Cc:
Date: Sun, 23 Jun 2013 20:06:31 +0530
Subject: Coconut oil
Harvard University A New Look at Coconut Oil
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
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.
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
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="" alpha-lipoproteins="" and="" feeding.="" higher="" lipoproteins="" of="" oil="" p="" pre-beta="" relative="" significantly="" sunflower="" to="">
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="" 154.7="" 170.9="" 2.69.="" 3.08="" and="" baseline="" cholesterol="" decreased="" diet.="" dl="" experimental="" from="" in="" increase="" ldl-c="" mg="" on="" p="" ratios="" the="" to="" total="" was="">
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).
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.
Ctd.......
