How the Wrong Science Is Making People Sick: The Truth About Saturated Fat, Animal Fat and Coconut Oil

This article is written by Dr. Fabian Dayrit, president of the Integrated Chemists of the Philippines and the chairman of the Asian and Pacific Coconut Community’s Scientific Advisory Committee for Health, and is in response to the recent viral advisory published by the American Heart Association (AHA) warning the public against the use of coconut oil due to its saturated fat content.

 

Abstract

The 2017 AHA Presidential Advisory attacked coconut oil using studies that did not involve coconut oil. A careful review of the fatty acid composition of coconut oil and animal fat shows that: first, coconut oil has a vastly different fatty acid profile from animal fats; second, coconut oil has negligible cholesterol content while animal fats are high in cholesterol; and third, animal fats are actually not saturated fats. This casts doubt on the basis of the almost 60-year anti-saturated fat campaign which was focused on animal fat. Although the AHA Presidential Advisory claimed that it had new studies to present, it actually just reanalyzed old papers and selected the studies, some dating from the 1960s and 1970s, which agreed with its position and labeled these as “high quality.” It then rejected the studies which gave contrary conclusions, such as studies on HDL as a beneficial cardiovascular marker and the Minnesota Coronary Survey (MCS). The MCS study is important because it is a research project which Ancel Keys himself undertook but which failed to support his saturated fat-heart disease hypothesis. In passing judgment that coconut oil has “no known offsetting favorable effects,” the AHA has ignored evidence from thousands of years of its use in the tropics and Pacific islands that demonstrate its healthful properties, and the repeated observation that people who shifted from a coconut diet to a Western diet have gotten sick. The AHA produced no evidence that coconut oil causes heart disease. The AHA attack against coconut oil is a repeat of previous negative campaigns that have made the Americans obese and sick.

 

Introduction

On June 15, 2017, the American Heart Association published its AHA Presidential Advisory entitled “Dietary Fats and Cardiovascular Disease.” Although the title mentioned dietary fats, it was actually an attack on coconut oil. Although this Advisory tried to appear authoritative and objective, a detailed analysis shows that it is full of errors and biases.

 

1. AHA attacked coconut oil using studies that did not involve coconut oil.

Although the AHA Presidential Advisory claimed that it would present the “most recent studies, on the effects of dietary saturated fat intake,” it in fact just recycled old studies and reinterpreted them using statistical arguments. Four of the studies dated from the 1960s and 1970s and had been previously criticized for being poorly executed. But more to the point, all of these studies are irrelevant to coconut oil because none of them used coconut oil as a test material: these studies used animal fat and AHA just assumed that animal fat and coconut oil are the same. They are not!

Table 1 compares the fatty acid profiles and cholesterol content of coconut oil, butter, beef fat (tallow), and hog fat (lard). The following conclusions are clear:

1. Coconut oil has a vastly different fatty acid profile from animal fats and to assume a similarity is simply incorrect. Further, coconut oil is about 63% medium-chain fat while beef and hog fat do not contain any medium-chain fat (butter contains 9% medium-chain fat);
2. Coconut oil has negligible cholesterol content while animal fats are high in cholesterol; and
3. Animal fats are actually not saturated fats as Keys mistakenly assumed: in fact, animal fats contain comparable proportions of saturated fat and unsaturated fat.

Unfortunately, most studies, including those used by AHA, assume that animal fats are saturated fats and that coconut oil and animal fats are similar. In fact, animal fat is actually composed of long-chain saturated fat with lots of unsaturated fat. On this basis alone, we can say that the whole AHA campaign against saturated fat is based on the wrong definition of saturated fat and the warning against coconut oil is not valid. This represents over 50 years of defective dietary recommendations and false information!

The AHA provided an incomplete fatty acid profile of coconut oil in the table that it presented by not listing capoic acid (C6), caprylic acid (C8), and capric acid (C10) as components of coconut oil (Figure 1). These fatty acids, together with lauric acid (C12), are medium-chain fatty acids, and the AHA has consistently ignored medium-chain fatty acids as a distinct metabolic group from long-chain fatty acids. The correct fatty acid profile of coconut oil is given in Table 1.

Figure 1. Reproduction of part of the fatty acid table from the AHA Presidential Advisory (AHA page e4). AHA excluded capoic acid (C6), caprylic acid (C8), and capric acid (C10) as components of coconut oil and lumped all saturated fats into one group.
t1

 

Table 1. Fatty acid profile and cholesterol content of coconut oil and various animal fats.

t2
1 Codex Alimentarius 210-1999, amended 2015. Median values are calculated.
2 USDA Food Composition Databases. https://ndb.nal.usda.gov/

The AHA Presidential Advisory is clearly full of errors.

 

2. The AHA ignored studies that were unfavorable to its position.

AHA selected information that was in favor of its agenda and ignored other facts that were unfavorable, in particular, those pertaining to LDL and HDL, and the Minnesota Coronary Survey.

Regarding LDL, the AHA stated that “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.” (AHA page e13) This statement is scientifically unacceptable because the evidence of the link between LDL and CVD is only a correlation and its causality has not been proven. The AHA advisory cited two papers, neither of which presented convincing evidence that coconut oil was linked to CVD. In fact, one of the papers that AHA cited contradicted its position regarding coconut oil stating that: although coconut oil raised LDL cholesterol, “observational evidence suggests that consumption of coconut flesh or squeezed coconut in the context of traditional dietary patterns does not lead to adverse cardiovascular outcomes.”

The AHA tried to further discredit coconut oil by ignoring the beneficial effects of coconut oil on HDL claiming that: “changes in HDL cholesterol caused by diet or drug treatments can no longer be directly linked to changes in CVD, and therefore, the LDL cholesterol-raising effect should be considered on its own.” (AHA page e13) The justification for this statement was based on a study that showed that a genetic variant rendered HDL as an unreliable marker for protection against heart disease. However, this genetic variant was found in only 2.6% of the population. Similarly, a recent paper reported that extremely high HDL levels may increase the risk of death but this was found in only 0.4% of men and 0.3% of women. Clearly, these examples represent a minority of the population and are outliers. Extremely high and low HDL (and LDL) levels are unhealthy but this does not negate the value of HDL as a beneficial cardioprotective marker for coconut oil.

The Minnesota Coronary Survey (MCS) was a study that Keys himself designed and implemented together with Ivan Frantz Jr. MCS was meant to finally prove Keys’s saturated fat-heart disease hypothesis using a large number of subjects (n=9,423), a long feeding period (4.5 years, from 1968-1973), a high level of dietary control, and double blind randomized design. This study was conducted at the same time that Keys was coordinating the Seven Countries Study and would have provided powerful validation for his saturated fat-heart disease hypothesis.

In the end, Keys did not participate in the publication of the results of the MCS study. A partial report was made in a 1989 paper with Frantz as lead author but without Keys as co-author. This work remained hidden until 2016 – forty-three years after its completion – when the raw data were unearthed and turned over to Ramsden and co-workers, who then analyzed the data. The main conclusion from the MCS study was that a high omega-6 diet effectively lowered serum cholesterol, but also increased the risk of heart disease, a result that was the opposite of what Keys desired.

The AHA eliminated the MCS study from its list of “high quality” core studies because of its “short duration, large percentage of withdrawals from the study, and intermittent treatment, which is not relevant to clinical practice.” (AHA page e7) They conveniently ignored the fact that the MCS study was longer than some of the “high quality” studies that it cited and was likely better designed and implemented (by Keys himself). The AHA concern regarding subject withdrawals had already been adequately addressed previously by Broste and Frantz. The AHA also critiqued the use of “lightly hydrogenated corn oil margarine in the polyunsaturated fat diet” which would have contained trans-fat, which is known to raise cholesterol. Ramsden and co-workers addressed this concern in their paper by pointing out that both Keys and Frantz were well aware of this problem and had already devised diets from previous studies which achieved reductions in cholesterol. The MCS study should remain an important study for consideration notwithstanding the AHA objection.

The AHA Presidential Advisory is clearly biased.

 

3. Coconut has always been part of a healthy traditional tropical and Pacific island diet.

The AHA Presidential Advisory complained that: “A recent survey reported that 72% of the American public rated coconut oil as a ‘healthy food’ compared with 37% of nutritionists. This disconnect between lay and expert opinion can be attributed to the marketing of coconut oil in the popular press.” (AHA page e13)

Obviously, the AHA is of the opinion that the perception of coconut oil as a health food is just a health fad and that, as previously mentioned, it has “no known offsetting favorable effects.” Coconut oil may be a fad in the US, but it has been part of a healthy traditional diet in the tropics and Pacific islands for thousands of years. The AHA probably believes that a healthy diet can only be proven within the confines of its clinics and laboratories and not in the real world where people actually consume the food. The AHA does not realize that people cannot live on a tropical island and not consume coconut every day, and that despite this, do not suffer from heart disease. The AHA is obviously unaware of the numerous published studies that document how Pacific island inhabitants who shifted from a coconut diet to a Western diet became more prone to heart disease and obesity. The AHA wants us to miss the forest for the trees: There is no evidence that coconut oil causes heart disease; instead, they want to focus only on LDL.

At the same time that the AHA is attacking coconut oil, it has been promoting a high omega-6 diet. In 2009, AHA issued a science advisory which endorsed a minimum of 10% omega-6 in the diet, contrary to the recommendations of international health agencies to limit total omega-6 + omega-3 fat consumption to about 8%, and to keep an omega-6 to omega-3 ratio of no more than 5:1. The excessive consumption of omega-6 fat and deficiency in omega-3 fat may be one of the major contributors to the epidemic of obesity and diabetes in the US. It is soybean oil, an omega-6 fat, which has profited the most from the AHA support for a high omega-6 diet and warning against coconut oil.

In 1987, the American Soybean Association launched a “truth-in-labeling campaign” to demonize coconut oil to “increase market share for soybean oil.” This campaign, which came to be known as the Tropical Oils War, severely damaged the coconut industry. Today, soybean oil accounts for 55% of the edible vegetable oil consumption in the US and the soybean industry has been funding the AHA in the guise of supporting its health campaign to further increase its market share. In exchange, AHA is once again using defective science that demonizes coconut oil and makes Americans obese and sick.

 

References

Sacks FM, Lichtenstein AH, Wu JHY, Appel LJ, Creager MA, Kris-Etherton PM, Miller M, Rimm EB, Rudel LL, Robinson JG, Stone NJ, Van Horn LV (2017). Dietary Fats and Cardiovascular Disease, A Presidential Advisory From the American Heart Association. Circulation 135: e1-e24.

The studies that the AHA selected as “high quality” were the following: a. Morris et al. Controlled trial of soya-bean oil in myocardial infarction. Lancet 1968; 2: 693–699; b. Dayton et al. A controlled clinical trial of a diet high in unsaturated fat in preventing complications of atherosclerosis. Circulation 1969; 40 (suppl II): 1–63; c. Leren. The Oslo Diet-Heart Study: eleven-year report. Circulation 1970;42:935–942; d. Turpeinan et al. Dietary prevention of coronary heart disease: the Finnish Mental Hospital Study. Int J Epidemiol 1979; 8: 99–118.

Here is an example of a critique of the Finnish Mental Health Hospital study: Pietinen P, Ascherio A, Korhonen P, Hartman AM, Willett WC, Albanes D, Virtamo J (1997). Intake of Fatty Acids and Risk of Coronary Heart Disease in a Cohort of Finnish Men. Am. J. Epidemiol. 145 (10): 876-887.

Sampling of references: a. Bach & Babayan. Medium-chain triglycerides: an update. Am J Clin Nutr 1982; 36: 950-962; b. Schonfeld P, Wojtczak L (2016). Short- and medium-chain fatty acids in the energy metabolism – the cellular perspective. Journal of Lipid Research 57: 943-954; c. Huang CB, Altimova Y, Myers TM, Ebersole JL. Short- and medium-chain fatty acids exhibit antimicrobial activity for oral microorganisms. Arch Oral Biol. 2011; 56(7): 650–654.

Eyres L, Eyres MF, Chisholm A, Brown RC. Coconut oil consumption and cardiovascular risk factors in humans. Nutrition Reviews 2016; 74(4): 267–280.

a. Voight BF et al. Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study. Lancet 2012; 380: 572–80; b. Hewing B, Moore KJ, Fisher EA. HDL and Cardiovascular Risk. Time to Call the Plumber? Circ Res. 2012; 111: 1117-1120.

Madsen CM, Varbo A, Nordestgaard BG. Extreme high high-density lipoprotein cholesterol is paradoxically associated with high mortality in men and women: two prospective cohort studies. European Heart Journal 2017; 38: 2478–2486.

Frantz ID Jr, Keys A. R01 HE 0986-03 Research Grant Application: Effect of a Dietary Change on Human Cardiovascular Disease “The Minnesota Coronary Survey”. 1967.

Frantz ID Jr., Dawson EA, Ashman PL, Gatewood LC, Bartsch GE, Kuba K, Brewer ER. Test of Effect of Lipid Lowering by Diet on Cardiovascular Risk. The Minnesota Coronary Survey. Arteriosclerosis 1989; 9:129-135.

O’Connor A. A Decades-Old Study, Rediscovered, Challenges Advice on Saturated Fat. New York Times, April 13, 2016. http://well.blogs.nytimes.com/2016/04/13/a-decades-old-study-rediscovered-challenges-advice-on-saturated-fat/?_r=0

Ramsden CE, Zamora D, Majchrzak-Hong S, R Faurot KR, Broste SK, Frantz RP, Davis JM, Ringel A, Suchindran CM, Hibbeln JR. Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73). BMJ 2016;353:i1246.

Broste SK. Lifetable Analysis of the Minnesota Coronary Survey. MS thesis, 1981. University of Minnesota.

Gunn BF, Baudouin L, Olsen KM. Independent Origins of Cultivated Coconut (Cocos nucifera L.) in the Old World Tropics. PLoS ONE 2011; 6(6): e21143.

Prior I. Epidemiology of cardiovascular diseases in Asian-Pacific region. Singapore Medical Journal 1973; 14(3): 223-227.

a. Galanis DJ, McGarvey ST, Quested C, Sio B, Afele-Fa’Amuli S. Dietary Intake of Modernizing Samoans: Implications for Risk of Cardiovascular Disease. Journal of the American Dietetic Association 1999; 99(2): 184–190; b. World Health Organization. Diet, food supply and obesity in the Pacific.2003. WHO Regional Office for the Western Pacific. ISBN 92 9061 044 1.

Harris WS, Mozaffarian D, Rimm E, Kris-Etherton P, Rudel LL, Appel LJ, Engler MM, Engler MB, Sacks F. Omega-6 Fatty Acids and Risk for Cardiovascular Disease. Circulation 2009; 119: 902-907.

a. Simopoulos AP. The importance of the ratio of omega-6/omega-3 essential fatty acids. Biomed Pharmacother 2002; 56(8): 365-79; b. Simopoulos AP. The Importance of the Omega-6/Omega-3 Fatty Acid Ratio in Cardiovascular Disease and Other Chronic Diseases. Exp Biol Med 2008; 233(6): 674-688; c. Simopoulos AP. Genetic variants in the metabolism of omega-6 and omega-3 fatty acids: their role in the determination of nutritional requirements and chronic disease risk. Exp Biol Med 2010; 235: 785–795.
American Soybean Association website. https://soygrowers.com/about-asa/highlights/1980s/

US Department of Agriculture Economic Research Service. ERS Oilseed Yearbook 2014.

Bayer and LibertyLink Soybeans Help Protect Hearts in America’s Heartland. https://www.cropscience.bayer.us/news/press-releases/2017/03022017-bayer-and-libertylink-soybeans-help-protect-hearts-in-americas-heartland

Glenn Alea Elected PFCS President

The Philippine Federation of Chemistry Societies (PFCS), the umbrella organization for the different chemistry societies in the country, is pleased to announce the election of Dr Glenn Alea as its President, assuming the post on 19 July 2017, and succeeding Dr Armando Guidote. Dr Alea is a graduate of De La Salle University (DLSU) in Manila, where he obtained his BS (1987), MS (1993), and PhD (1998) degrees in chemistry. His MS thesis is on natural products involving the isolation, characterization, and structural elucidation of terpenes from the soft coral Clavularia inflata. He did his research at the James Cook University in North Queensland, Australia. From 1994 to 1998, he was a PhD fellow of the Department of Science and Technology – Engineering and Science Education Program (DOST-ESEP). He was a research fellow from 1997 to 1998 at the Southampton University in the United Kingdom doing organic synthesis. His dissertation involved the synthesis and characterization of tetrathiafulvalene derivatives and macrocycles containing sugar units.

Dr Alea’s research interests include the syntheses of tetrathiafulvalene macrocycles, cobaltadithiolene complexes, pyrazinamide and isoniazid derivatives, phthalimide derivatives, and thiazolidinedione derivatives. His papers have been published in various journals and presented in local and international conferences.

Dr Alea has been with the Chemistry Department of DLSU since 1987 and has more than twenty years of teaching experience to his name, rising from assistant lecturer to associate professor. Among his iconic projects is the DLSU Chemistry Challenge, a chemistry quiz-bee type contest for high school students, which he initiated in the year 2000. He has been the Department Chair since 2015, and is in charge of the strategic direction, management, and coordination of the academic programs in line with the Department’s mission-vision. Come September 2017, Dr Alea shall become Dean of DLSU’s College of Science.

In addition to his role in the PFCS, Dr Alea is also the Vice President for Internal Affairs of the Integrated Chemists of the Philippines (ICP), the accredited professional organization (APO) of registered chemists and registered chemical technicians recognized by the Professional Regulation Commission, since being first elected in 2011. He also became a member of the three-person CPD Council for Chemistry in 2017.

He is married to the former Cristina Hinagpis and they have two children, Alzea and Yana. In his free time, Dr Alea plays badminton with members of DLSU’s chemistry community.

ICP Board Election 2017: Results

The ICP Election 2017 Committee is pleased to announce the results of the elections for ICP Board of Directors. The newly elected board members (in bold) who will serve from 2017 to 2020 are:

Academe
Glenn Alea, PhD (140)
Abstain (5)

Government
Ms. Nenita Marayag (126)
Abstain (19)

Industry
Ms. Teresita Corpuz (34)
Ms. Priscilla Alice Samonte (96)
Abstain (15)

Ballots received:
Valid: 145
Invalid: 5
Total: 150

We would like to thank all those who voted / participated in this election. Let us all continue to support the different activities of the ICP.

Sincerely,
ICP Election 2017 Committee
Rosalinda Torres, PhD (Chair)
Lilibeth Coo, PhD (Member)
Ms. Edna Mijares (Member)

Coconut Oil: Bringing History, Common Sense and Science Together

This article is written by Dr. Fabian Dayrit, president of the Integrated Chemists of the Philippines and the chairman of the Asian and Pacific Coconut Community’s Scientific Advisory Committee for Health, and is in response to the recent viral advisory published by the American Heart Association (AHA) warning the public against the use of coconut oil due to its saturated fat content.

 

Abstract

The modern Western diet has suffered the damaging effects of trans fats, much of it from soybean oil. It is suffering another blow, this time from the damaging effects of an excess of omega-6 fats, again from soybean oil.

The vast majority of epidemiological studies do not distinguish between coconut oil and animal fat, and simply refer to them collectively as “saturated fat.” This is a fatal mistake for two reasons: first, the fatty acid profiles of coconut oil and animal fat are very different, and second, coconut oil hardly has any cholesterol while animal fats contain a lot of cholesterol. This means that the results based on animal fat cannot be applied to coconut oil.

Contrary to the claim of the AHA, there is abundant evidence to show that coconut oil and a coconut diet do not raise the incidence of heart disease and are, in fact, part of many healthy traditional diets. Many populations who shifted from a traditional coconut diet to a Western diet have suffered worse health outcomes. However, the historical and scientific evidence in support of coconut oil may not be enough to convince the AHA which favors a high omega-6 diet.

 

Introduction

Only wholeness leads to clarity.”  -Schiller
 

The 2017 AHA Presidential Advisory has failed to see the forest for the trees. It has failed to see the worsening epidemics of obesity and metabolic disease, but has focused instead on the details of the meta-analysis of LDL and r values as if these were more important. The AHA has failed to bring the science together with the reality; there is no wholeness in their analysis.

Food is made up of three principal biochemical groups: protein, carbohydrate and fat. Assuming that one needs to maintain a certain level of energy, a food group cannot be decreased without compensation with another group. The “low fat” recommendation promoted by the AHA and the Dietary Guidelines for Americans since 1980 has resulted in an increase in refined carbohydrates: the American average fat consumption dropped from over 40% to 33% while carbohydrate consumption increased and obesity more than doubled from 14% to 36.5% (CDC, 2017). Worldwide obesity has likewise more than doubled since 1980, and by 2014, 13% were obese (WHO, 2016). Meanwhile, heart disease, the principal concern of the AHA and the justification of the Dietary Guidelines, has remained as the #1 cause of mortality.

The AHA and the Dietary Guidelines have led the Americans – and the rest of the world – astray with its warning against fat, especially saturated fat. However, if we go back to the time before the Dietary Guidelines made the world obese, we will find the answer and rediscover what traditional food cultures have been consuming for millennia: the coconut. This essay will show that, contrary to the claims of the AHA, the evidence for coconut oil is based on science and validated by the experience of people.

 

The modern diet

WHO recommends that the total energy from fat should not exceed 30% along with a shift in fat consumption away from saturated to unsaturated fat and the elimination of industrial trans fats (WHO, 2015). This works out to about 70 grams or about 75 mL of fat. Since we should aim for a healthy total fat diet, how much of each type of fat should we consume? How much saturated fat is desirable and what type should this be? How much unsaturated fat should one have?  How can we eliminate industrial trans fats completely? Since there is a trend to decrease the amount of carbohydrates in the diet how should we replace these calories?

It was the rising popularity of coconut oil that may have prompted the AHA to issue its Presidential Advisory. In its discussion of coconut oil, they said: “A recent survey reported that 72% of the American public rated coconut oil as a ‘healthy food’ compared with 37% of nutritionists. This disconnect between lay and expert opinion can be attributed to the marketing of coconut oil in the popular press.” The AHA then issued a warning against coconut oil: “[B]ecause coconut oil increases LDL cholesterol, a cause of CVD, and has no known offsetting favorable effects, we advise against the use of coconut oil” (Sacks et al., 2017).

In addition, the AHA unilaterally disposed of the importance of HDL to cancel the favorable effects of coconut oil, an issue that was tackled in the second article in this series (Dayrit, 2017b). The stated objective of the AHA is to limit the consumption of coconut oil down to 6%. This essay will answer these allegations and show that the claims of the AHA are wrong.

 

The trans fats fiasco

Coconut oil used to enjoy robust consumption in the US from the 1900s up to 1940, when the war interrupted the importation of coconut. During the war, trans fats, much of it from soybean oil, were used to replace coconut oil in food products (Shurtleff & Aoyagi, 2007). After the war, US importation of coconut oil remained low because of the soybean lobby that wanted to retain its market dominance. By 1999, it was estimated that trans fats in the American diet had reached 2.6% of calories (Allison et al., 1999). In 2006, it was estimated that trans fats may have been responsible for 72,000 to 228,000 myocardial infarctions and deaths from CHD in the US (accounting for 6% to 19%) (Mozaffarian et al., 2006).

Over 30 years after the warning against trans fats was first made, the FDA finally set a compromise rule where a manufacturer can declare “zero trans-fats” if the product contains less than 0.5 grams trans fatty acids per serving (FDA, 2003). This ruling actually does not eliminate trans fats from the food supply; it just hides it.

What is equally lamentable is the AHA’s tepid warning against trans fats. Despite the substantial harm that industrial trans fats have made to heart health, the AHA has not issued any advisory against trans fats in the same way that it has attacked saturated fat and coconut oil.

 

The high omega-6 fiasco

Linoleic acid (C18:2) and linolenic acid (C18:3) are both essential fatty acids. However, international nutrition institutions recommend that only a limited amount should be taken and that a particular ratio should be maintained (Table 1).

Table 1. Recommendations for daily intake (in grams) of omega-6 and omega-3, and omega-6 to omega-3 ratio from international institutions.

Agency Linoleic acid (C18:2)

Omega-6

Linolenic acid (C18:3)

Omega-3

Healthy ratio

Omega-6 : Omega-3

European Scientific Committee on Food1 2%

5 g*

6.4 g**

0.5%

1 g*

1.6 g**

5 : 1
European Food Safety Authority2 10 g 2 g 5 : 1
World Health Organization3 5-8% 1-2% 5 : 1

1 SCF, 1992.  2 EFSA, 2009.  3 FAO/WHO, 2008.
* recommendation for women ** recommendation for men

The American Soybean Association is a very powerful industry lobby (https://soygrowers.com/). Soybean oil is a high omega-6 oil, being made up of about 54% C18:2 (Codex, 2015). It was estimated that from 1909 to 1999 the per capita consumption of soybean oil in the US increased over 1,000 times from 0.01 to 11.6 kg/yr and by 1999, the average American consumption of C18:2 was 7.2% of total calories, with an omega-6 to omega-3 ratio of 10:1 (Blasbalg et al., 2011). The modern American diet has become a high omega-6 fat diet.

In 2009, AHA issued a “Science Advisory” in a paper entitled: “Omega-6 Fatty Acids and Risk for Cardiovascular Disease” (Harris et al., 2009). This paper summarized and defended the health benefits of omega-6 fatty acids. However, the ASA Science Advisory ignored the important issue of how much omega-6 fat should be consumed in the diet, and what the ratio of omega-6 to omega-3 fat should be. Numerous papers have pointed out that a high omega-6 diet and a high omega-6 to omega-3 ratio are linked to heart disease, cancer, inflammatory diseases, and others (Simopoulos 2002, 2008, 2010; Lands, 2012). The AHA Science Advisory dodged both important issues and one might surmise that AHA does not want to set a limit for this fat.

However, the AHA acknowledged that other health agencies have set limits to omega-6 in the diet (Table 1), but it defended its position of not specifying a limit by proclaiming: “The American Heart Association places primary emphasis on healthy eating patterns rather than on specific nutrient targets.”

This statement is highly irresponsible: since an excess of omega-6 fat is clearly linked to CHD, how can the AHA not issue a warning? This is also highly hypocritical and suspicious: the AHA refused to set a target for omega-6 fat and yet aggressively set a target of 6% for saturated fat in its Presidential Advisory (Sacks et al., 2017). Why the double standard? Is the AHA protecting omega-6 fats?

This omega-6 fiasco will become a replay of the trans fats disaster, with soybean oil as the beneficiary. Heart disease will remain the #1 cause of death in the US (and the world!).

 

Canola oil for coconut oil?

Aside from soybean oil, canola oil is the other beneficiary of the AHA warning. Since the 1990s, the agroindustry giant Calgene, which is convinced of the beneficial health properties of lauric acid, has been undertaking genetic engineering experiments on canola oil to produce a high lauric acid GMO, called Laurical 35, which contains 37% lauric acid and 34% oleic acid (Shahidi et al., 2007). As the Canola website declared: “Domestically produced high-laurate canola oil could potentially replace some of the $400 million of tropical oil imported annually, primarily from the Philippines, Malaysia and Indonesia” (Ag Innovation News, 2003). Thus, while the AHA warns against coconut oil, Calgene is set to enter the lauric oil market with a GM product.

 

Coconut oil, saturated fat, and animal fat: a serious misunderstanding

The vast majority of epidemiological studies do not distinguish between coconut oil and animal fat, and simply refer to them collectively as “saturated fat.” This is a serious misunderstanding. Coconut oil is 65% medium-chain saturated fat while the different types of animal fat contain from 40 to 50% long-chain saturated fat, with the rest being mono- and polyunsaturated fat. In addition, coconut oil contains from zero to 3 mg cholesterol per kg (Codex, 2015), while animal fat contains various amounts of cholesterol depending on animal source (USDA, 2017). (Table 2)

Polyunsaturated fat oxidizes readily with heat and, in the presence of cholesterol, will produce oxidized cholesterol. Oxidized cholesterol has been shown to accelerate the development of atherosclerosis leading to heart disease (Staprans et al., 2000). This will not happen with coconut oil because there is only a small proportion of unsaturated fat and very little cholesterol. This is a mistake that Ancel Keys made; it is a mistake that many researchers who followed him have made. Therefore, the so-called “high quality” studies that the AHA Presidential Advisory judged as acceptable evidence against coconut oil cannot be admitted as evidence because of this fatal mistake (Sacks et al., 2017).

 

Table 2. Comparison of fatty acid profile and cholesterol content of coconut oil and various types of animal fat: butter, beef fat and lard.

1 Codex, 2015
2 USDA

 

Historical use of the coconut

Contrary to the claim of the AHA, there is abundant evidence to show that coconut oil and a coconut diet do not raise the incidence of heart disease and are, in fact, part of many healthy traditional diets.  In the remainder of this essay, we will discuss the historical and traditional consumption of the coconut, health statistics of coconut-consuming populations, and a comparison with the Western (mainly American) diet.

The coconut is one of the most ancient and widespread of edible fruits in the world (Lutz, 2011). It is part of the diet and culinary tradition of virtually all countries where the coconut grows. It is also unparalleled in its overall usefulness as a portable source of food and water and many other useful applications. The settling of the Pacific islands was made possible by the coconut (Gunn et al., 2011). This is affectionately described by Henri Hiro, indigenous advocate for the Polynesian people, in a poem which is found in the Bishop Museum in Hawaii:

“Traveling companion of the Polynesians,
coconut tree, indispensable support
For a happy and fulfilled life;
coconut tree of peace, coconut tree of harmony,
eternal coconut tree, with you
life is there.”
 

Indeed, the coconut is widely revered in many cultures as the “Tree of Life.”

Miguel de Loarca, a Spanish explorer in the Philippines during the 16th century, observed that “The cocoanuts furnish a nutritious food when rice is scarce” (Blair & Robertson, 1906). It was so useful that the Spanish government in the Philippines decreed the planting of coconuts as a source of raw material and as food for the people, especially during drought.

Among some food cultures in the Pacific islands, the coconut accounts for up to 60% of fat intake. There is no report that the coconut has caused ill-health or disease, except for the occasional death from a falling coconut.

 

Health of coconut-consuming populations

Studies on the influence of dietary coconut oil on heart disease and other health factors have shown that there is no negative effect from coconut oil consumption compared with other oils and that in some cases, better health outcomes can be attributed to coconut oil.

Numerous studies have documented the absence of negative effects from coconut oil. Prior and co-workers (1981) reported that Polynesians from Pukapuka and Tokelau both consume a high saturated fat diet from coconut oil, 34% and 63%, respectively, and yet vascular disease was uncommon in both populations and there was no evidence of harmful effects in these populations due to their diet.  A small study of 32 CHD patients and 16 matched healthy controls from the Indian state of Kerala showed that coconut and coconut oil did not play any role in the causation of CHD in this state (Kumar, 1997). A similar study conducted in West Sumatra, Indonesia, involving 93 CHD patients with a control group showed that consumption of coconut was not a predictor for CHD (Lipoeto et al., 2004).

The association between coconut oil consumption and lipid profiles was studied in a cohort of 1,839 Filipino women (age 35–69 years) over a 22-year period, from 1983 to 2005. Lipid analysis showed that the mean TC, LDL, and triglyceride levels and TC/HDL ratio of the women were within the desirable limits set by WHO and that coconut oil intake may enhance HDL levels (Feranil et al., 2011).

A direct comparison between coconut oil and sunflower oil, a polyunsaturated oil, used as cooking oil was conducted to determine their effect on lipid profile, antioxidant and endothelial status in patients with stable coronary artery disease. This study was conducted for 2 years with 100 coronary artery disease patients and 100 in the healthy control group with 98% follow-up. The results showed that there was no statistically significant difference in the anthropometric, biochemical, vascular function, and cardiovascular events in both groups indicating that coconut oil does not pose any additional risk for heart disease compared with a polyunsaturated fat (Vijayakumar et al., 2016).

On the other hand, there are studies that show better health outcomes in populations that consume coconut oil or a coconut-based diet. In the Philippines, people from the Bicol province who have the highest consumption of coconut showed comparatively low levels of atherosclerosis and heart disease compared with people from other regions in the Philippines who consume less coconut in their diet (Florentino & Aguinaldo, 1987).

The type of fat has a strong influence on obesity. Rural populations of Vanuatu consume fat from traditional sources, which includes coconut, while urban Vanuatu populations consume fat from imported foods, such as oil, margarine, butter, and meat. Despite the fact that rural Vanuatu populations consumed more total calories than the urban population, they had half the prevalence of obesity and diabetes (WHO, 2003).

In the US, it is interesting to note that the states with high coconut consumption – Hawaii and Florida – showed lower rates of heart disease compared to the national average in 2014 (heart disease rate per 100,000): US average (167.0); Hawaii (136.7); Florida (151.3) (KFF, 2017).  Similarly, Cuba, a coconut-consuming country that has been spared the Western diet, had a mortality rate from heart disease of 144.8 from 1986 to 1997 (Cañero, 1999).

In summary, dietary studies on populations that consume coconut or coconut oil show no evidence of a higher incidence of heart disease and a number of studies report more favorable health outcomes.

 

From a traditional coconut diet to a Western diet

A number of studies have shown that populations that shifted from a traditional coconut diet to a Western diet report poorer health status. In 1973, Ian Prior saw the unique opportunity to observe in detail a real time experiment of the effect that diet can have on Polynesians who migrated from their islands to New Zealand. He recorded mortality from heart disease, hypertensive heart disease, and blood lipids, among others. He concluded his paper with this statement: “The high price being paid by the New Zealand Maori, in terms of morbidity and mortality from a range of cardiovascular and metabolic disorders and the contrast with the picture seen among atoll dwellers, gives a clear indication of how exposure to the ways and diet of Western society can influence health and disease patterns” (Prior, 1973).

A 1999 comparative study among American and Western Samoans showed that a shift to a modern diet increased their carbohydrate and protein consumption and decreased their overall fat, in particular, saturated fat. This shift was identified as the cause of their increased incidence of obesity and cardiovascular disease (Galanis et al. 1999). WHO (2003) reported that Pacific islanders “were 2.2 times more likely to be obese and 2.4 times more likely to be diabetic if they consumed fat from imported foods rather than from traditional fat sources.”  Among the most commonly consumed imported fats were vegetable oil and margarine which replaced coconut oil.

 

Will there be a science-based conclusion?

In 2016, Eyres and co-workers conducted an assessment of the literature to verify the merits of the claim that coconut consumption had favorable effects on cardiovascular risk factors. After reviewing 8 clinical trials and 13 observational studies, they concluded that: “Observational evidence suggests that consumption of coconut flesh or squeezed coconut in the context of traditional dietary patterns does not lead to adverse cardiovascular outcomes.” Strangely, they ended their paper with this statement: “However, due to large differences in dietary and lifestyle patterns, these findings cannot be applied to a typical Western diet” (Eyres et al., 2016).

Despite the exacting standards of science that Eyres and co-workers applied, why can’t these findings be applied to a typical Western diet? The authors did not provide an explanation. With this statement, the authors have effectively put science aside.

This set of three essays has provided evidence from science and from millennia of people’s experience which provide a holistic picture of the health properties of coconut oil. These essays have also pointed out specific aspects where the AHA and the Dietary Guidelines have perpetuated errors, many of which date back to the bias of Ancel Keys against saturated fat. The mistake of assuming that animal fat and coconut oil are similar means that much of the basis for the warnings against saturated fat are erroneous. In addition, recent discoveries regarding small dense LDL and oxidized LDL mean that conclusions from many LDL studies are questionable. Truly, wholeness leads to clarity.

These should be enough basis to reverse the AHA’s campaign against coconut oil, but its real reasons may not be based on science but on its bias for a high omega-6 diet. #

 

References

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Allison DB, Egan SK, Barraj LM, Caughman C, Infante M, Heimbach JT (1999). Estimated intakes of trans fatty and other fatty acids in the US population. J Am Diet Assoc 99: 166-174.

Blair EH, Robertson JA (1906). The Philippine Islands 1493-1803. Vol 5, p 167. Translation of the writings of Miguel de Loarca (1582 – 1583).

Blasbalg TL, Hibbeln JR, Ramsden CE, Majchrzak SF, Rawlings RR (2011). Changes in consumption of omega-3 and omega-6 fatty acids in the United States during the 20th century. Am J Clin Nutr 93: 950–62.

[CDC] Center for Disease Control (2017). Health, United States, 2016. https://www.cdc.gov/nchs/data/hus/hus16.pdf#056

Cañero AH (1999). Mortality from ischemic heart disease in Cuba.  The role of diet and serum cholesterol. Revista Cubana de Cardiología y Cirugía Cardiovascular 13(1): 8-12.

[Codex] Codex Alimentarius 210-1999, amended 2015.

Dayrit F (2017a). The Warning on Saturated Fat: From Defective Experiments to Defective Guidelines.

Dayrit F (2017b). A Half-Truth is Not the Whole Truth: The AHA Position on Saturated Fat.

[EFSA] European Food Safety Authority (2009). Scientific Opinion: Labelling reference intake values for n-3 and n-6 polyunsaturated fatty acids. The EFSA Journal. 1176, 1–11.

Eyres L, Eyres MF, Chisholm A, Brown RC (2016). Coconut oil consumption and cardiovascular risk factors in humans. Nutrition Reviews 74(4): 267–280.

[FAO/WHO] Interim Summary of Conclusions and Dietary Recommendations on Total Fat & Fatty Acids, in Expert Consultation on Fats and Fatty Acids in Human Nutrition. Nov. 10-14, 2008: Geneva.

[FDA] Food and Drug Administration. Food Labeling; Trans Fatty Acids in Nutrition Labeling; Final Rule and Proposed Rule. Federal Register. July 11, 2003.

Feranil AB, Duazo PL, Kuzawa CW, Adair LS (2011). Coconut oil predicts a beneficial lipid profile in pre-menopausal women in the Philippines. Asia Pac. J. Clin. Nutr. 20(2): 190–195.

Florentino RF, Aguinaldo AR (1987). Diet and Cardiovascular Disease in the Philippines. Phil. J. Coconut Stud. 13(2): 56-70.

Galanis DJ, McGarvey ST, Quested C, Sio B, Afele-Fa’Amuli S (1999). Dietary Intake of Modernizing Samoans: Implications for Risk of Cardiovascular Disease. Journal of the American Dietetic Association. 99(2): 184–190.

Gunn BF, Baudouin L, Olsen KM (2011). Independent Origins of Cultivated Coconut (Cocos nucifera L.) in the Old World Tropics. PLoS ONE 6(6): e21143.

Harris WS, Mozaffarian D, Rimm E, Kris-Etherton P, Rudel LL, Appel LJ, Engler MM, Engler MB, Sacks F (2009). Omega-6 Fatty Acids and Risk for Cardiovascular Disease. Circulation 119: 902-907.

[KFF] Kaiser Family Foundation (2017). Number of Heart Disease Deaths per 100,000 Population by Gender, Timeframe 2014. http://www.kff.org/other/state-indicator/heart-disease-death-rate-by-gender/?currentTimeframe=0&sortModel=%7B%22colId%22:%22Location%22,%22sort%22:%22asc%22%7D

Kumar PD (1997). The role of coconut and coconut oil in coronary heart disease in Kerala, South India. Tropical Doctor 27: 215-217.

Lands B (2012). Consequences of Essential Fatty Acids. Nutrients 4: 1338-1357;

Lipoeto NI, Agus Z, Oenzil F, Wahlqvist ML, Wattanapenpaiboon N (2004). Dietary intake and the risk of coronary heart disease among the coconut-consuming Minangkabau in West Sumatra, Indonesia. Asia Pac. J. Clin. Nutr. 13(4):377-384.

Lutz D (2011). Deep history of coconuts decoded. Washington University of St. Louis, June 24, 2011.  https://source.wustl.edu/2011/06/deep-history-of-coconuts-decoded/

Mozaffarian D, Katan MB, Ascherio A, Stampfer MJ, Willett WC (2006). Trans Fatty Acids and Cardiovascular Disease. N Engl J Med 354: 1601-13.

Prior I (1973). Epidemiology of cardiovascular diseases in Asian-Pacific region. Singapore Medical Journal  14(3): 223-227.

Prior IA, Davidson F, Salmond CE, Czochanska Z (1981). Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapuka and Tokelau Island studies. Am. J. Clin. Nutr. 34: 1552-1561.

[SCF]  Scientific Committee on Food, Commission of the European Communities. Reports of the Scientific Committee for Food: Nutrient and energy intakes for the European Community. 1992.

Sacks FM, Lichtenstein AH, Wu JHY, Appel LJ, Creager MA, Kris-Etherton PM, Miller M, Rimm EB, Rudel LL, Robinson JG, Stone NJ, Van Horn LV (2017). Dietary Fats and Cardiovascular Disease, A Presidential Advisory from the American Heart Association. Circulation. 135: e1-e24.

Shurtleff W, Aoyagi A (2007). History of Soy Oil Hydrogenation and of Research on the Safety of Hydrogenated Vegetable Oils. (http://www.soyinfocenter.com/HSS/hydrogenation1.php. downloaded July 3, 2017).

Shahidi F, Hamam F, Zhong Y (2007). High-laurate canola oil in production of structured lipids. Proceedings IRC Wuhan, vol 5, p 237-238.

Simopoulos AP (2002). The importance of the ratio of omega-6/omega-3 essential fatty acids. Biomed Pharmacother 56(8): 365-79.

Simopoulos AP (2008). The Importance of the Omega-6/Omega-3 Fatty Acid Ratio in Cardiovascular Disease and Other Chronic Diseases. Exp Biol Med 233(6): 674-688.

Simopoulos AP (2010). Genetic variants in the metabolism of omega-6 and omega-3 fatty acids: their role in the determination of nutritional requirements and chronic disease risk. Exp Biol Med 235: 785–795.

Staprans I, Pan XM, Rapp JH, Grunfeld C, Feingold KR (2000). Oxidized Cholesterol in the Diet Accelerates the Development of Atherosclerosis in LDL Receptor– and Apolipoprotein E–Deficient Mice. Arteriosclerosis, Thrombosis, and Vascular Biology. 20: 708-714.

[USDA] United States Department of Agriculture (2017). United States Department of Agriculture. Food Composition Databases. https://ndb.nal.usda.gov/; (downloaded: May 15, 2017).

Vijayakumar M, Vasudevan DM, Sundaram KR, Krishnan S, Vaidyanathan K, Nandakumar S, Chandrasekhar R, Mathew N (2016). A randomized study of coconut oil versus sunflower oil on cardiovascular risk factors in patients with stable coronary heart disease. Ind. Heart J. 68: 498-506.

[WHO] World Health Organization (2003). Diet, food supply and obesity in the Pacific. WHO Regional Office for the Western Pacific. ISBN 92 9061 044 1.

[WHO] World Health Organization (2015). Healthy Fact Sheet No. 394, updated Sept. 2015. (http://www.who.int/mediacentre/factsheets/fs394/en/. downloaded March 1, 2017)

[WHO] World Health Organization (2016). Obesity and overweight. Fact sheet No. 311. (http://www.who.int/mediacentre/factsheets/fs311/en/. downloaded July 4, 2017)

 

A Half-Truth is Not the Whole Truth: The AHA Position on Saturated Fat

This article is written by Dr. Fabian Dayrit, president of the Integrated Chemists of the Philippines and the chairman of the Asian and Pacific Coconut Community’s Scientific Advisory Committee for Health, and is in response to the recent viral advisory published by the American Heart Association (AHA) warning the public against the use of coconut oil due to its saturated fat content.

 

Abstract

This second in this series of papers will present the biases in the American Heart Association’s 2017 Presidential Advisory with respect to saturated fat. Although important differences in the metabolic properties of specific SFA have been known since the 1960s, the AHA still considers all SFA as one group having the same properties. There is abundant research available that supports the designation of C6 to C12 fatty acids as medium-chain fatty acids (MCFA). This is particularly relevant to coconut oil, which is made up of about 65% MCFA. Ignoring the evidence, AHA simply labels coconut oil as SFA. The AHA promotes half-truths, not the whole truth.

Abbreviations: AHA: American Heart Association; CHD: coronary heart disease; CVD: cardiovascular disease; HDL: high-density lipoprotein; LCFA: long-chain fatty acid; LDL: low-density lipoprotein; MCFA: medium-chain fatty acid; MCT: medium-chain triglyceride; oxLDL: oxidized low-density lipoprotein; PUFA: polyunsaturated fatty acid; oxLDL: oxidized low-density lipoprotein; SFA: saturated fatty acid

 

 Introduction

On June 16, 2017, the American Heart Association issued its AHA Presidential Advisory which repeated its recommendation to “shift from saturated to unsaturated fats” (Sacks et al., 2017). While this advisory did not present any new data, it provided a re-analysis of old data which selectively rejected some studies which it claims did not satisfy “rigorous criteria for causality,” while reinforcing those which were favorable to its conclusions.

The first paper in this series (Dayrit, 2017) showed that the scientific basis upon which the AHA made its recommendations is flawed and the Dietary Guidelines for Americans, which has been recommending a low-saturated fat diet for 35 years, has made Americans obese even as heart disease – the supposed concern of the AHA – has remained the top health problem.

This second article will focus on “saturated fatty acids,” the fat that AHA wants us to minimize. This article will analyze the 2017 AHA Presidential Advisory and provide counter evidence from the scientific literature, including clinical studies, to show that much of the confusion that we have today regarding the role of these fats in a healthy diet stems from the selective use of scientific information regarding saturated fat. The 2017 AHA Presidential Advisory provided only half the truth on saturated fat.

 

SFA, MCFA and LCFA

Saturated fatty acids (SFAs) generally refer to the following linear carboxylic acids: caproic (C5H11CO2H, C6), caprylic (C7H15CO2H, C8), capric (C9H19CO2H, C10), lauric (C11H23CO2H, C12), myristic (C13H27CO2H, C14), palmitic (C15H31CO2H, C16:0), and stearic (C17H35CO2H; C18:0). SFAs share the same structural features, but differ in their molecular size. Figure 1 shows their chemical structure and their % composition in coconut oil. Because of the apparent similarity in their chemical structures, SFAs are often assumed to possess the same biochemical and physiological properties. This is not true.

Coconut oil is an important chemical feedstock for the oleochemical industry*. It is hydrolyzed and separated into its individual fatty acids. Lauric acid (C12), the main component of coconut oil, has the highest commercial value and is used in the manufacture of various surfactants. There was a need to find applications for the other fatty acids. In the 1960s, a new synthetic group of fats was developed – “medium-chain triglyceride” (MCT) – which was made up mainly of C8 and C10. This commercial mixture was later called “MCT oil” and the main component fatty acids, C8 and C10, were called “medium-chain fatty acids” (MCFA). Initial feeding studies on rats showed that MCT oil was non-toxic and did not lead to weight gain compared with lard (Senior, 1968). Human clinical trials later showed that MCT oil was useful for patients with lipid disorders and for weight loss and it became commercially available in the mid-1960s (Harkins & Sarett, 1968). Since then, MCT oil has been widely used in clinical practice as a special dietary oil and has been classified by the US FDA as GRAS (generally recognized as safe) (FDA, 2012). Because of its wide commercial availability and safety, medical researchers use MCT oil in their research. Consequently, most medical researchers consider MCFA to include C8 and C10 only; by exclusion, they use the term “long-chain” fatty acids (LCFA) to mean the longer SFAs, C12 and longer.

*The oleochemical industry uses fatty acids from vegetable and animal fats for various applications, such as polymers, surfactants, paints, coatings, engine lubricants, and others.

Figure 1. Chemical structure of saturated fatty acids and their % composition in coconut oil (Codex, 2015).

This historical account clearly shows that the classification of MCFA as C8 and C10 was based on the commercial availability of MCT oil and not on scientific considerations, and its wide use in clinical research reinforced this. However, based on biochemical and physiological properties, the classification of MCFA should include the fatty acids from C6 to C12.**

**It is relevant to mention here that commercial products with a composition that includes C6 to C12 are now available for special dietary purposes, such as a ketone diet (see later).

Numerous researchers consider MCFAs to include the fatty acids from C6 to C12 based on their metabolic properties (Bach & Babayan, 1982; St. Onge & Jones, 2002; McCarty & DiNicolantonio, 2016; Schonfeld & Wojtczak, 2016; TMIC, 2017). MCFAs possess special properties that differentiate them from LCFAs. This section will highlight some of the special characteristics of MCFAs in general, and C12 in particular, will show why using only the single category of “saturated fatty acid” is a half-truth.

 

SFAs in various fats and oils

All biological organisms and cells utilize different fatty acids to produce lipids that are characteristic of the organism and cell type to fulfill its structural or functional requirements. The fatty acid profiles of the various vegetable oils are characteristic of the plant source (Codex, 2015). Coconut oil has a characteristic fatty acid profile that differs from other vegetable oils in terms of its fatty acid profile: almost 50% is C12, about 65% is C6 to C12, and 92% is saturated. In contrast, the fatty acid profiles of all other vegetable oils start mainly with C16 and contain a significant proportion of unsaturated fatty acids. For example, soybean oil and corn oil both contain over 50% C18:2 (linoleic acid, an omega-6 fatty acid) and over 80% total unsaturated fat. Even animal fats, such as beef fat and lard, contain a substantial amount of unsaturated fat. For example, both beef fat and lard contain about 60% total unsaturated fatty acids even though these are often referred to as “saturated fat”. Clearly, the fatty acid composition of coconut oil is very different from those of animal fats, including butter (Figure 2).

Another feature that sets the group of MCFAs (C6 to C12) apart is that they are not generally present in human abdominal fat and liver fat, and they are not constituents of serum lipids, whether as triglycerides or phospholipids. Analysis of fats in the liver using mass spectral imaging analysis did not detect any MCFA; the smallest fatty acid found was C14 (Debois et al., 2009). This is consistent with the claims that MCFAs (C6 to C12) comprise a separate category from LCFA and that the use of “SFA” as a common label for this group is incomplete.

 

Figure 2. Fatty acid composition of various lipids: vegetable oils, animal fat, and human storage and structural lipids.


1 Codex 2013; 2015
 


2 Gunstone, 1996; Mansson, 2008
 


3 Kotronen et al., 2010
 

Another distinguishing characteristic of the group of MCFA (C6 to C12) is that they are rarely found attached to cholesterol as fatty acid ester derivatives. Plasma cholesterol is attached to long chain saturated and unsaturated fatty acid esters, in particular C16:0, C18:0, C18:1, C18:2, and C20:4 (AOCS, 2014). That is, LCFA and PUFA are involved with the circulation of cholesterol around the blood stream and cholesterol deposited in arterial plaques, not MCFA.

 

Metabolic properties of SFAs

The metabolic properties of the various SFAs clearly show differences between MCFA and LCFA. Here, we describe three major steps: first, lipase hydrolysis to release the free fatty acid; second, transport of the free fatty acid across the membrane to enter the cell; and third, mitochondrial oxidation to produce energy.

The first step involves the release of fatty acids from the triglyceride, a process called hydrolysis. In a study of various triglycerides using rat pancreatic lipase, C12 was found to be released most rapidly, followed by C4 (butyrate) (Mattson & Volpenhein, 1969).

The second limiting step in the metabolism of SFAs is the rate at which it can cross the membranes of cells where they can be metabolized. MCFA can cross the membrane rapidly while LCFA and PUFA require carnitine (Bremer, 1983; Schafer et al., 1997; Hamilton, 1998). The third step is fatty acid oxidation. In human liver mitochondria, C12 is more rapidly and completely oxidized compared with C18 (DeLany et al., 2000). This is one reason why coconut oil is not fattening and is better for metabolic energy than other vegetable oils.

Thus, a detailed accounting of the steps in the metabolism of SFAs shows that their properties and behavior are not the same. MCFA (C6 to C12) are clearly different from LCFA (C14 and longer).

 

Ketogenesis

Ketogenesis refers to the production of ketone bodies (KBs) – beta-hydroxybutyrate (BHB), acetoacetate (Acac) and acetone – from the metabolism of fat mainly in the liver. Ketone bodies are energy-rich molecules that are released by the liver into circulation to be used by other tissues and organs, such as the heart, brain and muscles (Krebs, 1970; Liu, 2008). This is the basis for the ketogenic diet.

There are three ways of inducing ketogenesis: first, by ingestion of MCFAs; second, by taking a very high-fat diet (greater than 80%) using on a long-chain vegetable oil, such as corn oil or soybean oil (Akkaoui 2009); and third, by fasting.

Upon ingestion and entering the small intestine, fatty acids are channeled either to the portal vein going directly to the liver, or are repackaged into other lipid bodies (called chylomicrons) to enter the bloodstream. MCFAs pass directly through the portal vein to the liver where they are converted into ketone bodies. Thus, MCFAs provide the most convenient and rapid way of producing ketone bodies. LCFAs and PUFAs are packaged into chylomicrons and are bound to cholesterol and circulate around the bloodstream after which they are deposited in the liver (Bach & Babayan, 1982).

 

The unique properties of C12

C12 has special properties that are not shared even by other MCFAs: its distribution in the small intestine is variable; and it has strong antimicrobial properties.

Distribution in intestine. C12 is unique because its distribution between the portal vein and lymphatic system depends on the feeding condition (You et al., 2008). Under normal conditions, most of the C12 is channeled to the portal vein. However, a concentrated injection of C12 has been shown to distribute about half to the portal vein and half to the lymphatic system (Sigalet et al., 1997). Ingestion of C12 together with proteins may direct more C12 to the lymphatic system (Schonfeld & Wojtczak, 2016) (Figure 3). This special behavior of C12 was foretold as early as the 1950s, when some researchers suggested the additional categories of “intermediate-chain fatty acids” (Schon et al., 1955; Goransson, 1965; Knox et al., 2000), and “transition fatty acid” (You et al., 2008).

 

Figure 3. Hydrolysis of triglycerides and distribution of various fatty acids between the portal vein and bloodstream. Depending on the dietary condition, C12 can be distributed to both in varying amounts.

 

Antimicrobial properties. C12 is recognized as the most effective antimicrobial fatty acid. C12 and its monoglyceride, monolaurin, have significant antimicrobial activity against gram positive bacteria and a number of fungi and viruses. Considering its antimicrobial property, it is an important property that some C12 can enter the bloodstream to provide antimicrobial protection. Because C12 and monolaurin are non-toxic and inexpensive, many food and cosmetic products use these compounds as antimicrobial agents. Interestingly, some antimicrobial natural products have been discovered that have a C12 group attached. Other MCFAs, C8 and C10, have limited antimicrobial activity; LCFAs have very little, if any, antimicrobial activity (Dayrit, 2015).

 

To summarize the discussion thus far: MCFA (C6 to C12) have very different biochemical and physiological properties from LCFA (C14 to C18). However, not once did the 2017 AHA Presidential Advisory refer to the existence of MCFA and LCFA and simply used the general category of SFA. This is not scientifically justifiable, and for a scientific society like the AHA, this is inexcusable.

 

“Saturated fat” and “animal fat” in the scientific literature

The vast majority of epidemiological studies, starting from Ancel Keys (1957) to the present, have failed to distinguish MCFA and LCFA and make their conclusions using the gross category of SFA. Unlike PUFAs, which are differentiated as omega-6 and omega-3, most epidemiologists, except those who study coconut oil in the diet, ignore the differences between MCFA and LCFA. In fact, most doctors and nutritionists commit the error of lumping animal fats and coconut oil into one category. Is it any wonder then that the wrong dietary advice has been made for coconut oil and C12?

There are, however, a few papers that have specifically addressed C12. In 2003, Mensink and co-workers combined the results of 60 controlled trials into a single analysis (called a meta-analysis) and calculated the effects of the amount and type of fat on the ratio of total cholesterol to HDL (high-density lipoprotein), as well as to lipids. They reported that C12 increased HDL so that the net effect was to decrease the ratio of total cholesterol to HDL, a beneficial result. On the other hand, the LCFAs C14 and C16:0 had little effect on the ratio, while C18:0 reduced the ratio slightly. This is certainly a favorable result for C12.

Interestingly, the 2017 AHA Presidential Advisory also disposed of the beneficial properties of HDL without adequate proof, proclaiming that now CHD would be all about LDL: “…changes in HDL-cholesterol caused by diet or drug treatments can no longer be directly linked to changes in CVD, and therefore, the LDL-cholesterol-raising effect should be considered on its own.”

Since HDL is generally considered a standard lipid indicator, it is incumbent upon the AHA to provide definitive evidence to support its claim that HDL is now useless as a predictor of CHD.

Today, several types of LDL particles are known. LDL particles can be small and dense LDL (sdLDL) or large and buoyant (lbLDL). sdLDL is more susceptible to oxidation producing oxidized LDL (oxLDL). Thus sdLDL is more atherogenic and has been shown to be a strong predictor of CHD, while large buoyant LDL is not (Toft-Petersen et al., 2011; Hoogeveen et al., 2014).

In a 10-year study in Finland on 1,250 subjects, the various types of lipoproteins – LDL, HDL, and oxLDL – were measured. The study concluded that oxLDL, in proportion to LDL and HDL, was a strong risk factor of all-cause mortality independent of confounding factors (Linna et al., 2012). Furthermore, it has also been reported that the ratio of triglyceride to HDL is also a predictor for coronary disease (da Luz et al., 2008). If this is the case, HDL should remain an important lipid parameter, contrary to the AHA proclamation.

In the case of LDL, the absence of data on sdLDL and oxLDL in early studies involving LDL measurements makes their conclusions questionable. Correlations which have been made between LDL and CHD cannot therefore be considered reliable.

 

Conclusion

The warnings against saturated fat started with Ancel Keys. Keys never showed any appreciation for the physiologic differences between medium-chain fat and long-chain fat. The AHA has adopted this position to ignore the distinction between MCFA and LCFA despite numerous advances in their science. Detailed comparison of the fatty acid composition shows that coconut oil is very different from animal fat and studies that assume that they are similar are therefore in error. These may be one of the reasons why the Dietary Guidelines have not worked.

To this conclusion, we can apply the warning that Benjamin Franklin once made:

Half a truth is often a great lie.”
 

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