A New Look at Coconut Oil

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A New

Look at Coconut Oil

By

*Mary G. Enig, Ph.D. <#author>*

Abstract

Coconut

oil has a unique role in the diet as an important physiologically functional

food. The health and nutritional benefits that can be derived from consuming

coconut oil have been recognized in many parts of the world for centuries.

Although the advantage of regular consumption of coconut oil has been

under-appreciated by the consumer and producer alike for the recent two or

three decades, its unique benefits should be compelling for the health minded

consumer of today. A review of the diet/heart disease literature relevant to

coconut oil clearly indicates that coconut oil is at worst neutral with respect

to atherogenicity of fats and oils and, in fact, is likely to be a beneficial

oil for prevention and treatment of some heart disease.

Additionally,

coconut oil provides a source of anti-microbial lipid for individuals with

compromised immune systems and is a non-promoting fat with respect to chemical

carcinogenesis.

I.

Introduction

Mr.

Chairman and members of the ASEAN Vegetable Oils Club, I would like to thank

you for inviting me to participate in this Lauric Oils Symposium. I am pleased

to have the opportunity to review with you some information that I hope will

help redress some of the anti-tropical oils rhetoric that has been so

troublesome to your industry.

I will

be covering two important areas in my presentation. In the first part, I would

like to review the history of the major health challenge facing coconut oil

today. This challenge is based on a supposed negative role played by saturated

fat in heart disease. I hope to dispel any acceptance of this notion with the

information I will present to you today. I will show you how both animal

studies and human studies have exonerated coconut oil of causing the problem.

In the

second part of my talk I will suggest some new directions where important

positive health benefits are seen for coconut oil. These benefits stem from

coconut oil's use as a food with major anti-microbial and anti-cancer benefits.

I will present to you some of the rationale for this effect and some of the

supporting literature.

The

health and nutritional benefits derived from coconut oil are unique and

compelling. Although the baker and food processor have recognized the

functional advantages of coconut oil in their industries, over most competing

oils, for many years, I believe these benefits are under-appreciated today by

both the producer and the consumer. It is time to educate and reeducate all t

hose who harbor this misinformation.

Historically,

coconuts and their extracted oil have served man as important foods for

thousands of years. The use of coconut oil as a shortening was advertised in

the United States in popular cookbooks at the end of the 19th century. Both the

health-promoting attributes of coconut oil and those functional properties

useful to the homemaker were recognized 100 years ago. These same attributes,

in addition to some newly discovered ones, should be of great interest to both

the producing countries as well as the consuming countries.

II.

Origins of the Diet/Heart Hypothesis

Although

popular literature of epidemiological studies usually attribute an increased

risk of coronary heart disease (CHD) to elevated levels of serum cholesterol,

which in turn are thought to derive from a dietary intake of saturated fats and

cholesterol. But, saturated fats may be considered a major culprit for CHD only

if the links between serum cholesterol and CHD, and between saturated fat and

serum cholesterol are each firmly established. Decades of large-scale tests and

conclusions there from have purported to establish the first link. In fact,

this relationship has reached the level of dogma. Through the years metabolic

ward and animal studies have claimed that dietary saturated fats increase serum

cholesterol levels, thereby supposedly establishing the second link. But the

scientific basis for these relationships has now been challenged as resulting

from large-scale misinterpretation and misrepresentation of the data. (Enig

1991, Mann 1991, Smith 1991, Ravnskov 1995)

Ancel

Keys is largely responsible for starting the anti-saturated fat agenda in the

United States. From 1953 to 1957 Keys made a series of statements regarding the

atherogenicity of fats. These pronouncements were:

" All fats raise serum cholesterol;

Nearly half of total fat comes from vegetable fats and oils; No

difference between animal and

vegetable fats in effect on CHD (1953);

Type of fat makes no difference; Need to reduce margarine and

shortening (1956); All fats

are comparable; Saturated fats raise and

polyunsaturated fats lower serum cholesterol; Hydrogenated vegetable

fats are the problem;

Animal fats are the problem

(1957-1959). "

As can

be seen, his findings were inconsistent.

What

was the role of the edible oil industry in promoting the diet/heart hypothesis?

It is

important to realize that at that time (1960s) the edible oil industry in the

United States seized the opportunity to promote its polyunsaturates. The

industry did this by developing a health issue focusing on Key's anti-saturated

fat bias. With the help of the edible oil industry lobbying in the United

States, federal government dietary goals and guidelines were adopted

incorporating this mistaken idea that consumption of saturated fat was causing

heart disease. This anti-saturated fat issue became the agenda of government

and private agencies in the US and to an extent in other parts of the world.

This is the agenda that has had such a devastating effect on the coconut

industry for the past decade. Throughout the 1960s, the 1970s, the 1980s, and

the 1990s, the anti-saturated fat rhetoric increased in intensity.

What

are some of the contradictions to the hypothesis blaming saturated fat?

Recently,

an editorial by Harvard's Walter Willett, M.D. in the 'American Journal of

Public Health' (1990) acknowledged that even though

" the focus of dietary recommendations

is usually a reduction of saturated fat intake, no relation between

saturated fat intake and

risk of CHD was observed in the most

informative prospective study to date. "

Another

editorial, this time by Framingham's William P. Castelli in the

'Archives

of Internal Medicine'(1992), declared for the record that

" ...in Framingham, Mass, the more

saturated fat one ate, the more cholesterol one ate, the /more calories

one ate/, the lower the

person's serum cholesterol... the opposite

of what the equations provided by Hegsted at al (1965) and Keys

et al (1957) would predict... "

Castelli

further admitted that

" ...In Framingham, for example, we

found that the people who ate the most cholesterol, ate the most saturated

fat, ate the most calories, weighed the least, and were the most

physically active. "

III.

Coconut Oil and the Diet/Heart Hypothesis

For the

past several decades you have heard about animal and human studies feeding

coconut oil that purportedly showed increased indices for cardiovascular risk.

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.

How did

coconut oil get such a negative reputation?

The

question then is, how did coconut oil get such a negative reputation? The

answer quite simply is, initially, the significance of those changes that

occurred during animal feeding studies were misunderstood. The wrong

interpretation was then repeated until ultimately the misinformation and

disinformation took on a life of its own.

The

problems for coconut oil started four decades ago when researchers fed animals

hydrogenated coconut oil that was purposefully altered to make it completely

devoid of any essential fatty acids. The hydrogenated coconut oil was selected

instead of hydrogenated cottonseed, corn or soybean oil because it was a soft

enough fat for blending into diets due to the presence of the lower melting

medium chain saturated fatty acids.

The

same functionality could not be obtained from the cottonseed, corn or soybean

oils if they were made totally saturated, since all their fatty acids were long

chain and high melting and could not be easily blended nor were they as readily

digestible.

The

animals fed the hydrogenated coconut oil (as the only fat source) naturally

became essential fatty acid deficient; their serum cholesterol levels

increased. Diets that cause an essential fatty acid deficiency always produce

an increase in serum cholesterol levels as well as an increase in the

atherosclerotic indices. The same effect has also been seen when other

essential fatty acid deficient, highly hydrogenated oils such as cottonseed,

soybean, or corn oils have been fed; so it is clearly a function of the

hydrogenated product, either because the oil is essential fatty acid (EFA)

deficient or because of /trans/ fatty acids (TFA).

What

about the studies where animals were fed with unprocessed coconut oil?

Hostmark

et al (1980) compared the effects of diets containing 10% coconut fat and 10%

sunflower oil on lipoprotein distribution in male Wistar rats. Coconut oil

feeding produced significantly lower levels (p=<0.05) of pre-beta

lipoproteins (VLDL) and significantly higher (p=<0.01) alpha-lipoproteins

(HDL) relative to sunflower oil feeding.

Awad

(1981) compared the effects of diets containing 14% coconut oil, 14% safflower

oil or a 5% " control " (mostly soybean) oil on accumulation of

cholesterol in tissues in male Wistar rats. The synthetic diets had 2% added

corn oil with a total fat of 16% Total tissue cholesterol accumulation for

animals on the safflower diet was six times greater than for animals fed the

coconut oil, and twice that of the animals fed the control oil.

A

conclusion that can be drawn from some of this animal research is that feeding

hydrogenated coconut oil devoid of essential fatty acids (EFA) in a diet

otherwise devoid of EFA leads to EFA deficiency and potentiates the formation

of atherosclerosis markers. It is of note that animals fed regular coconut oil

have less cholesterol deposited in their livers and other parts of their

bodies.

What

about the studies where coconut oil is part of the normal diet of human beings?

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 below the acceptable lower limit) and the

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

considered quite undesirable. As noted above, Kurup and Rajmohan (1995) studied

the addition of coconut oil alone to previously mixed fat diets and report no

significant difference.

Previously,

Prior et al (1981) had shown that islanders with high intake 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.

What

about the studies where coconut oil was deliberately fed to human beings?

Some of

the studies reported thirty and more years ago should have cleared coconut oil

of any implication in the development of coronary heart disease (CHD).

For

example, when Frantz and Carey (1961) fed an additional 810 kcal/day fat

supplement for a whole month to males with high normal serum cholesterol

levels, there was no significant difference from the original levels even

though the fat supplement was hydrogenated coconut oil.

Halden

and Lieb (1961) also showed similar results in a group of

hyperchole-sterolemics when coconut oil was included in their diets.

Original

serum cholesterol levels were reported as 170 to 370 mg/dl.

Straight

coconut oil produced a range from 170 to 270 mg/dl. Coconut oil combined with

5% sunflower oil and 5% olive oil produced a range of 140 to 240 mg/dl.

Earlier,

Hashim and colleagues (1959) had shown quite clearly that feeding a fat

supplement to hypercholesterolemics, where half of the supplement (21% of

energy) was coconut oil (and the other half was safflower oil), resulted in

significant reductions in total serum cholesterol. The reductions averaged -29%

and ranged from -6.8 to -41.2%.

And

even earlier, Ahrens and colleagues (1957) had shown that adding coconut oil to

the diet of hypercholesterolemics lowers serum cholesterol from, e.g., 450

mg/dl to 367 mg/dl. This is hardly a cholesterol-raising effect.

Bierenbaum

et al (1967) followed 100 young men with documented myocardial infarction for 5

years on diets with fat restricted to 28% of energy. There was no significant

difference between the two different fat mixtures (50/50 corn and safflower

oils or 50/50 coconut and peanut oils), which were fed as half of the total fat

allowance; both diets reduced serum cholesterol. This study clearly showed that

7% of energy as coconut oil was as beneficial to the 50 men who consumed it as

for the 50 men who consumed 7% of energy as other oils such as corn oil or

safflower. Both groups fared better than the untreated controls.

More

recently, Sundram et al (1994) fed whole foods diets to healthy

normo-cholesterolemic males, where approximately 30% of energy was fat.

Lauric

acid (C12:0) and myristic acid (C14:0) from coconut oil supplied approximately

5% of energy. Relative to the baseline measurements of the subjects prior to

the experimental diet, this lauric and myristic acid-rich diet showed an

increase in total serum cholesterol from 166.7 to 170.0 mg/dl (+1.9%), a

decrease in low density lipoprotein cholesterol (LDL-C) from 105.2 to 104.4

mg/dl (-0.1%), an increase in high density lipoprotein cholesterol (HDL-C) from

42.9 to 45.6 mg/dl (+6.3%). There was a 2.4% decrease in the LDL-C/HDL-C ratio

from 2.45 to 2.39. These findings indicate a favorable alteration in serum lipoprotein

balance was achieved when coconut oil was included in a whole food diet at 5%

of energy.

Tholstrup

et al (1994) report similar results with whole foods diets high in lauric and myristic

acids from palm kernel oil. The HDL cholesterol levels increased significantly

from baseline values (37.5 to 46.0 mg/dl, P<0.01) and the LDL-C/HDL-C ratios

decreased from 3.08 to 2.69. The increase in total cholesterol was from 154.7

(baseline) to 170.9 mg/dl on the experimental diet.

Ng et

al (1991) fed 75% of the fat ration as coconut oil (24% of energy) to 83 adult

normocholesterolemics (61 males and 22 females). Relative to baseline values,

the highest values on the experimental diet for total cholesterol was increased

17% (169.6 to 198.4 mg/dl), HDL cholesterol was increased 21.4% (44.3 to 53.8

mg/dl), and the LDL-C/HDL-C ratio was decreased 3.6% (2.51 to 2.42).

When

unprocessed coconut oil is added to an otherwise normal diet, there is frequently

no change in the serum cholesterol although some studies have shown a decrease

in total cholesterol. For example, when Ginsberg et al provided an

" Average American " diet with 2-3 times more myristic acid (C14:0),

4.5 times more lauric acid (C12:0), and 1.2 times more palmitic and stearic

acid (C16:0 and C18:0) than their " Mono[unsaturated] " diet and the

National Cholesterol Education Program " Step 1 " diet, there was no

increase in serum cholesterol, and in fact, serum cholesterol levels for this diet

group fell approximately 3% from 177.1 mg% to 171.8 mg% during the 22 week

feeding trial.

It

appears from many of the research reports that the effect coconut oil has on

serum cholesterol is the opposite in individuals with low serum cholesterol values

and those with high serum values. We see that there may be a raising of serum

total cholesterol, LDL cholesterol and especially HDL cholesterol in

individuals with low serum cholesterol. On the other hand there is lowering of

total cholesterol and LDL cholesterol in hypercholesterolemics as noted above.

Studies

that supposedly showed a /hypercholesterolemic/ effect of coconut oil feeding,

in fact, usually only showed that coconut oil was not as effective at lowering

the serum cholesterol as was the more unsaturated fat 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% 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).

Should

coconut oil be used to prevent coronary heart disease?

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 is suggestive that there is a causative role for the herpes virus and

cytomegalovirus in the initial formation of atherosclerotic plaques and the

recloging 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.

Perhaps

more important than any effect of coconut oil on serum cholesterol is the

additional effect of coconut oil on the disease fighting capability of the

animal or person consuming the coconut oil.

IV.

Coconut Oil and Cancer

Lim-Sylianco

(1987) has reviewed 50 years of literature showing anti-carcinogenic effects

from dietary coconut oil. These animal studies show quite clearly the

nonpromotional effect of feeding coconut oil.

In a

study by Reddy et al (1984) straight coconut oil was more inhibitory than MCT

oil to induction of colon tumors by azoxymethane.

Chemically

induced adenocarcinomas differed 10-fold between corn oil(32%) and coconut oil

(3%) in the colon. Both olive oil and coconut oil developed the low levels (3%)

of the adenocarcinomas in the colon, but in the small intestine animals fed

coconut oil did not develop any tumors while 7% of animals fed olive oil did.

Studies

by Cohen et al (1986) showed that the nonpromotional effects of coconut oil

were also seen in chemically induced breast cancer. In this model, the slight

elevation of serum cholesterol in the animals fed coconut oil was protective as

the animals fed the more polyunsaturated oil had reduced serum cholesterol and

more tumors. The authors noted that " ...an overall inverse trend was

observed between total serum lipids and tumor incidence for the 4 [high fat]

groups. "

This is

an area that needs to be pursued.

V.

Coconut Oil Anti-microbial Benefits

I would

now like to review for you some of the rationale for the use of coconut oil as

a food that will serve as the raw material to provide potentially useful levels

of anti-microbial activity in the individual.

The

lauric acid in coconut oil is used by the body to make the same

disease-fighting fatty acid derivative monolaurin that babies make from the

lauric acid they get from their mothers= milk. The monoglyceride monolaurin is

the substance that keeps infants from getting viral or bacterial or protozoal

infections. Until just recently, this important benefit has been largely

overlooked by the medical and nutrition community.

Recognition

of the antimicrobial activity of the monoglyceride of lauric acid (monolaurin)

has been reported since 1966. The seminal work can be credited to Jon Kabara.

This early research was directed at the virucidal effects because of possible

problems related to food preservation. 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

US Public Health Service with selected prototypes or recognized representative

strains of enveloped human viruses. The envelope of these viruses is a lipid

membrane.

Kabara

(1978) and others have reported that certain fatty acids (e.g., medium-chain

saturates) and their derivatives (e.g., monoglycerides) can have adverse

effects on various microorrganisms: those microorganism that are inactivated

include bacteria, yeast, fungi, and enveloped viruses.

The

medium-chain saturated fatty acids and their derivatives act by disrupting the

lipid membranes of the organisms (Isaacs and Thormar 1991)(Isaacs et al 1992).

In particular, enveloped viruses are inactivated in both human and bovine milk

by added fatty acids (FAs) and monoglycerides (MGs)(Isaacs et al 1991) as well

as by endogenous Fas and MGs (Isaacs et al 1986, 1990, 1991, 1992; Thormar et

al 1987).

All

three monoesters of lauric acid are shown to be active Anti-microbials, i.e.,

alpha-, alpha'-, and beta-MG. Additionally, it is reported that the

anti-microbial effects of the FAs and MGs are additive and total concentration

is critical for inactivating viruses (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-10) or myristic acid (C-14).

The

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. In effect, it is reported that the fatty acids and

monoglycerides produce their killing/inactivating effect by lysing the (lipid

bilayer) plasma membrane. However, there is evidence from recent studies that

one antimicrobial effect is related to its interference with signal

transduction (Projan et al 1994).

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 anti-viral, anti-microbial,

and anti-protozoal monoglycerides and fatty acids such as monolaurin and its

precursor lauric acid.

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

non-toxic 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 (envelop) viruses are dependent on host lipids for their lipid

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

accounts for the variability of fatty acids in the virus envelop and also

explains the variability of glycoprotein expression.

Loss of

lauric acid from the American diet

Increasingly,

over the past 40 years, the American diet has undergone major changes. Many of

these changes involve changes of fats and oils.

There

has been an increasing supply of the partially hydrogenated 'trans'-containing

vegetable oils and a decreasing amount of the lauric acid-containing oils. As a

result, there has been an increased consumption of 'trans' fatty acids and linoleic

acid and a decrease in the consumption of lauric acid. This type of change in

diet has an effect on the fatty acids the body has available for metabolic

activities.

VI.

Lauric Acid in Foods

The

coconut producing countries

Whole

coconut as well as extracted coconut oil has been a mainstay in the food supply

in many countries in parts of Asia and the Pacific Rim throughout the

centuries. Recently though, there has been some replacement of coconut oil by

other seed oils. This is unfortunate since the benefits gained from consuming

an adequate amount of coconut oil are being lost.

Based

on the per capita intake of coconut oil in 1985 as reported by Kaunitz (1992),

the per capita daily intake of lauric acid can be approximated. For those major

producing countries such as the Philippines, Indonesia, and Sri Lanka, and

consuming countries such as Singapore, the daily intakes of lauric acid were

approximately 7.3 grams (Philippines), 4.9 grams (Sri Lanka), 4.7 grams

(Indonesia), and 2.8 grams (Singapore). In India, intake of lauric acid from

coconut oil in the coconut growing areas (e.g., Kerala) range from about 12 to

20 grams per day (Eraly 1995), whereas the average for the rest of the country

is less than half a gram. An average high of approximately 68 grams of lauric

acid is calculated from the coconut oil intake previously reported by Prior et

al (1981) for the Tokelau Islands. Other coconut producing countries may also

have intakes of lauric acid in the same range.

The US

experience

In the

United States today, there is very little lauric acid in most of the foods.

During the early part of the 20th Century and up until the late 1950s many

people consumed heavy cream and high fat milk. These foods could have provided

approximately 3 grams of lauric acid per day to many individuals. In addition,

desiccated coconut was a popular food in homemade cakes, pies and cookies, as

well as in commercial baked goods, and 1-2 tablespoons of desiccated coconut

would have supplied 1-2 grams of lauric acid. Those foods made with the coconut

oil based shortenings would have provided additional amounts.

Until

two years ago, some of the commercially sold popcorn, at least in movie

theaters, had coconut oil as the oil. This means that for those people lucky

enough to consume this type of popcorn the possible lauric acid intake was 6

grams or more in a three (3) cup order.

Some

infant formulas (but not all) have been good sources of lauric acid for

infants. However, in the past 3-4 years there has been reformulation with a

loss of a portion of coconut oil in these formulas, and a subsequent lowering

of the lauric acid levels.

Only

one US manufactured enteral formula contains lauric acid (e.g., Impact7); this

is normally used in hospitals for tube feeding; it is reported to be very

effective in reversing severe weight loss in AIDS patients, but it is

discontinued when the patients leave the hospital because it is not

sufficiently palatable for oral use. The more widely promoted enteral formulas

(e.g., Ensure7, Nutren7) are not made with lauric oils, and, in fact, many are

made with partially hydrogenated oils.

There

are currently some candies sold in the US that are made with palm kernel oil,

and a few specialty candies made with coconut oil and desiccated coconut. These

can supply small amounts of lauric acid.

Cookies

such as macaroons, if made with desiccated coconut, are good sources of lauric

acid, supplying as much as 6 grams of lauric acid per macaroon (Red Mill).

However, these cookies make up a small portion of the cookie market. Most

cookies in the United States are no longer made with coconut oil shortenings;

however, there was a time when many US cookies (e.g., Pepperidge Farm) were

about 25% lauric acid.

Originally,

one of the largest manufacturers of cream soups used coconut oil in the

formulations. Many popular cracker manufacturers also used coconut oil as a

spray coating. These products supplied a small amount of lauric acid on a daily

basis for some people.

How

much lauric acid is needed?

It is

not known exactly how much food made with lauric oils is needed in order to

have a protective level of lauric acid in the diet. Infants probably consume

between 0.3 and 1 gram per kilogram of body weight if they are fed human milk

or an enriched infant formula that contains coconut oil. This amount appears to

have always been protective. Adults could probably benefit from the consumption

of 10 to 20 grams of lauric acid per day. Growing children probably need about

the same amounts as adults.

VII.

Recommendations

The

coconut oil industry needs to make the case for lauric acid now. It should not

wait for the rapeseed industry to promote the argument for including lauric

acid because of the increased demand for laurate. In fact lauric acid may prove

to be a conditionally essential saturated fatty acid, and the research to

establish this fact around the world needs to be vigorously promoted.

Although

private sectors need to fight for their commodity through the offices of their

trade associations, the various governments of coconut producing countries need

to put pressure on WHO, FAO, and UNDP to recognizes the health importance of

coconut oil and the other coconut products. Moreover, those representatives who

are going to do the persuading need to believe that their message is

scientifically correct -- because it is.

Among

the critical foods and nutrition " buzz words " for the 21st Century is

the term " functional foods. " Clearly coconut oil fits the designation

of a very important functional food.

 

References

Awad

AB. Effect of dietary lipids on composition and glucose utilization by rat

adipose tissue. /Journal of Nutrition/ 111:34-39, 1981.

Bierenbaum

JL, Green DP, Florin A, Fleishman AI, Caldwell AB.

Modified-fat

dietary management of the young male with coronary disease: a

five-year report. /Journal of the American Medical Association/ 202:1119-1123;1967.

Blackburn

GL, Kater G, Mascioli EA, Kowalchuk M, Babayan VK, kBistrian BR. A

reevaluation of coconut oil's effect on serum cholesterol and atherogenesis.

/The Journal of the Philippine Medical Association/ 65:144-152;1989.

Castelli

WP. Editorial: Concerning the possibility of a nut... /Archives of

Internal Medicine/ 152:1371-2;1992.

Cohen

LA, Thompson DO, Maeura Y, Choi K, Blank M, Rose DP. Dietary fat and

mammary cancer. I. Promoting effects of different dietary fats on N-nitrosomethylurea-induced

rat mammary tumorigenesis. /Journal of the National

Cancer Institute/ 77:33;1986.

Cohen

LA, Thompson DO, Choi K, Blank M, Rose DP. Dietary fat and mammary cancer.

II. Modulation of serum and tumor lipid composition and tumor prostaglandins

by different dietary fats: Association with tumor incidence

patterns. /Journal of the National Cancer Institute/ 77:43;1986.

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*About

the Author*

Mary G.

Enig, PhD**Mary G. Enig, PhD* is an expert of international renown in the field

of lipid biochemistry. She has headed a number of studies on the content and

effects of 'trans' fatty acids in America and Israel, and has successfully

challenged government assertions that dietary animal fat causes cancer and heart

disease. Recent scientific and media attention on the possible adverse health

effects of 'trans' fatty acids has brought increased attention to her work. She

is a licensed nutritionist, certified by the Certification Board for Nutrition

Specialists, a qualified expert witness, nutrition consultant to individuals,

industry and state and federal governments, contributing editor to a number of

scientific publications, Fellow of the American College of Nutrition and President

of the Maryland Nutritionists Association. She is the author of over 60

technical papers and presentations, as well as a popular lecturer. Dr. Enig is

currently working on the exploratory development of an adjunct therapy for AIDS

using complete medium chain saturated fatty acids from whole foods. She is Vice-President of the

Weston A Price Foundation and Scientific Editor of 'Wise Traditions' as well as

the author of 'Know Your Fats: The Complete Primer for Understanding the

Nutrition of Fats, Oils, and Cholesterol', Bethesda Press, May 2000. She is the

mother of three healthy children brought up on whole foods including butter,

cream, eggs and meat. See her website at http://www.enig.com/trans.html

 

 

Radiating

UNCONDITIONAL LOVE & Truth

To ALL who share our circle, our

universe, our love, our trust.

May

I always be found worthy.

Gratitude

& Thankfulness to All of Us

aSoaringHawk

Look at everything as though you were seeing it either for the

first or last time. Then your time on earth will be filled with joy &

glory.

Thank you for YOU!