a good idea or not.  But treating symptoms after they occur is smarter than keeping the immune system depressed all the time so we'll have fewer symptoms if we get hurt.

An MCT and coconut oil study by Carlson et al had similar results. The paper puts a positive spin on their effect, but it doesn't sound like it was actually beneficial.  The abstract says that the groups fed MCTs or coconut oil "demonstrated biochemical essential fatty acid deficiency" in addition to having a reduced inflammatory response to an endotoxin challenge. It says that the fish oil (Omega 3) group had a higher response to the challenge (suggesting that Omega 3 does not interfere with the body's initial response to injury, and may enhance it). The addition of MCTs to the fish oil group reduced this stronger response, so the MCTs may be offsetting the effect of the Omega 3.

There's also a very strange study where a mix of coconut oil, fructose, and hydrogenated fat was used to induce obesity in pigs, and it was observed later that the obese pigs had more beneficial bacteria in their vijayjays than the lean pigs (Newell-Fugate et al). The researchers attributed this gynecological triumph to the coconut oil, which is a very doubtful conclusion since coconut oil was not the only difference between the high fat diet and the control diet. In any case, intentionally getting fat with coconut oil is not a smart way to prevent vaginal infections.

There are studies saying that lauric acid applied to the skin can prevent acne (Nakatsuji et al, Huang et al). That's those undeniable antimicrobial properties at work, but topical applications are a world apart from actually eating the stuff.  It's obviously good news if it's true, although it's reported that putting coconut oil on the skin can cause acne in some people (AnnMarie) and just simply eating the stuff can cause outbreaks (Healthy Home Economist).  It's possible that some kind of allergic reaction may be involved in these cases.

Some of the other inflammation studies cited by the pro-coconuters aren't relevant because the study design was too wide or too narrow, like a multiple-ingredient glass-dish study by Ratheesh et al and an antioxidant study by Vysakh et al. There is no indication that the antioxidants in coconut oil are better than the antioxidants from any other source.

Chronic inflammation. The Omega 3 fats help prevent and eliminate chronic inflammation, and play a role in the resolution of acute inflammation (Calder, Mittal et al).  What does coconut oil do for chronic inflammation? That's definitely bad news. Coconut oil promoters don't tell you about this:

Haghikia et al found that lauric acid had a strong inflammation-promoting effect. Its effect on the gut flora disrupted the immune system of mice, and worsened the symptoms of multiple sclerosis.  Caprylic and capric acid promoted inflammation to a lesser degree. A negative effect was also observed on human cells in a glass dish.  The paper is difficult to understand, but there are plain-English discussions at Science Daily, Ben Greenfield Fitness, and Medical News Daily.  The direct negative impact on the immune system that was observed in this study reinforces the notion that a weakened immune response might be involved in the acute inflammation studies that were discussed earlier.

Radonjic et al found that an MCT-based diet could have an adverse effect on the inflammatory and metabolic status of men with upper body obesity. Gupta et al and Fritsche also report that lauric acid has strong inflammatory effects and that saturated fats in general promote inflammation. This seems to be generally accepted in the scientific community. But there's a silver lining to the cloud. Several of the sources listed here report that Omega 3 fats and propionic acid can reduce the inflammatory effects of lauric acid and other saturated fats. But contrary to what one of the sources says, propionic acid is NOT plentiful in vegetables.  It's primarily produced by bacteria in the gut (Nutrition Journal), and lauric acid's negative impact on gut flora might affect its production.

The cautions about individual components of coconut oil not necessarily performing the same way as whole coconut oil do apply here.  But the proportion of lauric acid in coconut oil is so high (about half the total) and the dose in the Haghikia study was so low (equivalent to a human eating two tablespoons of coconut oil a day) that a little concern may be warranted.

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Ketones and brain function

The brain normally uses blood sugar (glucose) as its energy supply, but when there's not enough glucose the body will use fat stores to produce ketones that the brain can use as an alternate energy source.  But medium chain triglycerides metabolize more easily than other types of fat, and tend to be transformed into ketones immediately and promptly burned for energy instead of being stored as body fat (Nutrition Review).

There is a reasonable amount of evidence that ketones can help improve brain function with certain types of neurological disorders including epilepsy (McNally & Hartman) and Alzheimer's disease, which involves an inability to use glucose normally (Henderson).  It's possible that ketones may be helpful with other types of neurological disease including Parkinsons disease, traumatic brain injury, and stroke (Maciej et al). It's been mentioned in connection with autism as well. But we can't assume that they'll do anything special for a brain that's functioning normally.

The traditional way to produce ketones is through a high-fat, low-carbohydrate ketogenic diet (Wikipedia), which keeps the glucose level low and forces the body to rely on ketones for energy. But medium chain triglycerides produce substantial amounts of ketones without the need for glucose suppression, which is a unique attribute; the metabolism of other fats doesn't normally have this result. Any kind of ketogenic diet requires the restriction of carbs and proteins, but the MCT ketogenic diet is slightly less strict than the traditional ketogenic diet  (Matthew's Friends).

This is the only claim about coconut oil that currently looks like it might actually have some validity to it. Research is still in the early stages (Snopes) but there is hope that it will eventually lead to new medicines for the treatment of brain disorders. The caprylic triglycerides in particular are the primary focus of MCT research, although capric triglycerides are also strongly ketogenic (Alzconnected). Unfortunately there is good reason to think that we shouldn't get our hopes up too high. A medically formulated MCT supplement called Axona appears to be only moderately effective, and a modified version called AC-1204 failed a clinical drug trial (Vocativ, Business Insider). Some people are attempting to use coconut oil as a cheaper substitute, which is not expected to produce better results (DeDea).  There are other lines of Alzheimers research that might be more productive than MCTs, particularly a hormone/protein called klotho (Science Daily, Los Angeles Times).

It's not clear how much future research we can expect on coconut oil and Alzheimers, since a clinical trial on the subject was cancelled in 2017 due to lack of participation.  They wanted to recruit 65 participants but could only find 21 (, Alzheimers Society). It looks like they did three years of work with the limited pool that they did attract before they ran out of money, but no results have been published.

The medical community and organizations like the Alzheimers Association do not encourage the use of coconut oil as a "do it yourself" treatment due to concerns about safety and effectiveness. The Alzheimers Society says that coconut oil could actually be detrimental to Alzheimers patients because it might increase the amount of an undesirable protein. 

As mentioned earlier, only a small percentage of the fat in coconut oil is expected to behave like an MCT. So even if MCTs actually turn out to be useful for brain disorders, a specially formulated MCT oil will probably be preferred over coconut oil, because you'd need a lot more coconut oil (with a lot more fat calories) to get the same results. 

An excessively high level of ketones in the body can be dangerous or even fatal. People on this forum thread reported alarming heart symptoms from consuming as little as two tablespoons of coconut oil per day. But this is a forum for people who are already on a ketogenic diet, and adding coconut oil may have resulted in an undesirably high level of ketones in the body.  People with a more normal diet who consume coconut oil are probably less likely to have problems. But it would be wise to consider the potential risks along with the potential benefits, and to be alert for problems related to blood pressure and heart function.  It's very doubtful whether inducing ketosis in the body could prevent neurological disease or improve the functioning of a healthy brain. 

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The bottom line

Coconut oil is just fat, people. Look at it the same way you would look at any other kind of cooking oil. MCTs metabolize a little differently than other fats but they're still just fat, not a magic potion. Coconut oil doesn't contain very much real MCT, and a healthy person doesn't need MCT in their diet anyway because the body can manufacture them if it needs them. 

Coconut oil might have modest benefits in some circumstances and it might be detrimental in others. But like any other fat it's not likely to do any harm if you don't go crazy with it, and watch your calorie consumption in general. It's fine to use some coconut oil if you like the taste and don't have a major risk factor like heart disease. 

But it's silly to eat it just because somebody with amazing marketing skills has convinced millions that it's a miracle food. There is absolutely no reason to give it to your bird, and your bird will be better off if you give it nutritious foods instead of empty fat calories. If you really really really want your bird to eat some coconut fat, give it a piece of coconut meat instead of the processed oil.  At least the bird will get some desirable nutrients that way, and it will be less likely to cause diarrhea.

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Semi-related topic: red palm oil (RPO)

We don't hear too much any more about red palm oil, also known as dende oil, since the RPO fad has mostly been superseded by the coconut oil fad.  But RPO has also been hyped as a marvelously healthy oil for both humans and birds. Dr. Oz pimped it rather belatedly in 2013, with all the quackery that is his hallmark (Science Based Medicine, McGill Office for Science and Society).  Alas, this hype wasn't justified either.  It can be argued that RPO is marginally less undesirable than coconut oil as a food for birds, but not much more than that. 

RPO is made from Elaeis guineensis, the same palm fruit that palm kernel oil comes from (which was discussed earlier).  But RPO is made from the fruit pulp, while palm kernel oil comes from the nut. Their fatty acid profile is quite different. Contrary to what some hype sites will tell you, RPO does not have the medium chain triglycerides (MCTs) found in coconut oil and palm kernel oil (MPOB). So MCTs were never the basis for the RPO hype; instead they rave about its nutrient content, along with miscellaneous claims about some unremarkable phytochemicals. Unlike most processed oils, which deliver empty fat calories and virtually nothing else, red palm oil contains a large amount of beta carotene (which the body processes into Vitamin A) and a moderate amount of Vitamin E.  Apparently that's all you get as far as nutrient content is concerned.  The original palm fruit contained some protein, minerals, and other vitamins (see the nutritional analysis in the Fruit article), but all this is stripped away when the fruit is processed into oil.  Processed oils are always nutritionally poorer than the original food source that they came from.

The RPO hype ignores the fact that Vitamin A is plentiful in vegetables and fruit, and Vitamin E is plentiful in most plant foods. The presence of these vitamins in RPO has real value in poor countries where calories are hard to come by, RPO is relatively cheap, and many people can't afford to buy both vegetables and cooking oil. But it's hard to justify the need for this oil in the Western world, where vegetables are a lot cheaper and more easily available than RPO is, and we need to reduce our calorie consumption not raise it. Like all oils, RPO is essentially 100% fat.  100 grams of RPO contains 929 calories, versus 10-100 calories in 100 grams of most vegetables (USDA Database, NutritionData).

Vitamin A. Exactly how much Vitamin A is in RPO?  That's kind of hard to say, but it's a lot. There isn't a standard, generic USDA analysis for RPO like there is for most foods. Most of the product labels just tell you a percentage of the Vitamin A requirement, with so much variation between them that it almost seems like a random number.  The few that tell you the number of IUs also vary wildly.  For example, Tropical Traditions says it has 8480 IU per tablespoon (14 grams), and that this is 200% of the daily value. Alaffia says it has 18,900 IU per tablespoon and this is 420% of the daily value. The daily value (which is not the same thing as the RDA) is 5,000 IU for everyone over the age of 4 (NIH), so the percents on the label are inaccurate.

Scientific sources indicate that red palm oil that has been refined to the point that it's reasonably edible but still retains its red color has roughly 500 ppm of carotenes, and that 80% of this is beta carotene (the only type that's relevant to Vitamin A) (Rao, AOCS).  That translates to 40,000 mcg of beta carotene in 100 grams of RPO, which is reasonably in line with the amounts reported for palm fruit in my fruit article. At the current USDA conversion rate of mcg*1.66=IU, that's 66,400 IU of Vitamin A in 100 grams of RPO.

100 grams of carrots has 16,705 IU of Vitamin A (NutritionData), so RPO has four times as much on a weight-for-weight basis.  But 100 grams of carrots has 41 calories, while 100 grams of RPO has 929.  Carrots give you 407 IU of Vitamin A per calorie, while RPO gives you 71.  Carrots are obviously a better deal for those who need to control their calorie intake.

Saturated fat. What about RPO's fatty acid profile?  The Malaysian Palm Oil Board says that the amount of desirable Omega 3 fats (C18:3) is close to zero. RPO is about 10% Omega 6 (C18:2), 39% Omega 9 (C18:1), and 50% saturated fat. This high level of saturated fat is not desirable. Most of the saturated fat is palmitic acid (C16:0), which is thought to be worse for your heart than other types of saturated fat (Harvard Health). Also see Chen et al for a study on how increased palm oil consumption correlates with increased heart disease. The Human Food Project has a plain-English report on a study by Laugerette et al, who found that mice on a high-fat diet did worse on palm oil than on any other fat that was tested, including dairy fat. It's not easy to do worse than dairy fat, but palm oil succeeded.

The comments that were made earlier about coconut oil and palm kernel oil also apply to red palm oil:  the countries that use a lot of it (primarily in Africa) tend to have a worse heart disease rate overall than the US and other Western countries. Smallstarter lists the African countries with the highest red palm oil consumption, and it's fun to see where they stand on World Health Ranking's heart disease mortality chart. The numbers will change as new data becomes available, but currently the rate per 100,000 is Angola 120.88; Benin 113.55; Cameroon 93.85; Cote D'Ivoire 98.02; Congo 111.88; Ghana 96.73; Guinea 94.03; Liberia 68.54; Nigeria 77.49; Sierra Leone 115.75; USA 77.97; UK 60.10; Canada 56.36; Australia 54.89. 

Vitamin E and tocotrienols.  RPO's Vitamin E content isn't nearly as spectacular as its Vitamin A content, but it does have a modest claim to fame because of the type of Vitamin E in it. Vitamin E comes in several different forms, and the most common form is tocopherol. Tocotrienols are a less common form, with four subtypes called alpha, beta, gamma, and delta. There have been limited studies indicating that tocotrienols may provide some special benefits, especially the delta form. Predictably, this was followed by an explosion of 'alternative' hype, with eager supplement makers ready and willing to sell you tocotrienol supplements (Life Extension Vitamin Institute). And never mind that there are questions about the bioavailability of tocotrienols (Fu et al).

RPO is the best food source of gamma and delta tocotrienol (Peatarian Review), but if you're interested in getting it you're really better off buying the supplements, and hoping that the bottle actually contains what it says on the label.  The recommended dosage varies (ExcelVite), but says that 80g of red palm oil (about 6 tablespoons) per day will provide a "biologically effective" amount. At 9.3 calories per gram, this means that you need to consume more than 700 calories every day of a food that contributes nothing to your nutrient needs except for calories, Vitamin A and Vitamin E, and basically drops a saturated fat bomb on your heart.  You're better off using that part of the calorie budget on foods that also provide nutrients like protein and calcium.

Parrots and palm fruit. There are a number of large parrots that are known to eat palm fruit in the wild, but details are lacking on how big a part of their diet it is, which parrots are eating fruit from which palms, and whether they're eating the fruit pulp, the seed, or both. Many wild parrots that feed on fruit are primarily interested in the seed, and throw the lower-calorie fruit pulp away.  But in general it looks like palm fruit is a high-calorie fatty fruit, so parrots consider the fruit pulp to be worthwhile whether they also eat the seed or not.

RPO is made from Elaeis guineensis, an African palm species, and African grey parrots do eat the fruit from this tree. Parrots who eat palm fruit on other continents will obviously be feeding on different palm species, whose fatty acid profile might be considerably different. For example, the fat content of Acrocomia aculeata is 70% Omega 9 (Lescano et al). This tree is also called the macaw palm, and its fruit is eaten by the blue-throated macaw. Evidently the blue-throat is eating the pulp not the seed - the bird is thought to be a seed disperser for the palm, and it couldn't be a disperser if it was eating the seed.  The hyacinth macaw has a bill strong enough to crush the nut and eat it, suggesting that smaller macaws aren't strong enough to eat the nut, and have to make do with the fruit pulp (Smith). See the Fruit article for more information on fruit eating by wild parrots.

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