Coconut Health Benefits

COCONUT AND ITS ANTI-BACTERIAL FUNCTIONS

Lauric acid, the major fatty acid from the fat of the coconut, has been recognized for its unique properties in food use, which are related to its antiviral, antibacterial, and antiprotozoal functions. Desiccated coconut is about 69% coconut fat, as is creamed coconut. Approximately 50% of the fatty acids in coconut fat are lauric acid. Lauric acid is a medium chain fatty acid, which has the additional beneficial function of being formed into monolaurin in the human or animal body. Monolaurin is the antiviral, antibacterial, and antiprotozoal monoglyceride used by the human or animal to destroy lipid-coated viruses such as HIV, herpes, cytomegalovirus, influenza, various pathogenic bacteria, including listeria monocytogenes and helicobacter pylori, and protozoa such as giardia lamblia. Some studies have also shown some antimicrobial effects of the free lauric acid.

Also, approximately 6-7% of the fatty acids in coconut fat are capric acid. Capric acid is another medium chain fatty acid, which has a similar beneficial function when it is formed into monocaprin in the human or animal body. Monocaprin has also been shown to have antiviral effects against HIV and is being tested for antiviral effects against herpes simplex and antibacterial effects against chlamydia and other sexually transmitted bacteria.

Adapted from: Coconut: In Support of Good Health in the 21st Century by Mary G. Enig, Ph.D., F.A.C.N.
Full story: http://coconutoil.com/coconut_oil_21st_century

MONOLAURIN AND AIDS

Monolaurin is an antiviral, antibacterial, and antiprotozoal monoglyceride that your body makes from the lauric acid in the fat in motherís milk, in cowís milk, and lauric fats such as coconut oil and palm kernel oil. The largest and easiest source of lauric acid is coconut oil (and or course whole coconut products). There is extensive scientific literature on its efficacy. Lauric acid is turned into monolaurin in the gut and this is what keeps infants fed human milk from getting sick even when they exposed to lipid coated viruses and various pathogenic organisms.

The AIDS virus is killed by monolaurin. Why it is not more extensively used is probably related to the fact that most people donít understand what it does and why it does it, even when you explain the effects. There have been some reported benefits for several years from both monolaurin capsules and coconut; however, this has all been anecdotal reporting and there have not been any properly conducted clinical trial.

Source: Know Your Fats. The Complete Primer for Understanding the Nutrition of Fats, Oils and Cholesterol. Enig, Mary, G. Ph.D. 2000.

COCONUT AS THE NATURAL SOURCE OF LAURIC ACID

LAURIC ACID

Lauric acid or dodecanoic acid, its chemical name, is the most potent fatty acid there is. Most of it is naturally found in coconut oil. More than half of the fatty acids found in coconut oil is lauric (C12). Together with caprylic acid (C8) and capric acid (C10), these three make up the medium chain fatty acid (MCFA) content of coconut oil.

MCFAs are the “antimicrobial powerhouse” behind coconut oil’s ability to cure and prevent a growing list of disease and illness. Lauric, capric and caprylic acids and their respective monoglycerides, monolaurin, monocaprin and monocaprylin, all exhibit antimicrobial activity that boosts your immune system. Of all the MCFAs, lauric (C12) acid appears to have the greatest overall effect.

Below are just some of the microorganisms destroyed by this mighty MCFA.

  • AIDS virus (HIV)
  • Chlamydia pneumoniae
  • Herpes simplex virus II
  • Gram-positive organisms
  • Hepatitis C virus
  • Group A, B, F, and G streptococci
  • Helicobacter pylor
  • Measles virusi
  • Listeria monocytogenes
  • Leukemia virus
  • Streptococcus agalactiae
  • Influenza virus
  • Staphylococcus aureus
  • Epstein-Barr virus
  • Hemophilus influenzae
  • Sarcoma virus
  • Escherichia coli (E. coli)

Lauric acid is not just about killing bacteria, viruses, fungi and other harmful organisms. This magnificent MCFA tends to improve cholesterol ratio by increasing HDL (good) cholesterol. It also enhances the ability of your pancreas to secrete insulin.

Source: http://www.coconut-oil-central.com/lauric-acid.html


Coconut Milk

COCONUT OIL HAS LOWER FAT CALORIES THAN OTHER OILS AND FATS

Coconut oil is the world’s only, low calorie fat. Coconut oil has at least 2.56% fewer calories per gram of fat than other fats and oils. The coconut oil contains only 6.8 calories per gram versus 9 calories per gram for other oils. It is unique among oils in that it promotes weight loss.

Coconut oil is thermogenic. The special fats in coconut oil called medium chain fatty acids (MCFAs) are not stored in your body as fat. It raises the bodyís metabolism, and even prevents the accumulation of fat by burning calories and converting fat into energy. Coconut oil is natural fat burner and bodyís energy booster since its digestion is different from that of carbohydrates and bodyís energy booster since its digestion is different from that of carbohydrates and protein. It is ideal for weight loss.

Calorie Chart

Source: COCONUT: PHILIPPINES. Villafuerte-Abonal, Lalaine. 2007.

HEALTH FACTS ABOUT COCONUTS

  • Coconut oil has lower calories than any other fats.
  • MCFAs in coconut oil promote thermogenesis which increases the bodyís metabolism.
  • MCFA in coconut oil is faster to digest and has better solubility in biological fluids.
  • Coconut oil is used to facilitate absorption of calcium and magnesium, both of which are essential for bone development.
  • MCFA in coconut oil can destroy illness-causing viruses, fungi and bacteria easily on contact similar to the colostrums of motherís milk.
  • Lauric acid in coconut oil is good for geriatic patients as it contributes to faster surgical recovery.
  • MCFAs in coconut oil can kill gram-positive cocci.
  • Capric and lauric acid in coconut oil can kill Candida albicans, a common yeast infection found in those who have used antibiotic excessively.

COCONUT CONTAINS ZERO TRANS FATS

What is trans-fat?

Trans-fat, also called Trans fatty acids (TFA), is formed when hydrogen is added to a vegetable oil to make a more solid fat like shortening or margarine. This process is called hydrogenation, and it is used to increase the shelf life and maintain the flavor and texture of foods.

Trans-fats behave like saturated fats by raising the ìbadî cholesterol, low-density lipoprotein (LDL), which may increase risk of coronary heart disease (CHD), a leading cause of death in the United States.

Source: Trans Fat Fact Sheet. USDA. http://www.fns.usda.go
Full story: http://www.fns.usda.gov


Shredded Coconut

COCONUT IS GOOD FOR DIABETICS

Blood sugar is an important issue for anyone who is concerned about heart disease, overweight, hypoglycaemia, and especially diabetes because it affects all of these conditions.

Carbohydrates in our foods are broken down in the digestive tract and converted into glucose (blood sugar). Meals that contain a high concentration of carbohydrates, particularly simple carbohydrates such as sugar and refined flours, cause a rapid rise in blood sugar. Since elevated blood sugar can lead to a coma and death, insulin is frantically pumped into the blood stream to avoid this. If insulin is produced in adequate amounts blood sugar is soon brought back down to normal. This is what happens in most individuals. However, if insulin is not produced quickly enough or if the cells become desensitized to the action of insulin, blood glucose can remain elevated for extended periods of time. This is what happens in diabetes.

Dietary fiber helps moderate swings in blood sugar by slowing down the absorption of sugar into the blood stream. This helps keep blood sugar and insulin levels under control. Coconut fiber has been shown to be very effective in moderating blood sugar and insulin levels. For this reason, coconut is good for diabetics.

Diabetics are encouraged to eat foods that have a relatively low glycemic index. The glycemic index is a measure of how foods affect blood sugar levels. The higher the glycemic index, the greater an effect a particular food has on raising blood sugar. So diabetics need to eat foods with a low glycemic index. When coconut is added to foods, including those high in starch and sugar, it lowers the glycemic index of these foods. This was clearly demonstrated by T. P. Trinidad and colleagues in a study published in the British Journal of Nutrition in 2003. In their study, both normal and diabetic subjects were given a variety of foods to eat. Some of the types of food included cinnamon bread, granola bars, carrot cake, and brownies, all foods that a diabetic must ordinarily limit because of their high sugar and starch content. It was found that as the coconut content of the foods increased, the blood sugar response between the diabetic and non-diabetic subjects became nearly identical. In other words, coconut moderated the release of sugar into the bloodstream so that there was no spike in blood glucose levels. As the coconut content in the foods decreased, the diabetic subjectsí blood sugar levels became elevated, as would normally be expected from eating foods high in sugar and white flour. This study showed that adding coconut to foods lowers the glycemic index of the foods and keeps blood sugar levels under control. Sweet foods such as cookies and cakes made using coconut flour do not affect blood sugar levels like those made with wheat flour. This is good news for diabetics who want a treat now and then without adversely affecting their blood sugar.

Source: Coconut Flour: A Low Carb, Gluten-Free, Alternative to Wheat by Bruce Fife, ND.
Full story: http://www.coconutresearchcenter.org/newsletter-sample.htm

CAN COCONUT OIL BE ATHEROGENIC?

According to the universally accepted Lipid-Heart Theory, high saturated fats cause hypercholesterolemia and coronary heart disease. Coronary morbidity and mortality are said to be highest in the countries and peoples consuming the highest amounts of saturated fats. Coconut oil, with its saturated medium chain fats, has been especially condemned for this reason. The true facts are just the opposite. The countries consuming the highest amounts of coconut oil ñ the Polynesians, Indonesians, Sri Lankans, Indians, Filipinos ñ have not only low serum cholesterol but also low coronary heart disease rates – morbidity and mortality.

The reason why coconut oil cannot be atherogenic is basic. Coco oil consists predominantly of 65% medium chain fatty acids (MCFA) and MCFAs are metabolized rapidly in the liver to energy and do not participate in the biosynthesis and transport of cholesterol. Coconut oil, in fact, tends to raise the HDL and lower the LDL:HDL ratio. Coco oil is not deposited in adipose tissues and therefore does not lead to obesity. It is primarily an energy supplier and as fast a supplier of energy as sugar.

MCFAs therefore differ in their metabolism from all the long chain fatty acids, whether saturated or unsaturated.

The pathogenesis of atherosclerosis has recently taken a complete paradigm shift – from a simple deposition of cholesterol and cholesterol esters to an inflammatory condition where numerous genetically dependent factors – dyslipoproteinemias, dysfunctions of endothelial and other cells leading to invasions of the subendothelial region by macrophages, smooth muscle cells, leukocytes and T cells ñ all interplay in a scenario still not fully understood. This will be discussed at length and whatever role fat deposition plays appears late in atherogenesis and secondary to oxidation process and the overriding role of the dysfunctional endothelium. Coconut oil has no role at all to play in this highly complex and still ill understood process.

Adapted from: COCONUT OIL: Atherogenic or Not? By Conrado S. Dayrit, MD, FPCC, FPCP, FACC. Philippine Journal Of Cardiology. July-September 2003, Volume 31 Number 3:97-104.
Full story PDF: http://www.coconutoil.com/DayritCardiology.pdf



Shredded Coconut

COCONUT CONTAINS HIGH AMOUNT OF DIETARY FIBER

Fiber Chart
HEALTH BENFITS OF DIETARY FIBER
  • Aids weight control and reduces risk of developing obesity.
  • Forms a vital part of the diet by adding mass to the stool which eases elimination.
  • Soluble dietary fibers can be useful for controlling blood glucose in patients with diabetes.
  • Soluble dietary fiber also inhibits cholesterol absorption from small intestines thereby reducing serum cholesterol.
  • Plays a key role in preventing cancer of the large intestines commonly called colon cancer.

Sources: USDA National Nutrient Database for Standard Reference Release

COCONUT FOR WEIGHT MANAGEMENT

Effects of dietary coconut oil on the biochemical and anthropometric profiles of women presenting abdominal obesity.

Assunão ML, Ferreira HS, dos Santos AF, Cabral CR Jr, Florêncio TM.

Faculdade de Nutricão, Universidade Federal de Alagoas, Maceió, AL 57072-970, Brazil.

Abstract

The effects of dietary supplementation with coconut oil on the biochemical and anthropometric profiles of women presenting waist circumferences (WC) >88 cm (abdominal obesity) were investigated. The randomised, double-blind, clinical trial involved 40 women aged 20-40 years. Groups received daily dietary supplements comprising 30 mL of either soy bean oil (group S; n = 20) or coconut oil (group C; n = 20) over a 12-week period, during which all subjects were instructed to follow a balanced hypocaloric diet and to walk for 50 min per day. Data were collected 1 week before (T1) and 1 week after (T2) dietary intervention. Energy intake and amount of carbohydrate ingested by both groups diminished over the trial, whereas the consumption of protein and fiber increased and lipid ingestion remained unchanged. At T1 there were no differences in biochemical or anthropometric characteristics between the groups, whereas at T2 group C presented a higher level of HDL (48.7 +/- 2.4 vs. 45.00 +/- 5.6; P = 0.01) and a lower LDL:HDL ratio (2.41 +/- 0.8 vs. 3.1 +/- 0.8; P = 0.04). Reductions in BMI were observed in both groups at T2 (P < 0.05), but only group C exhibited a reduction in WC (P = 0.005). Group S presented an increase (P < 0.05) in total cholesterol, LDL and LDL:HDL ratio, whilst HDL diminished (P = 0.03). Such alterations were not observed in group C. It appears that dietetic supplementation with coconut oil does not cause dyslipidemia and seems to promote a reduction in abdominal obesity.

Source: Pubmed. US National Library of Medicince. http://www.ncbi.nlm.nih.gov/pubmed/19437058
Full story: http://www.ncbi.nlm.nih.gov/pubmed/19437058



Coconut Products

Coconut Products and Their Uses

Each component of the coconut, from husk and fiber to the natural extracts has an extremely valuable route to market, which contributes to increasing the value of the crop. Able to outlive any man who plants it, the coconut tree’s ability to supply an abundance of essential nutrients has earned it the titles of 'Jewel of the Tropics', 'King of Trees' and 'The Tree of Life'. Some of the most valuable products are gathered below, but the list is by no means comprehensive.

Activated Carbon Filtration

Extensive research in this field is producing multiple industry applications for activated carbon produced from coconut husks and shells. Traditional uses in water purification for both groundwater and drinking water filtration are being joined by applications in nuclear plants, solvent recovery and utilization in catalytic converters.

  • A high carbon content makes coconut shells a perfect source to produce activated carbon
  • Coconut based activated carbon has the most microporous pore structure, and has the highest hardness compared to other types of activated carbon. This makes it the best carbon for water filtration
  • It generates the least ash during production
  • The carbon can be reactivated
Lauric Acid

Coconut Oil contains 50% lauric acid, most commonly used in soap production and manufacturing cosmetics. In humans, lauric acid is converted into monolaurin, a compound which has antiviral, antimicrobial and antifungal properties.

Biodiesel

Coco-Biodiesel is created by processing pure coconut oil and converting it to a diesel-like product. It is set to become a more prominent part of the worldwide biofuel blend as pressure mounts on international governments to employ cleaner burning and non-toxic alternative fuels from renewable sources. Biodiesels will reduce greenhouse gas emissions, and can be used in diesel engines without modifications.

  • Brazil is one of the world’s largest biofuel consumers and has 10 million flex-fuel cars on its roads
  • The global consumption of ethanol and biodiesel is projected to reach 135 billion gallons by the year 2018
  • Coconut oil burns more slowly than diesel engines, reducing engine wear and lubricating the engine more efficiently
Fibers

Coconut husk fibers, also known as coir, come from the large outer casing that surrounds the hard brown nut. These tough fibers are used to make mats, packaging, mattresses and brushes. It can even be rubberized and used as an eco-friendly alternative to plastics, an application car manufacturer Ford is currently researching.

Husks and Shells

The husks and shells have historically been used as charcoal and as a potting medium for growing saplings. However, the most recent demand, and one that looks set to grow, is the use of the husks and shell as biomass fuel.

  • Biomass energy is responsible for over 75 per cent of the world’s renewable energy, and demand for woody biomass is increasing rapidly
  • Global demand for biomass products is estimated to increase by 600 per cent over the next 20 years, according to the International Institute for Environment and Development
Milk

Coconut milk is made by pressing the flesh of the coconut or by passing hot water or milk through grated coconut.

There is a high demand for this product within the food industry, particularly in the Asian market where it features in many traditional dishes.

The milk is a premium cooking product in Western markets and is being added to shopping baskets more readily as consumers develop a taste for Eastern flavors.

Water

The sweet water from young coconuts is a refreshing, nutrient-packed liquid ubiquitous in tropical countries like Brazil, Indonesia and India where coconut trees are indigenous.

Coconut water is expanding beyond its traditional markets. Beverage giants PepsiCo and Coca-Cola, and a host of smaller niche suppliers, are promoting the product to a wider global market.

  • The latest available data shows that the market for coconut water in key demographics grew by 26% annually between 2007-11
  • Although still in its infancy, the coconut water market in the United States was valued at $350m in 2012 and continues to experience super-normal growth
  • Brazil, with the world’s fifth biggest population (196m people), is the largest market for packaged coconut water, where it accounts for 70% of total beverage volume sales
  • More than 200 brands are now in the global marketplace, including major players Vita Coco, Zico (Coca-Cola has a stake in the company) and O.N.E. (PepsiCo's investment). PepsiCo also owns Amacoco, Brazil's largest coconut water producer
  • Celebrities have played a major role in boosting the commercial profile of coconut water brands; Vita Coco has chosen Rihanna to front its international marketing and Madonna has invested directly in the company.
Oil

Coconut oil is a stable and well-established commodity that has been traded globally for more than fifty years.

Extracted from the dried white flesh of the coconut, coconut oil is a multi-purpose liquid that can be used as a cholesterol cutting cooking oil, healthcare product and biofuel feedstock.

  • The oil is anti-viral, anti-bacterial, anti-fungal and anti-microbial
  • Coconut oil products have been shown to tackle Alzheimer’s, tooth decay and all manner of medical conditions
  • It is increasingly popular in the pharmaceutical industry which is ploughing millions of dollars into further research of its medicinal properties
  • The price of coconut oil has more than doubled over the last decade and exports of virgin coconut oil to major Western markets have doubled in the last year


VCO

The Truth About Coconut Oil

American Coconut Association Statement
We collectively respect the American Heart Association (AHA) and its general research in advancing heart health; however, we respectfully disagree with their findings on coconut oil. The statement from the AHA has created some confusion and sharing of misinformation. Knowledge is power and it is important to clarify a few important points. Coconut oil was never positioned as low in saturated fats and not all saturated fats are equal. The AHA did not qualify or differentiate between the medium chain fatty acids (MCTs) found in coconut from the long chain triglycerides found in animal fats. In addition, coconut oil contains no cholesterol, while animal fats do.

The saturated fats found in coconut oil is fairly unique in that in that they are made up of short and medium chain fatty acids, which are metabolized differently in the body than the longer chain fatty acids that make up the saturated fats in animal sources.

Studies have demonstrated that MCTs are absorbed directly into the blood stream and are converted to ketones in the liver, where they are then burned as energy rather than absorbed in the body. MCTs make up the majority of fatty acids in coconut oil – around 65% – and do not act in the same way in the body as longer chain saturated fatty acids. The MCTs in high-quality coconut oil like organic virgin coconut oil (which is made from fresh and cold-pressed coconut meat) have been shown to increase metabolism.

As a society of informed consumers, education and sharing of accurate, science backed information is one of our most powerful tools. There are numerous articles from leading experts in the nutrition, medical, and holistic fields, as well as, scientific studies with in depth information supporting the benefits of coconut oil. We encourage you to explore these works to make the best decision for your own personal health and wellness

www.ncbi.nlm.nih.gov/pubmed/26545671
United Coconut Associations of the Philippines, Inc.
UNITED COCONUT ASSOCIATION OF THE PHILIPPINES (UCAP) ON THE AMERICAN HEART ASSOCIATION (AHA)WARNING ON SATURATED FAT

JUNE 21, 2017: The AHA issued last June 15 a Presidential Advisory on Dietary Fats and Cardiovascular Disease(CVD), effectively a warning on saturated fat. This has gone viral with coconut oil unfortunately on the receiving end because coconut oil is a saturated fat. With a respectable body like AHA, any warning on cardiovascular health gets a lot of weight on people’s perception.

Such warning on coconut oil, however, is not new at all. It has been there for the last 35 years and in eight editions of the Dietary Guidelines for Americans. While the warning is on saturated fats, notably animal fats, coconut oil was included because saturated fats generally connote coconut oil and vice• versa. Coconut oil is not a home-grown oil in the US. Despite the guidelines calling for reduction in the intake of saturated fats, data indicate heart disease remains the leading cause of death in the US, thus a total failure.

It all started from a saturated fat-cholesterol-heart disease hypothesis that Ansel Keys proposed back in 1957 that aimed to show a direct correlation between cholesterol and heart disease. However, this was never proven even to this day. Researches done to prove the hypothesis were fatally flawed and biased against coconut oil. For example, the human feeding studies used hydrogenated coconut oil while the observational studies included coconut oil which was only a minor part of the population’s diet. Keys knew beforehand that hydrogenated oils raise serum cholesterol and triglycerides. Other studies such as the Minnesota Coronary Survey, the Sydney Heart Study, and the Women’s Health Initiative were rejected by AHA because results refuted the hypothesis.

Lately, the US Dietary Guidelines has recommended low-fat and low-saturated fat in the diet. The recommendation has increased the incidence of rising obesity, diabetes and other metabolic diseases as this resulted into higher consumption of sugar and carbohydrates. Moreover, the Guidelines also resulted into a diet high in omega-6 fatty acid and low omega-3 fatty acid at a ratio of 15:1, far from the ideal 4:1. Such a high ratio is blamed for CVD, cancer and chronic inflammatory and autoimmune diseases.

There have been no indications that saturated fats or coconut oil as having caused inflammation, therefore not a culprit in CVD. Alternatively, there is much less consumption of coconut oil in food in the US where the main vegetable oils used are soybean oil and corn oil. Besides, more recent and updated studies reveal dietary cholesterol is not the culprit in cardiovascular disease, but inflammation.

The 2017 AHA Presidential Advisory selectively cited old research that is supportive of their intent to correlate saturated fats with CVD. It failed to distinguish medium-chain saturated fats and long-chain saturated fats. Coconut oil is mostly medium-chain saturated fats, which is the healthy type of fat.

The website of The Coconut Research Center (coconutresearchcenter.org) compiles thousands of studies on coconut oil and cardiovascular health and other ailments. This resource will provide an overwhelming amount of research to support coconut oil as a healthy oil.

We call on readers and users of coconut oil to be discerning of this advisory, and the news articles who draw the wrong conclusion to misinform consumers. More recent and updated studies establish that there is no direct correlation between coconut oil and CVD.

Truly, history is repeating itself. The smear campaign against coconut oil is a rehash of the anti-tropical oils campaign waged by the American Soybean Association in the 1980s. The anti-coconut oil sentiment is back and this time has gone viral because of technology.

There is a motive behind the AHA Presidential Advisory and it is being used to misinform the public. We urge users of coconut oil to draw on their personal experiences. Recognize its health benefits, and join us in overcoming the malicious campaign on coconut oil.

Refer: United Coconut Association of the Philippines 4f Coconut Center, 291 Dansalan St. Bgy. Barangka llaya, Mandaluyong City Tel: (+63-2) 5310351 Email:ucap@ucap.org.ph


Coconut Oil: The Truth Behind the American Heart Association Advisory on Saturated Fats Are Bad for Heart Health

By Dr. Bruce Fife, CN, ND

The AMA (AHA) report is written specifically to denounce coconut oil using deceptive tactics. There is nothing new here, it is the same old argument that saturated fats raise cholesterol and the evil cholesterol is going to kill you.

You cannot say LDL is bad and HDL is good. It is more complex than that. There are actually two types of LDL: one small and dense the other large and soft. The large LDL is a good cholesterol the type used to make bile, hormones, and vitamin D–it is essential to life! The small dense LDL is the type that becomes oxidized and can be harmful, as all oxidized lipids can be. Eating coconut oil (and other saturated fats) increases both HDL and the “good” LDL, thus lowering the risk of heart disease. This is one of the reasons why populations that eat a lot of coconut oil have the lowest heart disease rates in the world.

Articles and studies criticizing coconut oil (and other saturated fats) do not make the distinction between the two types of LDL and simply call them all bad–this is bad science! The authors purposely do this to slant the article in an effort to deceive the reader–most of whom do not understand that that are two types of LDL.

The AMA (AHA) report is simply a marketing gimmick sponsored by the pharmaceutical industry to keep the outdated and false cholesterol-heart disease hypothesis alive and promote the sales of cholesterol drugs.

The Warning on Saturated Fat: From Defective Experiments to Defective Guidelines

Dr. Fabian M. Dayrit Professor, Ateneo de Manila University, Philippines Chairman, Scientific Advisory Committee for Health, Asian and Pacific Coconut Community June 19, 2017

Abstract

Coconut oil has been adversely affected by the current dietary guidelines that advocate a lowering of total fat and the replacement of saturated fat with polyunsaturated fat. This recommendation has its origins in the saturated fat-cholesterol-heart disease hypothesis that Ancel Keys first proposed in 1957. This hypothesis became an official recommendation with the publication of the Dietary Guidelines for Americans in 1980 and has been adopted by many other countries and international agencies. The dietary recommendations also warn against coconut oil. Recently, the American Heart Association re-issued this warning in its 2017 Presidential Advisory. However, a critical review of the experiments that Keys conducted has revealed experimental errors and biases that cast serious doubt on the correctness of his hypothesis and the warnings against coconut oil. Further, the recommendation to decrease saturated fat recommendation effectively means an increase in unsaturated fat in the diet. The actual result has been an increase in omega-6 fats and a high omega-6 to omega-3 fat ratio. This unhealthy ratio has been linked to heart disease, the very disease that the AHA wants to target, as well as cancer and inflammatory diseases. Defective experiments have led to defective guidelines. This first paper in this series of papers will present these errors and biases and address the points raised by the AHA.

Abbreviations: AHA: American Heart Association; CHD: coronary heart disease; CVD: cardiovascular disease; HFCS: high fructose corn syrup; MCS: Minnesota Coronary Survey; PUFA: polyunsaturated fatty acid; SDHS: Sydney Diet Heart Study; SFA: saturated fatty acid

Introduction: the Dietary Guidelines

The Vital Statistics of the United States 1976 listed “diseases of heart” as the leading cause of death in the US (USDHHS, 1980). From 1980 to 2015, there were eight editions of the Dietary Guidelines for Americans which sought to address the problem of heart disease. In all eight editions of the Dietary Guidelines, there was one warning that was consistent: “Decrease overall fat intake and replace saturated fat with unsaturated fat.” However, in 2016, heart disease continued to be the leading cause of death in the US (CDC, 2016).In its 2017 Presidential Advisory, the American Heart Association continued to emphatically recommend that “lowering intake of saturated fat and replacing it with unsaturated fats, especially polyunsaturated fats, will lower the incidence of CVD (Sacks et al., 2017).

Albert Einstein famously defined insanity as: “doing the same thing over and over again and expecting different results.” This essay aims to show how the Dietary Guidelines and the AHA recommendation are examples of insanity.

The warning against “saturated fat” is virtually the same recommendation that Ancel Keys made in the 1950s. The Keys hypothesis, generally known as the saturated fat- cholesterol-heart disease hypothesis, states that saturated fats raise serum cholesterol which in turn increases the risk for heart disease. Although the saturated fats that are most often studied are animal fats, coconut oil is often included in this warning because it is a saturated fat.

This first paper will discuss the basis for the recommendations against coconut oil and saturated fat. We will review of the work of Ancel Keys which reveals several errors that invalidate his strictures against coconut oil.

Errors in the Keys experiments

Keys committed several serious errors that cast doubt on the validity of his saturated fat-cholesterol-heart disease hypothesis with respect to coconut oil. He conducted both human feeding and observational studies. In his human feeding studies, Keys used hydrogenated coconut oil, while in his observational studies coconut oil was only a minor component of the population’s diet. Finally, Keys was never able to unambiguously prove his hypothesis and refused to acknowledge results that contradicted his hypothesis.

Keys used hydrogenated coconut oil in his human feeding studies

In 1957,Keys published two important papers, one in the Journal of Nutrition (Anderson, Keys & Grande, 1957) and the other in Lancet (Keys, Anderson, Grande, 1957) on controlled feeding studies using schizophrenic patients from the Hastings State Hospital, businessmen in Minnesota, and Japanese coalminers in Shime, Japan. These were relatively small, short-term feeding studies with the number of subjects ranging from 16 to 66. In these studies, Keys wanted to compare the effects on serum cholesterol of feeding monounsaturated and polyunsaturated fats versus saturated fats. For sources of unsaturated fats, he used corn oil, olive oil, cottonseed oil, safflower oil, and sardine oil. For sources of saturated fats, he used butterfat, margarine and hydrogenated coconut oil (Hydrol) in the Minnesota experiment and margarine in the Shime experiment.

The use of hydrogenated fats – margarine and Hydrol – in this feeding study casts doubt on the validity of the conclusions of this work regarding the effects of coconut oil. It was already known in the 1920s that hydrogenation of vegetable oils produced trans fats (Hilditch & Vidyarthi, 1929). In 1957, the same year when both Keys papers came out, it was reported that trans fats were deposited in various human tissues, such as adipose tissues, liver, aortic tissue, and atheroma of those who died of atherosclerosis (Johnston, Johnson, Kummerow, 1957). In a 1961 paper on hydrogenated fats, Keys himself noted that hydrogenated oils raised serum cholesterol and triglycerides (Anderson, Grande, Keys, 1961). Therefore, the increase in serum cholesterol that Keys observed may have been due to the trans fats in margarine and hydrogenated coconut oil and this would make his conclusions invalid. The use of hydrogenated coconut oil may also have biased Keys’s judgment against coconut oil.

The Seven Countries Study was not a representative study

Keys described the evolution of the Seven Countries Study in a book that he published in 1980. Keys conducted initial studies on CHD in 1947 in Minnesota on healthy businessmen and professionals. In 1952, this study expanded to include Italy and Spain, in 1956, Japan and Finland. The aim of these studies was to identify dietary and lifestyle factors in apparently healthy middle-aged men that contributed to CHD. However, this study had two built-in limitations which would give results that are not representative. First, to ensure higher probability of successful follow-up (every 5 years), the study targeted rural populations so that 11 of the 16 cohorts studied were rural populations. For the US, since the stability of rural populations could not be assured, the American subjects selected were railroad men and to balance this effect, Italian railroad men were also selected. Second, the basis for the selection of the seven countries was not systematic but was decided by the availability of collaborators. As Keys himself stated, it was the availability of research collaborators that became the deciding factor in the selection of subject areas (Keys, 1980). It is clear that there was no scientific basis for the selection of the seven countries and these limitations should have been declared so that sweeping generalizations could be avoided.

The Seven Countries Study was begun in 1956 and ended with the publication of the 1986 paper (Keys et al., 1986). The most important conclusions from the Seven Countries Study were given as follows:

“Death rates were related positively to average percentage of dietary energy from saturated fatty acids, negatively to dietary energy percentage from monounsaturated fatty acids …. All death rates were negatively related to the ratio of monounsaturated to saturated fatty acids… Oleic acid accounted for almost all differences in monounsaturates among cohorts. All-cause and coronary heart disease death rates were low in cohorts with olive oil as the main fat.”

There are a number of important things that should be noted regarding the Seven Countries Study: First, this study cannot be claimed to be representative for all types of oils and for all groups of people. Second, the beneficial oil claimed in the Seven Countries Study was olive oil and it should be compared only to the other fats and oils that were consumed, which was mainly animal fat. Interestingly, although Japan showed very low death rates, olive oil consumption in Japan was negligible (Pitts et al., 2007). Third, this study assumed that all saturated fats have the same properties regardless of chain length. This assumption is not valid given what is known today regarding the individual properties of saturated fatty acids (this will be discussed in a succeeding article).

Coconut oil was not a significant part of the diet in the Seven Countries Study

Coconut oil was not a significant part of the diet in any of the seven countries and it was not mentioned in the 1986 Keys paper. Based on the consumption record for the year 1961, the estimated amount of animal fat consumed in Northern and Southern Europe was 67.5% and 35.7%, respectively, while for coconut oil, it was 5.9% and 1.6%. In the US, the amount of animal fat in the diet was 51% versus 3% for coconut oil (FAOSTAT, 2006; Pitts et al., 2007). Clearly, coconut oil was an insignificant part of the diet in Europe and the US so how did coconut oil get included in the health warnings on heart disease?

The Low-fat Diet and Obesity

The first official recommendation on saturated fat was contained in the first Dietary Guidelines for Americans which was jointly issued by the US Department of Agriculture and the US Department of Health and Human Services in 1980 and updated every 5 years. From the first to the eighth edition of Dietary Guidelines, the recommendation on saturated fat remained fundamentally the same: consume a low fat diet and avoid saturated fat. In the 2010 edition, the recommendation was made more specific: “consume less than 10% of calories from saturated fatty acids by replacing them with monounsaturated and polyunsaturated fatty acids.”

Cohen and co-workers (2015) conducted a comprehensive analysis of the food consumption patterns together with the body weight and body mass index of the US adult population using data from the US National Health and Nutrition Examination Survey (NHANES). They found that Americans in general have been following the nutrition advice from the Dietary Guidelines. In particular from 1971 to 2011, consumption of fats dropped from 45% to 34% of total caloric intake, but this was accompanied by an increase in carbohydrate consumption from 39% to 51%. The result was a dramatic increase in the percentage of overweight or obese Americans from 42% to 66% over the same period. It is surprising that the AHA would continue to recommend the “low-fat diet” in light of the obesity epidemic among Americans.

Keys failed to prove his Saturated Fat-Cholesterol-Heart Disease Hypothesis

Since the Seven Countries Study was an observational study, Keys wanted to do a study where he could carefully control the diet of the subjects. In 1967, Ivan Frantz, Jr. and Ancel Keys undertook a project entitled “Effect of a Dietary Change on Human Cardiovascular Disease,” also called the “Minnesota Coronary Survey” (MCS). This study was funded by the US National Heart, Lung and Blood Institute and was undertaken from 1968 to 1973. MCS was meant to be a landmark study because of the large number of subjects (n=9,423), the length of the feeding study (5 years), the high level of dietary control, and the double blind randomized design. MCS used residents in a nursing home and patients in six state mental hospitals in Minnesota. This enabled the study to carefully control and document the food that was actually consumed. This study sought to test whether replacement of saturated fat (animal fat, margarines and shortenings) with vegetable oil rich in linoleic acid (mainly corn oil) will reduce all-cause death, and CHD in particular, by lowering serum cholesterol. Coronary atherosclerosis and myocardial infarcts were also checked in 149 autopsies conducted (Ramsden et al., 2016). This study was conducted at the same time that Keys was coordinating the Seven Countries Study and would have provided powerful validation of the saturated fat- cholesterol-heart disease hypothesis.

Unfortunately, Keys did not publish the results of this study. A partial release of the results of MCS study was made in a 1989 paper in the journal Arteriosclerosis with Frantz as lead author. This paper made the modest conclusion that: “For the entire study population, no differences between the treatment (high linoleic acid group) and control (high saturated fat group) were observed for cardiovascular events, cardiovascular deaths, or total mortality.” (Frantz et al., 1989). Interestingly, although Keys was a co-proponent of the MCS study, his name did not appear as a co-author in the Arteriosclerosis paper; he was not even mentioned in the Acknowledgment.

The full data were discovered in the basement of the home of Frantz by his son, Robert, who turned them over to Ramsden and co-workers, who then analyzed and interpreted the data (O’Connor, 2016). The key results from the MCS study were reported by Ramsden and co-workers (2016) and are summarized as follows:

  • The group that consumed the high linoleic acid diet showed significant reduction in serum cholesterol compared with those on the saturated fat group.
  • However, there was no difference in mortality among the groups.
  • There was a higher risk of death in subjects who showed reduction in serum cholesterol level.
  • The main conclusions from this study are as follows: a high linoleic acid diet effectively lowers serum cholesterol but this increases the risk of CHD.

    The results of the MCS study did not give the expected results and directly contradicted the conclusions of the Seven Countries Study which Keys had published in a few years earlier in 1986. This might explain why it was published in a journal of limited circulation which gave it less exposure. It is clear that a wider distribution of the results of the 1989 paper, with Keys properly included as co-author, would have been fatal to the saturated fat-cholesterol-heart disease hypothesis and to the scientific basis of Dietary Guidelines, which was going into its third edition.

    The recovered MCS study is not the only example of an unreported study which had negative results. The Sydney Diet Heart Study (SDHS) was conducted from 1966 to 1973, almost at the same time as the MCS study, with the same objectives and similar study design to evaluate the effectiveness of replacing dietary saturated fat with linoleic acid for the prevention of CHD and all-cause mortality. This was a single blinded, parallel group, randomized controlled trial involving 458 men aged 30-59 years with a recent coronary event. The intervention involved replacement of dietary saturated fats (from animal fats, common margarines, and shortenings) with omega-6 linoleic acid (from safflower oil and safflower oil polyunsaturated margarine). The primary outcome was all-cause mortality and the secondary outcomes were CHD and death from heart disease. The results of this study were contrary to expectation: the unsaturated fat group had higher rates of death than the animal fat group, both in terms of all-cause mortality and CVD mortality. Similar to the recovered MCS study, the SDHS data were not reported but were recovered for analysis by Ramsden and co-workers almost 40 years after it was conducted (Ramsden et al., 2013).

    In addition to the hidden MCS and SDHS studies, there are a number of published studies that contradicted the saturated heart-cholesterol-heart disease hypothesis. A six-year dietary study of 21,930 Finnish men, aged 50-69 years, concluded that there was no association between the intake of saturated fat and monounsaturated fat with the risk of coronary death (Pietinen et al., 1997). A dietary study of 80,082 women in the US Nurses’ Health Study, aged 34–59 years, with a 14-year follow-up, failed to come up with an unambiguous conclusion on the link between saturated fat and CHD (Hu et al., 1999). A study involving 58,453 Japanese men and women, aged 40-79 years, with a 14- year follow-up, gave an inverse association between SFA intake and mortality from total cardio vascular disease and concluded that replacing SFA with PUFA would have no benefit for the prevention of heart disease (Yamagishi et al., 2010).

    One would think that these studies should be enough evidence to prove that the saturated fat-cholesterol-heart disease hypothesis is wrong. Unfortunately, the 2017 AHA Presidential Advisory did not cite these studies and instead went out of its way to discredit the results of the Minnesota Coronary Survey and the Sydney Diet Heart Study so that they could remove these studies from the “totality of the scientific evidence (that) satisfy rigorous criteria for causality.”

    In 1981, Steven Broste, who was then a MS student at the University of Minnesota, analyzed the MCS data and addressed the difficulties that the AHA used to reject this study. These issues included withdrawals and uneven feeding periods of subjects. After making the appropriate statistical corrections, Broste still came to the conclusion that: “the experimental diet of the MCS may actually have been harmful in some way to patients who were exposed to it for at least one year” (Broste, 1981, p 85), and that “the experimental diet of the MCS, and reductions in cholesterol that resulted from the diet, were counterproductive… cholesterol reductions were generally associated with increased mortality, especially among males and older patients” (Broste, 1981, p 97).Broste’s conclusions were consistent with those of Frantz and co-workers (1989) and Ramsden and co-workers (2016). Contrary to the claims of the AHA, the MCS results are valid: low serum cholesterol increases the risk of CHD. It is unfortunate that the AHA chose to dismiss the results of the MCS and SHDS studies as lacking in scientific rigor.

    High PUFA consumption and high omega-6 to omega-3 ratio: A dietary disaster

    The low-fat and low-saturated fat recommendation of the Dietary Guidelines may be the reason for rising obesity, diabetes, and other metabolic diseases among Americans. The low-fat recommendation has effectively increased the consumption of sugar and carbohydrates. Since 1980, consumption of fats fell by 11% of total caloric intake (from 45% to 34%), while consumption of carbohydrates rose by 12% (from 39% to 51%) (Cohen et al., 2015). The consumption of soybean oil, a high omega-6 polyunsaturated oil, more than doubled during the same period and now accounts for over 90% of vegetable oil consumption in the US (Index Mundi, 2016). Because soybean oil is a polyunsaturated oil, it is susceptible to the formation of free radicals, malondialdehyde, trans fats, and polymeric material during frying (Brühl, 2014).

    The other major problem with the Dietary Guidelines is that it has resulted in a diet with excessive omega-6 fatty acid resulting in an average omega-6 to omega-3 ratio of about 15:1. Such a high ratio has been blamed for cardiovascular disease, cancer, and chronic inflammatory, and autoimmune diseases. The ideal omega-6 to omega-3 ratio is about 4:1 (Simopoulos 2002, 2008, 2010).

    AHA should worry about the impact of too much soybean oil – not coconut oil – on the American diet. It should also rethink its support for the Dietary Guidelines.

    From defective experiments to defective guidelines

    Despite its widespread adoption, the saturated fat-cholesterol-heart disease hypothesis has been shown to be incorrect. Ancel Keys committed a number of errors and was unable to unambiguously demonstrate a causal link for the role of saturated fat in heart disease. The twenty-five year old, 8-edition Dietary Guidelines for Americans, which has a great influence on international guidelines, has failed to address the problem of heart disease. Defective experiments can only lead to defective guidelines, and defective guidelines can only result in poor health outcomes.

    References:

  • Anderson JT, Grande F, Keys A (1961). Hydrogenated Fats in the Diet and Lipids in the Serum of Man. J. Nutr. 75: 388-394.
  • Anderson JT, Keys A, Grande F (1957). The effects of different food fats on serum cholesterol concentration in man. J Nutr. 62: 421-444.
  • Broste SK (1981). Lifetable Analysis of the Minnesota Coronary Survey. MS thesis, University of Minnesota.
  • Brühl L (2014). Fatty acid alterations in oils and fats during heating and frying. Eur. J. Lipid Sci. Technol. 116: 707-715.
  • [CDC] Center for Disease Control. 2016. https://www.cdc.gov/dhdsp/data_statistics/fact_sheets/docs/fs_heart_disease.pdf[Codex] Codex Alimentarius 210-1999, amended 2015; Codex Alimentarius 33-1981, amended 2013.
  • Cohen E, Cragg M, deFonseka J, Hite A, Rosenberg M, Zhou B (2015). Statistical review of US macronutrient consumption data, 1965–2011: Americans have been following dietary guidelines, coincident with the rise in obesity. Nutrition 31: 727–732.
  • [FAOSTAT] Food and Agriculture Organisation Statistics Data. 2006. World lipid availability, Kg/capita/year, 1961. Food Balance Sheets, Rome: FAO.
  • Frantz Jr. ID, Dawson EA, Ashman PL, Gatewood LC,Bartsch GE, Kuba K, Elizabeth R. Brewer ER (1989). Arteriosclerosis 9:129-135.
  • Hilditch TP, Vidyarthi NL (1929). The products of partial hydrogenation of higher monoethylenic esters. Proc. Roy. Soc. A, 122(790): 552-563.
  • Hu FB, Stampfer MJ, Manson JE, Ascherio A, Colditz GA, Speizer FE, Hennekens CH, C Willett WC (1999). Dietary saturated fats and their food sources in relation to the risk of coronary heart disease in women. Am. J. Clin. Nutr. 70:1001–1008.
  • Index Mundi (2016). http:// www.indexmundi.com/
  • Keys A, Anderson JT, Grande F (1957). Prediction of serum-cholesterol responses of man to changes in fats in the diet. Lancet 959-966.
  • Keys A, Aravanis C, Blackburn H, Buzina R, Djordjević BS, Dontas AS, Fidanza F, Karvonen MJ, Kimura N, Menotti A, Mohacek I, Nedeljkovic S, Puddu V, Punsar S, Taylor HL, van Buchem FSP (1980). Seven Countries. A Multivariate Analysis of Death and Coronary Heart Disease. Harvard University Press, Cambridge, Massachusetts.
  • Keys A, Menotti A, Karvonen MJ, Aravanis C, Blackburn H, Buzina R, Djordjevic BS, Dontas AS, Fidanza F, Keys MH, Kromhout D, Nedeljkovic S, Punsar S, Seccareccia F, Toshima H (1986). The diet and 15-year death rate in the Seven Countries Study. Am. J. Epidemiol. 124(6): 903-915.
  • O’Connor A (2016). 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
  • 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.
  • Pitts M, Dorling D, Pattie C (2007). Oil for Food: The Global Story of Edible Lipids. Journal of World- Systems Research, Volume XIII, Number 1, Pages 12-32. ISSN 1076-156X.
  • Ramsden CE, Zamora D, Leelarthaepin B, Majchrzak-Hong SF, Faurot KR, Suchindran CM, Ringel A, Davis JM, Hibbeln JR (2013). Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis. BMJ 2013;346:e8707.
  • Ramsden CE, Zamora D, Majchrzak-Hong S, R Faurot KR, Broste SK, Frantz RP, Davis JM, Ringel A, Suchindran CM, Hibbeln JR (2016). Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73). BMJ 2016;353:i1246 http://dx.doi.org/10.1136/bmj.i1246.
  • 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.
  • 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.
  • [USDA] United States Department of Agriculture (2017). United States Department of Agriculture. Food Composition Databases. https://ndb.nal.usda.gov/; (downloaded: May 15, 2017).
  • [USDHHS] U.S. Department of Health and Human Services. 1980. Vital Statistics of the United States 1976. Volume II- Mortality. Part A. National Center for Health Statistics. Hyattsville, Maryland.
  • 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.
  • Yamagishi K, Iso H, Yatsuya H, Tanabe N, Date C, Kikuchi S, Yamamoto A, Inaba Y, Tamakoshi A, (JACC Study Group) (2010). Dietary intake of saturated fatty acids and mortality from cardiovascular disease in Japanese: the Japan Collaborative Cohort Study for Evaluation of Cancer Risk (JACC) Study. Am. J. Clin. Nutr. 92:759-765.

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

    Dr. Fabian M. Dayrit Professor, Ateneo de Manila University, Philippines Chairman, Scientific Advisory Committee for Health, Asian and Pacific Coconut Community

    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

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

    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.

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

  • Article 2 Fig 1

    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.†

    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)

    † 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).

    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.

    Article 2 Fig 2

    Article 2 Fig 2a

    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.

    Article 2 Fig 3

    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.

    “Sa tur ated fa t” an d “a ni mal 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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    Coconut Oil: Bringing History, Common Sense and Science Together

    Dr. Fabian M. Dayrit Professor, Department of Chemistry, Ateneo de Manila University, Philippines Chairman, Scientific Advisory Committee for Health, Asian and Pacific Coconut Community

    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 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: “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” (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 hadreached 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.