By way of introduction, my name is Dr. Alvin Berger. I hold a MS, Ph. D, Post-doctoral NIH Fellowship, two Adjunct Professorships in Nutrition, and 30 years of industrial experience heading up nutrition and lipid (fat, oil) programs for large multi-national companies. Of all the fats I have studied over these many years, saturated fat as a class, but particularly coconut oil, is the most controversial. It is either considered a miracle fat or a poison. Let’s delve into the history and then the science supporting each position.
Historical aspects of fat consumption in humans: As a species, man is physiologically an omnivore, eating mixtures of fats, proteins, and carbohydrates, depending on availability of each source for survival purposes. Fat would have been a preferred energy source for early man, hunters and gatherers, and hunters prior to food industrialization (throughout the 1800s), since it provides more than twice the caloric density of carbohydrates and proteins. Also, some fats are essential meaning they cannot be made in the human body and must be consumed in the diet, such as linoleic (a fatty acid component of skin ceramides) and alpha-linolenic acids (ALA). Fats such as EPA and DHA, present in marine and algal oils, are conditionally essential, meaning some should be consumed intact in the diet, because for a variety of reasons, they are typically only minimally converted from dietary precursors, including ALA. These types of fats were important for the development and advancement of the human brain relative to other species, as DHA is a major structural component of our brains and the most abundant brain and retinal lipid [1]. Fats with missing double bonds (a non-methylene interrupted double bond position, termed NMIFA including Delta-5 NMIFAs) may also have been widely consumed in ancient diets as components of conifers and animals eating conifers, but have now been largely eliminated from our food supply during the course of industrialization. Delta-5 anti-inflammatory oils are now sold for skin use by SciaEssentials.com.
Saturated Fats 101
Now turning to saturated fats, fats such as butter and lard were considered a great energy source during World War II years, where the glycerin component was also used to make explosives [2].
In the 1980s, soybean oil (another interesting story) accounted for more than 70% of edible oil consumption and palm and coconut oils accounted for only 4% (coconutresearchcenter.org). Driven by endorsements from the Amercian Soybean Association and the consumer crusader Phil Sokolof, we experienced the tropical oil scare or tropical grease campaign. During this period, oils such as coconut oil and palm oils were considered to be poisoning America, and they proposed warnings on product labels.
The Dietary Guidelines for Americans Committee (DGAC) are a set of consumption guidelines published by the U.S. Department of Health and Human Services and U.S. Department of Agriculture (USDA), compiled by leading academic nutrition experts reviewing peer-reviewed literature. The 8th Edition, covering 2015-2020, recommends limiting calories from saturated fats (less than 10% of calories from saturated fat), consuming fat free or low fat dairy, and eating lean meats (source). Their conclusions are consistent with those of the American Heart Association (AHA), citing evidence that saturated fats are detrimental to heart health. They rely on the so-called lipid hypothesis, stating that there is a direct relationship between the amount of saturated fat and cholesterol in the diet and the incidence of coronary heart disease, as proposed by Ancel Keys in the late 1950’s. Numerous subsequent studies have questioned his data and the conclusions from his “Seven Countries Study” which relied on “fat disappearance” in an epidemiological study. Rather than saturated fat, Key’s famous graph associating fat and saturated intake with heart disease death across seven countries, could also be fitted to sugar consumption and mortality, in these same countries (source). Nathan Pritikin was a strong and respected advocate for low fat diets, although he recognized the many flaws in this approach (lack of energy, people could not stay on the diets). His diet called for elimination of sugar and processed foods, but it was the reduction in fat that received the most attention.
The latest guidelines recognize that some whole foods such as nuts rich in oils, or some fat-rich whole grains, and some monounsaturated (MUFA) and polyunsaturated (PUFA) oils are healthy (see page 25), but specifically calls out the tropical oils coconut oil, palm kernel oil (PKO), and palm oil as fats to avoid because of their high fat content. Saturated fats should be limited to 10% of calories per the latest guidelines. Oils are otherwise recommended to be consumed at a level of 27 grams (5 teaspoons), as part of a 2000 calorie diet. Cholesterol is associated with saturated fats in non-plant sources. It is noteworthy that the DGAC now recommends dropping limits on dietary cholesterol, citing no appreciable relationship between dietary cholesterol and serum cholesterol or clinical cardiovascular events in general populations; very early studies in rabbits were actually studying oxidized dietary cholesterol.
In sharp contrast to these DGAC recommendations, groups embracing so called “keto” and “paleo” lifestyles (and many other related terms), feel the DGA should be recommending much higher fat intakes, and not demonize saturated fats and tropical fats. They emphasize that decreasing our fat intake and saturated fat intake led to increased added sugar intake, did not decreased caloric intake, and worsened obesity, diabetes, and metabolic syndrome incidence.
Coconut Oil and Its History of Use
Coconut oil has been used as a food ingredient and in folk medicine for millennia in tropical regions where coconut trees grow (India, Phillippines, Sri Lanka, Malaysia, Polynesia, Indonesia). The oil attracted attention of European traders in the late 19th century, during a time of increased demand for edible oils and soap stock. Europeans established coconut plantations in the Caribbean, Southeast Asia, and South Pacific from 1890s-1920s and coconut oil was widely used as a cooking oil in Europe and the United States until 1940. During WWII, supply of coconut oil was cut off to the USA and the soy industry boomed (Coconut Oil Boom, Laura Cassiday, INFORM 27: 6-13, 2016). There are two main types of coconut oil. Copra is produced by crushing dried coconut kernels to extract the oil, and the oil may then be refined, bleached, and deodorized (RBD). Virgin coconut oil (VCO) is made by pressing shredded wet coconut kernels to squeeze out the oil and coconut milk to from an emulsion. VCO has higher concentrations of tocopherols, tocotrienols (forms of Vitamin E), and healthy polyphenols. Apart from the oil of coconuts, Pacific Islanders used to cook with coconut meat. Now that they cook with coconut oil, they have the worst rates of obesity in the world, although other factors can be involved. In Kerala State in India, they widely consume coconut oil, and have the highest average blood cholesterol level in India (Gupta et al. 2017)
Coconut Oil in the Recent Press: Poison or Miracle Fat
Coconut oil is either the panacea that helps everything from bad hair and mental grogginess to obesity and hemorrhoids; or a poison according to Karin Michels, an epidemiologist at the Harvard TH Chan school of public health (source). Michels poured scorn on the superfood movement and singled out the fad for coconut oil in particular, calling the substance “one of the worst things you can eat” that was as good for wellbeing as “pure poison.” Michels made her comments in a recent lecture entitled “Coconut oil and other nutritional errors” at the University of Freiburg, where she holds a second academic position as director of the Institute for Prevention and Tumor Epidemiology. The speech, delivered in German (translated here), has now been watched nearly a million times on YouTube! Michels based her warning on the high proportion of saturated fat in coconut oil, which is known to raise LDL (bad) cholesterol, and risk of cardiovascular disease. Coconut oil has 80-86%% saturated fat, twice the amount found in lard.
Last year [3], the AHA reviewed the evidence on coconut oil among other foodstuffs. While three quarters of the US public considered coconut oil to be healthy, the review noted that only 37% of nutritionists agreed that coconut oil was healthy. The authors attributed the gulf in perception to the marketing of coconut oil in the popular press. “Because coconut oil increases LDL cholesterol, a cause of cardiovascular disease [and stroke], and has no known offsetting favorable effects, we advise against the use of coconut oil,” the review concluded. Other organizations have issued similar warnings. “Coconut oil can be included in the diet, but as it is high in saturated fats should only be included in small amounts and as part of a healthy balanced diet,” the British Nutrition Foundation said. “There is to date no strong scientific evidence to support health benefits from eating coconut oil.” Despite the advice, promotions from health food shops and celebrity endorsements from Gwyneth Paltrow and others have helped sales of coconut oil surge. In the US, coconut oil sales appear to have peaked in 2015 at $229m.
Not all nutrition experts agree that coconut oil is harmful and should be avoided (source). Saturated fats in general tend to have been studied in flawed animal models and the aforementioned flawed Keys studies. They raise total cholesterol, but also raise good HDL cholesterol; and the type of LDL (bad) cholesterol raised, tends to be of the large, buoyant type, which is less strongly associated with CVD than small dense LDL particles.
A meta-analysis (compilation of different clinical studies) of 21 studies published in 2010 in the American Journal of Clinical Nutrition (AJCN) concluded that the “consumption of saturated fat had no observable correlation to heart issues.” It included 347,747 people, followed for an average of 14 years [4].
In another notable meta-analysis, the Prospective Urban Rural Epidemiology (“PURE”) study, offered a modern view of what a daily diet should look like, with higher fat-to-carb ratios than the long-standing status quo. Self-reported dietary data from 135,335 people in 18 countries was collected between January 2003 and March 2013, and grouped according to amount of carbohydrate, fat, and protein consumed. After tracking participants’ health over a seven-year period, researchers found that those with the highest intake of dietary fat (35% of daily calories; low relative to some countries) were 23% less likely to have died than those with the lowest intake of fat (10% of daily calories). Oppositely, for carbohydrates, those with the highest intake (77% of daily calories) were 28% more likely to have died than those with the lowest intake (46% of daily calories). From these findings the authors’ main conclusion is that “high carbohydrate intake was associated with higher risk of total mortality, whereas total fat and individual types of fat were related to lower total mortality” [5].“ Since the Harvard publication, contrarians are speaking out on the internet. Coconut oil has been safely used for hundreds of years and has been shown to have a number of health-promoting properties,” says Stephen D. Anton PhD, Associate Professor at the University of Florida’s Institute on Aging. “Specifically, coconut oil has been shown to increase the ratio of HDL to LDL and lower overall cholesterol count.”
Opinions of Dr. Berger on Coconut Oils for Nutritional and Personal Care Use
Nutrition: Early rodent studies testing coconut oil were flawed in that the coconut oil was often hydrogenated producing deleterious trans fatty acids; fed in excessive amounts without essential omega 3s; and to rodent species that are poor models for studying cholesterol metabolism (carry most cholesterol in their HDL particles rather than their LDL particles). We can also agree that the early Keys studies was flawed and that subsequent meta analyses and epidemiological studies were flawed or overstated against saturated fats including coconut oil.
I still do not encourage my customers and patients to consume more than 1-3 tablespoons coconut oil per day (see link).
Here is why:
Coconut oil is not a ketogenic fat: Despite what is in the lay press and being sold, recent work confirms that coconut oil is not a ketogenic fat [6]. This is not surprising because coconut oil only contains 10-15% of ketogenic C8/10 medium chain fatty acids (as medium chain triglycerides, MCTs), and 50+ percent C12 or lauric acid (similar compositionally to PKO). For more about MCTS, please see this link. In early textbooks, C12 was considered to be a long chain fatty acid (LCFA). In some more recent text books C12 (lauric acid), perhaps guided by commercial interests and publications, has been considered a MCFA, so that coconut oil can then be claimed to be ketogenic and anti-microbial. Lauric acid is metabolized mostly like other long chain fats in being oxidized or stored in body fat, rather than being preferentially converted to ketone bodies. Some parties claim coconut oil is ketogenic because they have a vested commercial interest, and others are are sponsored by Palm and Coconut oil Boards. In the recent study by Vandenberghe et al., nine healthy adults consumed 2 X 20 mL portions per day of emulsified MCT oils, consisting of coconut oil, C8 MCT oil, C10 MCT oil, C8/10 55:35 MCT oil, or coconut oil diluted 50:50 with the C8/10 or C8 oils. Blood was sampled every 30 min for 8 hours in a cross-over design. C8 MCT oils were the most ketogenic of the MCTs with highest blood ketones. Other MCT oils tested were less ketogenic than C8. A dose-response could only be shown for C8 MCT, suggesting it is C8 in MCTs that drives the ketogenic response. C10 was not a very ketogenic. Coconut oil alone had a minor effect on increasing ketones, and only after 4-8 hours when no meal was provided (during this same time with food, C8 MCT was 3.4-fold more potent). Coconut oil mixed with C8 MCT oil reduced the ketogenicity of C8 MCT oil by 75% as expected. Coconut oil was not more ketogenic after 7-8 hours than the control-some increase in ketones due to fasting observed.
Coconut oil is not antimicrobial in vivo: Despite the plethora of internet claims and some scientific literature, the so-called “anti-microbial” properties of lauric acid and lauric acid bound to glycerol, have not been demonstrated in vivo (in living people). When PKO or coconut oil is consumed, the C12 is bound to glycerol to form triglycerides. The C12 as a free fatty acid or monglyceride is generated during digestion when acted upon by lipases, and the rapidly re-esterified to triglycerides and carried in chylomicron particles in the lymph system, and eventually deposited into fat adipose tissues. So, there are several issues in claiming C12 is antimicrobial. First, any killing properties of lauric acid were demonstrated for the free acid or monoglyceride form (MAG), not the digested triglyceride (TAG) form. Second, the anti-microbial properties of lauric acid as a FFA or MAG were found to occur in test tubes or other experimental ex vivo systems outside the living body. Third, people confuse the well-established food preservative microbial-killing properties of lauric acid as a FFA or MAG, with the ability to kill organisms in vivo in humans. Fourth, with the recognition that many microbes are good for us in the human gut (and on the skin), it is a vast over-simplification to speak of “anti-microbial” properties so broadly. Fifth, assuming there were anti-microbial properties, we need to establish, in vivo, not only that harmful organisms are killed, but that the level of killing has physiological relevance. Last, what dose of lauric acid would be needed to have positive anti-microbial properties in vivo. So called “oil pulling” or swishing coconut oil in the mouth to kill microbes, popular in traditional Indian culture and now the USA, has no proven efficacy beyond anectodes. Claims made for coconut oil having benefits for the skin are in some cases also flawed, because there is focus on the anti-microbial properties of lauric acid, without recognition that lauric acid in the free form or MAG form would only be generated upon skin lipase action, which is largely of microbial nature.
Coconut oil can have a soapy taste and other QC issues: Since soap is sodium dodecyl (C12) sulfate (SDS), or sodiumlauroylsulfate, if lauric acid is present as a free fatty acid (free fatty acids do occur in coconut oils), and has opportunity to react with sodium and sulfate, then soaps are formed. In our household, we have had soapy coconut oil in the house, and the taste was quite terrible. It is published that coconut oil in contact with water generates rancid coconut oil that is not suitable for oral and cosmetic applications. Coconut oil can also be adulterated, with PKO or RBD coconut oil added to virgin coconut oil to cut costs.
Crude Coconut Oil May Not Be Healthier Than Processed Coconut Oil
Polycyclic aromatic hydrocarbons (PAHs) are formed by combustion and thermal decomposition (pyrolysis) of organic substances in coconut shells. Some PAHs are highly carcinogenic such as benzo-[a]-pyrene and dibenzo-[a,h]-anthracene. It is reported that crude, less refined coconut oils can have higher levels of PAHs and that PAHs are mostly or completely removed during oil refining [7]. Processing of palm oils is also reported to decrease PAHs in most cases. Moreover, in developing countries of South Asia, PAH concentrations are strongly influenced by the monsoonal rainfall system in the region and it has been supported by many studies that higher concentrations were measured during the winter season as compared to summer. Biomass burning (household and brick kilns activities), open burning of solid wastes and industrial and vehicular emissions were categorized as major sources of PAHs in the region [8]. I have heard from reliable sources, that burning of car tires in the vicinity of coconut oil production, also generates PAHs. So PAHs can become incorporated into coconut oils from a variety of sources. Overall, then the consumer purchasing virgin or less processed coconut oils, must have a deep understanding of the source they are purchasing and ask to see analytical results on PAHs and other contaminants.
References:
- Crawford, M.A., The early development and evolution of the human brain. Ups J Med Sci Suppl, 1990. 48: p. 43-78.
- Walker, T.B. and M.J. Parker, Lessons from the War on Dietary Fat. Journal of the American College of Nutrition, 2014. 33(4): p. 347-351.
- Sacks, F.M., et al., Dietary Fats and Cardiovascular Disease: A Presidential Advisory From the American Heart Association. Circulation, 2017. 136(3): p. e1-e23.
- Mensink, R.P., et al., Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials. Am J Clin Nutr, 2003. 77(5): p. 1146-55.
- Dehghan, M., et al., Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. The Lancet, 2017. 390(10107): p. 2050-2062.
- Vandenberghe, C., et al., Tricaprylin Alone Increases Plasma Ketone Response More Than Coconut Oil or Other Medium-Chain Triglycerides: An Acute Crossover Study in Healthy Adults. Current Developments in Nutrition, 2017. 1(4): p. e000257-e000257.
- Wijeratne, M., U. Samarajeewa, and M. Rodrigo, Polycyclic aromatic hydrocarbons in coconut kernal products. Journal of the National Science Foundation of Sri Lanka 1996. 24(4): p. 285-297.
- Hamid, N., et al., A Review on the Abundance, Distribution and Eco-Biological Risks of PAHs in the Key Environmental Matrices of South Asia. Rev Environ Contam Toxicol, 2017. 240: p. 1-30.