A New Look at Coconut Oil - Health and Nutritional Benefits from Coconut Oil: An

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A New Look at Coconut Oil

http://www.westonaprice.org/knowyourfats/coconut_oil.html

By Mary G. Enig, Ph.D.

 

Health and Nutritional Benefits from Coconut Oil: An Important Functional

Food for the 21st Century

 

Presented at the AVOC Lauric Oils Symposium, Ho Chi Min City, Vietnam, 25

April 1996

 

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

underappreciated 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 antimicrobial lipid for individuals with compromised immune

systems and is a nonpromoting 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 antimicrobial and anticancer

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 underappreciated 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 therefrom 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

anticarcinogenic 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 Antimicrobial 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 antimicrobial 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 microorganisms: those microorganisms 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 antimicrobials,

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

antimicrobial 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