Coconut the good fat

[Guest guest]

http://www.livecoconutoil.com/maryenig.htm

 

 

 

 

 

 

Coconut: In Support of Good

Health in the 21st Century

 

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

 

 

Dr. Enig has

authored numerous journal publications, mainly on fats and oils

research and nutrient/drug interactions, and is a well-known invited

lecturer at scientific meetings and a popular interviewee on TV and

radio shows about nutrition. She was an early and articulate critic of

the use of trans fatty acids and advocated their inclusion in

nutritional labeling. The scientific mainstream is now challenging the

food product industry's use of trans-containing partially hydrogenated

vegetable oils.

 

She received her Ph.D. in Nutritional Sciences from the University

of Maryland, College Park, and is a Fellow of The American College of

Nutrition, a member of The American Society for Nutritional Sciences,

and President of the Maryland Nutritionists Association.

 

 

 

 

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

reported that the antimicrobial 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.m 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;

(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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