Opening the Coconut Oil Can of Worms Part Two

THE EVIDENCE

Risk of heart disease

There is a lack of large, well-controlled human studies exhibiting that coconut oil causes either a reduction or an increase in cardiovascular disease. On the other hand most randomized controlled trials on the subject agree that the ingestion of coconut oil causes increased RISK FACTORS for heart disease. Consuming coconut oil raises total cholesterol, LDL-cholesterol and HDL-cholesterol and its removal from the diet reduces those same levels (7,35,36,37,38).

Whole coconut products tell a slightly different story. Coconut oil proponents point out that in places where coconuts naturally grow and where large quantities of coconut products are consumed, the residents enjoy low rates of heart disease. For instance, on Kitava, a traditional Melanesian island, the diet in 1993 centered around sweet potatoes with added fruits, greens, nuts, corn, beans and whole coconut. Residents’ rates of stroke and heart disease were very low (2). Research in 1981 on residents of a Polynesian island, Pukapuka, and those of the Tokelau island group, found that the local diet included substantial amounts of whole coconuts. The cholesterol levels of these populations were high, reflecting the high level of fat in their diet. Their rate of heart disease was uncertain as that portion of the analysis of this study was inadequate and inconclusive (3).

It is important to remember that whole coconut is metabolized in the body very differently than the extracted oil. Whole coconut flesh contains soluble and insoluble fiber and protein, all of which moderate blood cholesterol levels. In addition, the diets eaten on the tropical islands were essentially plant-based. They included no dairy products and meat was eaten very infrequently. Moreover the fiber content was very high. Studies show that even ingesting psyllium fiber along with coconut oil results in significantly less of an increase in blood LDL-cholesterol compared to eating coconut oil alone (4). The island diets were also high in protective omega-3 fats as well as being low in sodium and cholesterol. These people were physically active, did not smoke and were free from obesity, diabetes and high blood pressure. The influence of these healthy lifestyle factors would certainly play a major role in the prevention of cardiovascular disease and the maintenance of overall health in the islanders (2,3).

Another study looked at eating whole coconut product with a twist. This double-blind randomized 2004 study fed defatted coconut flakes to people with moderately-raised blood cholesterol. It demonstrated that eating this coconut by-product resulted in a 7 to 10% reduction of their blood total cholesterol and LDL-cholesterol (1). In this case the lack of fat in the product used would undoubtedly influence changes in cholesterol levels.
And then there are MCT oils which are composed of solely medium chain triglycerides. (Triglycerides are compounds containing three chains of fatty acids). Some studies have shown that MCTs raise cholesterol by about the same amount as olive oil (40). Advocates of coconut oil cite references to this research, suggesting that coconut oil is full of MCFAs and would have the same effect as MCT oil. However, MCT oil is composed of pure MCFAs, about 50% each of caprylic and capric acid, while coconut oil contains only about 15% of these two medium chain fatty acids. It is clear that research on MCTs cannot be extrapolated to coconut oil whose main component is the longer chain fatty acids, lauric, myristic and palmitic which have potent LDL raising effects (5,6,7).

Let’s boil all this research down to some practical information that we can use in our lives.
Coconut oil increases levels of total cholesterol and LDL cholesterol, known risk factors for heart disease.
MCT oil does not cause such a large increase in harmful cholesterol as coconut oil but it is not at all the same entity as coconut oil and should not be considered as such.
Eating limited amounts of coconut in its whole form can be part of a healthy diet.

Bottom line – Eating coconut oil does not decrease heart disease.

 

Increasing HDL

A 2016 review shows that the level of HDL (“good” cholesterol) in the blood is significantly higher when eating coconut oil (7). This might be considered a health benefit of coconut oil. However, new insight into the activity of HDL tells a different story.

Though high HDL is linked with less cardiovascular disease, it is not the driving force behind heart disease protection. An offshoot of the Framingham Study monitored cholesterol levels and cardiovascular disease risk for 3,590 participants and concluded that high LDL and/or high TG (triglycerides) are the lipid components predictive of heart disease risk regardless of the HDL level (8). There is increasing evidence that it is the quality and not the quantity of HDL that is important. High functioning HDL particles have the ability to remove cholesterol from the body as waste and to normalize artery wall endothelial function thereby reducing oxidation and inflammation. However, in a state of chronic inflammation such as occurs in cardiovascular disease, atherosclerosis, metabolic disorder, chronic renal disease, diabetes or arthritis, the HDL is not functioning well. Transport of cholesterol out of the body by HDL is interrupted and the HDL particles actually support oxidation of cholesterol and fuel the inflammatory process. (9,32,33,34). The association of high HDL with less cardiovascular disease stems from healthy people whose HDL is working well.

This finding has been corroborated in numerous ways. For example, people who genetically have lifelong high HDL levels do not have a lower risk of heart attack (11). Drugs such as torcetrapib, administered to increase HDL levels, have not been shown to have any effect on atherosclerotic plaques in the carotid or coronary arteries nor have they shown any improvement in cardiovascular outcomes. In fact torcetrapib actually increased cardiovascular events and total mortality, leading to its discontinuation (9,12,13,14,15). Another drug, niacin, increases HDL by up to 25% but two large randomized controlled trials have shown that niacin does not decrease the incidence of cardiovascular events and may also have significant adverse effects (16).

Bottom line – The increase in HDL from coconut does not translate into a health benefit.

 

Treating or preventing Alzheimer’s Disease

Alzheimer’s Disease is another area in which health claims for coconut oil are rampant however such assertions are not supported by any large peer-reviewed clinical trials. “Any positive findings are based on small clinical trials and on anecdotal evidence.” (19).

There have been some human studies undertaken using caprylic acid (a MCFA) to improve cognitive function. The theory is that caprylic acid induces a mild ketosis which increases energy in the brain by bypassing the slow glucose metabolism that is a feature of Alzheimer’s Disease. Further well-designed and executed research is needed to substantiate this effect. However, any consequence of a high level of caprylic acid cannot be transferred to coconut oil which contains only about 7% caprylic acid (20).

A randomized, double-blind, placebo-controlled study looked at Alzheimer’s Disease using, not coconut oil, but a proprietary blend of MCTs and LCTs. Slight improvement was seen in some patients, but only in those who did not harbour the gene mutation ApoE4 that increases risk of Alzheimer’s Disease. Even within this group lacking ApoE4 the beneficial effect disappeared once the study was properly randomized (21).

Searches of the literature reveal no human studies using coconut oil itself in people suffering from cognitive impairment or in healthy people (20).

Bottom line – At this point in time there is no reason to believe that coconut oil is of any use in preventing or treating Alzheimer’s Disease.

 

Promoting weight loss

The main research cited by coconut oil supporters for its benefits in weight loss was completed in 2003 by scientists at Cornell University Medical School. Researchers compared the effects of diets rich in MCFAs to those high in LCFAs upon losing weight and found that people eating more MCFAs lost an extra pound of weight after a month compared to participants consuming more LCFAs. Delving into the details of this research makes it clear that the MCFAs used in this study came not from coconut oil, with its low level of 15% MCFAs, but from a manufactured MCT oil which was composed of 100% MCFAs. Lead researcher Dr. Marie-Pierre St-Onge herself states that using her research to say that coconut oil increases weight loss is a “very liberal extrapolation of what we’ve actually studied” (22).

Subsequent studies have made similar claims. Still, the devil is in the details and when these studies are looked at closely the sources of confusion come into focus. In many instances the product used in the investigation is once again not coconut oil but MCTs (Medium Chain Triglycerides). Research in the past has suggested that MCTs can cause a slight increase in metabolic rate and higher thermogenesis (heat production) during digestive processes that might encourage weight loss (51,52,53). However we are well aware that results from MCTs cannot be applied to coconut oil. More recent trials show no increase in thermogenesis using actual coconut oil consumption when compared to consumption of corn oil (50). Furthermore, other research shows that ingestion of MCFAs can have a deleterious effect on the blood lipid profile, increasing total cholesterol, triglycerides and LDL while leaving HDL unchanged (23).

If you look at studies that actually use coconut oil itself, there are some that claim to show that coconut oil is associated with weight loss (42,43). When the methods of these studies are examined however the studies come up short. An “open label” study performed in 2011 looked at twenty men and women eating two tablespoons of coconut oil daily, observing that the men lost about an inch off their waist measurement. This study had no control group, the participants were well aware of what they were ingesting and they were monitored regularly for results (42). The problem here is that the process of being under observation induces people to improve the activity that is being monitored, skewing the results (44). The first controlled trial of the effect of coconut oil on waistlines was accomplished in 2015 and involved over 100 men and women. For the first three months all participants received intensive nutritional information and on average experienced some weight loss. In the second three months half ingested one tablespoon of coconut oil daily and half did nothing different. The coconut oil group was encouraged to eat fruit with their coconut oil. At the end of the second three months the coconut oil group had lost an average of one extra inch off their waists. In this trial the placebo effect becomes a factor in those who were actively doing “something” (taking the coconut oil) (45). In addition, though the amount of fruit eaten was not taken into account, those that did eat more fruit would benefit from the anti-obesity effects of fruit, introducing another confounding factor into the results (46).

A study that did include other fats for comparison divided participants into three groups and added the same daily amount of dairy fat, coconut oil or beef fat (tallow) to their diets. At the end of the trial subjects showed no difference in their hunger, satisfaction after the meal or on how much they consumed at their next meal (47). A 2009 randomized double-blind trial compared the daily ingestion of two tablespoons of coconut oil to two tablespoons of soybean oil in women with abdominal obesity and resulted in no significant difference in their abdominal body fat. Adversely there was a significant increase in insulin resistance in the coconut oil group, a metabolic state that leads to diabetes and is associated with many other chronic diseases (48). Surprisingly this negative result occurred even though the women were advised to increase their fruit and vegetable intake, cut down on sugar and animal fat and walk for 50 minutes a day four days a week. And finally in 2017 one more placebo-controlled study on coconut oil’s effect on the waistline revealed no significant changes in weight or the amount of body fat in Caucasian postmenopausal women. The coconut oil did raise total cholesterol, LDL-cholesterol and HDL-cholesterol however the TC/HDL ratio after ingestion of both oils was unaffected (49).

Current perspective on this subject concludes that there is a lack of consistent evidence for any beneficial effect of coconut oil on weight loss and further research, especially long-term clinical trials are warranted (54). One thing that we can be sure of is that the regular addition of coconut oil to a healthy low-fat whole-food plant-based diet will cause weight gain.

Bottom line – Coconut oil offers no benefits for losing weight.

 

Immune-modulating effects

Lauric acid and its metabolite, monolaurin, are the ingredients in coconut oil claimed to boost the immune system. Lauric acid has shown some antibacterial and antiviral properties in the lab. Used topically monolaurin may be effective at preventing skin infections. However, the amount of monolaurin produced after ingesting coconut oil is low. No well-designed human studies have demonstrated anti-infective effects of coconut oil in humans (20).

Bottom line – Coconut oil has negligible effects on the human immune system.

 

Diabetes

In 1992 a study of lauric acid showed that it could increase insulin secretion in mouse pancreatic cells. No human studies have observed this result and other studies on pure sources of MCFAs are inconclusive (24).

A 2009 study showed a 30% reduction in insulin sensitivity when LCFAs were fed to rats compared to no change in insulin activity after feeding with MCFAs (25). However, subsequent studies concluded that both LCFAs and MCFAs increase insulin resistance through different mechanisms (26). Once again human studies are lacking.

Bottom line – Coconut oil cannot prevent or treat diabetes.

 

SUMMING IT ALL UP…

Coconut oil is an oil, an extracted fat concentrate, a processed food, not a whole food. Separating oil from its whole food source removes its fiber-, vitamin- and mineral-rich package and changes the product from nutrient dense to calorie dense. Concentrated nutrients are processed much differently by the body than nutrients in their natural whole state.

All oils, including coconut oil, are pure fat. Over 90% of the fat in coconut oil is saturated fat.

Coconut oil has virtually no nutritional value. It contains no protein, carbohydrate, fiber, minerals or vitamins (except for a tiny amount of Vitamin K, about 0.07 mcg in 1 tablespoon of coconut oil). Virgin coconut oil contains some polyphenols but they are in insignificant amounts. Much better sources are fruits, vegetables and whole grains (27).

Though MCFAs seem to be more easily absorbed and have less of an effect on LDL (bad cholesterol), coconut oil is composed of only about 15% MCFAs along with about 75% of LCFAs that are notoriously LDL-raising.

Regrettably, much of the reportedly beneficial MCFA content of coconut oil is isolated and removed from the oil before it is packaged up for sale. MCFAs are used in medication and beauty products as antimicrobials, stabilizers and lubricants (28).

There are some examples of native populations that eat coconut and live a healthy life relatively free of cardiovascular disease. In these cases, it is not coconut oil that is being consumed but whole coconuts. Coconut is likely their only cardiovascular risk factor in an otherwise healthy lifestyle.

Coconut oil increases lipid factors that raise the risk of cardiovascular disease.

Coconut oil does not provide benefits for Alzheimer’s Disease, diabetes, weight loss or the immune system.

The evidence for the many other health claims for coconut oil is anecdotal or derived from small, poorly designed studies, many of which have been only performed only on animals. Future study will clarify the effect, if any, of coconut oil on diseases such as cancer, infections, kidney disease, diabetes and osteoporosis. We must wait for large randomized controlled studies designed specifically to show cause and effect for each condition for which health claims from coconut oil are made.

Lastly, a quick warning… do not cook with coconut oil. Coconut oil reaches its smoke point at a very low temperature. This is the point at which the fat breaks down and free radicals form. These free radicals cause inflammation and cell wall damage that can be an underlying factor in cardiovascular disease and cancer.

 

IN CONCLUSION

The claims of health benefits for coconut oil are not supported by robust scientific evidence. We know that coronary artery disease is reduced most effectively when trans-fatty acids and saturated fatty acids are replaced by unsaturated fatty acids (30,31). Well controlled studies repeatedly substantiate the fact that the saturated fatty acids in coconut oil increase total cholesterol, LDL and HDL (29). While the increase in HDL is of uncertain clinical relevance, the increase in LDL is known to increase atherosclerotic cardiovascular risk (17). Recent lipid recommendations in both Canada and the USA are focused not on increasing HDL but on lowering LDL-cholesterol as their primary goal with a secondary goal of non-HDL-cholesterol or apoB targets (17,18). The evidence is clear that it is the lowering of LDL that leads to lower cardiovascular risk not the raising of HDL.

In 2017 the European Atherosclerosis Society completed an astoundingly extensive review of current clinical and genetic evidence regarding the association between LDL cholesterol and atherosclerotic cardiovascular disease. This comprehensive analysis encompassed over 200 different studies including controlled, randomized trials along with prospective cohort studies, genetic studies and Mendelian randomization studies. These studies involved more than 2 million participants with over 20 million person-years of follow-up. Their conclusion is … “Consistent evidence from numerous and multiple different types of clinical and genetic studies unequivocally establishes that LDL causes atherosclerotic cardiovascular disease.” (41).

The British Nutrition Foundation states that, due to existing knowledge regarding saturated fatty acids and their detrimental effects on the heart and vascular system along with the evidence that coconut oil raises blood cholesterol levels, frequent use of coconut oil is not advised (20). They also point out the lack of large, well-controlled human studies published in peer-reviewed journals demonstrating any health benefits of coconut oil.

The USA NLA (National Lipid Association) Expert Panel advises that “ …if coconut oil is used as part of a daily eating plan and/or in food preparation, it is recommended that it be used within the context of a healthy dietary pattern.” They further state that one tablespoon of virgin coconut oil would contribute a significant portion of the recommended total daily saturated fat limit of less than 7% of energy (17).

The last bit of advice comes from Cochrane, a global independent network of researchers who are free from commercial sponsorship and other conflicts of interest. Their work is recognized as the international gold-standard for high quality, trusted information. In 2015 they performed a review of fifteen randomized controlled trials encompassing 59,000 participants. These trials met their strict criteria for trial design and looked directly at the effect of replacing saturated fat with carbohydrate, polyunsaturated fat or monounsaturated fat on cardiovascular disease and mortality. The advice from Cochrane is permanent reduction of dietary saturated fat (32).

Health Canada, the AHA (American Heart Association) and the World Health Organization all share the same opinion. High levels of dietary saturated fat, such as those found in coconut oil, are destructive to heart health and promote heart disease. At present the best advice is to heed this warning and keep intake of all saturated oils, including coconut oil, to less than 7% of total calorie intake.

 

SOURCES:

1 Trinidad, T.P., Loyola, A.S., Mallillin, A.C., Valdez, D.H., Askali, F.C., Castillo, J.C., Resaba, R.L., Masa, D.B. The cholesterol-lowering effect of coconut flakes in humans with moderately raised serum cholesterol. J Med Food. 2004 Summer; 7(2):136-40.

2 Lindeberg, S., Lundh, B. Apparent absence of stroke and ischaemic heart disease in a traditional Melanesian island: a clinical study in Kitava. J Intern Med. 1993 Mar;2 33(3): 269-275.

3 Prior, I.A., Davidson, F., Salmond, C.E., Czochanska, Z. Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapuka and Tokelau island studies. Am J Clin Nutr. 1981 Aug; 34(8):1552-61.

4 Ganji, V., Kies, C.V. Psyllium husk fiber supplementation to the diets rich in soybean or coconut oil: hypocholesterolemic effect in healthy humans. Int J Food Sci Nutr. 1996 Mar; 47(2):103-110.

5 Zock, P.L., Blom, W.A., Nettleton, J.A., Hornstra, G. Progressing Insights into the Role of Dietary Fats in the Prevention of Cardiovascular Disease. Curr Cardiol Rep. 2016 Nov; 18(11):111.

6 Mensink, R.P., Zock, P.L., Kester, A.D., Katan, M.B. 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 May; 77(5) :1146-1155.

7 Eyres, L., Eyres, M.F., Chisholm, A., Brown, R.C. Coconut oil consumption and cardiovascular risk factors in humans. Nutr Rev. 2016 Apr; 74(4):267-280.

8 Bartlett, J., Predazzi, I.M., Williams, S.M., et al. Is isolated low high-density lipoprotein cholesterol a cardiovascular disease risk factor? New insights from the Framingham Offspring Study. Circ Cardiovasc Qual Outcomes. Published online May 10, 2016.

9 März, W., Kleber, M.E., Scharnagl, H., Speer, T., Zewinger, S. et al. HDL cholesterol: reappraisal of its clinical relevance. Clin Res Cardiol. 2017 Sep; 106(9): 663-675.

10 Ali, K.M., Wonnerth, A., Huber, K., Wojta, J. Cardiovascular disease risk reduction by raising HDL cholesterol – current therapies and future opportunities. Br J Pharmacol. 2012 Nov; 167(6): 1177–1194.

11 Voight, B.F., Peloso, G.M., Orho-Melander, M., Frikke-Schmidt, R. et al. Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study. Lancet. 2012 Aug 11; 380(9841): 572–580.

12 Barter, P.J., Caulfield, M. Effects of Torcetrapid in Patients at high risk for coronary events. N Engl J Med 2007 Nov 22; 357 (21); 2109-1222

13 Clark, R.W., Sutfin, T.A., Ruggeri, R.B., Willauer, A.T. et al. Raising high-density lipoprotein in humans through inhibition of cholesteryl ester transfer protein: an initial multidose study of torcetrapib. Arteriosclerosis, Thrombosis, and Vascular Biology January, 2004; 24 (3): 490–497.

14 Lloyd-Jones, D.M. Niacin and HDL – Time to Face Facts. N Engl J Med July 2014; 371(3).

15 Barter, P. Lessons learned from the Investigation of Lipid Level Management to Understand its Impact in Atherosclerotic Events (ILLUMINATE) trial. Am J Cardiol. 2009 Nov 16; 104(10 Suppl):10E-5E.

16 Mani, P., Rohatgi, A. Niacin Therapy, HDL Cholesterol, and Cardiovascular Disease: Is the HDL Hypothesis Defunct? Curr Atheroscler Rep. 2015 Aug; 17(8):43.

17 Jacobson, T.A., Maki, K.C., Orringer, C.E., Jones, P.H., Kris-Etherton, P, et al. Expert Panel. National Lipid Association Recommendations for Patient-Centered Management of Dyslipidemia: Part 2. J Clin Lipidol. 2015 Nov-Dec; 9(6 Suppl):S1-122.e1.

18 Anderson, T.J., Gregoire, J., Pearson, G.J., Barry, A.R., Couture, P., Dawes, M. Francis, G.A. et al. Society Guidelines – 2016 Canadian Cardiovascular Society Guidelines for the Management of Dyslipidemia for the Prevention of Cardiovascular Disease in the Adult. Can J Card 2016; 32: 1263e to 1282.

19 Fernando, W.M., Martins, I.J., Goozee, K.G., Brennan, C.S., Jayasena, V., Martins, R.N. The role of dietary coconut for the prevention and treatment of Alzheimer’s disease: potential mechanisms of action. Br J Nutr. 2015 Jul 14; 114(1):1-14.

20 Lockyer, S., Stanner, S. Facts Behind the Headlines: Coconut oil – a nutty idea? Nutrition Bulletin – British Nutrition Foundation February 2016; 41 (1): 42-54.

21 Henderson, S.T., Vogel, J.L., Barr, L.J., Garvin, F., Jones, J.J., Costantini, L.C. Study of the ketogenic agent AC-1202 in mild to moderate Alzheimer’s disease: a randomized, double-blind, placebo-controlled, multicenter trial. Nutr Metab (Lond). 2009 Aug 10; 6:31.

22 St. Onge, M.-P., Ross, R., Parsons,W.D., Jones, P.J.H. Medium-Chain Triglycerides Increase Energy Expenditure and Decrease Adiposity in Overweight Men. Obesity March 2003; 11(3): 395-402.

23 Kern, M., Lagomarcino, N.D., Misell, L.M., Schuster, V. The effect of medium-chain triacylglycerols on the blood lipid profile of male endurance runners. J Nutr Biochem. 2000 May; 11(5):288-292.

24 Garfinkel, M., Lee, S., Opara, E.C., Akwari, O.E. Insulinotropic potency of lauric acid: a metabolic rationale for medium chain fatty acids (MCF) in TPN formulation. J Surg Res. 1992; 52(4):328-333.

25 Wein, S., Wolffram, S., Schrezenmeir, J., Gasperiková, D., Klimes, I., Seböková, E. Medium-chain fatty acids ameliorate insulin resistance caused by high-fat diets in rats. Diabetes Metab Res Rev. 2009; 25(2):185-194.

26 De Vogel-van den Bosch, J., van den Berg, S.A., Bijland, S., et al. High-fat diets rich in medium- versus long-chain fatty acids induce distinct patterns of tissue specific insulin resistance. J Nutr Biochem. 2011; 22(4):366-371.

27 FAQs: Coconut oil. British Nutrition Foundation. October, 2016.

28 Pharmaceutical and cosmetic uses of palm and lauric products. Journal of the American Oil Chemists’ Society 1985; 62(2).

29 Voon, P.T., Ng, T.K., Lee, V.K., and Nesaretnam, K. Diets high in palmitic acid (16:0), lauric and myristic acids (12:0 + 14:0), or oleic acid (18:1) do not alter postprandial or fasting plasma homocysteine and inflammatory markers in healthy Malaysian adults. Am J Clin Nutr. 2011; 94: 1451–1457

30 Hu, F.B., Manson, J.E., Willett, W.C. Types of dietary fat and risk of coronary heart disease: a critical review. J Am Coll Nutr. 2001; 20: 5–19.

31 Jakobsen, M.U., O’Reilly, E.J., Heitmann, B.L., Pereira, M.A. et al. Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. Am J Clin Nutr. 2009 May; 89(5): 1425–1432.

32 Hooper, L., Martin, N., Abdelhamid, A., Davey Smith, G. Reduction in saturated fat intake for cardiovascular disease. Cochrane Database Syst Rev. 2015 Jun 10 ;(6):CD011737.

33 Nicholls, S.J., Lundman, P., Harmer, J.A., Cutri, B., Griffiths, K.A., Rye, K.A., Barter, P.J., Celermajer, D.S. Consumption of saturated fat impairs the anti-inflammatory properties of high-density lipoproteins and endothelial function. J Am Coll Cardiol. 2006 Aug 15; 48(4):715-720.

35 Ng, C.K., Chan, A.P., Cheng, A. Impairment of endothelial function–a possible mechanism for atherosclerosis of a high-fat meal intake. Ann Acad Med Singapore. 2001 Sep; 30(5):499-502.

36 Vafeiadou, K., Weech, M., Altowaijri, H., Todd, S., Yaqoob, P., Jackson, K.G., Lovegrove, J.A. Replacement of saturated with unsaturated fats had no impact on vascular function but beneficial effects on lipid biomarkers, E-selectin, and blood pressure: results from the randomized, controlled Dietary Intervention and VAScular function (DIVAS) study. Am J Clin Nutr. 2015 Jul; 102(1): 40-48.

37 Hu, F.B., Meir, M.D., Stampfer, J., Manson, J.E. et al. Dietary Fat Intake and the Risk of Coronary Heart Disease in Women. N Engl J Med 1997; 337:1491-1499

38 Briggs, M.A., Petersen, K.S., Kris-Etherton, P.M. Saturated Fatty Acids and Cardiovascular Disease: Replacements for Saturated Fat to Reduce Cardiovascular Risk. Healthcare (Basel). 2017 Jun; 5(2): 29.

39 Harris, M., Hutchins,A., Fryda, L. The Impact of Virgin Coconut Oil and High-Oleic Safflower Oil on Body Composition, Lipids, and Inflammatory Markers in Postmenopausal Women. J Med Food. 2017 Apr; 20(4):345-351.

40 St-Onge, M.-P., Bosarge, A., Goree, L. L.T., Darnell, B. Medium Chain Triglyceride Oil Consumption as Part of a Weight Loss Diet Does Not Lead to an Adverse Metabolic Profile When Compared to Olive Oil. J Am Coll Nutr. 2008 Oct; 27(5): 547–552.

41 Ference, B.A., Ginsberg, H.N., Graham, I. et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. Eur Heart J April 4, 2017.

42 Liau KM, Lee YY, Chen CK, Rasool AHG. An open-label pilot study to assess the efficacy and safety of virgin coconut oil in reducing visceral adiposity. ISRN Pharmacology. 2011;2011:1-7.

43 Cardoso DA, Moreira AS, De oliveira GM, Raggio luiz R, Rosa G. A coconut extra virgin oil-rich diet increases HDL cholesterol and decreases waist circumference and body mass in coronary artery disease patients. Nutrición Hospitalaria. 2015;32(5):2144-2152.

44 Robinson E, Hardman CA, Halford JC, Jones A. Eating under observation: a systematic review and meta-analysis of the effect that heightened awareness of observation has on laboratory measured energy intake. American Journal of Clinical Nutrition. 2015;102(2):324-337.

45 Fontaine KR, Williams MS, Hoenemeyer TW, Kaptchuk TJ, Dutton GR. Placebo effects in obesity research. Obesity (Silver Spring). 2016;24(4):769-771.

46 Sharma SP, Chung HJ, Kim HJ, Hong ST. Paradoxical effects of fruit on obesity. Nutrients. 2016;8(10).

47 Poppitt S, Strik C, Macgibbon A, Mcardle B, Budgett S, Mcgill A-T. Fatty acid chain length, postprandial satiety and food intake in lean men. Physiology & Behavior. 2010;101(1):161-167.

48 Assunção ML, Ferreira HS, Dos santos AF, Cabral CR, Florêncio TM. Effects of dietary coconut oil on the biochemical and anthropometric profiles of women presenting abdominal obesity. Lipids. 2009;44(7):593-601.

49 Harris M, Hutchins A, Fryda L. The impact of virgin coconut oil and high-oleic safflower oil on body composition, lipids, and inflammatory markers in postmenopausal women. J Med Food. 2017;20(4):345-351.

50 LaBarrie, J., St-Onge, M. –P. A coconut oil-rich meal does not enhance thermogenesis compared to corn oil in a randomized trial in obese adolescents. Insights Nutr Metab. 2017; 1(1): 30–36.

51 Dulloo, A.G,Fathi, M., Mensi, N., Girardier, L. Twenty-four-hour energy expenditure and urinary catecholamines of humans consuming low-to-moderate amounts of medium-chain triglycerides: a dose-response study in a human respiratory chamber. Eur J Clin Nutr. 1996 Mar; 50(3): 152-158.

52 St.-Onge, M.-P., Jones, P.J. Greater rise in fat oxidation with medium-chain triglyceride consumption relative to long-chain triglyceride is associated with lower initial body weight and greater loss of subcutaneous adipose tissue. Int J Obes Relat Metab Disord. 2003 Dec; 27(12):1565-71.

53 Scalfi,L.,, Coltorti, A., Contaldo, F. Postprandial thermogenesis in lean and obese subjects after meals supplemented with medium-chain and long-chain triglycerides. Am J Clin Nutr. 1991 May; 53(5):1130-1133.

54 Clegg, M.E.. They say coconut oil can aid weight loss, but can it really? European Journal of Clinical Nutrition 2017; 71: 1139–1143