Complete history on coconut oil & heart disease

[Guest guest]

coconut, in support of good health- http://www.apcc.org.sg/special.htm -

The research over four decades concerning coconut oil in the diet and heart

disease is quite clear: coconut oil has been shown to be beneficial.

See section V.

Elaine

 

 

Coconut: In Support of Good Health in the 21st Century

by

Mary G. Enig, Ph.D., F.A.C.N.

12501 Prosperity Drive, Suite 340, Silver Spring, MD, 20904-1689 USA

Tel: (301) 680-8600 Fax: (301) 680-8100

Abstract

 

Coconuts play a unique role in the diets of mankind because they are the

source of important physiologically functional components. These

physiologically functional components are found in the fat part of whole

coconut, in the fat part of desiccated coconut, and in the extracted coconut

oil. Lauric acid, the major fatty acid from the fat of the coconut, has

long been recognized for the unique properties that it lends to nonfood uses

in the soaps and cosmetics industry. More recently, lauric acid has been

recognized for its unique properties in food use, which are related to its

antiviral, antibacterial, and antiprotozoal functions. Now, capric acid,

another of coconut's fatty acids has been added to the list of coconut's

antimicrobial components. These fatty acids are found in the largest

amounts only in traditional lauric fats, especially from coconut. Also,

recently published research has shown that natural coconut fat in the diet

leads to a normalization of body lipids, protects against alcohol damage to

the liver, and improves the immune system's anti-inflammatory response.

Clearly, there has been increasing recognition of health- supporting

functions of the fatty acids found in coconut. Recent reports from the U.S.

Food and Drug Administration about required labeling of the trans fatty

acids will put coconut oil in a more competitive position and may help

return to its use by the baking and snack food industry where it has

continued to be recognized for its functionality. Now it can be recognized

for another kind of functionality: the improvement of the health of

mankind.

 

I. INTRODUCTION

Mr. Chairman and members of the Asian Pacific Coconut Community, I would

like to thank you for inviting me to once again speak to this gathering of

delegates on the occasion of your 36th session as you celebrate the 30th

anniversary of APCC.

 

When I addressed the 32nd COCOTECH meeting in Cochin, India, I covered two

areas of interest to the coconut community. In the first part, I reviewed

the major health challenge facing coconut oil at that time, which was based

on a supposed negative role played by saturated fat in heart disease. I

hope that my talk was able to dispel any acceptance of that notion. In the

second part of my talk I suggested that there were some new positive health

benefits from coconut that should be recognized. These benefits stemmed

from coconut's use as a food with major functional properties for

antimicrobial and anti-cancer effects.

 

In my presentation today, I will bring you up to date about the new

recognition of functional foods as important components in the diet.

Additionally, I would like to briefly review the state of the

anti-saturated fat situation and bring you up to date on some of the

research that compares the beneficial effects of saturated fats with those

of omega-6 polyunsaturates, as well as the beneficial effects of the

saturated fats relative to the detrimental effects of the partially

hydrogenated fats and the trans fatty acids. In particular I will review

some of the surprising beneficial effects of the special saturates found in

coconut oil as they compare with those of the unsaturates found in some of

the other food oils. Components of coconut oil are increasingly being shown

to be beneficial. Increasingly, lauric acid, and even capric acid, have

been the subject of favorable scientific reports on health parameters.

 

II. FUNCTIONAL PROPERTIES OF LAURIC FATS AS ANTIMICROBIALS

Earlier this year, at a special conference entitled, " Functional Foods For

Health Promotion: Physiologic Considerations " ; EXPERIMENTAL BIOLOGY '99,

Renaissance Washington Hotel, Washington, DC Saturday, April 17, 1999, which

was sponsored by the International Life Sciences Institute, ILSI NORTH

AMERICA, Technical Committee on Food Components for Health Promotion, the

term " functional foods " was defined as " a functional food provides a health

benefit over and beyond the basic nutrients. "

 

This is exactly what coconut and its edible products such as desiccated

coconut and coconut oil do. As a functional food, coconut has fatty acids

that provide both energy (nutrients) and raw material for antimicrobial

fatty acids and monoglycerides (functional components) when it is eaten.

Desiccated coconut is about 69% coconut fat, as is creamed coconut. Full

coconut milk is approximately 24% fat.

 

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. (Reuters, London June 29, 1999) See below for details.

 

The food industry has, of course, long been aware that the functional

properties of the lauric oils, and especially coconut oil, are unsurpassed

by other available commercial oils. Unfortunately, in the U.S., both during

the late 1930s and again during the 1980s and 1990s, the commercial

interests of the U.S. domestic fats and oils industry were successful in

driving down usage of coconut oil. As a result, in the U.S. and in other

countries where the influence from the U.S. is strong, the manufacturer has

lost the benefit of the lauric oils in its food products. As we will see

from the data I will present in this talk, it is the consumer who has lost

the many health benefits that can result from regular consumption of coconut

products.

 

The antiviral, antibacterial, and antiprotozoal properties of lauric acid

and monolaurin have been recognized by a small number of researchers for

nearly four decades: this knowledge has resulted in more than 20 research

papers and several U.S. patents, and this past year it resulted in a

comprehensive book chapter, which reviewed the important aspects of lauric

oils as antimicrobial agents (Enig 1998). In the past, the larger group of

clinicians and food and nutrition scientists has been unaware of the

potential benefits of consuming foods containing coconut and coconut oil,

but this is now starting to change.

 

Kabara (1978) and others have reported that certain fatty acids (FAs) (e.g.,

medium-chain saturates) and their derivatives (e.g., monoglycerides (MGs))

can have adverse effects on various microorganisms: those microorganisms

that are inactivated include bacteria, yeast, fungi, and enveloped viruses.

Additionally, it is report-ed that the antimicro----bial effects of the FAs

and MGs are additive, and total concentration is critical for inactivating

virus-es (Isaacs and Thormar 1990).

 

The properties that determine the anti-infective action of lipids are

related to their structure: e.g., monoglycerides, free fatty acids. The

monoglycerides are active; diglycerides and triglycerides are inactive. Of

the saturated fatty acids, lauric acid has greater antiviral activity than

either caprylic acid (C-8), capric acid (C-10), or myristic acid (C-14). In

general, it is reported that the fatty acids and monoglycerides produce

their killing/inactivating effect by lysing the plasma membrane lipid

bilayer. The antiviral action attributed to monolaurin is that of

solubilizing the lipids and phospholipids in the envelope of the virus,

causing the disintegration of the virus envelope. However, there is

evidence from recent studies that one antimicrobial effect in bacteria is

related to monolaurin's interference with signal transduction (Projan et al

1994), and another antimicrobial effect in viruses is due to lauric acid's

interference with virus assembly and viral maturation (Hornung et al 1994).

 

Recognition of the antiviral aspects of the antimicrobial activity of the

monoglyceride of lauric acid (monolaurin) has been reported since 1966.

Some of the early work by Hierholzer and Kabara (1982) that showed virucidal

effects of monolaurin on enveloped RNA and DNA viruses was done in

conjunction with the Center for Disease Control of the U.S. Public Health

Service. These studies were done with selected virus prototypes or

recognized representative strains of enveloped human viruses. The envelope

of these viruses is a lipid membrane, and the presence of a lipid membrane

on viruses makes them especially vulnerable to lauric acid and its

derivative monolaurin.

 

The medium-chain saturated fatty acids and their derivatives act by

disrupting the lipid membranes of the viruses (Isaacs and Thormar 1991;

Isaacs et al 1992). Research has shown that enveloped viruses are

inactivated in both human and bovine milk by added fatty acids and

monoglycerides (Isaacs et al 1991), and also by endogenous fatty acids and

monoglycerides of the appropriate length (Isaacs et al 1986, 1990, 1991,

1992; Thormar et al 1987).

 

Some of the viruses inactivated by these lipids, in addition to HIV, are the

measles virus, herpes simplex virus-1 (HSV-1), vesicular stomatitis virus

(VSV), visna virus, and cytomegalovirus (CMV). Many of the pathogenic

organisms reported to be inactivated by these antimicrobial lipids are those

known to be responsible for opportunistic infections in HIV-positive

individuals. For example, concurrent infection with cytomegalovirus is

recognized as a serious complication for HIV+ individuals (Macallan et al

1993). Thus, it would appear to be important to investigate the practical

aspects and the potential benefit of an adjunct nutritional support regimen

for HIV-infected individuals, which will utilize those dietary fats that are

sources of known antiviral, antimicrobial, and antiprotozoal monoglycerides

and fatty acids such as monolaurin and its precursor lauric acid.

 

Until now, no one in the mainstream nutrition community seems to have

recognized the added potential of antimicrobial lipids in the treatment of

HIV-infected or AIDS patients. These antimicrobial fatty acids and their

derivatives are essentially nontoxic to man; they are produced in vivo by

humans when they ingest those commonly available foods that contain adequate

levels of medium-chain fatty acids such as lauric acid. According to the

published research, lauric acid is one of the best " inactivating " fatty

acids, and its monoglyceride is even more effective than the fatty acid

alone (Kabara 1978, Sands et al 1978, Fletcher et al 1985, Kabara 1985).

 

The lipid-coated (envelope) viruses are dependent on host lipids for their

lipid constituents. The variability of fatty acids in the foods of

individuals as well as the variability from de novo synthesis accounts for

the variability of fatty acids in the virus envelope and also explains the

variability of glycoprotein expression, a variability that makes vaccine

development more difficult.

 

Monolaurin does not appear to have an adverse effect on desirable gut

bacteria, but rather on only potentially pathogenic microorganisms. For

example, Isaacs et al (1991) reported no inactivation of the common

Escherichia coli or Salmonella enteritidis by monolaurin, but major

inactivation of Hemophilus influenzae, Staphylococcus epidermidis and Group

B gram positive streptococcus.

 

The potentially pathogenic bacteria inactivated by monolaurin include

Listeria monocytogenes, Staphylococcus aureus, Streptococcus agalactiae,

Groups A,F & G streptococci, gram-positive organisms, and some gram-negative

organisms if pretreated with a chelator (Boddie & Nickerson 1992, Kabara

1978, Kabara 1984, Isaacs et al 1990, Isaacs et al 1992, Isaacs et al 1994,

Isaacs & Schneidman 1991, Isaacs & Thormar 1986, Isaacs & Thormar 1990,

Isaacs & Thormar 1991, Thormar et al 1987, Wang & Johnson 1992).

 

Decreased growth of Staphylococcus aureus and decreased production of toxic

shock syndrome toxin-1 was shown with 150 mg monolaurin per liter (Holland

et al 1994). Monolaurin was 5000 times more inhibitory against Listeria

monocytogenes than ethanol (Oh & Marshall 1993). Helicobacter pylori is

rapidly inactivated by medium-chain monoglycerides and lauric acid, and

there appears to be very little development of resistance of the organism to

the bactericidal effects (Petschow et al 1996) of these natural

antimicrobials.

 

A number of fungi, yeast, and protozoa are inactivated or killed by lauric

acid or monolaurin. The fungi include several species of ringworm (Isaacs

et al 1991). The yeast reported is Candida albicans (Isaacs et al 1991).

The protozoan parasite Giardia lamblia is killed by free fatty acids and

monoglycerides from hydrolyzed human milk (Hernell et al 1986, Reiner et al

1986, Crouch et al 1991, Isaacs et al 1991). Numerous other protozoa were

studied with similar findings; these findings have not yet been published

(Jon J. Kabara, private communication, 1997).

 

Research continues in measuring the effect of the monoglyceride derivative

of capric acid monocaprin as well as the effects of lauric acid. Chlamydia

trachomatis is inactivated by lauric acid, capric acid, and monocaprin

(Bergsson et al 1998), and hydrogels containing monocaprin are potent in

vitro inactivators of sexually transmitted viruses such as HSV-2 and HIV-1

and bacteria such as Neisseria gonorrhoeae (Thormar 1999).

 

III. ORIGINS OF THE ANTI-SATURATED FAT AGENDA

The coconut industry has suffered more than three decades of abusive

rhetoric from the consumer activist group Center for Science in the Public

Interest (CSPI), from the American Soybean Association (ASA) and other

members of the edible oil industry, and from those in the medical and

scientific community who learned their misinformation from groups like CSPI

and ASA. I would like to review briefly the origins of the anti-saturated

fat, anti-tropical oil campaigns and hopefully give you some useful insight

into the issues.

 

When and how did the anti-saturated fat story begin? It really began in

part in the late 1950s, when a researcher in Minnesota announced that the

heart disease epidemic was being caused by hydrogenated vegetable fats. The

edible oil industry's response at that time was to claim it was only the

saturated fat in the hydrogenated oils that was causing the problem. The

industry then announced that it would be changing to partially hydrogenated

fats and that this would solve the problem.

 

In actual fact, there was no change because the oils were already being

partially hydrogenated, and the levels of saturated fatty acids remained

similar, as did the levels of the trans fatty acids. The only thing that

really changed was the term for hydrogenation or hardening listed on the

food label.

 

During this same period, a researcher in Philadelphia reported that

consuming polyunsaturated fatty acids lowered serum cholesterol. This

researcher, however, neglected to include the information that the lowering

was due to the cholesterol going into the tissues, such as the liver and the

arteries. As a result of this research report and the acceptance of this new

agenda by the domestic edible oils industries, there was a gradual increase

in the emphasis on replacing " saturated fats " in the diet and on the

consuming of larger amounts of the " polyunsaturated fats. " As many of you

probably know, this strong emphasis on consuming polyunsaturates has

backfired in many ways: the current adjustments being recommended in the

U.S. by groups such as the National Academy of Sciences replace the

saturates with monounsaturates instead of with polyunsaturates and replace

polyunsaturates with monounsaturates.

 

Early promoters of the anti-saturated fat ideas included companies such as

Corn Products Company (CPC International) through a book written by

Jeremiah Stamler in 1963, with the professional edition published in 1966 by

CPC. This book took some of the earliest pejorative stabs at the tropical

oils. In 1963, the only tropical fat or oil singled out as high in

saturated fats was coconut oil. Palm oil had not entered the U.S. food

supply to any extent, had not become a commercial threat to the domestic

oils, and was not recognized in any of the early texts. An observation by

the editorial staff of Consumer Reports noted that

" ...in 1962...one writer observed, the average American now fears fat

(saturated fat, that is) 'as he once feared witches.' "

 

In 1965, a representative of Procter and Gamble told the American Heart

Association to change its Diet/Heart statement, removing any reference to

the trans fatty acids. This altered official document encouraged the

consumption of partially hydrogenated fats. In the 1970s, this same Procter

and Gamble employee served as nutrition chairman in two controlling

positions for the National Heart Lung and Blood Institute's Lipid Research

Clinic (LRC) trials and as director of one of the LRC centers. These LRC

trials were the basis for the 1984 NIH Cholesterol Consensus

 

Conference, which in turn spawned the National Cholesterol Education Program

(NCEP). This program encourages consumption of margarine and partially

hydrogenated fats, while admitting that trans should not be consumed in

excess.

 

The official NCEP document states that " ...coconut oil, palm oil, and palm

kernel oil...should be avoided... "

In 1966, the U.S. Department of Agriculture documents on fats and oils

talked about how unstable the unsaturated fats and oils were. There was no

criticism of the saturated fats. That criticism of saturated fat was to

come later to this agency when it came under the influence of the domestic

edible fats and oils industry, and when it developed the U.S. Dietary

Guidelines. These Dietary Guidelines became very anti-saturated fat and

remain so to this day. Nevertheless, as we will learn later in my talk,

there has started some reversal of the anti-saturated fat stance in the

works in this agency in 1998.

 

In the early 1970s, although a number of researchers were voicing concerns

about the trans fats, the edible oil industry and the U.S. Food and Drug

Administration (FDA) were engaging in a revolving-door exchange that would

(i) promote the increasing consumption of partially hydrogenated vegetable

oils, (ii) would condemn the saturated fats, and (iii) hide the trans issue.

As an example of this " oily " exchange, in 1971 the FDA's general counsel

became president of the edible oil trade association, and he in turn was

replaced at the FDA by a food lawyer who had represented the edible oil

industry.

 

From that point on, the truth about any real effects of the dietary fats had

to play catch-up. The American edible oil industry sponsored " information "

to educate the public, and the natural dairy and animal fats industries were

inept at countering any of that misinformation. Not being domestically

grown in the U.S., coconut oil, palm oil, and palm kernel oil were not

around to defend themselves at that time. The government agencies

responsible for disseminating information ignored those protesting " lone

voices, " and by the mid-1980s, American food manufacturers and consumers had

made major changes in their fats and oils usage -- away from the safe

saturated fats and headlong into the problematic trans fats.

 

Enig and Fallon (1998/1999) have reviewed the above history in " The Oiling

of America " published in the Australian magazine Nexus. The magazine has

placed this review on the internet and it can be viewed or downloaded from

the Nexus website. The internet addresses for the websites are

http://www.peg.apc.org/~nexus/OilingAmerica.1.html and

http://www.peg.apc.org/~nexus/OilingAmerica.2.html.

 

IV. THE DAMAGING ROLE OF THE U.S. CONSUMER ACTIVIST GROUP CSPI

Some of the food oil industry (especially those connected with the American

Soybean Association (ASA)) and some of the consumer activists (especially

the Center for Science in the Public Interest (CSPI) and also the American

Heart Savers Association) further eroded the status of natural fats when

they sponsored the major anti-saturated fat, anti-tropical oils campaign in

the late 1980s.

 

Actually, an active anti-saturated fat bias started as far back as 1972 in

CSPI. But beginning in 1984, this very vocal consumer activist group

started its anti-saturated fat campaign in earnest. In particular, at this

time, the campaign was against the " saturated " frying fats, especially those

being used by fast-food restaurants. Most of these so-called saturated

frying fats were tallow based, but also included was palm oil in at least

one of the hotel/restaurant chains.

 

Then in a " News Release " in August 1986, CSPI criticized what it called

" Deceptive Vegetable Oil Labeling: Saturated Fat Without The Facts, "

referring to " palm, coconut, and palm kernel oil " as " rich in

artery-clogging saturated fat. "

 

CSPI further announced that it had petitioned the Food and Drug

Administration to stop allowing labeling of foods as having " 100% vegetable

shortening " if they contained any of the " tropical oils. " CSPI also asked

for mandatory addition of the qualifier " a saturated fat " when coconut, palm

or palm kernel oils were named on the food label.

In 1988, CSPI published a booklet called " Saturated Fat Attack. " This

booklet contained lists of processed foods " surveyed " in Washington, DC

supermarkets. The lists were used for developing information about the

saturated fat in the products. Section III is entitled " Those Troublesome

Tropical Oils, " and it contains statements encouraging pejorative labeling.

There were lots of substantive mistakes in the booklet, including errors in

the description of the biochemistry of fats and oils and completely

erroneous statements about the fat and oil composition of many of the

products.

 

At the same time CSPI was conducting its campaign in 1986, the American

Soybean Association began its anti-tropical oil campaign by sending

inflammatory letters, etc., to soybean farmers. The ASA took out

advertisements to promote a " [tropical] Fat Fighter Kit. " The ASA hired a

Washington DC " nutritionist " to survey supermarkets to detect the presence

of tropical oils in foods.

 

Then early in 1987, the ASA petitioned the FDA to require labeling of

" Tropical Fats, " and by mid-1987, the Soybean Digest continued an active and

increasing anti-tropical oils campaign. At about the same time (June 3,

1987), the New York Times published an editorial, " The Truth About

Vegetable Oil, " in which it called palm, palm kernel, and coconut oils " the

cheaper, artery-clogging oils from Malaysia and Indonesia " and claimed that

U.S. federal dietary guidelines opposed tropical oils, although it is not

clear that this was so. The " artery-clogging " terminology was right out of

CSPI.

 

Two years later in 1989, the ASA held a press conference with the help of

the CSPI in Washington DC in an attempt to counter the palm oil group's

press conference of 6 March. The ASA " Media Alert " stated that the National

Heart Lung and Blood Institute and National Research Council " recommend

consumers avoid palm, palm kernel and coconut oils. " Only months before

these press conferences, millionaire Phil Sokolof, the head of the National

Heart Savers Association (NHSA), purchased the first of a series of

anti-saturated fats and anti-tropical fats advertisements in major

newspapers. No one has found an overt connection between Sokolof (and his

NHSA) and the ASA, but the CSPI bragged about being his advisor.

 

 

V. WHAT ABOUT HEART DISEASE AND COCONUT OIL?

The research over four decades concerning coconut oil in the diet and heart

disease is quite clear: coconut oil has been shown to be beneficial. This

research leads us to ask the question, " should coconut oil be used to both

prevent and treat coronary heart disease? "

 

This statement is based on several reviews of the scientific literature

concerning the feeding of coconut oil to humans. Blackburn et al (1988)

have reviewed the published literature of " coconut oil's effect on serum

cholesterol and atherogenesis " and have concluded that when " ...[coconut oil

is] fed physiologically with other fats or adequately supplemented with

linoleic acid, coconut oil is a neutral fat in terms of atherogenicity. "

 

After reviewing this same literature, Kurup and Rajmohan (1995) conducted a

study on 64 volunteers and found " ...no statistically significant alteration

in the serum total cholesterol, HDL cholesterol, LDL cholesterol, HDL

cholesterol/total cholesterol ratio and LDL cholesterol/HDL cholesterol

ratio of triglycerides from the baseline values... " A beneficial effect of

adding the coconut kernel to the diet was noted by these researchers.

 

Kaunitz and Dayrit (1992) have reviewed some of the epidemiological and

experimental data regarding coconut-eating groups and noted that the

" available population studies show that dietary coconut oil does not lead to

high serum cholesterol nor to high coronary heart disease mortality or

morbidity. " They noted that in 1989 Mendis et al reported undesirable lipid

changes when young adult Sri Lankan males were changed from their normal

diets by the substitution of corn oil for their customary coconut oil.

Although the total serum cholesterol decreased 18.7% from 179.6 to 146.0

mg/dl and the LDL cholesterol decreased 23.8% from 131.6 to 100.3 mg/dl, the

HDL cholesterol decreased 41.4% from 43.4 to 25.4 mg/dl (putting the HDL

values very much below the acceptable lower limit of 35 mg/dl) and the

LDL/HDL ratio increased 30% from 3.0 to 3.9. These latter two changes are

considered quite undesirable. Mendis and Kumarasunderam (1990) also

compared the effect of coconut oil and soy oil in normolipidemic young

males, and again the coconut oil resulted in an increase in the HDL

cholesterol, whereas the soy oil reduced this desirable lipoprotein. As

noted above, Kurup and Rajmohan (1995), who studied the addition of coconut

oil alone to previously mixed fat diets, had reported no significant

difference from baseline.

 

Previously, Prior et al (1981) had shown that islanders with high intakes of

coconut oil showed " no evidence of the high saturated fat intake having a

harmful effect in these populations. " When these groups migrated to New

Zealand, however, and lowered their intake of coconut oil, their total

cholesterol and LDL cholesterol increased, and their HDL cholesterol

decreased. Statements that any saturated fat is a dietary problem is not

supported by evidence (Enig 1993).

 

Studies that allegedly showed a " hypercholesterolemic " effect of coconut oil

feeding, usually only showed that coconut oil was not as effective at

lowering the serum cholesterol as was the more unsaturated fat to which

coconut oil was being compared. This appears to be in part because coconut

oil does not " drive " cholesterol into the tissues as does the more

polyunsaturated fats. The chemical analysis of the atheroma shows that the

fatty acids from the cholesterol esters are 74% unsaturated (41% of the

total fatty acids is polyunsaturated) and only 24% are saturated. None of

the saturated fatty acids were reported to be lauric acid or myristic acid

(Felton et al 1994).

 

There is another aspect to the coronary heart disease picture. This is

related to the initiation of the atheromas that are reported to be blocking

arteries. Recent research shows that there is a causative role for the

herpes virus and cytomegalovirus in the initial formation of atherosclerotic

plaques and the reclogging of arteries after angioplasty. (New York Times

1991) What is so interesting is that the herpes virus and cytomegalovirus

are both inhibited by the antimicrobial lipid monolaurin, but monolaurin is

not formed in the body unless there is a source of lauric acid in the diet.

Thus, ironically enough, one could consider the recommendations to avoid

coconut and other lauric oils as contributing to the increased incidence of

coronary heart disease.

 

Chlamydia pneumoniae, a gram-negative bacteria, is another of the

microorganisms suspected of playing a role in atherosclerosis by provoking

an inflammatory process that would result in the oxidation of lipoproteins

with induction of cytokines and production of proteolystic enzymes, a

typical phenomena in atherosclerosis (Saikku 1997). Some of the pathogenic

gram-negative bacteria with an appropriate chelator have been reported to be

inactivated or killed by lauric acid and monolaurin as well as capric acid

and monocaprin (See above, Bergsson et al 1997 and Thormar et al 1999).

However, the microorganisms most frequently identified as probable causative

infecting agents are in the herpes virus family and include cytomegalovirus,

type 2 herpes simplex (HSV-2), and Coxsackie B4 virus. The evidence for a

causative role for cytomegalovirus is the strongest (Ellis 1997, Visseren et

al 1997, Zhou et al 1996, Melnick et al 1996, Epstein et al 1996, Chen &

Yang 1995), but a role for HSV-2 is also shown (Raza-Ahmad et al 1995). All

members of the herpes virus family are reported to be killed by the fatty

acids and monoglycerides from saturated fatty acids ranging from C-6 to C-14

(Isaacs et al 1991), which include approximately 80% of the fatty acids in

coconut oil.

In spite of what has been said over the past four or more decades about the

culpability of the saturated fatty acids in heart disease, they are

ultimately going to be held blameless. More and more research is showing

the problem to be related to oxidized products. One protection man has

against oxidized products is the naturally saturated fats such as coconut

oil.

 

VI. THE LATEST ON THE TRANS FATTY ACIDS

Both the United States and Canada will soon require labeling of the trans

fatty acids, which will put coconut oil in a more competitive position than

it has been in the past decade. A fear of the vegetable oil manufacturers

has always been that they would have to label trans fatty acids. The

producers of trans fatty acids have relied on the anti-saturated fat crusade

to protect their markets. However, the latest research on saturated fatty

acids and trans fatty acids shows the saturated fatty acids coming out ahead

in the health race.

 

It has taken this last decade, from 1988 to 1998, to see changes in

perception. During this period, the trans fatty acids have taken a deserved

drubbing. Research reports from Europe have been emerging since the seminal

report by Mensink and Katan in 1990 that the trans fatty acids raised the

low density lipoprotein (LDL) cholesterol and lowered the high density

lipoprotein (HDL) cholesterol in serum. This has been confirmed by studies

in the U.S. (Judd et al 1994, Khosla and Hayes 1996, Clevidence 1997).

 

In 1990, the lipids research group at the University of Maryland published a

paper (Enig et al 1990) correcting some of the erroneous data sponsored by

the food industry in the 1985 review by the Life Sciences Research Office of

Federation of American Societies for Experimental Biology (LSRO-FASEB)

(Senti 1985) of the trans fatty acids.

Also, in 1993, a group of researchers at Harvard University, led by

Professor Walter Willett, reported a positive relationship between the

dietary intake of the trans fatty acids and coronary heart disease in a

greater than 80,000 cohort of nurses who had been followed by the School of

Public Health at Harvard University for more than a decade.

 

Pietinen and colleagues (1997) evaluated the findings from the large cohort

of Finnish men who were being studied for a cancer prevention study. After

controlling for the appropriate variables including several coronary risk

factors, the authors observed a significant positive association between the

intake of trans fatty acids and the risk of death from coronary disease.

There was no association between intakes of saturated fatty acids, or

dietary cholesterol and the risk of coronary deaths. This is another

example of the differences between the effects of the trans fatty acids and

the saturated fatty acids and further challenge to the dietary cholesterol

hypothesis.

 

The issue of the trans fatty acids as a causative factor in remains

underexplored, but recent reports have found a connection. Bakker and

colleagues (1997) studied the data for the association between breast-cancer

incidence and linoleic acid status across European countries since animal

and ecological studies had suggest a relationship. They found that the mean

fatty acid composition of adipose did not show an association with omega-6

linoleic acid and breast, colon or prostate cancer. However, cancers of the

breast and colon were positively associated with the trans fatty acids.

Kohlmeier and colleagues (1997) also reported that data from the EURAMIC

study showed adipose tissue concentration of trans fatty acids having a

positive association with postmenopausal breast cancer in European women.

 

In 1995 a British documentary on the trans fatty acids aired on a major

television station in the U.K. This documentary included an expose of the

battle between the edible oil industry and some of the major researchers of

the trans fatty acids. Just this year, this same documentary has been aired

on television in France where it was requested by a major television

station.

 

Several of the early researchers into the trans problems, Professor Fred

Kummerow and Dr. George Mann, have continued their research and/or writing

(Mann 1994). The popular media has continued to press the issue of the

amounts of trans in the foods, for which there are still no comprehensive

government data bases, and a recent published paper from a U.S. Department

of Agriculture researcher states:

 

" Because trans fatty acids have no known health benefits and strong

presumptive evidence suggests that they contribute markedly to the risk of

developing CHD, the results published to date suggest that it would be

prudent to lower the intake of trans fatty acids in the U.S. diet. " (Nelson

1998).

Professor Meir Stampfer from Harvard University refers to trans fats as " one

of the major nutritional issues of the nation, " contending that " they have a

large impact " and " ...we should completely eliminate hydrogenated fats from

the diet " (Gottesman 1998).

 

Lowering the trans fatty acids in the foods in the U.S. can only be done by

returning to the use of the natural unhydrogenated and more saturated fats

and oils.

 

Predictions can be made regarding the future of the trans fatty acids. Our

ability to predict has been pretty good; for example when Enig Associates

started producing the marketing newsletter Market Insights written by Eric

Enig, we predicted that trans fatty acids would eventually be swept out of

the market. It appears that this prediction may be close to coming true.

 

Also in the early 1990s, Market Insights predicted that CSPI would change

its mind about the trans fatty acids, which it had spent years defending.

CSPI did change its mind, and in fact went on the attack regarding the

trans, but CSPI never admitted that it had originally been promoting the

trans or that the high levels of trans found in the fried foods in the fast

food and other restaurants and in many other foods are directly due to CSPI

lobbying. While its change was welcome, CSPI's revisionist version of its

own history of support of partially hydrogenated oils and trans fatty acids

would have fit perfectly into George Orwell's " 1984 "

 

VII. COMPARISON OF SATURATED FATS WITH THE TRANS FATS

The statement that trans fatty acids are like saturated fatty acids is not

correct for biological systems. A listing of the biological effects of

saturated fatty acids in the diet versus the biological effects of trans

fatty acids in the diet is in actuality a listing of the good (saturated)

versus the bad (trans).

 

When one compares the saturated fatty acids and the trans fatty acids, we

see that

(1) saturated fatty acids raise HDL cholesterol, the so-called good

cholesterol, whereas the trans fatty acids lower HDL cholesterol (Mensink

and Katan 1990, Judd et al 1994);

(2) saturated fatty acids lower the blood levels of the atherogenic

lipoprotein [a], whereas trans fatty acids raise the blood levels of

lipoprotein [a] (Khosla and Hayes 1996, Hornstra et al 1991, Clevidence et

al 1997);

(3) saturated fatty acids conserve the elongated omega-3 fatty acids

(Gerster 1998), whereas trans fatty acids cause the tissues to lose these

omega-3 fatty acids (Sugano and Ikeda 1996);

(4) saturated fatty acids do not inhibit insulin binding, whereas trans

fatty acids do inhibit insulin binding;

(5) saturated fatty acids are the normal fatty acids made by the body, and

they do not interfere with enzyme functions such as the delta-6-desaturase,

whereas trans fatty acids are not made by the body, and they interfere with

many enzyme functions such as delta-6-desaturase;

and

(6) some saturated fatty acids are used by the body to fight viruses,

bacteria, and protozoa, and they support the immune system, whereas trans

fatty acids interfere with the function of the immune system.

 

VIII. WHAT ABOUT THE UNSATURATED FATS?

The arteries of the heart are also compromised by the unsaturated fatty

acids. When the fatty acid composition of the plaques (atheromas) in the

arteries has been analyzed, the level of saturated fatty acids in the

cholesterol esters is only 26 percent compared to that in the unsaturated

fatty acids, which is 74 percent. When the unsaturated fatty acids in the

cholesterol esters in these plaques are analyzed, it is shown that 38

percent are polyunsaturated and 36 percent are monounsaturated. Clearly the

problem in not with the saturated fatty acids.

 

As an aside, you need to understand that the major role of cholesterol in

heart disease and in cancer is as the body's repair substance, and that

cholesterol is a major support molecule for the immune system, an important

antioxidant, and a necessary component of neurotransmitter receptors. Our

brains do not work very well without adequate cholesterol. It should be

apparent to scientists that the current approach to cholesterol has been

wrong.

 

The pathway to cholesterol synthesis starts with a molecule of acetyl CoA

that comes from the metabolism of excess protein forming ketogenic amino

acids and from the metabolism of excess carbohydrate, as well as from the

oxidation of excess fatty acids. Grundy in 1978 reported that the degree

of saturation of the fat in the diet did not affect the rate of synthesis of

cholesterol. Research reported in 1997 (Jones 1997), however, showed that

the polyunsaturated fatty acids in the diet increase the rate of cholesterol

synthesis relative to other fatty acids. Furthermore, research reported in

1993 (Hodgsons et al 1993) had shown that dietary intake of the omega-6

polyunsaturated fatty acid linoleic acid was positively related to coronary

artery disease.

 

Thus, those statements made by the consumer activists in the United States

to the effect that the saturated fatty acids increase cholesterol synthesis

is without any foundation. What happens when there is an increase or a

decrease of cholesterol in the serum is more like a shift from one

compartment to another as the body tries to rectify the potential damage

from the excess polyunsaturated fatty acids. Research by Dr. Hans Kaunitz

reported in 1978 clearly showed the potential problems with excess

polyunsaturated fatty acids.

 

IX. RESEARCH SHOWING BENEFICIAL EFFECTS OF EATING THE MORE SATURATED FATS

One major concern expressed by the nutrition community is related to whether

or not people are getting enough elongated omega-3 fatty acids in their

diets. The elongated omega-3 fatty acids of concern are eicosapentaenoic

acid (EPA) and docosahexaenoic acid (DHA). Some research has shown that

(the basic omega-3 fatty acid) -linolenic acid is not readily converted to

the elongated forms in humans or animals, especially when there is ingestion

of the trans fatty acids and the consequent inhibition of the

delta-6-desaturase enzyme. One recent study (Gerster 1998), which used

radioisotope-labeled -linolenic acid to measure this conversion in adult

humans, showed that if the background fat in the diet was high in saturated

fat, the conversion was approximately 6% for EPA and 3.8% for DHA, whereas

if the background fat in the diet was high in omega-6 polyunsaturated fatty

acids (PUFA), the conversion was reduced 40-50%.

Nanji and colleagues (1995) report that a diet enriched in saturated but not

unsaturated fatty acids reversed alcoholic liver injury in their animals,

which was caused by dietary linoleic acid. These researchers conclude that

this effect may be explained by the down-regulation of lipid peroxidation.

This is another example of the need for adequate saturated fat in the diet.

Cha and Sachan (1994) studied the effects of saturated fatty acid and

unsaturated fatty acid diets on ethanol pharmacokinetics. The hepatic enzyme

alcohol dehydrogenase and plasma carnitines were also evaluated. The

researchers concluded that dietary saturated fatty acids protect the liver

from alcohol injury by retarding ethanol metabolism, and that carnitine may

be involved.

 

Hargrove and colleagues (1999) noted the work of Nanji et al and postulated

that they would find that diets rich in linoleic acid would also cause acute

liver injury after acetaminophen injection. In the first experiment, two

levels of fat (15 g/100 g protein and 20 g/100 g protein) were fed using

corn oil or beef tallow. Liver enzymes indicating damage were significantly

elevated in all the animals except for those animals fed the higher level of

beef tallow. These researchers concluded that " diets with high [linoleic

acid] may promote acetaminophen-induced liver injury compared to diets with

more saturated and monounsaturated fatty acids. "

 

 

X. RESEARCH SHOWING GENERAL BENEFICIAL EFFECTS FROM FEEDING COCONUT OIL

Research that compares coconut oil feeding with other oils to answer a

variety of biological questions is increasingly finding beneficial results

from the coconut oil.

Obesity is a major health problem in the United States and the subject of

much research. Several lines of research dealing with metabolic effects of

high fat diets have been followed. One study used coconut oil to enrich a

high fat diet and the results reported were that the " coconut-oil enriched

diet is effective in...[producing]...a decrease in white fat stores. "

(Portillo et al 1998)

 

Cleary et al (1999) fed genetically obese animals high fat diets of either

safflower oil or coconut oil. Safflower oil-fed animals had higher hepatic

lipogenic enzyme activities than did coconut oil fed animals. When the

number of fat cells were measured, the safflower oil-fed also had more fat

cells than the coconut oil-fed.

 

Many of the feeding studies produce results at variance with the popular

conception. High fat diets have been used to study the effects of different

types of fatty acids on membrane phospholipid fatty acid profiles. When

such a study was performed on mice, the phospholipid profiles were similar

for diets high in linoleic acid from high-linoleate sunflower oil relative

to diets high in saturated fatty acids from coconut oil. However, those

animals fed the diets high in oleic acid (from the high-oleate sunflower

oil) or high in elongated omega-3 fatty acids (from menhaden oil) were not

only different from the other two diets, but they also resulted in enlarged

spleens in the animals. (Huang and Frische 1992)

 

Oliart-Ros and colleagues (1998), Instituto Technologico de Veracruz,

Mexico, reported on effects of different dietary fats on sucrose-induced

cardiovascular syndrome in rats. The most significant reduction in

parameters of the syndrome was obtained by the n-3 PUFA-rich diet. These

researchers reported that the diet thought to be PUFA-deficient presented a

tissue lipid pattern similar to the n-3 PUFA-rich diet (fish oil), which

surprised and puzzeled them. When questioned, it turned out that the diet

was not really PUFA-deficient, but rather just a normal coconut oil

(nonhydrogenated), which conserved the elongated omega-3 and normalized the

omega-6-to-omega-3 balance.

 

A recent study measured the effect of high-fat diets, fed for more than

three months to the neonatal pig, on the HMG-CoA reductase enzyme's function

and gave some surprises. There were two feeding protocols: one with the

added cholesterol and one without added cholesterol, but both with coconut

oil. The hepatic reductase activity, which was the same in all groups at

the beginning of the feeding on the third day and similar on the 42nd day,

was increased with and without added cholesterol on the 13th day and then

decreased on the 25th day. The data was said to suggest that dietary

cholesterol suppressed hepatic reductase activity in the young pigs

regardless of their genetic background, that the stage of development was a

dominant factor in its regulation, and that both dietary and endogenously

synthesized cholesterol was used primarily for tissue building in very young

pigs. (McWhinney et al 1996) The feeding of coconut oil did not in any way

compromise the normal development of these animals.

 

When compared with feeding coconut oil, feeding two different soybean oils

to young females caused a significant decrease in HDL cholesterol. Both

soybean oils, one of which was extracted from a new mutant soybean thought

to be more oxidatively stable, were not protective of the HDL levels (Lu Z

et al 1997).

 

Trautwein et al (1997) studied cholesterol-fed hamsters on different oil

supplements for plasma, hepatic, and biliary lipids. The dietary oils

included butter, palm stearin, coconut oil, rapeseed oil, olive oil, and

sunflowerseed oil. Plasma cholesterol concentrations were higher (9.2

mmol/l) for olive oil than for coconut oil (8.5 mmol/l), hepatic cholesterol

was highest in the olive oil group, and none of the diet groups differed for

biliary lipids. Even in this cholesterol-sensitive animal model, coconut

oil performed better than olive oil.

 

Smit and colleagues (1994) had also studied the effect of feeding coconut

oil compared with feeding corn oil and olive oil in rats and measured the

effect on biliary cholesterol. Bile flow was not different between the

three diets, but the hepatic plasma membranes showed more cholesterol and

less phospholipid from corn and olive oil feeding relative to coconut oil

feeding.

 

Several studies (Kramer et al 1998) have pointed out problems with canola

oil feeding in newborn piglets, which result in the reduction in number of

platelets and the alteration in their size. There is concern for similar

effects in human infants. These undesirable effects can be reversed when

coconut oil or other saturated fat is added to the feeding regimen (Kramer

et al 1998).

 

Research has shown that coconut oil is needed for good absorption of fat and

calcium from infant formulas. The soy oil (47%) and palm olein (53%)

formula gave 90.6% absorption of fat and 39% absorption of calcium, whereas

the soy oil (60%) and coconut oil (40%) gave 95.2% absorption of fat and

48.4% absorption of calcium (Nelson et al 1996). Both fat and calcium are

needed by the infant for proper growth. These results clearly show the

folly of removing or lowering the coconut oil in infant formulas.

 

XI. RESEARCH SHOWING A ROLE FOR COCONUT IN ENHANCING IMMUNITY AND

MODULATING METABOLIC FUNCTIONS

Coconut oil appears to help the immune system response in a beneficial

manner. Feeding coconut oil in the diet completely abolished the expected

immune factor responses to endotoxin that were seen with corn oil feeding.

This inhibitory effect on interleukin-1 production was interpreted by the

authors of the study as being largely due to a reduced prostaglandin and

leukotriene production (Wan and Grimble 1987). However, the damping may be

due to the fact that effects from high omega-6 oils tend to be normalized by

coconut oil feeding. Another report from this group (Bibby and Grimble

1990) compared the effects of corn oil and coconut oil diets on tumor

necrosis factor-alpha and endotoxin induction of the inflammatory

prostaglandin E2 (PGE2) production. The animals fed coconut oil did not

produce an increase in PGE2, and the researchers again interpreted this as a

modulatory effect that brought about a reduction of phospholipd arachidonic

acid content. A study from the same research group (Tappia and Grimble

1994) showed that omega-6 oil enhanced inflammatory stimuli, but that

coconut oil, along with fish oil and olive oil, suppressed the production of

interleukin-1.

 

Several recent studies are showing additional helpful effects of consuming

coconut oil on a regular basis, thus supplying the body with the lauric acid

derivative monolaurin. Monolaurin and the ether analogue of monolaurin have

been shown to have the potential for damping adverse reactions to toxic

forms of glutamic acid (Dave et al 1997). Lauric acid and capric acid have

been reported to have very potent effects on insulin secretion (Garfinkel et

al 1992). Using a model system of murine splenocytes, Witcher et al 1996

showed that monolaurin induced proliferation of T cells and inhibited the

toxic shock syndrome toxin-1 mitogenic effects on T cells.

Monserrat and colleagues (1995) showed that a diet rich in coconut oil could

protect animals against the renal necrosis and renal failure produced by a

diet deficient in choline (a methyl donor group). The animals had less or

no mortality and increased survival time as well as decreased incidence or

severity of the renal lesions when 20% coconut oil was added to the

deficient diet. A mixture of hydrogenated vegetable oil and corn oil did

not show the same benefits.

The immune system is complex and has many feedback mechanism to protect it,

but the wrong fat and oils can compromise these important mechanisms. The

data from the several studies show the helpful effects of coconut fat.

Additionally, there are anecdotal reports that consumption of coconut is

beneficial for individuals with the chronic fatigue and immune dysfunction

syndrome known as CFIDS.

 

XII. U.S. PATENTS FOR MEDICAL USES OF LAURIC OILS, MEDIUM-CHAIN FATTY ACIDS,

AND THEIR DERIVATIVES SUCH AS MONOLAURIN

A number of patents have been granted in the United States for medical uses

of lauric oils, lauric acid, and monolaurin. Although one earlier patent

was granted to Professor Kabara more than three decades ago, the rest of

these patents have been granted within the past decade.

In 1989 a patent was issued to the New England Deaconess Hospital (Bistrian

et al 1989) for the invention titled " Kernel Oils and Disease Treatment. "

This treatment required lauric acid as the primary fatty acid source with

lauric oils constituting up to 80% of the diet " using naturally occurring

kernel oils. "

In 1991 and 1995, two patents were issued to the group of researchers whose

work has been reviewed above. The first invention (Isaacs et al 1991) was

directed to antiviral and antibacterial activity of both fatty acids and

monoglycerides, primarily against enveloped viruses. The claims were for " a

method of killing enveloped viruses in a host human...wherein the enveloped

viruses are AIDS viruses...[or]...herpes viruses...[and the]...compounds

selected from the group consisting of fatty acids having from 6 to 14 carbon

atoms and monoglycerides of said fatty acids...[and]...wherein the fatty

acids are saturated fatty acids. "

The second patent (Isaacs et al 1995) was a further extension of the earlier

one. This patent also included discussion of the inactivation of envelop

viruses and specifically cited monoglycerides of caproic, caprylic, capric,

lauric, and myristic acid. These fatty acids make up more than 80% of

coconut oil. Also included in this patent was a listing of susceptible

viruses and some bacteria and protozoa.

Although these latter patents may provide the owners of the patents with the

ability to extract royalties from commercial manufacturers of monoglycerides

and fatty acids, they cannot require royalties from the human

gastrointestinal tract when it is the " factory " that is doing the

manufacturing of the monoglycerides and fatty acids. Clearly though, these

patents serve to illustrate to us that the health-giving properties of

monolaurin and lauric acid are well-recognized by some individuals in the

research arena, and they lend credence to our appropriate choice of lauric

oils for promoting health and as adjunct treatment of viral diseases.

 

XIII. HOW CAN WE GET SUFFICIENT COCONUT FAT INTO THE FOOD SUPPLY IN THE

U.S. AND

OTHER COUNTRIES THAT NEED ITS BENEFITS?

I would like to review for you my perception of the status regarding the

coconut and coconut products market in the North American countries such as

the United States and Canada at the end of the 20th century and the

beginning of the 21st century.

 

Coconut products are trying to regain their former place in several small

markets. The extraction of oil from fresh coconut has been reported in the

past decade and my impression is that this is being considered as a

desirable source of minimally processed oil, which produces an oil with

desirable characteristics for the natural foods market.

There have been some niche markets for coconut products developing during

the past half-decade. These are represented primarily by the natural foods

and health foods producers. Some examples are the new coconut butters

produced in the U.S. and Canada by Omega Nutrition and Carotec, Inc. And,

this is no longer as small a market as it has been in past years.

Desiccated coconut products, coconut milk, and even coconut oil are

appearing on the shelves of many of these markets. After years of packaging

coconut oil for skin use only, one of the large suppliers of oils to the

natural foods and health foods stores has introduced coconut oil for food

use, and it has appeared within the last few months on shelves in the

Washington, DC metropolitan area along with other oils. I believe I

indirectly had something to do with this turn of events.

 

XIV. CONCLUSIONS AND RECOMMENDATIONS

As we come close to the end of the year 1999 and set our sights on what

could happen in the year 2000 and beyond, there is much to be gained from

pursuing the functional properties of coconut for improving the health of

humanity.

On the occasion of the 30th anniversary of the Asian Pacific Coconut

Community, at this 36th meeting of APCC, I wanted to bring you a message

that I hope will encourage you to continue your endeavors on behalf of all

parts of the coconut industry. Coconut products for inedible and especially

edible uses are of the greatest importance for the health of the entire

world.

Some of what I have been telling you, most of you already know. But in

saying these things for the record, it is my intention to tell those who did

not know all the details until they heard or read this paper about the

positive properties of coconut.

Coconut oil is a most important oil because it is a lauric oil. The lauric

fats possess unique characteristics for both food industry uses and also for

the uses of the soaps and cosmetic industries. Because of the unique

properties of coconut oil, the fats and oils industry has spent untold

millions to formulate replacements from those seed oils so widely grown in

the world outside the tropics. While it has been impossible to truly

duplicate coconut oil for some of its applications, many food manufacturers

have been willing to settle for lesser quality in their products. Consumers

have also been willing to settle for a lesser quality, in part because they

have been fed so much misinformation about fats and oils.

Desiccated coconut, on the other hand, has been impossible to duplicate, and

the markets for desiccated coconut have continued. The powdered form of

desiccated coconut now being sold in Europe and Asia has yet to find a

market in the U.S., but I predict that it will become an indispensable

product in the natural foods industry. Creamed coconut, which is desiccated

coconut very finely ground, could be used as a nut butter.

APCC needs to promote the edible uses of coconut, and it needs to promote

the reeducation of the consumer, the clinician, and the scientist. The

researcher H. Thormar (Thormar et al 1999) concluded his abstract with the

statement that monocaprin " ...is a natural compound found in certain

foodstuffs such as milk and is therefore unlikely to cause harmful side

effects in the concentrations used. " It is not monocaprin that is found in

milk, but capric acid. It is likely safe at most any level found in food.

However, the levels in milk fat are at most 2 percent whereas the levels in

coconut fat are 7 percent.

One last reference for the record. Sircar and Kansra (1998) have reviewed

the increasing trend of atherosclerotic disease and type-2 diabetes mellitus

in the Indians from both the subcontinent of India and abroad. They note

that over the time when there has been an alarming increase in the

prevalence of these diseases, there has been a replacement of traditional

cooking fats with refined vegetable oils that are promoted as

heart-friendly, but which are being found to be detrimental to health.

These astute researchers suggest that it is time to return to the

traditional cooking fats like ghee, coconut oil, and mustard oil.

There are a number of areas of encouragement. The nutrition community in

the United States is slowly starting to recognize the difference between

medium chain saturated fatty acids and other saturated fatty acids. We

predict now that the qualities of coconut, both for health and food

function, will ultimately win out.

 

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