quinta-feira, 20 de outubro de 2011

Óleo de Coco

PROPRIEDADES DO ÓLEO DE COCO PDF Imprimir E-mail

Obs.: Veja matérias complementares em português a seguir (após as referências)


Mary Enig Ph.D.
on the Effects of Coconut Oil on Serum Cholesterol Levels and HDLs
(sobre os efeitos do óleo de coco e os níveis séricos de colesterol HDL)
http://www.coconutoil.com/enig_cholesterol.htm
http://www.westonaprice.org/knowyourfats/coconut_oil.html

The following article is taken from Report 14, Keep Hope Alive.

Dr. Mary Enig MS (Nutritional Sciences), Ph.D. did original research
that showed a positive link between vegetable oil and cancer and a
negative correlation for animal fat. She originated comprehensive
analysis of transfatty acid components of over 200 foods. transfatty
acids are formed when vegetable oils are hydrogenated or heated to
high temperatures. With high temperatures, transfatty acids are fats
that are twisted, which alter their natural "cis" shape. She studied
how the transfatty acids from foods affected the liver's mixed
function oxidase enzyme system that metabolizes drugs and
environmental pollutants in the body. An important finding of this
latter study was that laboratory animals fed experimental diets
containing transfatty acids have altered activity of this enzyme
system. These results were partly responsible for the review of
the "Health Aspects of Dietary transfatty Acids" held by the
Federation of American Societies for Experimental Biology, Life
Sciences Research Office, at the request of the Food and Drug
Administration. Mary Enig has had 17 articles published in
scientific journals since 1976. In 1986, she was appointed by the
Governor of Maryland to the "State Advisory Council on Nutrition."
She was contributing editor to "Clinical Nutrition" magazine and
consulting editor for the "Journal of the American College of
Nutrition." She has given over 50 seminars and lectures on since
1979 on foods and nutrition topics.

In an article published in the Indian Coconut Journal, Sept., 1995,
Dr. Enig stated that "Ancel Keys is largely responsible for starting
the anti-saturated fat agenda in the United States." She quoted Keys
as saying that "All fats raise serum cholesterol; saturated fats
raise and polyunsaturated fats lower serum cholesterol; Hydrogenated
fats are the problem; Animal fats are the problem." Enig stated: "As
can be seen, his findings were inconsistent."

Enig also stated: "The problems for coconut oil started four decades
ago when researchers fed animals hydrogenated coconut oil that was
purposely altered to make it completely devoid of any essential
fatty acids... The animals fed the hydrogenated coconut oil (as the
only fat source) naturally became essential fatty acid deficient;
their serum cholesterol increased. Diets that cause an essential
fatty acid deficiency always produce an increase in serum
cholesterol levels as well as in increase in the atherosclerotic
indices. The same effect has also been seen when other ...highly
hydrogenated oils such as cottonseed, soybean or corn oils have been
fed; so it is clearly a function of the hydrogenated products,
either because the oil is essential fatty acid (EFA) deficient or
because of transfatty acids."

What about studies where animals were fed unprocessed coconut oil?
Enig wrote: "Hostmark et al (1980) compared the effects of diets
containing 10% coconut oil 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 feeding." (Editor's note: HDLs are considered the good
cholesterol as they prevent deposits of LDL cholesterol on artery
walls.) She also cited a study by Awad (1981) on Wistar rats fed a
diet of either 14% (natural) coconut oil or 14% safflower oil. She
stated:"Total tissue cholesterol accumulation for animals on the
safflower diet was six times greater than for animals fed the
[unhydrogenated] coconut oil. A conclusion that can be drawn from
some of the animal research is that feeding hydrogenated coconut oil
devoid of essential fatty acids (EFA) ...potentate 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." Enig also referred to epidemiological
studies done by Kaunitz and Dayrit (1992) on coconut eating
societies who found that "available population studies show that
dietary coconut oil does not lead to high serum cholesterol nor to
high coronary heart disease.." It is noteworthy that hydrogenated
coconut oil was not consumed by these coconut eating societies; they
only consumed natural coconut oil.

Kaunitz and Dayrit noted in 1989 that Mendis et al reported when Sri
Lankan males were changed from their normal diet of natural coconut
oil to corn oil, their LDL cholesterol declined 23.8% which is good
news, but their HDL cholesterol declined 41.4% which is bad news.
This created a more unfavorable LDL/HDL ratio meaning that on the
corn oil diet there would be more cholesterol depositing on the
artery walls than on the coconut oil diet. In plain English, a diet
using liquid corn oil will lead to cholesterol deposits faster than
a diet using natural coconut oil. Natural coconut oil, by increasing
the good HDL cholesterol, may help prevent atherosclerosis and heart
disease. Enig cited several other studies in her article that showed
that natural coconut oil (not hydrogenated coconut oil) had health
benefits markers indicating that coconut oil was more beneficial in
preventing heart disease than most vegetable oils. Enig also cited
the research of Tholstrup et al (1994) on natural (NOT hydrogenated)
palm kernel oil which is high in lauric acid and also contains
myristic acid. Tholstrup found that with palm kernel oil, "HDL
cholesterol levels increased significantly from baseline values."

Enig reported in her article that the effects of coconut oil on
persons with low cholesterol levels was the opposite of persons with
high cholesterol levels. Of persons with low total cholesterol
counts, she wrote that "there may be a rising of serum cholesterol,
LDL cholesterol and especially HDL cholesterol." In persons with
high cholesterol levels, "there is lowering of total cholesterol and
LDL cholesterol." The studies she cited showed that in both groups
the LDL/HDL ratio moved in a favorable direction. In persons with
AIDS or immune-compromised from other causes, the conclusions of
this research are profound. It means everything the public has been
told about vegetable oils on television for the past 15 years has
been half truths and leading the public to the wrong conclusions.
The public has been led to believe that tropicals will clog your
arteries and cause heart disease. In fact, the opposite is true;
natural tropical oils will help prevent hardening of the arteries
while most liquid vegetable oils will increase hardening of the
arteries! In a phone call to Mary Enig in April, 1997, she told me
that the worst oil to use for any purpose is Canola oil. When used
in cooking, it produces the very high levels of transfatty acids.

Mary Enig Ph.D. on Natural Coconut Oil for AIDS and Other Viral
Infections
On July 19, 1995, Enig was quoted in an article published in The
HINDU, India's National Newspaper as stating that coconut oil is
converted by the body into "Monolaurin" a fatty acid with anti-viral
properties that might be useful in the treatment of AIDS. The staff
reporter for The HINDU wrote about Enig's presentation at a press
conference in Kochi and wrote the following:

"There was an instance in the US in which an infant tested HIV
positive had become HIV negative. That it was fed with an infant
formula with a high coconut oil content gains significance in this
context and at present an effort was on to find out how the 'viral
load' of an HIV infected baby came down when fed a diet that helped
in the generation of Monolaurin in the body."

The reporter commented on Enig's observations that "Monolaurin
helped in inactivating other viruses such as measles, herpes,
vesicular stomatitis and Cytomegalovirus (CMV) and that research
undertaken so far on coconut oil also indicated that it offered a
certain measure of protection against cancer-inducing substances. "

In another article published in the Indian Coconut Journal, Sept.,
1995, Dr. Enig stated:

"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 strains of enveloped viruses. The envelope of these
viruses is a lipid membrane."

Enig stated in her article that Monolaurin, of which the precursor
is lauric acid, disrupted the lipid membranes of envelope viruses
and also inactivated bacteria, yeast and fungi. She wrote: "Of the
saturated fatty acids, lauric acid has greater anti-viral activity
than either caprylic acid (C-10) or myristic acid (C-14). The action
attributed to Monolaurin is that of solubilizing the lipids ...in
the envelope of the virus causing the disintegration of the virus
envelope." In India, coconut oil is fed to calves to treat
Cryptosporidium as reported by Lark Lands Ph.D. in her upcoming
book "Positively Well" (1).

While HHV-6A was not mentioned by Enig, HHV-6A is an enveloped virus
and would be expected to disintegrate in the presence of lauric acid
and/or Monolaurin. Some of the pathogens reported by Enig to be
inactivated by Monolaurin include HIV, measles, vercular stomatitis
virus (VSV), herpes simplex virus (HSV-1), visna, cytomegalovirus
(CMV), Influenza virus, Pneumonovirus, Syncytial virus and Rubeola.
Some bacteria inactivated by Monolaurin include listeria,
Staphylococcus aureus, Streptococcus agalactiae, Groups A, B, F and
G streptococci, Gram-positive organisms; and gram-negative
organisms, if treated with chelator.

Enig reported that only one infant formula "Impact" contains lauric
acid while the more widely promoted formulas like "Ensure" do not
contain lauric acid and often contain some hydrogenated fats
(transfatty acids). A modified ester of lauric acid, Monolaurin
(available in capsules), is sold in health food stores and is
manufactured by Ecological Formulas, Concord, CA.

Enig on a Therapeutic Dose
Based on her calculations on the amount of lauric acid found in
human Mother's milk, Dr. Enig suggests a rich lauric acid diet would
contain about 24 grams of lauric acid daily for the average adult.
This amount could be found in about 3.5 tablespoons of coconut oil
or 10 ounces of "Pure Coconut Milk." Coconut Milk is made in Sri
Lanka and imported into the United States. It can be found in health
food stores and in local grocery stores in the International Foods
section or in specialty grocery stores that sell products imported
from Thailand, the Philippines or East India. About 7 ounces of raw
coconut daily would contain 24 grams of lauric acid. 24 grams of
lauric acid is the therapeutic daily dose for adults suggested by
Mary Enig based on her research of the lauric acid content of
mother's milk. (1)

1. Positively Well, by Lark Lands Ph.D. Her new book discusses
lauric acid and suggests many treatment options for persons with
AIDS or CFIDS and may be ordered by calling 905-672-7470 or 800-542-
8102

Scientific Research on the Anti-Viral Effects of Lauric Acid:
Mary Enig cites 24 references in her 7 page article on "Lauric Acid
for HIV-infected Individuals," a few of which are as follows:

1. Issacs, C.E. et al. Inactivation of enveloped viruses in human
bodily fluids by purified lipids. Annals of the New York Academy of
Sciences 1994;724:457-464.

2. Kabara, J.J. Antimicrobial agents derived from fatty acids.
Journal of the American Oil Chemists Society 1984;61:397-403.

3. Hierholzer, J.C. and Kabara J.J. In vitro effects on Monolaurin
compounds on enveloped RNA and DNA viruses. Journal of Food Safety
1982;4:1-12.

4. Wang, L.L. And Johnson, E.A. Inhibition of Listeria monocytogenes
by fatty acids and monoglycerides. Appli Environ Microbiol 1992;
58:624-629.

5. Issacs, CE et al. Membrane-disruptive effect of human milk:
inactivation of enveloped viruses. Journal of Infectious Diseases
1986;154:966-971.

6. Anti-viral effects of monolaruin. JAQA 1987;2:4-6 7. Issacs CE et
al. Antiviral and antibacterial lipids in human milk and infant
formula feeds. Archives of Disease in Childhood 1990;65:861-864.
 
 

The Oiling of America

by Mary Enig, PhD, and Sally Fallon
http://www.westonaprice.org/knowyourfats/oiling.html
In 1954 a young researcher from Russia named David Kritchevsky published a paper describing the effects of feeding cholesterol to rabbits. Cholesterol added to vegetarian rabbit chow caused the formation of atheromas—plaques that block arteries and contribute to heart disease. Cholesterol is a heavy weight molecule—an alcohol or a sterol—found only in animal foods such as meat, fish, cheese, eggs and butter. In the same year, according to the American Oil Chemists Society, Kritchevsky published a paper describing the beneficial effects of polyunsaturated fatty acids for lowering cholesterol levels. Polyunsaturated fatty acids are the kind of fats found in large amounts in highly liquid vegetable oils made from corn, soybeans, safflower seeds and sunflower seeds. (Monounsaturated fatty acids are found in large amounts in olive oil, palm oil and lard; saturated fatty acids are found in large amounts in fats and oils that are solid at room temperature, such as butter, tallows and coconut oil.)

Rise of Coronary Heart Disease in the 20th Century

Scientists of the period were grappling with a new threat to public health—a steep rise in heart disease. While turn-of-the-century mortality statistics are unreliable, they consistently indicate that heart disease caused no more than ten percent of all deaths, considerably less than infectious diseases such as pneumonia and tuberculosis. By 1950, coronary heart disease, or CHD, was the leading source of mortality in the United States, causing more than 30% of all deaths. The greatest increase came under the rubric of myocardial infarction (MI)—a massive blood clot leading to obstruction of a coronary artery and consequent death to the heart muscle. MI was almost nonexistent in 1910 and caused no more than three thousand deaths per year in 1930. By 1960, there were at least 500,000 MI deaths per year in the US. What life-style changes had caused this increase?
One change was a decrease in infectious disease, following the decline of the horse as a means of transport, the installation of more sanitary water supplies and the advent of better housing, all of which allowed more people to reach adulthood and the heart attack age. The other was a dietary change. Since the early part of the century, when the Department of Agriculture had begun to keep track of food "disappearance" data—the amount of various foods going into the food supply—a number of researchers had noticed a change in the kind of fats Americans were eating. Butter consumption was declining while the use of vegetable oils, especially oils that had been hardened to resemble butter by a process called hydrogenation, was increasing—dramatically increasing. By 1950 butter consumption had dropped from eighteen pounds per person per year to just over ten. Margarine filled in the gap, rising from about two pounds per person at the turn of the century to about eight. Consumption of vegetable shortening—used in crackers and baked goods—remained relatively steady at about twelve pounds per person per year but vegetable oil consumption had more than tripled—from just under three pounds per person per year to more than ten.
The statistics pointed to one obvious conclusion—Americans should eat the traditional foods that nourished their ancestors, including meat, eggs, butter and cheese, and avoid the newfangled vegetable-oil-based foods that were flooding the grocers' shelves; but the Kritchevsky articles attracted immediate attention because they lent support to another theory—one that militated against the consumption of meat and dairy products. This was the lipid hypothesis, namely that saturated fat and cholesterol from animal sources raise cholesterol levels in the blood, leading to deposition of cholesterol and fatty material as pathogenic plaques in the arteries. Kritchevsky's rabbit trials were actually a repeat of studies carried out four decades earlier in St. Petersburg, in which rabbits fed saturated fats and cholesterol developed fatty deposits in their skin and other tissues—and in their arteries. By showing that feeding polyunsaturated oils from vegetable sources lowered serum cholesterol in humans, at least temporarily, Kritchevsky appeared to show that animals findings were relevant to the CHD problem, that the lipid hypothesis was a valid explanation for the new epidemic and that by reducing animal products in the diet Americans could avoid heart disease.

The "evidence" for the lipid hypothesis

In the years that followed, a number of population studies demonstrated that the animal model—especially one derived from vegetarian animals—was not a valid approach for the problem of heart disease in human omnivores. A much publicized 1955 report on artery plaques in soldiers killed during the Korean War showed high levels of atherosclerosis, but another report—one that did not make it to the front pages—found that Japanese natives had almost as much pathogenic plaque—65% versus 75%—even though the Japanese diet at the time was lower in animal products and fat. A 1957 study of the largely vegetarian Bantu found that they had as much atheroma—occlusions or plaque buildup in the arteries—as other races from South Africa who ate more meat. A 1958 report noted that Jamaican Blacks showed a degree of atherosclerosis comparable to that found in the United States, although they suffered from lower rates of heart disease. A 1960 report noted that the severity of atherosclerotic lesions in Japan approached that of the United States. The 1968 International Atherosclerosis Project, in which over 22,000 corpses in 14 nations were cut open and examined for plaques in the arteries, showed the same degree of atheroma in all parts of the world—in populations that consumed large amounts of fatty animal products and those that were largely vegetarian, and in populations that suffered from a great deal of heart disease and in populations that had very little or none at all. All of these studies pointed to the fact that the thickening of the arterial walls is a natural, unavoidable process. The lipid hypothesis did not hold up to these population studies, nor did it explain the tendency to fatal clots that caused myocardial infarction.
In 1956, an American Heart Association (AHA) fund-raiser aired on all three major networks. The MC interviewed, among others, Irving Page and Jeremiah Stamler of the AHA, and researcher Ancel Keys. Panelists presented the lipid hypothesis as the cause of the heart disease epidemic and launched the Prudent Diet, one in which corn oil, margarine, chicken and cold cereal replaced butter, lard, beef and eggs. But the television campaign was not an unqualified success because one of the panelists, Dr. Dudley White, disputed his colleagues at the AHA. Dr. White noted that heart disease in the form of myocardial infarction was nonexistent in 1900 when egg consumption was three times what it was in 1956 and when corn oil was unavailable. When pressed to support the Prudent Diet, Dr. White replied: "See here, I began my practice as a cardiologist in 1921 and I never saw an MI patent until 1928. Back in the MI free days before 1920, the fats were butter and lard and I think that we would all benefit from the kind of diet that we had at a time when no one had ever heard the word corn oil."
But the lipid hypothesis had already gained enough momentum to keep it rolling, in spite of Dr. White's nationally televised plea for common sense in matters of diet and in spite of the contradictory studies that were showing up in the scientific literature. In 1957, Dr. Norman Jolliffe, Director of the Nutrition Bureau of the New York Health Department initiated the Anti-Coronary Club, in which a group of businessmen, ranging in age from 40 to 59 years, were placed on the Prudent Diet. Club members used corn oil and margarine instead of butter, cold breakfast cereals instead of eggs and chicken and fish instead of beef. Anti-Coronary Club members were to be compared with a "matched" group of the same age who ate eggs for breakfast and had meat three times a day. Jolliffe, an overweight diabetic confined to a wheel chair, was confident that the Prudent Diet would save lives, including his own.
In the same year, the food industry initiated advertising campaigns that touted the health benefits of their products—low in fat or made with vegetable oils. A typical ad read: "Wheaties may help you live longer." Wesson recommended its cooking oil "for your heart's sake" a Journal of the American Medical Association ad described Wesson oil as a "cholesterol depressant." Mazola advertisements assured the public that "science finds corn oil important to your health." Medical journal ads recommended Fleishmann's unsalted margarine for patients with high blood pressure.
Dr. Frederick Stare, head of Harvard University's Nutrition Department, encouraged the consumption of corn oil—up to one cup a day—in his syndicated column. In a promotional piece specifically for Procter and Gamble's Puritan oil, he cited two experiments and one clinical trial as showing that high blood cholesterol is associated with CHD. However, both experiments had nothing to do with CHD, and the clinical trial did not find that reducing blood cholesterol had any effect on CHD events. Later, Dr. William Castelli, Director of the Framingham Study was one of several specialists to endorse Puritan. Dr. Antonio Gotto, Jr., former AHA president, sent a letter promoting Puritan Oil to practicing physicians—printed on Baylor College of Medicine, The De Bakey Heart Center letterhead. The irony of Gotto's letter is that De Bakey, the famous heart surgeon, coauthored a 1964 study involving 1700 patients which also showed no definite correlation between serum cholesterol levels and the nature and extent of coronary artery disease. In other words, those with low cholesterol levels were just as likely to have blocked arteries as those with high cholesterol levels. But while studies like De Bakey's moldered in the basements of university libraries, the vegetable oil campaign took on increased bravado and audacity.
The American Medical Association at first opposed the commercialization of the lipid hypothesis and warned that "the anti-fat, anti-cholesterol fad is not just foolish and futile... it also carries some risk." The American Heart Association, however, was committed. In 1961 the AHA published its first dietary guidelines aimed at the public. The authors, Irving Page, Ancel Keys, Jeremiah Stamler and Frederick Stare, called for the substitution of polyunsaturates for saturated fat, even though Keys, Stare and Page had all previously noted in published papers that the increase in CHD was paralleled by increasing consumption of vegetable oils. In fact, in a 1956 paper, Keys had suggested that the increasing use of hydrogenated vegetable oils might be the underlying cause of the CHD epidemic.
Stamler shows up again in 1966 as an author of Your Heart Has Nine Lives, a little self-help book advocating the substitution of vegetable oils for butter and other so-called "artery clogging" saturated fats. The book was sponsored by makers of Mazola Corn Oil and Mazola Margarine. Stamler did not believe that lack of evidence should deter Americans from changing their eating habits. The evidence, he stated, " . . was compelling enough to call for altering some habits even before the final proof is nailed down... the definitive proof that middle-aged men who reduce their blood cholesterol will actually have far fewer heart attacks waits upon diet studies now in progress." His version of the Prudent Diet called for substituting low-fat milk products such as skim milk and low-fat cheeses for cream, butter and whole cheeses, reducing egg consumption and cutting the fat off red meats. Heart disease, he lectured, was a disease of rich countries, striking rich people who ate rich food... including "hard" fats like butter.
It was in the same year, 1966, that the results of Dr. Jolliffe's Anti-Coronary Club experiment were published in the Journal of the American Medical Association. Those on the Prudent Diet of corn oil, margarine, fish, chicken and cold cereal had an average serum cholesterol of 220, compared to 250 in the meat-and-potatoes control group. However, the study authors were obliged to note that there were eight deaths from heart disease among Dr. Jolliffe's Prudent Diet group, and none among those who ate meat three times a day. Dr. Jolliffe was dead by this time. He succumbed in 1961 from a vascular thrombosis, although the obituaries listed the cause of death as complications from diabetes. The "compelling proof" that Stamler and others were sure would vindicate wholesale tampering with American eating habits had not yet been "nailed down."
The problem, said the insiders promoting the lipid hypothesis, was that the numbers involved in the Anti-Coronary Club experiment were too small. Dr. Irving Page urged a National Diet-Heart Study involving one million men, in which the results of the Prudent Diet could be compared on a large scale with the those on a diet high in meat and fat. With great media attention, the National Heart Lung and Blood Institute organized the stocking of food warehouses in six major cities, where men on the Prudent Diet could get tasty polyunsaturated donuts and other fabricated food items free of charge. But a pilot study involving 2,000 men resulted in exactly the same number of deaths in both the Prudent Diet and the control group. A brief report in Circulation, March 1968, stated that the study was a milestone "in mass environmental experimentation" that would have "an important effect on the food industry and the attitude of the public toward its eating habits." But the million-man Diet Heart Study was abandoned in utter silence "for reasons of cost." Its chairman, Dr. Irving Page, died of a heart attack.

Hydrogenation and trans fats

Most animal fats—like butter, lard and tallow—have a large proportion of saturated fatty acids. Saturated fats are straight chains of carbon and hydrogen that pack together easily so that they are relatively solid at room temperature. Oils from seeds are composed mostly of polyunsaturated fatty acids. These molecules have kinks in them at the point of the unsaturated double bonds. They do not pack together easily and therefore tend to be liquid at room temperature. Judging from both food data and turn-of-the-century cookbooks, the American diet in 1900 was a rich one—with at least 35 to 40 percent of calories coming from fats, mostly dairy fats in the form of butter, cream, whole milk and eggs. Salad dressing recipes usually called for egg yolks or cream; only occasionally for olive oil. Lard or tallow served for frying; rich dishes like head cheese and scrapple contributed additional saturated fats during an era when cancer and heart disease were rare. Butter substitutes made up only a small portion of the American diet, and these margarines were blended from coconut oil, animal tallow and lard, all rich in natural saturates.
The technology by which liquid vegetable oils could be hardened to make margarine was first discovered by a French chemist named Sabatier. He found that a nickel catalyst would cause the hydrogenation—the addition of hydrogen to unsaturated bonds to make them saturated—of ethylene gas to ethane. Subsequently the British chemist Norman developed the first application of hydrogenation to food oils and took out a patent. In 1909, Procter & Gamble acquired the US rights to the British patent that made liquid vegetable oils solid at room temperature. The process was used on both cottonseed oil and lard to give "better physical properties"—to create shortenings that did not melt as easily on hot days.
The hydrogenation process transforms unsaturated oils into straight "packable" molecules, by rearranging the hydrogen atoms at the double bonds. In nature, most double bonds occur in the cis configuration, that is with both hydrogen atoms on the same side of the carbon chain at the point of the double bond. It is the cis isomers of fatty acids that have a bend or kink at the double bond, preventing them from packing together easily. Hydrogenation creates trans double bonds by moving one hydrogen atom across to the other side of the carbon chain at the point of the double bond. In effect, the two hydrogen atoms then balance each other and the fatty acid straightens, creating a packable "plastic" fat with a much higher melting temperature. Although trans fatty acids are technically unsaturated, they are configured in such a way that the benefits of unsaturation are lost. The presence of several unpaired electrons presented by contiguous hydrogen atoms in their cis form allows many vital chemical reactions to occur at the site of the double bond. When one hydrogen atom is moved to the other side of the fatty acid molecule during hydrogenation, the ability of living cells to make reactions at the site is compromised or altogether lost. Trans fatty acids are sufficiently similar to natural fats that the body readily incorporates them into the cell membrane; once there their altered chemical structure creates havoc with thousands of necessary chemical reactions—everything from energy provision to prostaglandin production.
After the second world war, "improvements" made it possible to plasticize highly unsaturated oils from corn and soybeans. New catalysts allowed processors to "selectively hydrogenate" the kinds of fatty acids with three double bonds found in soy and canola oils. Called "partial hydrogenation," the new method allowed processors to replace cottonseed oil with more unsaturated corn and soy bean oils in margarines and shortenings. This spurred a meteoric rise in soybean production, from virtually nothing in 1900 to 70 million tons in 1970, surpassing corn production. Today soy oil dominates the market and is used in almost eighty percent of all hydrogenated oils.
The particular mix of fatty acids in soy oil results in shortenings containing about 40% trans fats, an increase of about 5% over cottonseed oil, and 15% over corn oil. Canola oil, processed from a hybrid form of rape seed, is particularly rich in fatty acids containing three double bonds and the shortening can contain as much as 50% trans fats. Trans fats of a particularly problematical form are also formed during the deodorization of canola oil, although they are not indicated on labels for the liquid oil.
Certain forms of trans fatty acids occur naturally in dairy fats. Trans-vaccenic acid makes up about 4% of the fatty acids in butter. It is an interim product which the ruminant animal then converts to conjugated linoleic acid, a highly beneficial anti-carcinogenic component of animal fat. Humans seem to utilize the small amounts of trans-vaccenic acid in butter fat without ill effects.
But most of the trans isomers in modern hydrogenated fats are new to the human physiology and by the early 1970's a number of researchers had expressed concern about their presence in the American diet, noting that their increasing use had paralleled the increase in both heart disease and cancer. The unstated solution was one that could be easily presented to the public: Eat natural, traditional fats; avoid newfangled foods made from vegetable oils; use butter, not margarine. But medical research and public consciousness took a different tack, one that accelerated the decline of traditional foods like meat, eggs and butter, and fueled continued dramatic increases in vegetable oil consumption.

Shenanigans at the AHA

Although the AHA had committed itself to the lipid hypothesis and the unproven theory that polyunsaturated oils afforded protection against heart disease, concerns about hydrogenated vegetable oils were sufficiently great to warrant the inclusion of the following statement in the organization's 1968 diet heart statement: "Partial hydrogenation of polyunsaturated fats results in the formation of trans forms which are less effective than cis, cis forms in lowering cholesterol concentrations. It should be noted that many currently available shortening and margarines are partially hydrogenated and may contain little polyunsaturated fat of the natural cis, cis form." 150,000 copies of the statement were printed but never distributed. The shortening industry objected strongly and a researcher named Fred Mattson of Procter and Gamble convinced Campbell Moses, medical director of the AHA, to remove it. The final recommendations for the public contained three major points—restrict calories, substitute polyunsaturates for saturates and reduce cholesterol in the diet.
Other organizations fell in behind the AHA in pushing vegetable oils instead of animal fats. By the early 1970's the National Heart Lung and Blood Institute, the AMA, the American Dietetic Association and the National Academy of Science had all endorsed the lipid hypotheses and the avoidance of animal fats for those Americans in the "at risk" category.
Since Kritchevsky's early studies, many other trials had shown that serum cholesterol can be lowered by increasing ingestion of polyunsaturates. The physiological explanation for this is that when excess polyunsaturates are built into the cell membranes, resulting in reduced structural integrity or "limpness," cholesterol is sequestered from the blood into the cell membranes to give them "stiffness." The problem was that there was no proof that lowering serum cholesterol levels could stave off CHD. That did not prevent the American Heart Association from calling for "modified and ordinary foods" useful for the purpose of facilitating dietary changes to newfangled oils and away from traditional fats. These foods, said the AHA literature, should be made available to the consumer, "reasonably priced and easily identified by appropriate labeling. Any existing legal and regulatory barriers to the marketing of such foods should be removed."

Shenanigans at the FDA

The man who made it possible to remove any "existing legal and regulatory barriers" was Peter Barton Hutt, a food lawyer for the prestigious Washington, DC law firm of Covington and Burling. Hutt once stated that "Food law is the most wonderful field of law that you can possibly enter." After representing the edible oil industry, he temporarily left his law firm to become the FDA's general council in 1971. The regulatory barrier to foods useful to the purpose of changing American consumption patterns was the Food, Drug and Cosmetic Act of 1938, which stated that "... there are certain traditional foods that everyone knows, such as bread, milk and cheese, and that when consumers buy these foods, they should get the foods that they are expecting... [and] if a food resembles a standardized food but does not comply with the standard, that food must be labeled as an 'imitation'".
The 1938 Food, Drug and Cosmetic Act had been signed into law partly in response to consumer concerns about the adulteration of ordinary foodstuffs. Chief among the products with a tradition of suffering competition from imitation products were fats and oils. In Life on the Mississippi, Mark Twain reports on a conversation overheard between a New Orleans cottonseed oil purveyor and a Cincinnati margarine drummer. New Orleans boasts of selling deodorized cottonseed oil as olive oil in bottles with European labels. "We turn out the whole thing—clean from the word go—in our factory in New Orleans... We are doing a ripping trade, too." The man from Cincinnati reports that his factories are turning out oleomargarine by the thousands of tons, an imitation that "you can't tell from butter." He gloats at the thought of market domination. "You are going to see the day, pretty soon, when you won't find an ounce of butter to bless yourself with, in any hotel in the Mississippi and Ohio Valleys, outside of the biggest cities... And we can sell it so dirt cheap that the whole country has got to take it... butter don't stand any show—there ain't any chance for competition. Butter's had its day—and from this out, butter goes to the wall. There's more money in oleomargarine than, why, you can't imagine the business we do."
In the tradition of Mark Twain's riverboat hucksters, Peter Barton Hutt guided the FDA through the legal and congressional hoops to the establishment of the FDA "Imitation" policy in 1973, which attempted to provide for "advances in food technology" and give "manufacturers relief from the dilemma of either complying with an outdated standard or having to label their new products as ‘imitation' ... [since ]... such products are not necessarily inferior to the traditional foods for which they may be substituted." Hutt considered the word "imitation" to be over simplified and inaccurate—"potentially misleading to consumers." The new regulations defined "inferiority" as any reduction in content of an essential nutrient that is present at a level of two percent or more of the US Recommended Daily Allowance (RDA). The new imitation policy meant that imitation sour cream, made with vegetable oil and fillers like guar gum and carrageenan, need not be labelled imitation as long as artificial vitamins were added to bring macro nutrient levels up to the same amounts as those in real sour cream. Coffee creamers, imitation egg mixes, processed cheeses and imitation whipped cream no longer required the imitation label, but could be sold as real and beneficial foods, low in cholesterol and rich in polyunsaturates.
These new regulations were adopted without the consent of Congress, continuing the trend instituted under Nixon in which the White House would use the FDA to promote certain social agendas through government food policies. They had the effect of increasing the lobbying clout of special interest groups, such as the edible oil industry, and short circuiting public participation in the regulatory process. They allowed food processing innovations regarded as "technological improvements" by manufacturers to enter the market place without the onus of economic fraud that might be engendered by greater consumer awareness and congressional supervision. They ushered in the era of ersatz foodstuffs, convenient counterfeit products—weary, stale, flat and immensely profitable.

Shenanigans in Congress

Congress did not voice any objection to this usurpation of its powers, but entered the contest on the side of the lipid hypothesis. The Senate Select Committee on Nutrition and Human Needs, chaired by George McGovern during the years 1973 to 1977, actively promoted the use of vegetable oils. "Dietary Goals for the United States," published by the committee, cited U.S. Department of Agriculture data on fat consumption, and stated categorically that "the overconsumption of fat, generally, and saturated fat in particular... have been related to six of the ten leading causes of death..." in the United States. The report urged the American populace to reduce overall fat intake and to substitute polyunsaturates for saturated fat from animal sources—margarine and corn oil for butter, lard and tallow. Opposing testimony included a moving letter—buried in the voluminous report—by Dr. Fred Kummerow of the University of Illinois, urging a return to traditional whole foods and warning against the use of soft drinks. In the early 1970's, Kummerow had shown that trans fatty acids caused increased rates of heart disease in pigs. A private endowment allowed him to continue his research—government funding agencies such as National Institutes of Health refused to give him further grants.
One unpublished study that was known to McGovern Committee members but not mentioned in its final report compared calves fed saturated fat from tallow and lard with those fed unsaturated fat from soybean oil. The calves fed tallow and lard did indeed show higher plasma cholesterol levels than the soybean oil-fed calves, and fat streaking was found in their aortas. Atherosclerosis was also enhanced. But the calves fed soybean oil showed a decline in calcium and magnesium levels in the blood, possibly due to inefficient absorption. They utilized vitamins and minerals inefficiently, showed poor growth, poor bone development and had abnormal hearts. More cholesterol per unit of dry matter was found in the aorta, liver, muscle, fat and coronary arteries, a finding which led the investigators to the conclusion the lower blood cholesterol levels in the soybean-oil fed calves may have been the result of cholesterol being transferred from the blood to other tissues. The calves in the soybean oil group also collapsed when they were forced to move around and they were unaware of their surroundings for short periods. They also had rickets and diarrhea.
The McGovern Committee report continued dietary trends already in progress—the increased use of vegetables oils, especially in the form of partially hydrogenated margarines and shortenings. In 1976, the FDA established GRAS (Generally Recognized as Safe) status for hydrogenated soybean oil. A report prepared by the Life Sciences Research Office of the Federation of American Scientists for Experimental Biology (LSRO-FASEB) concluded that "There is no evidence in the available information on hydrogenated soybean oil that demonstrates or suggests reasonable ground to suspect a hazard to the public when it is used as a direct or indirect food ingredient at levels that are now current or that might reasonably be expected in the future."

Enig speaks out

When Mary Enig, a graduate student at the University of Maryland, read the McGovern committee report, she was puzzled. Enig was familiar with Kummerow's research and she knew that the consumption of animal fats in America was not on the increase—quite the contrary, use of animal fats had been declining steadily since the turn of the century. A report in the Journal of American Oil Chemists—which the McGovern Committee did not use—showed that animal fat consumption had declined from 104 grams per person per day in 1909 to 97 grams per day in 1972, while vegetable fat intake had increased from a mere 21 grams to almost 60. Total per capita fat consumption had increased over the period, but this increase was mostly due to an increase in unsaturated fats from vegetable oils—with 50 percent of the increase coming from liquid vegetable oils and about 41 percent from margarines made from vegetable oils. She noted a number of studies that directly contradicted the McGovern Committee's conclusions that "there is ... a strong correlation between dietary fat intake and the incidence of breast cancer and colon cancer," two of the most common cancers in America. Greece, for example, had less than one-fourth the rate of breast cancer compared to Israel but the same dietary fat intake. Spain had only one-third the breast cancer mortality of France and Italy but the total dietary fat intake was slightly greater. Puerto Rico, with a high animal fat intake, had a very low rate of breast and colon cancer. The Netherlands and Finland both used approximately 100 grams of animal fat per capita per day but breast and colon cancer rates were almost twice in the Netherlands what they are in Finland. The Netherlands consumed 53 grams of vegetable fat per person compared to 13 in Finland. A study from Cali, Columbia found a fourfold excess risk for colon cancer in the higher economic classes, which used less animal fat than the lower economic classes. A study on Seventh-Day Adventist physicians, who avoid meat, especially red meat, found they had a significantly higher rate of colon cancer than non-Seventh Day Adventist physicians. Enig analyzed the USDA data that the McGovern Committee had used and concluded that it showed a strong positive correlation with total fat and vegetable fat and an essentially strong negative correlation or no correlation with animal fat to total cancer deaths, breast and colon cancer mortality and breast and colon cancer incidence—in other words, use of vegetable oils seemed to predispose to cancer and animal fats seemed to protect against cancer. She noted that the analysts for the committee had manipulated the data in inappropriate ways in order to obtain mendacious results.
Enig submitted her findings to the Journal of the Federation of American Societies for Experimental Biology (FASEB), in May, 1978, and her article was published in the FASEB's Federation Proceedings in July of the same year—an unusually quick turnaround. The assistant editor, responsible for accepting the article, died of a heart attack shortly thereafter. Enig's paper noted that the correlations pointed a finger at the trans fatty acids and called for further investigation. Only two years earlier, the Life Sciences Research office, which is the arm of FASEB that does scientific investigations, had published the whitewash that had ushered partially hydrogenated soybean oil onto the GRAS list and removed any lingering constraints against the number one ingredient in factory-produced food.

The food giants fight back

Enig's paper sent alarm bells through the industry. In early 1979, she received a visit from S. F. Reipma of the National Association of Margarine Manufacturers. Reipma was visibly annoyed. He explained that both his association and the Institute for Shortening and Edible Oils (ISEO) kept careful watch to prevent articles like Enig's from appearing in the literature. Enig's paper should never have been published, he said. He thought that ISEO was "watching out."
"We left the barn door open," he said, "and the horse got out."
Reipma also challenged Enig's use of the USDA data, claiming that it was in error. He knew it was in error, he said, "because we give it to them."
A few weeks later, Reipma paid a second visit, this time in the company of Thomas Applewhite, an advisor to the ISEO and representative of Kraft Foods, Ronald Simpson with Central Soya and an unnamed representative from Lever Brothers. They carried with them—in fact, waved them in the air in indignation—a two-inch stack of newspaper articles, including one that appeared in the National Enquirer, reporting on Enig's Federation Proceedings article. Applewhite's face flushed red with anger when Enig repeated Reipma's statement that "they had left the barn door open and a horse got out," and his admission that Department of Agriculture food data had been sabotaged by the margarine lobby.
The other thing Reipma told Enig during his unguarded visit was that he had called in on the FASEB offices in an attempt to coerce them into publishing letters to refute her paper, without allowing Enig to submit any counter refutation as was normally customary in scientific journals. He told Enig that he was "thrown out of the office"—an admission later confirmed by one of the FASEB editors. Nevertheless, a series of letters did follow the July 1978 article. On behalf of the ISEO, Applewhite and Walter Meyer of Procter and Gamble criticized Enig's use of the data; Applewhite accused Enig of extrapolating from two data points, when in fact she had used seven. In the same issue, John Bailar, Editor-in-Chief of the Journal of the National Cancer Institute, pointed out that the correlations between vegetable oil consumption and cancer were not the same as evidence of causation and warned against changing current dietary components in the hopes of preventing cancer in the future—which is of course exactly what the McGovern Committee did.
In reply, Enig and her colleagues noted that although the NCI had provided them with faulty cancer data, this had no bearing on the statistics relating to trans consumption, and did not affect the gist of their argument—that the correlation between vegetable fat consumption, especially trans fat consumption, was sufficient to warrant a more thorough investigation. The problem was that very little investigation was being done.
University of Maryland researchers recognized the need for more research in two areas. One concerned the effects of trans fats on cellular processes once they are built into the cell membrane. Studies with rats, including one conducted by Fred Mattson in 1960, indicated that the trans fatty acids were built into the cell membrane in proportion to their presence in the diet, and that the turnover of trans in the cells was similar to that of other fatty acids. These studies, according to J. Edward Hunter of the ISEO, were proof that "trans fatty acids do not pose any hazard to man in a normal diet." Enig and her associates were not so sure. Kummerow's research indicated that the trans fats contributed to heart disease, and Kritchevsky—whose early experiments with vegetarian rabbits were now seen to be totally irrelevant to the human model—had found that trans fatty acids raise cholesterol in humans. Enig's own research, published in her 1984 doctoral dissertation, indicated that trans fats interfered with enzyme systems that neutralized carcinogens and increased enzymes that potentiated carcinogens.

How much trans fat is "normal"?

The other area needing further investigation concerned just how much trans fat there was in a "normal diet" of the typical American. What had hampered any thorough research into the correlation of trans fatty acid consumption and disease was the fact that these altered fats were not considered as a separate category in any of the data bases then available to researchers. A 1970 FDA internal memo stated that a market basket survey was needed to determine trans levels in commonly used foods. The memo remained buried in the FDA files. The massive Health and Human Services NHANES II (National Health and Nutrition Examination Survey) survey, conducted during the years 1976 to 1980, noted the increasing US consumption of margarine, french fried potatoes, cookies and snack chips—all made with vegetable shortenings—without listing the proportion of trans fats.
Enig first looked at the NHANES II data base in 1987 and when she did, she had a sinking feeling. Not only were trans fats conspicuously absent from the fatty acid analyses, data on other lipids made no sense at all. Even foods containing no trans fats were listed with faulty fatty acid profiles. For example, safflower oil was listed as containing 14% linoleic acid (a double bond fatty acid of the omega-6 family) when in fact it contained 80%; a sample of butter crackers was listed as containing 34% saturated fat when in fact it contained 78%. In general, the NHANES II data base tended to minimize the amount of saturated fats in common foods.
Over the years, Joseph Sampagna and Mark Keeney, both highly qualified lipid biochemists at the University of Maryland, applied to the National Science Foundation, the National Institutes of Health, the US Department of Agriculture, the National Dairy Council and the National Livestock and Meat Board for funds to look into the trans content of common American foods. Only the National Livestock and Meat Board came through with a small grant for equipment; the others turned them down. The pink slip from National Institutes of Health criticized items that weren't even relevant to the proposal. The turndown by the National Dairy Council was not a surprise. Enig had earlier learned that Phil Lofgren, then head of research at the Dairy Council, had philosophical ties to the lipid hypothesis. Enig tried to alert Senator Mettzanbaum from Ohio, who was involved in the dietary recommendations debate, but got nowhere.
A USDA official confided to the Maryland research group that they "would never get money as long as they pursued the trans work." Nevertheless they did pursue it. Sampagna, Keeney and a few graduate students, funded jointly by the USDA and the university, spend thousands of hours in the laboratory analyzing the trans fat content of hundreds of commercially available foods. Enig worked as a graduate student, at times with a small stipend, at times without pay, to help direct the process of tedious analysis. The long arm of the food industry did its best to put a stop to the group's work by pressuring the USDA to pull its financial support of the graduates students doing the lipid analyses, which the University of Maryland received due to its status as a land grant college.
In December of 1982, Food Processing carried a brief preview of the University of Maryland research and five months later the same journal printed a blistering letter from Edward Hunter on behalf of the Institute of Shortening and Edible Oils. The University of Maryland studies on trans fat content in common foods had obviously struck a nerve. Hunter stated that the Bailar, Applewhite and Meyer letters that had appeared in Federation Proceedings five years earlier, "severely criticized and discredited" the conclusions reached by Enig and her colleagues. Hunter was concerned that Enig's group would exaggerate the amount of trans fats found in common foods. He cited ISEO data indicating that most margarines and shortenings contain no more than 35% and 25% trans respectively, and that most contain considerably less.
What Enig and her colleagues actually found was that many margarines indeed contained about 31% trans fat—later surveys by others revealed that Parkay margarine contained up to 45% trans—while many shortenings found ubiquitously in cookies, chips and baked goods contained more than 35%. She also discovered that many baked goods and processed foods contained considerably more fat from partially hydrogenated vegetable oils than was listed on the label. The finding of higher levels of fat in products made with partially hydrogenated oils was confirmed by Canadian government researchers many years later, in 1993.
Final results of Enig's ground-breaking compilation were published in the October 1983 edition of the Journal of the American Oil Chemists Society. Her analyses of more than 220 food items, coupled with food disappearance data, allowed University of Maryland researchers to confirm earlier estimates that the average American consumed at least 12 grams of trans fat per day, directly contradicting ISEO assertions that most Americans consumed no more that six to eight grams of trans fat per day. Those who consciously avoided animal fats typically consumed far more than 12 grams of trans fat per day.

Cat and mouse games in the journals

The ensuing debate between Enig and her colleagues at the University of Maryland, and Hunter and Applewhite of the ISEO, took the form of a cat and mouse game running through several scientific journals. Food Processing declined to publish Enig's reply to Hunter's attack. Science Magazine published another critical letter by Hunter in 1984, in which he misquoted Enig, but refused to print her rebuttal. Hunter continued to object to assertions that average consumption of trans fat in partially hydrogenated margarines and shortenings could exceed six to eight grams per day, a concern that Enig found puzzling when coupled with the official ISEO position that trans fatty acids were innocuous and posed no threat to public health.
The ISEO did not want the American public to hear about the debate on hydrogenated vegetable oils—for Enig this translated into the sound of doors closing. A poster presentation she organized for a campus health fair caught the eye of the dietetics department chairman who suggested she submit an abstract to the Society for Nutrition Education, many of whose members are registered dietitians. Her abstract concluded that "... meal plans and recipes developed for nutritionists and dieticians to use when designing diets to meet the Dietary Guidelines, the dietary recommendation of the American Heart Association or the Prudent Diet have been examined for trans fatty acid content. Some diet plans are found to contain approximately 7% or more of calories as trans fatty acids." The Abstract Review Committee rejected the submission, calling it "of limited interest."
Early in 1985 the Federation of American Societies for Experimental Biology (FASEB) heard more testimony on the trans fat issue. Enig alone represented the alarmist point of view, while Hunter and Applewhite of the ISEO, and Ronald Simpson, then with the National Association of Margarine Manufacturers, assured the panel that trans fats in the food supply posed no danger. Enig reported on University of Maryland research that delineated the differences in small amounts of naturally occurring trans fats in butter, which do not inhibit enzyme function at the cellular level, and man-made trans fats in margarines and vegetable shortenings which do. She also noted a 1981 feeding trial in which swine fed trans fatty acid developed higher parameters for heart disease than those fed saturated fats, especially when trans fatty acids were combined with added polyunsaturates. Her testimony was omitted from the final report, although her name in the bibliography created the impression that her research supported the FASEB whitewash.
In the following year, 1986, Hunter and Applewhite published an article exonerating trans fats as a cause of atherosclerosis in the prestigious American Journal of Clinical Nutrition, whose sponsors, by the way, include companies like Procter and Gamble, General Foods, General Mills, Nabisco and Quaker Oats. The authors once again stressed that the average per capita consumption of trans fatty acids did not exceed six to eight grams. Many subsequent government and quasi government reports minimizing the dangers of trans fats used the 1986 Hunter and Applewhite article as a reference.
Enig testified again in 1988 before the Expert Panel on the National Nutrition Monitoring System (NNMS). In fact she was the only witness before a panel, which began its meeting by confirming that the cause of America's health problems was the overconsumption of "fat, saturated fatty acids, cholesterol and sodium." Her testimony pointed out that the 1985 FASEB report exonerating trans fatty acids as safe was based on flawed data.
Behind the scenes, in a private letter to Dr. Kenneth Fischer, Director of the Life Sciences Research Office (LSRO), Hunter and Applewhite charged that "the University of Maryland group continues to raise unwarranted and unsubstantiated concerns about the intake of and imagined physiological effects of trans fatty acids and ... they continue to overestimate greatly the intake of trans acids by typical Americans." "No one other than Enig," they said, "has raised questions about the validity of the food fatty acid composition data used in NHANES II and... she has not presented sufficiently compelling arguments to justify a major reevaluating."
The letter contained numerous innuendos that Enig had mischaracterized the work of other researchers and had been less than scientific in her research. It was widely circulated among National Nutrition Monitoring System agencies. John Weihrauch, a USDA scientist, not an industry representative, slipped it surreptitiously to Dr. Enig. She and her colleagues replied by asking, "If the trade association truly believes ‘that trans fatty acids do not pose any harm to humans and animals'... why are they so concerned about any levels of consumption and why do they so vehemently and so frequently attack researchers whose findings suggest that the consumption of trans fatty acids is greater than the values the industry reports?"
Maryland researchers argued that trans fats should be included in food nutrition labels; the Hunter and Applewhite letter asserted that "there is no documented justification for including trans acids ... as part of nutrition labeling."
During her testimony Enig also brought up her concerns about other national food databases, citing their lack of information on trans. The Food Consumption Survey contained glaring errors—reporting, for example, consumption of butter in amounts nearly twice as great as what exists in the US food supply, and of margarine in quantities nearly half those known to exist in the food supply. "The fact that the data base is in error should compel the Congress to require correction of the data base and reevaluation of policy flowing from erroneous data," she argued, "especially since the congressional charter for NHANES was to compare dietary intake and health status and since this data base is widely used to do just that." Rather than "correction of the data base," [The] National Nutritional Monitoring System officials responded to Enig's criticism by dropping the whole section pertaining to butter and margarine from the 1980 tables.
Enig's testimony was not totally left out of the National Nutritional Monitoring System final report, as it had been from the FASEB report three years earlier. A summary of the proceedings and listing of panelists released in July of 1989 by Director Kenneth Fischer announced that a transcript of Enig's testimony could be obtained from Ace Federal Reporter in Washington DC. Unfortunately, his report wrongly listed the date of her testimony as January 20, 1988, rather than January 21, making her comments more difficult to retrieve.
The Enig-ISEO debate was covered by the prestigious Food Chemical News and Nutrition Week —both widely read by Congress and the food industry, but virtually unknown to the general public. National media coverage of dietary fat issues focused on the proceedings of the National Heart, Lung and Blood Institute as this enormous bureaucracy plowed relentlessly forward with the lipid hypothesis. In June of 1984, for example, the press diligently reported on the proceedings of the NHLBI's Lipid Research Clinics Conference, which was organized to wrap up almost 40 years of research on lipids, cholesterol and heart disease.
The problem with the 40 years of NHLBI-sponsored research on lipids, cholesterol and heart disease was that it had not produced many answers—at least not many answers that the NHLBI was pleased with. The ongoing Framingham Study found that there was virtually no difference in coronary heart disease "events" for individuals with cholesterol levels between 205 mg/dL and 294 mg/dL—the vast majority of the US population. Even for those with extremely high cholesterol levels—up to almost 1200 mg/dL, the difference in CHD events compared to those in the normal range was trivial. This did not prevent Dr. William Kannel, then Framingham Study Director, from making claims about the Framingham results. "Total plasma cholesterol" he said, "is a powerful predictor of death related to CHD." It wasn't until more than a decade later that the real findings at Framingham were published—without fanfare—in the Archives of Internal Medicine, an obscure journal. "In Framingham, Massachusetts," admitted Dr. William Castelli, Kannel's successor "the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower people's serum cholesterol... 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."
NHLBI's Multiple Risk Factor Intervention Trial (MRFIT) studied the relationship between heart disease and serum cholesterol levels in 362,000 men and found that annual deaths from CHD varied from slightly less than one per thousand at serum cholesterol levels below 140 mg/dL, to about two per thousand for serum cholesterol levels above 300 mg/dL, once again a trivial difference. Dr. John LaRosa of the American Heart Association claimed that the curve for CHD deaths began to "inflect" after 200 mg/dL, when in fact the "curve" was a very gradually sloping straight line that could not be used to predict whether serum cholesterol above certain levels posed a significantly greater risk for heart disease. One unexpected MRFIT finding the media did not report was that deaths from all causes—cancer, heart disease, accidents, infectious disease, kidney failure, etc.—were substantially greater for those men with cholesterol levels below 160 mg/dL.

Lipid Research Clinics Trial

What was needed to resolve the validity of the lipid hypothesis once and for all was a well-designed, long-term diet study that compared coronary heart disease events in those on traditional foods with those whose diets contained high levels of vegetable oils—but the proposed Diet-Heart study designed to test just that had been cancelled without fanfare years earlier. In view of the fact that orthodox medical agencies were united in their promotion of margarine and vegetable oils over animal foods containing cholesterol and animal fats, it is surprising that the official literature can cite only a handful of experiments indicating that dietary cholesterol has "a major role in determining blood cholesterol levels." One of these was a study involving 70 male prisoners directed by Fred Mattson — the same Fred Mattson who had pressured the American Heart Association into removing any reference to hydrogenated fats from their diet-heart statement a decade earlier. Funded in part by Procter and Gamble, the research contained a number of serious flaws: selection of subjects for the four groups studied was not randomized; the experiment inexcusably eliminated "an equal number of subjects with the highest and lowest cholesterol values;" twelve additional subjects dropped out, leaving some of the groups too small to provide valid conclusions; and statistical manipulation of the results was shoddy. But the biggest flaw was that the subjects receiving cholesterol did so in the form of reconstituted powder—a totally artificial diet. Mattson's discussion did not even address the possibility that the liquid formula diet he used might affect blood cholesterol differently than would a whole foods diet when, in fact, many other studies indicated that this is the case. The culprit, in fact, in liquid protein diets appears to be oxidized cholesterol, formed during the high-temperature drying process, which seems to initiate the buildup of plaque in the arteries. Powdered milk containing oxidized cholesterol is added to reduced fat milk—to give it body—which the American public has accepted as a healthier choice than whole milk. It was purified, oxidized cholesterol that Kritchevsky and others used in their experiments on vegetarian rabbits.
The NHLBI argued that a diet study using whole foods and involving the whole population would be too difficult to design and too expensive to carry out. But the NHLBI did have funds available to sponsor the massive Lipid Research Clinics Coronary Primary Prevention Trial in which all subjects were placed on a diet low in cholesterol and saturated fat. Subjects were divided into two groups, one of which took a cholesterol-lowering drug and the other a placebo. Working behind the scenes, but playing a key role in both the design and implementation of the trials, was Dr. Fred Mattson, formerly of Procter and Gamble.
An interesting feature of the study was the fact that a good part of the trial's one-hundred-and-fifty-million-dollar budget was devoted to group sessions in which trained dieticians taught both groups of study participants how to choose "heart-friendly" foods—margarine, egg replacements, processed cheese, baked goods made with vegetable shortenings, in short the vast array of manufactured foods awaiting consumer acceptance. As both groups received dietary indoctrination, study results could support no claims about the relation of diet to heart disease. Nevertheless, when the results were released, both the popular press and medical journals portrayed the Lipid Research Clinics trials as the long-sought proof that animal fats were the cause of heart disease. Rarely mentioned in the press was the ominous fact that the group taking the cholesterol-lowering drugs had an increase in deaths from cancer, stroke, violence and suicide.
LRC researchers claimed that the group taking the cholesterol-lowering drug had a 17% reduction in the rate of CHD, with an average cholesterol reduction of 8.5%. This allowed LRC trials Director Basil Rifkind to claim that "for each 1% reduction in cholesterol, we can expect a 2% reduction in CHD events." The statement was widely circulated even though it represented a completely invalid representation of the data, especially in light of the fact that when the lipid group at the University of Maryland analyzed the LRC data, they found no difference in CHD events between the group taking the drug and those on the placebo.
A number of clinicians and statisticians participating in a 1984 Lipid Research Clinics Conference workshop, including Michael Oliver and Richard Krommel, were highly critical of the manner in which the LRC results had been tabulated and manipulated. The conference, in fact, went very badly for the NHLBI, with critics of the lipid hypothesis almost outnumbering supporters. One participant, Dr. Beverly Teter of the University of Maryland's lipid group, was delighted with the state of affairs. "It's wonderful'" she remarked to Basil Rifkind, study coordinator, "to finally hear both sides of the debate. We need more meetings like this" His reply was terse and sour: "No we don't."

National Cholesterol Consensus Conference

Dissenters were again invited to speak briefly at the NHLBI-sponsored National Cholesterol Consensus Conference held later that year, but their views were not included in the panel's report, for the simple reason that the report was generated by NHLBI staff before the conference convened. Dr. Teter discovered this when she picked up some papers by mistake just before the conference began, and found they contained the consensus report, already written, with just a few numbers left blank. Kritchevsky represented the lipid hypothesis camp with a humorous five-minute presentation, full of ditties. Edward Ahrens, a respected researcher, raised strenuous objections about the "consensus," only to be told that he had misinterpreted his own data, and that if he wanted a conference to come up with different conclusions, he should pay for it himself.
The 1984 Cholesterol Consensus Conference final report was a whitewash, containing no mention of the large body of evidence that conflicted with the lipid hypothesis. One of the blanks was filled with the number 200. The document defined all those with cholesterol levels above 200 mg/dL as "at risk" and called for mass cholesterol screening, even though the most ardent supporters of the lipid hypothesis had surmised in print that 240 should be the magic cutoff point. Such screening would, in fact, need to be carried out on a massive scale as the federal medical bureaucracy, by picking the number 200, had defined the vast majority of the American adult population as "at risk." The report resurrected the ghost of Norman Jolliffe and his Prudent Diet by suggesting the avoidance of saturated fat and cholesterol for all Americans now defined as "at risk," and specifically advised the replacement of butter with margarine.
The Consensus Conference also provided a launching pad for the nationwide National Cholesterol Education Program, which had the stated goal of "changing physicians' attitudes." NHLBI-funded studies had determined that while the general population had bought into the lipid hypotheses, and was dutifully using margarine and buying low-cholesterol foods, the medical profession remained skeptical. A large "Physicians Kit" was sent to all doctors in America, compiled in part by the American Pharmaceutical Association, whose representatives served on the NCEP coordinating committee. Doctors were taught the importance of cholesterol screening, the advantages of cholesterol-lowering drugs and the unique benefits of the Prudent Diet. NCEP materials told every doctor in America to recommend the use of margarine rather than butter.

Cholesterol screening for everyone

In November of 1986, the Journal of the American Medical Association published a series on the Lipid Research Clinics trials, including "Cholesterol and Coronary Heart Disease: A New Era" by longtime American Heart Association member Scott Grundy, MD, PhD. The article is a disturbing combination of euphoria and agony—euphoria at the forward movement of the lipid hypothesis juggernaut, and agony over the elusive nature of real proof. "The recent consensus conference on cholesterol... implied that levels between 200 and 240. . carry at least a mild increase in risk, which they obviously do..." said Grundy, directly contradicting an earlier statement that "Evidence relating plasma cholesterol levels to atherosclerosis and CHD has become so strong as to leave little doubt of the etiologic connection." Grundy called for "... the simple step of measuring the plasma cholesterol level in all adults... those found to have elevated cholesterol levels can be designated as at high risk and thereby can enter the medical care system... an enormous number of patients will be included." Who benefits from "the simple step of measuring the plasma cholesterol level in all adults?" Why, hospitals, laboratories, pharmaceutical companies, the vegetable oil industry, margarine manufacturers, food processors and, of course, medical doctors. "Many physicians will see the advantages of using drugs for cholesterol lowering..." said Grundy, even though "a positive benefit/risk ratio for cholesterol-lowering drugs will be difficult to prove." The cost in the US of cholesterol screening and cholesterol-lowering drugs alone now stands at sixty billion dollars per year, even though a positive risk/benefit ratio for such treatment has never been established. Physicians, however, have "seen the advantages of using drugs for cholesterol lowering" as a way of creating patients out of healthy people.
Grundy was equally schizophrenic about the benefits of dietary modification. "Whether diet has a long term effect on cholesterol remains to be proved," he stated, but "Public health advocates furthermore can play an important role by urging the food industry to provide palatable choices of foods that are low in cholesterol, saturated fatty acids and total calories." Such foods, almost by definition, contain partially hydrogenated vegetable oils that imitate the advantages of animal fats. Grundy knew that the trans fats were a problem, that they raised serum cholesterol and contributed to the etiology of many diseases—he knew because a year earlier, at his request, Mary Enig had sent him a package of data detailing numerous studies that gave reason for concern, which he acknowledged in a signed letter as "an important contribution to the ongoing debate."
Other mouthpieces of the medical establishment fell in line after the Consensus Conference. In 1987 the National Academy of Science (NAS) published an overview in the form of a handout booklet containing a whitewash of the trans problem and a pejorative description of palm oil—a natural fat high in beneficial saturates and monounsaturates that, like butter, has nourished healthy population groups for thousands of years, and, also like butter, competes with hydrogenated fats because it can be used as a shortening. The following year the Surgeon General's Report on Nutrition and Health emphasized the importance of making low-fat foods more widely available. Project LEAN (Low-Fat Eating for America Now) sponsored by the J. Kaiser Family Foundation and a host of establishment groups such as the America Heart Association, the American Dietetic Association, the American Medical Association, the USDA, the National Cancer Institute, Centers for Disease Control and the National Heart, Lung and Blood Institute announced a publicity campaign to "aggressively promote foods low in saturated fat and cholesterol in order to reduce the risk of heart disease and cancer."

National Food Processors Association Conference

The following year, Enig joined Frank McLaughlin, Director of the Center for Business and Public Policy at the University of Maryland, in testimony before the National Food Processors Association. It was a closed conference, for NFPA members only. Enig and McLaughlin had been invited to give "a view from academia." Enig presented a number of slides and warned against singling out classes of fats and oils for special pejorative labeling. A representative from Frito-Lay took umbrage at Enig's slides, which listed amounts of trans fats in Frito-Lay products. Enig offered to redo the analyses if Frito-Lay would to fund the research. "If you'd talk different, you'd get money," he said.
Enig urged the association to endorse accurate labeling of trans fats in all food items but conference participants—including representatives from most of the major food processing giants—preferred a policy of "voluntary labeling" that did not unnecessarily alert the public to the presence of trans fats in their foods. To date they have prevailed in preventing the inclusion of trans fats on nutrition labels.
Enig's cat and mouse game with Hunter and Applewhite of the Institute of Shortening and Edible Oils continued throughout the later years of the 1980's. Their modus operandi was to pepper the literature with articles that downplayed the dangers of trans fats, to use their influence to prevent opposing points of view from appearing in print and to follow-up the few alarmist articles that did squeak through with "definitive rebuttals." In 1987 Enig submitted a paper on trans fatty acids in the US diet to the American Journal of Clinical Nutrition, as a reply to the erroneous 1985 FASEB report as well as to Hunter and Applewhite's influential 1986 article, which by even the most conservative analysis underestimated the average American consumption of partially hydrogenated fats. Editor-in-chief Albert Mendeloff, MD rejected Enig's rebuttal as "inappropriate for the journal's readership." His rejection letter invited her to resubmit her paper if she could come up with "new evidence." In 1991, the article finally came out in a less prestigious publication, the Journal of the American College of Nutrition, although Applewhite did his best to coerce editor Mildred Seelig into removing it at the last minute. Hunter and Applewhite submitted letters and then an article of rebuttal to the American Journal of Clinical Nutrition, which were published shortly thereafter. In the article, entitled "Reassessment of trans fatty acid availability in the US diet," Hunter and Applewhite argued that the amount of trans in the American diet had actually declined since 1984, due to the introduction of soft margarines and tub spreads. The media fell in line with their pronouncements, with numerous articles by food writers recommending low-trans tub spreads, made from polyunsaturated vegetable oils, as the sensible alternative to saturated fat from animal sources—not surprising as most newspapers rely on the International Food Information Council, an arm of the food processing industry, for their nutrition information.

Other research on trans fats

Enig and the University of Maryland group were not alone in their efforts to bring their concerns about the effect of partially hydrogenated fats before the public. Fred Kummerow at the University of Illinois, blessed with independent funding and an abundance of patience, carried out a number of studies that indicated that the trans fats increased risk factors associated with heart disease, and that vegetable-oil-based fabricated foods such as Egg Beaters cannot support life. George Mann, formerly with the Framingham project, possessed neither funding nor patience—he was, in fact, very angry with what he called the Diet/Heart scam. His independent studies of the Masai in Africa, whose diet is extremely rich in cholesterol and saturated fat, and who are virtually free of heart disease, had convinced him that the lipid hypothesis was "the public health diversion of this century... the greatest scam in the history of medicine." He resolved to bring the issue before the public by organizing a conference in Washington DC in November of 1991.
"Hundreds of millions of tax dollars are wasted by the bureaucracy and the self-interested Heart Association," he wrote in his invitation to participants. "Segments of the food industry play the game for profits. Research on the true causes and prevention is stifled by denying funding to the ‘unbelievers.' This meeting will review the data and expose the rascals."
The rascals did their best to prevent the meeting from taking place. Funding promised by the Greenwall Foundation of New York City was later withdrawn, so Mann paid most of the bills. A press release sent as a dirty trick to speakers and participants wrongly announced that the conference had been cancelled. Several speakers did in fact renege at the last minute on their commitment to attend, including the prestigious Dr. Roslyn Alfin-Slater and Dr. Peter Nixon of London. Dr. Eliot Corday of Los Angeles cancelled after being told that his attendance would jeopardize future funding.
The final pared-down roster included Dr. George Mann, Dr. Mary Enig, Dr. Victor Herbert, Dr. Petr Skrabenek, William B. Parsons, Jr., Dr. James McCormick, a physician from Dublin, Dr. William Stehbens from New Zealand, who described the normal protective process of arterial thickening at points of greatest stress and pressure, and Dr. Meyer Texon an expert in the dynamics of blood flow. Mann, in his presentation, blasted the system that had foisted the lipid hypothesis on a gullible public. "You will see," he said, "that many of our contributors are senior scientists. They are so for a reason that has become painfully conspicuous as we organized this meeting. Scientists who must go before review panels for their research funding know well that to speak out, to disagree with this false dogma of Diet/Heart, is a fatal error. They must comply or go unfunded. I could show a list of scientists who said to me, in effect, when I invited them to participate: ‘I believe you are right, that the Diet/Heart hypothesis is wrong, but I cannot join you because that would jeopardize my perks and funding.' For me, that kind of hypocritical response separates the scientists from the operators—the men from the boys."

90s see the nation well oiled

By the nineties the operators had succeeded, by slick manipulation of the press and of scientific research, in transforming America into a nation that was well and truly oiled. Consumption of butter had bottomed out at about 5 grams per person per day, down from almost 18 at the turn of the century. Use of lard and tallow had been reduced by two-thirds. Margarine consumption had jumped from less than 2 grams per person per day in 1909 to about 11 in 1960. Since then consumption figures had changed little, remaining at about 11 grams per person per day—perhaps because knowledge of margarine's dangers had been slowly seeping out to the public. However, most of the trans fats in the current American diet come not from margarine but from shortening used in fried and fabricated foods. American shortening consumption of 10 grams per person per day held steady until the 1960's, although the content of that shortening had changed from mostly lard, tallow and coconut oil—all natural fats—to partially hydrogenated soybean oil. Then shortening consumption shot up and by 1993 had tripled to over 30 grams per person per day.
But the most dramatic overall change in the American diet was the huge increase in the consumption of liquid vegetable oils, from slightly less than 2 grams per person per day in 1909 to over 30 in 1993—a fifteen fold increase.

Dangers of polyunsaturates

The irony is that these trends have persisted concurrently with revelations about the dangers of polyunsaturates. Because polyunsaturates are highly subject to rancidity, they increase the body's need for vitamin E and other antioxidants. Excess consumption of vegetable oils is especially damaging to the reproductive organs and the lungs—both of which are sites for huge increases in cancer in the US. In test animals, diets high in polyunsaturates from vegetable oils inhibit the ability to learn, especially under conditions of stress; they are toxic to the liver; they compromise the integrity of the immune system; they depress the mental and physical growth of infants; they increase levels of uric acid in the blood; they cause abnormal fatty acid profiles in the adipose tissues; they have been linked to mental decline and chromosomal damage; they accelerate aging. Excess consumption of polyunsaturates is associated with increasing rates of cancer, heart disease and weight gain; excess use of commercial vegetable oils interferes with the production of prostaglandins leading to an array of complaints ranging from autoimmune disease to PMS. Disruption of prostaglandin production leads to an increased tendency to form blood clots, and hence myocardial infarction, which has reached epidemic levels in America.
Vegetable oils are more toxic when heated. One study reported that polyunsaturates turn to varnish in the intestines. A study by a plastic surgeon found that women who consumed mostly vegetable oils had far more wrinkles than those who used traditional animal fats. A 1994 study appearing in the Lancet showed that almost three quarters of the fat in artery clogs is unsaturated. The "artery clogging" fats are not animal fats but vegetable oils.
Those who have most actively promoted the use of polyunsaturated vegetable oils as part of a Prudent Diet are well aware of their dangers. In 1971, William B. Kannel, former director of the Framingham study, warned against including too many polyunsaturates in the diet. A year earlier, Dr. William Connor of the American Heart Association issued a similar warning, and Frederick Stare reviewed an article which reported that the use of polyunsaturated oils caused an increase in breast tumors. And Kritchevsky, way back in 1969, discovered that the use of corn oil caused an increase in atherosclerosis.
As for the trans fats, produced in vegetable oils when they are partially hydrogenated, the results that are now in the literature more than justify concerns of early investigators about the relation between trans fats and both heart disease and cancer. The research group at the University of Maryland found that trans fatty acids not only alter enzymes that neutralize carcinogens, and increase enzymes that potentiate carcinogens, but also depress milk fat production in nursing mothers and decrease insulin binding. In other words, trans fatty acids in the diet interfere with the ability of new mothers to nurse successfully and increase the likelihood of developing diabetes. Unpublished work indicates that trans fats contribute to osteoporosis. Hanis, a Czechoslovakian researcher, found that trans consumption decreased testosterone, caused the production of abnormal sperm and altered gestation. Koletzko, a German pediatric researcher found that excess trans consumption in pregnant mothers predisposed them to low birth weight babies. Trans consumption interferes with the body's use of omega-3 fatty acids found in fish oils, grains and green vegetables, leading to impaired prostaglandin production. George Mann confirmed that trans consumption increases the incidence of heart disease. In 1995, European researchers found a positive correlation between breast cancer rates and trans consumption.
Until the 1995 study, only the disturbing revelations of Dutch researchers Mensink and Katan, in 1990, received front page coverage. Mensink and Katan found that margarine consumption increased coronary heart disease risk factors. The industry—and the press—responded by promoting tub spreads, which contain reduced amounts of trans compared to stick margarine. For the general population, these trans reductions have been more than offset by changes in the types of fat used by the fast food industry. In the early 1980's, Center for Science in the Public Interest campaigned against the use of beef tallow for frying potatoes. Before that they campaigned against the use of tallow for frying chicken and fish. Most fast food concerns switched to partially hydrogenated soybean oil for all fried foods. Some deep fried foods have been tested at almost 50% trans.
Epidemiologist Walter Willett at Harvard worked for many years with flawed data bases which did not identify trans fats as a dietary component. He found a correlation with dietary fat consumption and both heart disease and cancer. After his researchers contacted Enig about the trans data, they developed a more valid data base that was used in the analysis of the massive Nurses Study. When Willett's group separated out the trans component in their analyses, they were able to confirm greater rates of cancer in those consuming margarine and vegetable shortenings—not butter, eggs, cheese and meat. The correlation of trans fat consumption and cancer was never published, but was reported at the Baltimore Data Bank Conference in 1992.
In 1993 Willett's research group at Harvard found that trans contributed to heart disease, and this study was not ignored, but received much fanfare in the press. Willett's first reference in his report was Enig's work on the trans content of common foods.
The industry continues to argue that American trans consumption is a low six to eight grams per person per day, not enough to contribute to today's epidemic of chronic disease. Total per capita consumption of margarine and shortening hovers around 40 grams per person per day. If these products contain 30% trans (many shortenings contain more) then average consumption is about 12 grams per person per day. In reality, consumption figures can be dramatically higher for some individuals. A 1989 Washington Post article documented the diet of a teenage girl who ate 12 donuts and 24 cookies over a three day period. Total trans worked out to at least 30 grams per day, and possibly much more. The fat in the chips that teenagers consume in abundance may contain up to 48% trans which translates into 45.6 grams of trans fat in a small ten-ounce bag of snack chips—which a hungry teenager can gobble up in a few minutes. High school sex education classes do not teach American teenagers that the altered fats in their snack foods may severely compromise their ability to have normal sex, conceive, give birth to healthy babies and successfully nurse their infants.

Benefits of animal fats

Foods containing trans fat sell because the American public is afraid of the alternative—saturated fats found in tallow, lard, butter, palm and coconut oil, fats traditionally used for frying and baking. Yet the scientific literature delineates a number of vital roles for dietary saturated fats—they enhance the immune system, are necessary for healthy bones, provide energy and structural integrity to the cells, protect the liver and enhance the body's use of essential fatty acids. Stearic acid, found in beef tallow and butter, has cholesterol lowering properties and is a preferred food for the heart. As saturated fats are stable, they do not become rancid easily, do not call upon the body's reserves of antioxidants, do not initiate cancer, do not irritate the artery walls.
Your body makes saturated fats, and your body makes cholesterol—about 2000 mg per day. In general, cholesterol that the average American absorbs from food amounts to about 100 mg per day. So, in theory, even reducing animal foods to zero will result in a mere 5% decrease in the total amount of cholesterol available to the blood and tissues. In practice, such a diet is likely to deprive the body of the substrates it needs to manufacture enough of this vital substance; for cholesterol, like saturated fats, stands unfairly accused. It acts as a precursor to vital corticosteroids, hormones that help us deal with stress and protect the body against heart disease and cancer; and to the sex hormones like androgen, testosterone, estrogen and progesterone; it is a precursor to vitamin D, a vital fat-soluble vitamin needed for healthy bones and nervous system, proper growth, mineral metabolism, muscle tone, insulin production, reproduction and immune system function; it is the precursor to bile salts, which are vital for digestion and assimilation of fats in the diet. Recent research shows that cholesterol acts as an antioxidant. This is the likely explanation for the fact that cholesterol levels go up with age. As an antioxidant, cholesterol protects us against free radical damage that leads to heart disease and cancer. Cholesterol is the body's repair substance, manufactured in large amounts when the arteries are irritated or weak. Blaming heart disease on high serum cholesterol levels is like blaming firemen who have come to put out a fire for starting the blaze.
Cholesterol is needed for proper function of serotonin receptors in the brain. Serotonin is the body's natural "feel-good" chemical. This explains why low cholesterol levels have been linked to aggressive and violent behavior, depression and suicidal tendencies.
Mother's milk is especially rich in cholesterol and contains a special enzyme that helps the baby utilize this nutrient. Babies and children need cholesterol-rich foods throughout their growing years to ensure proper development of the brain and nervous system. Dietary cholesterol plays an important role in maintaining the health of the intestinal wall, which is why low-cholesterol vegetarian diets can lead to leaky gut syndrome and other intestinal disorders.
Animal foods containing saturated fat and cholesterol provide vital nutrients necessary for growth, energy and protection from degenerative disease. Like sex, animal fats are necessary for reproduction. Humans are drawn to both by powerful instincts. Suppression of natural appetites leads to weird nocturnal habits, fantasies, fetishes, bingeing and splurging.
Animal fats are nutritious, satisfying and they taste good. "Whatever is the cause of heart disease," said the eminent biochemist Michael Gurr in a recent article, "it is not primarily the consumption of saturated fats." And yet the high priests of the lipid hypothesis continue to lay their curse on the fairest of culinary pleasures—butter and Bernaise, whipped cream, souffles and omelets, full-bodied cheeses, juicy steaks and pork sausage.

Coming full circle—And yet, learning nothing

On April 30, 1996 a senior researcher named David Kritchevsky received the American Oil Chemists' Society's Research Award in recognition of his accomplishments as a "researcher on cancer and atherosclerosis as well as cholesterol metabolism." His accomplishments include co-authorship of more than 370 research papers, one of which appeared a month later in the American Journal of Clinical Nutrition. "Position paper on trans fatty acids" continued the debate on trans fats that began in the same journal with Hunter and Applewhite's 1986 attack on Enig's research. "A controversy has arisen about the potential health hazards of trans unsaturated fatty acids in the American diet," wrote Kritchevsky and his coauthors.
Actually the controversy dates back to 1954. In the rabbit studies that launched Kritchevsky on his career, the researcher actually found that cholesterol fed with Wesson oil "markedly accelerated" the development of cholesterol-containing low-density lipoproteins; and cholesterol fed with shortening gave cholesterol levels twice as high as cholesterol fed alone. Enig's work—and that of Kummerow and Mann and several others—merely confirmed what Kritchevsky ascertained decades ago but declined to publicize, that vegetable oils, and particularly partially hydrogenated vegetable oils, are bad news.
But the "Position paper on trans fatty acids" took no position at all. Studies have given contradictory results, said the authors, and the amount of trans in the average American diet is very difficult to determine. As for labeling, "There is no clear choice of how to include trans fatty acids on the nutrition label. The database is insufficient to establish a classification scheme for these fats." There may be problems with trans, says the senior researcher, but their use "helps to reduce the intake of dietary fats higher in saturated fatty acids. Also, vegetable fats are not a source of dietary cholesterol, unlike saturated animal fats." Kritchevsky and his coauthors conclude that physicians and nutritionists should "focus on a further decrease in total fat intake and especially the intake of saturated fat... A reduction in total fat intake simplifies the problem, because all fats in the diet decrease and choices are unnecessary." However, even senior scientists find that fence straddling is necessary. "We may conclude," wrote Kritchevsky and his colleagues, "that consumption of liquid vegetable oils is preferable to solid fats."

Footnote:

Early this year, 1998, a symposium entitled "Evolution of Ideas about the Nutritional Value of Dietary Fat" reviewed the many flaws in the lipid hypothesis and highlighted a study in which mice fed purified diets died within 20 days but whole milk kept the mice alive for several months. One of the participants was David Kritchevsky who noted that the use of low-fat diets and drugs in intervention trials, "did not affect overall CHD mortality." Ever with a finger in the wind, this influential Founding Father of the lipid hypothesis concluded thus: "Research continues apace and, as new findings appear, it may be necessary to reevaluate our conclusions and preventive medicine policies."

© 1999 Mary G. Enig, PhD and Sally Fallon.
First published in Nexus Magazine, Dec '98-Jan '99 and Feb '99-Mar '99.
Mary G. Enig, Ph.D. 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 the mother of three healthy children brought up on whole foods including butter, cream, eggs and meat.
Sally Fallon is the author of Nourishing Traditions: The Cookbook that Challenges Politically Correct Nutrition and the Diet Dictocrats (with Mary G. Enig, PhD), as well as of numerous articles on the subject of diet and health. She is President of the Weston A Price Foundation and founder of A Campaign for Real Milk. She is the mother of four healthy children raised on whole foods including butter, cream, eggs and meat.

References:

  1. D Kritchevsky, et al, "Effect of Cholesterol Vehicle in Experimental Atherosclerosis, Am J Physiol , July-September 1954, 178:30-32
     
  2. "Notice of Supelco-AOC Award to Kritchevsky," Inform, 1996, 7:315
     
  3. M Enig, Trans Fatty Acids in the Food Supply: A Comprehensive Report Covering 60 Years of Research , 2nd Edition, 1995, Enig Associates, Inc., Silver Spring, MD, pp 4-8
     
  4. D Groom, "Population Studies of Atherosclerosis," Annals of Int Med , July 1961, 55:1:51-62; W F Enos, et al, "Pathogenesis of Coronary Disease in American Soldiers Killed in Korea," JAMA , 1955, 158:912
     
  5. W Laurie, et al, "Atherosclerosis and its Cerebral Complications in the South African Bantu," Lancet , Feb 1958, pp 231-232
     
  6. W B Robertson, "Atherosclerosis and Ischaemic Heart Disease," Lancet, 1959, 1:444
     
  7. T Gordon, "Mortality Experience Among Japanese in the US, Hawaii and Japan," Pul Health Rep, 1957, 51:270; O J Pollak, "Diet and Atherosclerosis," Lancet, 1959, 1:444
     
  8. H C McGill, et al, "General Findings of the International Atherosclerosis Project," Laboratory Investigations, 1968, 18:(5):498
     
  9. R L Smith and E R Pinckney, The Cholesterol Conspiracy, 1991, Warren H Green, Inc. St. Louis, MO. p 125
     
  10. M De Bakey, et al, "Serum Cholesterol Values in Patients Treated Surgically for Atherosclerosis," JAMA, 1964, 189:9:655-59
     
  11. A Keys, "Diet and Development of Coronary Heart Disease," J Chron Dis, Oct 1956, 4(4):364-380
     
  12. G Cristakis, "Effect of the Anti-Coronary Club Program on Coronary Heart Disease Risk-Factor Status,"JAMA, Nov 7, 1966, 198:(6):129-35

    12a. Researchers at the University of Florida at Gainsborough found trans levels as high as 4.6% in processed canola oil. (S. O'Keefe and others. Journal of Food Lipids1994;1:165-176.) The conversion of omega-3 fatty acids to trans fats can be prevented by certain careful processing methods. (JL Sebedio and others. European Journal of Clinical Nutrition 2000 Feb;54(2):104-13.
     
  13. "Dietary Goals for the United States—Supplemental Views," prepared by the Staff of the Select Committee on Nutrition and Human Needs, United States Senate, November 1977, Government Printing Office, Washington, DC, pp 139-140
     
  14. R L Rizek, et al, "Fat in Today's Food Supply—Level of Use and Sources," J Am Oil Chem Soc, 1974, 51:244
     
  15. M G Enig, et al, "Dietary Fat and Cancer Trends—A Critique," Federation Proceedings, July 1978, 37:(9):2215-2220
     
  16. T H Applewhite, "Statistical ‘Correlations' Relating Trans-Fats to Cancer: A Commentary," Federation Proceedings, Oct 1979, 38:(11):2435-2439
     
  17. F A Kummerow, "Effects of Isomeric Fats on Animal Tissue, Lipid Classes and Atherosclerosis," Geometrical and Positional Fatty Acid Isomers, E. A. Emken and H. J. Dutton, eds, American Oil Chemists' Society, Champaign, IL, 1979, pp151-180; D Kritchevsky, "Trans Fatty Acid Effects in Experimental Atherosclerosis," Federation Proceedings, 1982, 41:2813
     
  18. M G Enig, Modification of Membrane Lipid Composition and Mixed-Function Oxidases in Mouse Liver Microsomes by Dietary Trans Fatty Acids, Doctoral Dissertation for the University of Maryland, 1984
     
  19. "New Focus on Trans Fatty Acids," Food Processing, December 1982, pp 64-66
     
  20. E J Hunter, "More on Those Trans Fatty Acids," Food Processing, May 1983, pp 35-36
     
  21. W M N Ratnayake, et al, "Fatty Acids in Some Common Food Items in Canada," J Am Coll Nutr, 1993, 12:(6):651-660
     
  22. M G Enig, et al, "Fatty Acid Composition of the Fat in Selected Food Items with Emphasis on Trans Components," J Am Oil Chem Soc, 1983, 60:(10):1788-1795
     
  23. J E Hunter, "Letter to the Editor," Science, 1984, 224:659
     
  24. C E Elson, et al, "The Influence of Dietary Unsaturated Cis and Trans and Saturated Fatty Acids on Tissue Lipids of Swine," Atherosclerosis, 1981, 40:115-137
     
  25. F R Senti, ed, Health Aspects of Dietary Trans Fatty Acids, Bethesda, MD, Life Sciences Research Office-Fed Am Soc Exp Biol, 1985
     
  26. J E Hunter and T Applewhite, "Isomeric Fatty Acids in the US Diet: Levels and Health Perspectives," Am J Clin Nutr, 1986, 44:707-717
     
  27. Ace Federal Reporter, Inc., Stenotype Reporters, 444 North Capitol Street, Suite 402, Washington, DC 20001 (202) 347-3700
     
  28. Food Chemical News, January 25, 1988, 29:(47):52; Nutrition Week, Community Nutrition Institute (CNI), June 16, 1988, p 6
     
  29. Smith, R and E R Pinckney, Diet, Blood Cholesterol and Coronary Heart Disease: A Critical Review of the Literature, Vol 2, 1991, Vector Enterprises, Sherman Oaks, CA
     
  30. Castelli, William, "Concerning the Possibility of a Nut..." Archives of Internal Medicine, Jul 1992, 152:(7):1371-1372
     
  31. "Multiple Risk Factor Intervention Trial; Risk Factor Changes and Mortality Results," JAMA, September 24, 1982, 248:(12):1465
     
  32. F H Mattson, et al, "Effect of Dietary Cholesterol on Serum Cholesterol in Men," Am J Clin Nutr, 1972, 25:589
     
  33. P Addis, Food and Nutrition News, March/April 1990, 62:(2):7-10
     
  34. "The Lipid Research Clinics Coronary Primary Prevention Trial Results. I. Reduction in Incidence of Coronary Heart Disease," JAMA, 1984, 251:359
     
  35. S M Grundy, "Cholesterol and Coronary Heart Disease: A New Era," JAMA, Nov 28, 1986, 256:(20):2849-2858
     
  36. "Letters to the Editor and Authors' Responses," J Am Coll Nutr, 1991, 10:5:510-521
     
  37. E J Hunter and T H Applewhite, "Reassessment of Trans Fatty Acid Availability in the US Diet," Am J Clin Nutr, 1991, 54:363-369
     
  38. F. A. Kummerow, "Nutritional Effects of Isomeric Fats: Their Possible Influence on Cell Metabolism or Cell Structure," Dietary Fats and Health, (E. G. Perkins and W. J. Visek, eds), Americna Oil Chemists' Society, Champaign, IL, 1983, pp 391-402; F. A. Kummerow, "Nutritional Aspects of Isomeric Fats," Lipids in Modern Nutrition, M Horisberger and U Bracco, eds, 1987, Nestle Nutrition, Vevey/Raven Press, New York
     
  39. Mann, G V, et al, "Atherosclerosis in the Maasai," Am J Epidemiol, 1972, 95:26-37
     
  40. Coronary Heart Disease, The Dietary Sense and Nonsense, George V Mann, ed, 1993, Veritas Society, London, p 1
     
  41. A general review of citations for problems with polyunsaturate consumption is found in E R Pinckney, and C Pinckney, The Cholesterol Controversy, 1973, Sherbourne Press, Los Angeles, pp127-131
     
  42. C V Felton, et al, "Dietary Polyunsaturated Fatty Acids and Composition of Human Aortic Plaques," Lancet, 1994, 344:1195
     
  43. D Kritchevsky, Medical Counterpoint, March 1969
     
  44. B B Teter, et al, "Milk Fat Depression in C57B1/6J Mice Consuming Partially Hydrogenated Fat," Journal of Nutrition, 1990, 120:818-824; Barnard, et al, "Dietary Trans Fatty Acids Modulate Erythrocyte Membrane Fatty Acid Composition and Insulin Binding in Monkeys," Journal of Nutritional Biochemistry, 1990, 1:190-195
     
  45. T Hanis, et al, "Effects of Dietary Trans Fatty Acids on Reproductive Perforamnce of Wistar Rats," British Journal of Nutrition, 1989, 61:519-529
     
  46. B Koletzko and J Muller, "Cis- and Trans-Isomeric Fatty Acids in Polasma Lipids of Newborn Infants and Their Mothers," Biology of the Neonate, 1990, 57:172-178
     
  47. D Horrobin, "The Regulation of Prostaglandin Biosynthesis by Manipultion of Essential Fatty Acid Metabolism," Reviews in Pure and Applied Pharmacological Sciences, 1983, 4:339-383
     
  48. G V Mann, "Metabolic Consequences of Dietary Trans Fatty Acids," The Lancet, 1994, 343:1268-1271
     
  49. L Kohlmeier, et al, "Stores of Trans Fatty Acids and Breast Cancer Risk, "Am J Clin Nutr, 1995, 61:896;A25

     
  50. R P Mensink and M Katan, "Effect of Dietary Trans Fatty Acids on High-Density and Low-Density Lipoprotein Cholesterol Levels in Healthy Subjects," N Eng J Med, 1990, 323:439-445
     
  51. M G Enig, et al, "Isomeric Trans Fatty Acids in the U.S. Diet," J Am Coll Nutr, 1990, 9:471-486
     
  52. W C Willett, et al, "Consumption of Trans-Fatty Acids in Relation to Risk of Coronary Heart Disease Among Women," Society for Epidemiology Research, June 1992, Annual Meeting, Abstract 249
     
  53. W C Willett, et al, "Intake of Trans Fatty Acids and Risk of Coronary Heart Disease Among Women," Lancet, 1993, 341:581-585
     
  54. J J Kabara, The Pharmacological Effects of Lipids, J J Kabara, ed, The American Oil Chemists' Society, Champaign, IL, 1978, 1-14; L A Cohen, et al, J Natl Cancer Inst, 1986, 77:43
     
  55. B A Watkins, et al, "Importance of Vitamin E in Bone Formation and in Chrondrocyte Function" Purdue University, Lafayette, IN, AOCS Proceedings, 1996; B A Watkins, and M F Seifert, "Food Lipids and Bone Health," Food Lipids and Health, R E McDonald and D B Min, eds, Marcel Dekker, Inc. New York, NY, p 101
     
  56. J F Mead, et al, Lipids: Chemistry, Biochemistry and Nutrition, Plenum Press, 1986, New York
     
  57. A A Nanji, et al, Gastroenterology, Aug 1995, 109(2):547-54; Y S Cha, and D S Sachan, J Am Coll Nutr, Aug 1994, 13(4):338-43
     
  58. M L Garg, et al, The FASEB Journal, 1988, 2:(4):A852; R M Oliart Ros, et al, Meeting Abstracts, AOCS Proceedings, May 1998, p 7, Chicago, IL
     
  59. L D Lawson and F Kummerow, "B-Oxidation of the Coenzyme A Esters of Vaccenic, Elaidic and Petroselaidic Acids by Rat Heart Mitochondria," Lipids, 1979, 14:501-503
     
  60. E M Cranton and J P Frackelton, "Free Radical Pathology in Age-Associated Diseases: Treatment with EDTA Chelation, Nutrition and Antioxidants," Journal of Holistic Medicine, Spring/Summer 1984, pp 6-37
     
  61. H Engelberg, "Low Serum Cholesterol and Suicide," Lancet, March 21, 1992, 339:727-728
     
  62. R B Alfin-Slater, and L Aftergood, "Lipids," Modern Nutrition in Health and Disease, 6th ed, 1980, R S Goodhart and M E Shils, eds, Lea and Febiger, Philadelphia, p 134
     
  63. M Gurr, "A Fresh Look at Dietary Recommendations," Inform, April 1996, 7:4:432-435
     
  64. AIN/ASCN Task Force on Trans Fatty Acids, "Position Paper on Trans Fatty Acids," Am J Clin Nutr, 1996, 63:663-670
     
  65. R M Lemmon, D Kritchevsky, et al, "The Effect of Delta-7-Cholestenol Feeding on the Cholesterol and Lipoproteins of Rabbit Serum," Archives of Biochemistry & Biophysics (NY), July 1954, 51:(1):1161-9; D Kritchevsky, et al, "Effect of Cholesterol Vehicle in Experimental Atherosclerosis, Am J Physiol, July-September 1954 178:30-32
     
  66. R E Olson, "Evolution of Ideas about the Nutritional Value of Dietary Fat: Introduction," J Nutr, 1998 128:421S-425S
  http://life-enthusiast.com/index/Articles/Enig/The_Oiling_of_America
 
An Interview With Dr. Raymond Peat
A Renowned Nutritional Counselor Offers His Thoughts About Thyroid
Disease  by Mary Shomon


http://thyroid.about.com/gi/dynamic/offsite.htm?
site=http://www.thyroid-info.com/articles/ray-peat.htm

http://thyroid.about.com/gi/dynamic/offsite.htm?
site=http://www.thyroid-info.com/articles/ray-peat.htm


Raymond Peat, Ph.D. is editor and researcher of a popular and well-
known monthly newsletter on nutritiona and health, as well as author
of a number of cutting-edge publications that look at aging,
nutrition, and hormones from a biochemical perspective. Dr. Peat has
a Ph.D. in Biology from the University of Oregon, with
specialization in physiology. He has taught at the University of
Oregon, Urbana College, Montana State University, National College
of Naturopathic Medicine, Universidad Veracruzana, the Universidad
Autonoma del Estado de Mexico, and Blake College. He also conducts
private nutritional counseling.

I had the privilege to conduct an interview with Ray Peat in
November of 2000, touching upon a few of the many interesting points
he raises in his various publications.


Mary Shomon: Why do women with treated hypothyroidism frequently
still have inappropriately high levels of cholesterol and high
triglycerides, and what can they do to help lower these levels?

Dr. Ray Peat: Often it's because they were given thyroxine, instead
of the active thyroid hormone, but hypertriglyceridemia can be
caused by a variety of things that interact with hypothyroidism.
Estrogen treatment is a common cause of high triglycerides, and
deficiencies of magnesium, copper, and protein can contribute to
that abnormality. Toxins, including some drugs and herbs, can
irritate or stimulate the liver to produce too much triglyceride.
T3, triiodothyronine, is the active thyroid hormone, and it is
produced (mainly in the liver) from thyroxine, and the female liver
is less efficient than the male liver in producing it, as is the
female thyroid gland. The thyroid gland, which normally produces
some T3, will decrease its production in the presence of increased
thyroxine. Therefore, thyroxine often acts as a "thyroid anti-
hormone," especially in women. When thyroxine was tested in healthy
young male medical students, it seemed to function "just like the
thyroid hormone," but in people who are seriously hypothyroid, it
can suppress their oxidative metabolism even more. It's a very
common, but very serious, mistake to call thyroxine "the thyroid
hormone."

High cholesterol is more closely connected to hypothyroidism than
hypertriglyceridemia is. Increased T3 will immediately increase the
conversion of cholesterol to progesterone and bile acids. When
people have abnormally low cholesterol, I think it's important to
increase their cholesterol before taking thyroid, since their
steroid-forming tissues won't be able to respond properly to thyroid
without adequate cholesterol.

Mary Shomon: You feel that progesterone can have anti-stress
effects, without harming the adrenal glands. Is progesterone therapy
something you feel is useful to many or most hypothyroid patients?
How can a patient know if she needs progesterone? Do you recommend
blood tests? And if so, at what point in a woman's cycle?

Dr. Ray Peat: Estrogen blocks the release of hormone from the
thyroid gland, and progesterone facilitates the release. Estrogen
excess or progesterone deficiency tends to cause enlargement of the
thyroid gland, in association with a hypothyroid state. Estrogen can
activate the adrenals to produce cortisol, leading to various
harmful effects, including brain aging and bone loss. Progesterone
stimulates the adrenals and the ovaries to produce more
progesterone, but since progesterone protects against the catabolic
effects of cortisol, its effects are the opposite of estrogen's.
Progesterone has antiinflammatory and protective effects, similar to
cortisol, but it doesn't have the harmful effects. In
hypothyroidism, there is a tendency to have too much estrogen and
cortisol, and too little progesterone.

The blood tests can be useful to demonstrate to physicians what the
problem is, but I don't think they are necessary. There is evidence
that having 50 or 100 times as much progesterone as estrogen is
desirable, but I don't advocate "progesterone replacement therapy"
in the way it's often understood. Progesterone can instantly
activate the thyroid and the ovaries, so it shouldn't be necessary
to keep using it month after month. If progesterone is used
consistently, it can postpone menopause for many years.

Cholesterol is converted to pregnenolone and progesterone by the
ovaries, the adrenals, and the brain, if there is enough thyroid
hormone and vitamin A, and if there are no interfering factors, such
as too much carotene or unsaturated fatty acids. Progesterone
deficiency is an indicator that something is wrong, and using a
supplement of progesterone without investigating the nature of the
problem isn't a good approach. The normal time to use a progesterone
supplement is during the "latter half" of the cycle, the two weeks
from ovulation until menstruation. If it is being used to treat
epilepsy, cancer, emphysema, migraine or arthritis, or something
else so serious that menstrual regularity isn't a concern, then it
can be used at any time. If progesterone is used consistently, it
can postpone menopause for many years.

Mary Shomon: What supplements do you feel are essential for most
people with hypothyroidism?

Dr. Ray Peat: Because the quality of commercial nutritional
supplements is dangerously low, the only supplement I generally
advocate is vitamin E, and that should be used sparingly.
Occasionally, I will suggest limited use of other supplements, but
it is far safer in general to use real foods, and to exclude foods
which are poor in nutrients. Magnesium is typically deficient in
hypothyroidism, and the safest way to get it is by using orange
juice and meats, and by using epsom salts baths; magnesium carbonate
can be helpful, if the person doesn't experience side effects such
as headaches or hemorrhoids.

Mary Shomon: Do you feel that there are any special considerations,
issues, or treatments for men with hypothyroidism?

Dr. Ray Peat: Thyroid supplements can be useful for prostate
hypertrophy and some cases of impotence and infertility.
Occasionally, a man who can't put on a normal amount of weight finds
that a thyroid supplement allows normal weight gain. Leg cramps,
insomnia and depression are often the result of hypothyroidism.
Heart failure, gynecomastia, liver disease, baldness and dozens of
other problems can result from hypothyroidism.

Mary Shomon: Many people describe how they are clinically
hypothyroid, with elevated TSH levels, but have extremely high pulse
rates. Do you have any thoughts as to what might be going on in that
situation?

Dr. Ray Peat: In hypothyroidism, thyrotropin-release hormone (TRH)
is usually increased, increasing release of TSH. TRH itself can
cause tachycardia, "palpitations," high blood pressure, stasis of
the intestine, increase of pressure in the eye, and hyperventilation
with alkalosis. It can increase the release of norepinephrine, but
in itself it acts very much like adrenalin. TRH stimulates prolactin
release, and this can interfere with progesterone synthesis, which
in itself affects heart function.

I consider even the lowest TSH within the "normal range" to be
consistent with hypothyroidism; in good health, very little TSH is
needed. When the thyroid function is low, the body often compensates
by over-producing adrenalin. The daily production of adrenalin is
sometimes 30 or 40 times higher than normal in hypothyroidism. The
adrenalin tends to sustain blood sugar in spite of the metabolic
inefficiency of hypothyroidism, and it can help to maintain core
body temperature by causing vasoconstriction in the skin, but it
also disturbs the sleep and accelerates the heart. During the night,
cycles of rising adrenalin can cause nightmares, wakefulness, worry,
and a pounding heart. Occasionally, a person who has chronically had
a heart rate of 150 beats per minute or higher, will have a much
lower heart rate after using a thyroid supplement for a few days. If
your temperature or heart rate is lower after breakfast than before,
it's likely that they were raised as a result of the nocturnal
increase of adrenalin and cortisol caused by hypothyroidism.

Mary Shomon: You have written that for some people, there is a
problem converting T4 to T3, but that diet can help. You recommend a
piece of fruit or juice or milk between meals, plus adequate
protein, can help the liver produce the hormone. Can you explain a
bit more about this idea and how it works?

Dr. Ray Peat: The amount of glucose in liver cells regulates the
enzyme that converts T4 to T3. This means that hypoglycemia or
diabetes (in which glucose doesn't enter cells efficiently) will
cause hypothyroidism, when T4 can't be converted into T3. When a
person is fasting, at first the liver's glycogen stores will provide
glucose to maintain T3 production. When the glycogen is depleted,
the body resorts to the dissolution of tissue to provide energy. The
mobilized fatty acids interfere with the use of glucose, and certain
amino acids suppress the thyroid gland. Eating carbohydrate
(especially fruits) can allow the liver to resume its production of
T3.

Mary Shomon: You have recommended if supplemental T3 is used, a
thyroid patients "nibble on a 10-15 mg Cytomel tablet throughout the
day." Can you explain why? Would compounded time-released T3 as
available in some compounding pharmacies do the same?

Dr. Ray Peat: Most hypothyroid people can successfully use a
supplement that contains four parts of thyroxine for each part of
T3, but some people need a larger proportion of T3 for best
functioning. The body normally produces several micrograms of T3
every hour, but if a large amount of supplementary thyroid is taken
in a short time, the liver quickly inactivates some of the excess
T3. Taking a few micrograms per hour provides what the body can use,
and doesn't suppress either the liver's or the thyroid's production
of the hormone.

I have only rarely talked to anyone who had good results with the so-
called time-release T3, and I have seen analyses of some samples in
which there was little or no T3 present. It is hard to compound T3
properly, and the conditions of each person's digestive system can
determine whether the T3 is released all at once, or not at all. I
don't think there is a valid scientific basis for calling
anything "time-release T3."

I have been told that the company which now owns the Armour name and
manufactures "Armour thyroid USP" has added a polymer to the
formula, and I think this would account for the stories I have heard
about its apparent inactivity. Some people have found that the
tablets passed through their intestine undigested, so I think it's
advisable to crush or powder the tablets.

Mary Shomon: You feel that excessive aerobic exercise can be a cause
of hypothyroidism. Can you explain this further? How much is too
much?

Dr. Ray Peat: I'm not sure who introduced the term "aerobic" to
describe the state of anaerobic metabolism that develops during
stressful exercise, but it has had many harmful repercussions. In
experiments, T3 production is stopped very quickly by even "sub-
aerobic" exercise, probably becaue of the combination of a decrease
of blood glucose and an increase in free fatty acids. In a healthy
person, rest will tend to restore the normal level of T3, but there
is evidence that even very good athletes remain in a hypothyroid
state even at rest. A chronic increase of lactic acid and cortisol
indicates that something is wrong. The "slender muscles" of
endurance runners are signs of a catabolic state, that has been
demonstrated even in the heart muscle. A slow heart beat very
strongly suggests hypothyroidism. Hypothyroid people, who are likely
to produce lactic acid even at rest, are especially susceptible to
the harmful effects of "aerobic" exercise. The good effect some
people feel from exercise is probably the result of raising the body
temperature; a warm bath will do the same for people with low body
temperature.

Mary Shomon: You feel that chronic protein deficiency is a common
cause of hypothyroidism. How much protein should people get (as much
as 70-100 grams a day?) and what types of protein, in order to
prevent hypothyroidism?

Dr. Ray Peat: The World Health Organization standard was revised
upward by researchers at MIT, and recently the MIT standard has been
revised upward again by military researchers; this is described in a
publication of the National Academy of Sciences (National Academy
Press, The Role of Protein and Amino Acids in Sustaining and
Enhancing Performance, 1999). When too little protein, or the wrong
kind of protein, is eaten, there is a stress reaction, with thyroid
suppression. Many of the people who don't respond to a thyroid
supplement are simply not eating enough good protein. I have talked
to many supposedly well educated people who are getting only 15 or
20 grams of protein per day. To survive on that amount, their
metabolic rate becomes extremely low. The quality of most vegetable
protein (especially beans and nuts) is so low that it hardly
functions as protein. Muscle meats (including the muscles of poultry
and fish) contain large amounts of the amino acids that suppress the
thyroid, and shouldn't be the only source of protein. It's a good
idea to have a quart of milk (about 32 grams of protein) every day,
besides a variety of other high quality proteins, including cheeses,
eggs, shellfish, and potatoes. The protein of potatoes is extremely
high quality, and the quantity, in terms of a percentage, is similar
to that of milk.

Mary Shomon: You talk about darkness and shorter days of winter as a
stress. It's known that more thyroid hormone is needed by some
patients during colder weather. Are there other things you recommend
patients do to "winterproof" their metabolism?

Dr. Ray Peat: Very bright incandescent lights are helpful, because
light acts on, and restores, the same mitochondrial enzymes that are
governed by the thyroid hormone. In squirrels, hibernation is
brought on by the accumulation of unsaturated fats in the tissues,
suppressing respiration and stimulating increased serotonin
production. In humans, winter sickness is intensified by those same
antithyroid substances, so it's important to limit consumption of
unsaturated fats and tryptophan (which is the source of serotonin).
When a person is using a thyroid supplement, it's common to need
four times as much in December as in July.

Mary Shomon: You have reported that pregnenolone can be helpful for
Graves' patients with exophthalmus. Can you explain further?

Dr. Ray Peat: Graves' disease and exophthalmos can occur with
hypothyroidism or euthyroidism, as well as with hyperthyroidism.
Pregnenolone regulates brain chemistry in a way that prevents
excessive production of ACTH and cortisol, and it helps to stabilize
mitochondrial metabolism. It apparently acts directly on a variety
of tissues to reduce their retention of water. In the last several
years, all of the people I have seen who had been diagnosed
as "hyperthyroid" have actually been hypothyroid, and benefitted
from increasing their thyroid function; some of these people had
also been told that they had Graves' disease.

Mary Shomon: You are a proponent of coconut oil for thyroid
patients. Can you explain why?

Dr. Ray Peat: An important function of coconut oil is that it
supports mitochondrial respiration, increasing energy production
that has been blocked by the unsaturated fatty acids. Since the
polyunsaturated fatty acids inhibit thyroid function at many levels,
coconut oil can promote thyroid function simply by reducing those
toxic effects. It allows normal mitochondrial oxidative metabolism,
without producing the toxic lipid peroxidation that is promoted by
unsaturated fats.

Mary Shomon: Do you have any thoughts for thyroid patients who are
trying to do everything right, and yet still can't lose any weight?

Dr. Ray Peat: Coconut oil added to the diet can increase the
metabolic rate. Small frequent feedings, each combining some
carbohydrate and some protein, such as fruit and cheese, often help
to keep the metabolic rate higher. Eating raw carrots can prevent
the absorption of estrogen from the intestine, allowing the liver to
more effectively regulate metabolism. If a person doesn't lose
excess weight on a moderately low calorie diet with adequate
protein, it's clear that the metabolic rate is low. The number of
calories burned is a good indicator of the metabolic rate. The
amount of water lost by evaporation is another rough indicator: For
each liter of water evaporated, about 1000 calories are burned.

Mary Shomon:You have talked about internal malnutrition as a problem
for many thyroid patients, due to insufficient digestive juices and
poor intestinal movements. Are there ways patients who are treated
for hypothyroidism can help alleviate this problem.

Dr. Ray Peat: The absorption and retention of magnesium, sodium, and
copper, and the synthesis of proteins, are usually poor in
hypothyroidism. Salt craving is common in hypothyroidism, and eating
additional sodium tends to raise the body temperature, and by
decreasing the production of aldosterone, it helps to minimize the
loss of magnesium, which in turn allows cells to respond better to
the thyroid hormone. This is probably why a low sodium diet
increases adrenalin production, and why eating enough sodium lowers
adrenalin and improves sleep. The lowered adrenalin is also likely
to improve intestinal motility.

Mary Shomon: You've mentioned eggs, milk and gelatin as good for the
thyroid. Can you explain a bit more about this?

Dr. Ray Peat: Milk contains a small amount of thyroid and
progesterone, but it also contains a good balance of amino acids.
For adults, the amino acid balance of cheese might be even better,
since the whey portion of milk contains more tryptophan than the
curd, and tryptophan excess is significantly antagonistic to thyroid
function. The muscle meats contain so much tryptophan and cysteine
(which is both antithyroid and potentially excitotoxic) that a pure
meat diet can cause hypothyroidism. In poor countries, people have
generally eaten all parts of the animal, rather than just the
muscles--feet, heads, skin, etc. About half of the protein in an
animal is collagen (gelatin), and collagen is deficient in
tryptophan and cysteine. This means that, in the whole animal, the
amino acid balance is similar to the adult's requirements. Research
in the amino acid requirements of adults has been very inadequate,
since it has been largely directed toward finding methods to produce
farm animals with a minimum of expense for feed. The meat industry
isn't interested in finding a diet for keeping chickens, pigs, and
cattle healthy into old age. As a result, adult rats have provided
most of our direct information about the protein requirements of
adults, and since rats keep growing for most of their life, their
amino acid requirements are unlikely to be the same as ours.

Mary Shomon: Do you think the majority of people with hypothyroidism
get too much or too little iodine? Should people with hypothyroidism
add more iodine, like kelp, seaweeds, etc.?

Dr. Ray Peat: 30 years ago, it was found that people in the US were
getting about ten times more iodine than they needed. In the
mountains of Mexico and in the Andes, and in a few other remote
places, iodine deficiency still exists. Kelp and other sources of
excess iodine can suppress the thyroid, so they definitely shouldn't
be used to treat hypothyroidism.

Mary Shomon: What are your thoughts for Graves'
disease/hyperthyroidism patients? Should they move ahead quickly to
get radioactive iodine treatment, or are there natural things they
might be able to try to temporarily - or even permanently - get a
remission?

Dr. Ray Peat: Occasionally, a person with a goiter will temporarily
become hyperthyroid as the gland releases its colloid stores in a
corrective process. Some people enjoy the period of moderate
hyperthyroidism, but if they find it uncomfortable or inconvenient,
they can usually control it just by eating plenty of liver, and
maybe some cole slaw or raw cabbage juice. Propranolol will slow a
rapid heart. The effects of a thyroid inhibitor, PTU,
propylthiouracil, have been compared to those of thyroidectomy and
radioactive iodine. The results of the chemical treatment are better
for the patient, but not nearly so profitable for the physician.

Besides a few people who were experiencing the unloading of a
goiter, and one man from the mountains of Mexico who became
hypermetabolic when he moved to Japan (probably from the sudden
increase of iodine in his diet, and maybe from a smaller amount of
meat in his diet), all of the people I have seen in recent decades
who were called "hyperthyroid" were not. None of the people I have
talked to after they had radioiodine treatment were properly studied
to determine the nature of their condition. Radioiodine is a foolish
medical toy, as far as I can see, and is never a proper treatment.

FOR MORE INFORMATION ABOUT RAY PEAT AND HIS PUBLICATIONS

For more information about Dr. Ray Peat, see the Publications Order
Page to order Ray Peat's monthly newsletter, or his books, which
include Progesterone in Orthomolecular Medicine, Generative Energy:
Protecting and Restoring the Wholeness of Life, Mind and Tissue:
Russian Research Perspectives on the Human Brain, Nutrition for
Women,and From PMS to Menopause: Female Hormones in Context. 
 

You Want a Food Loaded with Real Health Benefits? You Want Coconut Oil

By Ray Peat

This is a slightly modified version of Ray Peat's article which can be found at http://www.efn.org/~raypeat/
I have already discussed the many toxic effects of the unsaturated oils, and I have frequently mentioned that coconut oil doesn't have those toxic effects, though it does contain a small amount of the unsaturated oils.
Many people have asked me to write something on coconut oil. I thought I might write a small book on it, but I realize that there are no suitable channels for distributing such a book -- if the seed-oil industry can eliminate major corporate food products that have used coconut oil for a hundred years, they certainly have the power to prevent dealers from selling a book that would affect their market more seriously. For the present, I will just outline some of the virtues of coconut oil.
The unsaturated oils in some cooked foods become rancid in just a few hours, even at refrigerator temperatures, and are responsible for the stale taste of leftover foods. (Eating slightly stale food isn't particularly harmful, since the same oils, even when eaten absolutely fresh, will oxidize at a much higher rate once they are in the body, where they are heated and thoroughly mixed with an abundance of oxygen.)
The Premier Coconut Oil
for Health & Weight Loss
Learn what to look for in a quality coconut oil, and find out which one I now highly recommend because it meets these important requirements. And discover coconut oil's incredible health benefits to you such as:
  • Helps you lose weight, lowers cholesterol
  • Reduces your risk of heart disease and other diseases
  • Helps those with diabetes, thyroid, chronic fatigue
  • Improves Crohn's, IBS, and other digestive disorders
  • Boosts your daily energy
  • Rejuvenates your skin, prevents wrinkles
Coconut oil that has been kept at room temperature for a year has been tested for rancidity, and showed no evidence of it.
Since we would expect the small percentage of unsaturated oils naturally contained in coconut oil to become rancid, it seems that the other (saturated) oils have an antioxidative effect:
I suspect that the dilution keeps the unstable unsaturated fat molecules spatially separated from each other, so they can't interact in the destructive chain reactions that occur in other oils.
To interrupt chain-reactions of oxidation is one of the functions of antioxidants, and it is possible that a sufficient quantity of coconut oil in the body has this function. It is well established that dietary coconut oil reduces our need for vitamin E, but I think its antioxidant role is more general than that, and that it has both direct and indirect antioxidant activities.
Coconut oil is unusually rich in short and medium chain fatty acids. Shorter chain length allows fatty acids to be metabolized without use of the carnitine transport system. Mildronate protects cells against stress partly by opposing the action of carnitine, and comparative studies showed that added carnitine had the opposite effect, promoting the oxidation of unsaturated fats during stress, and increasing oxidative damage to cells.
I suspect that a degree of saturation of the oxidative apparatus by short-chain fatty acids has a similar effect -- that is, that these very soluble and mobile short-chain saturated fats have priority for oxidation, because they don't require carnitine transport into the mitochondrion, and that this will tend to inhibit oxidation of the unstable, peroxidizable unsaturated fatty acids.
When Albert Schweitzer operated his clinic in tropical Africa, he said it was many years before he saw any cases of cancer, and he believed that the appearance of cancer was caused by the change to the European type of diet. In the l920s, German researchers showed that mice on a fat-free diet were practically free of cancer.
Since then, many studies have demonstrated a very close association between consumption of unsaturated oils and the incidence of cancer.
Heart damage is easily produced in animals by feeding them linoleic acid; this "essential" fatty acid turned out to be the heart toxin in rape-seed oil.
The addition of saturated fat to the experimental heart-toxic oil-rich diet protects against the damage to heart cells.
Immuno-suppression was observed in patients who were being "nourished" by intravenous emulsions of "essential fatty acids," and as a result coconut oil is used as the basis for intravenous fat feeding, except in organ-transplant patients. For those patients, emulsions of unsaturated oils are used specifically for their immunosuppressive effects.
General aging, and especially aging of the brain, is increasingly seen as being closely associated with lipid peroxidation.
Several years ago I met an old couple, who were only a few years apart in age, but the wife looked many years younger than her doddering old husband. She was from the Philippines, and she remarked that she always had to cook two meals at the same time, because her husband couldn't adapt to her traditional food. Three times every day, she still prepared her food in coconut oil. Her apparent youth increased my interest in the effects of coconut oil.
In the l960s, Hartroft and Porta gave an elegant argument for decreasing the ratio of unsaturated oil to saturated oil in the diet (and thus in the tissues). They showed that the "age pigment" is produced in proportion to the ratio of oxidants to antioxidants, multiplied by the ratio of unsaturated oils to saturated oils. More recently, a variety of studies have demonstrated that ultraviolet light induces peroxidation in unsaturated fats, but not saturated fats, and that this occurs in the skin as well as in the lab.
Rabbit experiments, and studies of humans, showed that the amount of unsaturated oil in the diet strongly affects the rate at which aged, wrinkled skin develops. The unsaturated fat in the skin is a major target for the aging and carcinogenic effects of ultraviolet light, though not necessarily the only one.
In the l940s, farmers attempted to use cheap coconut oil for fattening their animals, but they found that it made them lean, active and hungry. For a few years, an antithyroid drug was found to make the livestock get fat while eating less food, but then it was found to be a strong carcinogen, and it also probably produced hypothyroidism in the people who ate the meat. By the late l940s, it was found that the same antithyroid effect, causing animals to get fat without eating much food, could be achieved by using soy beans and corn as feed.
Later, an animal experiment fed diets that were low or high in total fat, and in different groups the fat was provided by pure coconut oil, or a pure unsaturated oil, or by various mixtures of the two oils. At the end of their lives, the animals' obesity increased directly in proportion to the ratio of unsaturated oil to coconut oil in their diet, and was not related to the total amount of fat they had consumed. That is, animals which ate just a little pure unsaturated oil were fat, and animals which ate a lot of coconut oil were lean.
G. W. Crile and his wife found that the metabolic rate of people in Yucatan, where coconut is a staple food, averaged 25% higher than that of people in the United States.
In a hot climate, the adaptive tendency is to have a lower metabolic rate, so it is clear that some factor is more than offsetting this expected effect of high environmental temperatures. The people there are lean, and recently it has been observed that the women there have none of the symptoms we commonly associate with the menopause. By 1950, then, it was established that unsaturated fats suppress the metabolic rate, apparently creating hypothyroidism.
Over the next few decades, the exact mechanisms of that metabolic damage were studied. Unsaturated fats damage the mitochondria, partly by suppressing the reparatory enzyme, and partly by causing generalized oxidative damage. The more unsaturated the oils are, the more specifically they suppress tissue response to thyroid hormone, and transport of the hormone on the thyroid transport protein.
Plants evolved a variety of toxins designed to protect themselves from "predators," such as grazing animals. Seeds contain a variety of toxins, that seem to be specific for mammalian enzymes, and the seed oils themselves function to block protein digestive enzymes in the stomach. The thyroid hormone is formed in the gland by the action of a protein digestive enzyme, and the unsaturated oils also inhibit that enzyme. Similar protein digestive enzymes involved in clot removal and immune function appear to be similarly inhibited by these oils. Just as metabolism is "activated" by consumption of coconut oil, which prevents the inhibiting effect of unsaturated oils, other inhibited processes, such as clot removal and immune function, will probably tend to be restored by continuing use of coconut oil.
Brain tissue is very rich in complex forms of fats.
The experiment (around 1978) in which pregnant mice were given diets containing either coconut oil or unsaturated oil showed that brain development was superior in the young mice whose mothers ate coconut oil. Because coconut oil supports thyroid function, and thyroid governs brain development, including myelination, the result might simply reflect the difference between normal and hypothyroid individuals.
However, in 1980, experimenters demonstrated that young rats fed milk containing soy oil incorporated the oil directly into their brain cells, and had structurally abnormal brain cells as a result. Lipid oxidation occurs during seizures, and antioxidants such as vitamin E have some anti-seizure activity. Currently, lipid oxidation is being found to be involved in the nerve cell degeneration of Alzheimer's disease. Various fractions of coconut oil are coming into use as "drugs," meaning that they are advertised as treatments for diseases. Butyric acid is used to treat cancer, lauric and myristic acids to treat virus infections, and mixtures of medium-chain fats are sold for weight loss.
Purification undoubtedly increases certain effects, and results in profitable products, but in the absence of more precise knowledge, I think the whole natural product, used as a regular food, is the best way to protect health. The shorter-chain fatty acids have strong, unpleasant odors; for a couple of days after I ate a small amount of a medium-chain triglyceride mixture, my skin oil emitted a rank, goaty smell. Some people don't seem to have that reaction, and the benefits might outweigh the stink, but these things just haven't been in use long enough to know whether they are safe.
Treating any complex natural product as the drug industry does, as a raw material to be fractionated in the search for "drug" products, is risky, because the relevant knowledge isn't sought in the search for an association between a single chemical and a single disease. While the toxic unsaturated paint-stock oils, especially safflower, soy, corn and linseed (flaxseed) oils, have been sold to the public precisely for their drug effects, all of their claimed benefits were false.
When people become interested in coconut oil as a "health food," the huge seed-oil industry -- operating through their shills -- are going to attack it as an "unproved drug." While components of coconut oil have been found to have remarkable physiological effects (as antihistamines, antiinfectives/antiseptics, promoters of immunity, glucocorticoid antagonist, nontoxic anticancer agents, for example).
The cholesterol-lowering fiasco for a long time centered on the ability of unsaturated oils to slightly lower serum cholesterol. For years, the mechanism of that action wasn't known, which should have suggested caution. Now, it seems that the effect is just one more toxic action, in which the liver defensively retains its cholesterol, rather than releasing it into the blood.
Large scale human studies have provided overwhelming evidence that whenever drugs, including the unsaturated oils, were used to lower serum cholesterol, mortality increased, from a variety of causes including accidents, but mainly from cancer. Since the 1930s, it has been clearly established that suppression of the thyroid raises serum cholesterol (while increasing mortality from infections, cancer, and heart disease), while restoring the thyroid hormone brings cholesterol down to normal. In this situation, however, thyroid isn't suppressing the synthesis of cholesterol, but rather is promoting its use to form hormones and bile salts. When the thyroid is functioning properly, the amount of cholesterol in the blood entering the ovary governs the amount of progesterone being produced by the ovary, and the same situation exists in all steroid-forming tissues, such as the adrenal glands and the brain.
Progesterone and its precursor, pregnenolone, have a generalized protective function: antioxidant, anti-seizure, antitoxin, anti-spasm, anti-clot, anticancer, pro-memory, pro-myelination, pro-attention, etc. Any interference with the formation of cholesterol will interfere with all of these exceedingly important protective functions.
As far as the evidence goes, it suggests that coconut oil, added regularly to a balanced diet, lowers cholesterol to normal by promoting its conversion into pregnenolone.
Coconut-eating cultures in the tropics have consistently lower cholesterol than people in the U.S. Everyone that I know who uses coconut oil regularly happens to have cholesterol levels of about 160, while eating mainly cholesterol rich foods (eggs, milk, cheese, meat, shellfish). I encourage people to eat sweet fruits, rather than starches, if they want to increase their production of cholesterol, since fructose has that effect.
Many people see coconut oil in its hard, white state, and -- as a result of their training watching television or going to medical school -- associate it with the cholesterol-rich plaques in blood vessels. Those lesions in blood vessels are caused mostly by lipid oxidation of unsaturated fats, and relate to stress, because adrenaline liberates fats from storage, and the lining of blood vessels is exposed to high concentrations of the blood-borne material.
In the body, incidentally, the oil can't exist as a solid, since it liquefies at 76 degrees. (Incidentally, the viscosity of complex materials isn't a simple matter of averaging the viscosity of its component materials; cholesterol and saturated fats sometimes lower the viscosity of cell components.)
Most of the images and metaphors relating to coconut oil and cholesterol that circulate in our culture are false and misleading. I offer a counter-image, which is metaphorical, but it is true in that it relates to lipid oxidation, which is profoundly important in our bodies. After a bottle of safflower oil has been opened a few times, a few drops that get smeared onto the outside of the bottle begin to get very sticky, and hard to wash off.
This property is why it is a valued base for paints and varnishes, but this varnish is chemically closely related to the age pigment that forms "liver spots" on the skin, and similar lesions in the brain, heart, blood vessels, lenses of the eyes, etc. The image of "hard, white saturated coconut oil" isn't relevant to the oil's biological action, but the image of "sticky varnish-like easily oxidized unsaturated seed oils" is highly relevant to their toxicity.
The ability of some of the medium chain saturated fatty acids in coconut oil to inhibit the liver's formation of fat very likely synergizes with the pro-thyroid effect, in allowing energy to be used, rather than stored.
When fat isn't formed from carbohydrate, the sugar is available for use, or for
storage as glycogen. Therefore, shifting from unsaturated fats in foods to coconut oil involves several anti-stress processes, reducing our need for the adrenal hormones. Decreased blood sugar is a basic signal for the release of adrenal hormones.
Unsaturated oil tends to lower the blood sugar in at least three basic ways.
It damages mitochondria, causing respiration to be uncoupled from energy production, meaning that fuel is burned without useful effect. It suppresses the activity of the respiratory enzyme (directly, and through its anti-thyroid actions), decreasing the respiratory production of energy.
And it tends to direct carbohydrate into fat production, making both stress and obesity more probable. For those of us who use coconut oil consistently, one of the most noticeable changes is the ability to go for several hours without eating, and to feel hungry without having symptoms of hypoglycemia.
One of the stylish ways to promote the use of unsaturated oils is to refer to their presence in "cell membranes," and to claim that they are essential for maintaining "membrane fluidity." As I have mentioned above, it is the ability of the unsaturated fats, and their breakdown products, to interfere with enzymes and transport proteins, which accounts for many of their toxic effects, so they definitely don't just harmlessly form "membranes."
They probably bind to all proteins, and disrupt some of them, but for some reason their affinity for proteolytic and respiration-related enzymes is particularly obvious. (I think the chemistry of this association is going to give us some important insights into the nature of organisms).
Unsaturated fats are slightly more water-soluble than fully saturated fats, and so they do have a greater tendency to concentrate at interfaces between water and fats or proteins, but there are relatively few places where these interfaces can be usefully and harmlessly occupied by unsaturated fats, and at a certain point, an excess becomes harmful.
We don't want "membranes" forming where there shouldn't be membranes. The fluidity or viscosity of cell surfaces is an extremely complex subject, and the degree of viscosity has to be appropriate for the function of the cell. Interestingly, in some cells, such as the cells that line the air sacs of the lungs, cholesterol and one of the saturated fatty acids found in coconut oil can increase the fluidity of the cell surface.
In red blood cells, which have sometimes been wrongly described as "hemoglobin enclosed in a cell membrane," it has been known for a long time that lipid oxidation of unsaturated fats weakens the cellular structure, causing the cells to be destroyed prematurely.
Lipid oxidation products lower the rigidity of regions of cells considered to be membranes. But the red blood cell is actually more like a sponge in structure, consisting of a "skeleton" of proteins, which (if not damaged by oxidation) can hold its shape, even when the hemoglobin has been removed. Oxidants damage the protein structure, and it is this structural damage which in turn increases the "fluidity" of the associated fats.
So, it is probably true that in many cases the liquid unsaturated oils do increase "membrane fluidity," but it is now clear that in at least some of those cases the "fluidity" corresponds to the chaos of a damaged cell protein structure. (N. V. Gorbunov, "Effect of structural modification of membrane proteins on lipid-protein interactions in the human erythrocyte membrane," Bull. Exp. Biol. & Med. 116(11), 1364-67. 1993.
Although I had stopped using the unsaturated seed oils years ago, and supposed that I wasn't heavily saturated with toxic unsaturated fat, when I first used coconut oil I saw an immediate response, that convinced me my metabolism was chronically inhibited by something that was easily alleviated by "dilution" or molecular competition.
I had put a tablespoonful of coconut oil on some rice I had for supper, and half an hour later while I was reading, I noticed I was breathing more deeply than normal. I saw that my skin was pink, and I found that my pulse was faster than normal -- about 98, I think. After an hour or two, my pulse and breathing returned to normal.
Every day for a couple of weeks I noticed the same response while I was digesting a small amount of coconut oil, but gradually it didn't happen any more, and I increased my daily consumption of the oil to about an ounce. I kept eating the same foods as before, except that I added about 200 or 250 calories per day as coconut oil.
Apparently the metabolic surges that happened at first were an indication that my body was compensating for an anti-thyroid substance by producing more thyroid hormone; when the coconut oil relieved the inhibition, I experienced a moment of slight hyperthyroidism, but after a time the inhibitor became less effective, and my body adjusted by producing slightly less thyroid hormone.
But over the next few months, I saw that my weight was slowly and consistently decreasing. It had been steady at 185 pounds for 25 years, but over a period of six months it dropped to about 175 pounds. I found that eating more coconut oil lowered my weight another few pounds, and eating less caused it to increase.
The anti-obesity effect of coconut oil is clear in all of the animal studies, and in my friends who eat it regularly.
It is now hard to get it in health food stores, since Hain stopped selling it. The Spectrum product looks and feels a little different to me, and I suppose the particular type of tree, region, and method of preparation can account for variations in the consistency and composition of the product.
The unmodified natural oil is called "76 degree melt," since that is its natural melting temperature. One bottle from a health food store was labeled "natural coconut oil, 92% unsaturated oil," and it had the greasy consistency of old lard. I suspect that someone had confused palm oil (or something worse) with coconut oil, because it should be about 96% saturated fatty acids.
Raymond Peat, Ph.D.
P.O. Box 5764
Eugene, OR 97405

Feature an extensive list of frequently asked questions in the beginning of your book about the advantages of using virgin coconut oil. What makes virgin coconut oil more effective and advantageous than other oils on the market?
Virgin coconut oil's many health benefits come from the medium-chain length of its fatty acids, or triglycerides (MCTs). Most of the other edible oils on the market today are comprised of long-chain fatty acids. MCTs have many health benefits, including raising the body's metabolism, and fighting off pathogens such as viruses, bacteria, funguses and others.
Coconut oil is nature's richest source of MCTs outside of human breast milk. Virgin coconut oil is very stable oil that does not oxidize and break down quickly like other oils. It also has a shelf life of more than two years.
Typically, when one thinks about cooking oils, weight loss rarely comes to mind. Yet your book includes a number of stories about people who have done just that. What's the connection between virgin coconut oil and losing weight?
Well, the word is finally getting out that low-fat diets don't work. Our bodies need fat and depriving ourselves of it can actually lead to an increase in cravings for other foods, such as refined carbohydrates, that do lead to weight gain. Coconut oil is nature's richest source of MCTs that increase metabolic rates and lead to weight loss. MCTs promote what is called thermogenesis.
Thermogenesis increases the body's metabolism, producing energy. This phenomenon has been shown in many scientific studies. We have also found many people have underlying physical conditions that prevent them from losing weight. One of the most common is a low functioning thyroid. Also, many Americans today suffer from poor digestive health. Coconut oil really shines in these areas, improving thyroid function and digestive health.
Your book does a good job balancing the documented scientific research with lively testimonies that illustrate the benefits of virgin coconut oil. That approach makes for an easier read too. Some writers would've stayed away from using consumer testimonies, but you didn't. Why?
These testimonies are the main reason we wrote the book! It is the story of virgin coconut oil and how it has changed people's lives.
The world needs to hear these people's stories, which we receive on almost a daily basis. It is one thing to quote scientific studies, but quite another to hear the stories of people whose lives have actually been changed by a pure, unrefined coconut oil. This book is as much their story, as it is Marianita's and my story.
According to your book, virgin coconut oil has had its biggest impact on thyroid problems. How can thyroid problems be helped with coconut oil?
Hypothyroidism is truly one of the biggest epidemics of our time, and we have met so many people who have been told that their blood tests are normal, and yet find themselves with symptoms of hypothyroidism. There are very few options today offering any kind of hope of dealing with the underlying cause of this condition.
Probably the most dramatic results we have had reported to us are from those who have thyroid problems and have eliminated polyunsaturated oils from their diet, and started incorporating virgin coconut oil in its place. People's body temperatures increase, they have more energy and some, for the first time, are actually able to start losing weight.
Which skin problems can be helped the best by using virgin coconut oil?
We have had probably more testimonies in the area of skin health than any other one area. This is one benefit of coconut oil that has been well known even in the United States for quite some time.
When we first brought virgin coconut oil to the market to the United States in 2002, there were very few other quality coconut oils available, and the few that did exist were almost exclusively marketed for cosmetic purposes. As we began to publish the research on coconut oil as an edible oil -- that is considered a "functional food" by some like Dr. Mary Enig -- many people began to not only apply it to their skin but also consume it.
The result has been fantastic. We have seen reports of success for almost any kind of skin problem for those who both consume the oil and apply it to their skin. Skin problems related to fungal infections seem to be the most positively affected by the healing properties of Virgin Coconut Oil.
One of the more interesting parts of your book was the extended section on recipes. How did you find all those recipes?
All of the recipes were developed by a professional chef in California. Many of them were prepared in our own kitchen where the chef would come on a regular basis to cook for us. Marianita is a certified nutritionist in the Philippines and, of course, knows how to cook traditional Filipino foods with coconut oil. But we had to learn how to incorporate it into a more eclectic American-type menu once we moved back to the United States.
So we worked with the chef for many months developing the recipes. Unlike other coconut recipes that might simply take traditional recipes and just substitute coconut oil as an ingredient, our recipes were actually developed in the kitchen by our chef.
For those trying to get a certain amount of coconut oil into their diet each day, each recipe lists the amount of coconut oil per serving. So it is perfect for those on the coconut diet.
So many people have enjoyed great success adding coconut oil to the diets of their various pets, but no studies have been done to date. Is coconut oil beneficial to pets in different ways than ones enjoyed by their human caretakers?
We first noticed that many animals enjoyed eating coconut when we lived in the Philippines. Our dogs and cats on the farm would try to get the little bits of coconut out of the shell after they had been grated.
The people who made virgin coconut oil for us would take the coconut pulp after the oil had been extracted and feed it to their livestock. From the reports we have received from people here in the United States, the benefits to pets and animals are much the same as for humans. It increases metabolism, fights off infections and leads to a healthier coat of hair.
We have people giving it to race-track horses and one guy running a study right now is giving it to one of his sled-dog teams. The reports we are getting have been phenomenal!
In what way has virgin coconut oil changed your life the most?
Well, we are certainly grateful to the Lord in that it has kept our family healthy. But probably seeing how virgin coconut oil has changed so many other people's lives has affected me more than anything else. It humbles me to see how a completely natural product like this can give such incredible health to people, without being created in a laboratory or by years of labor and expense.
It is a God-given simple crop given to the people of the tropics and known as the "tree of life."
Part of your book is devoted to a memoir of living in the Philippines. You learned a great deal about living healthfully there. What do you miss most about those times?
I miss the simplicity of the agrarian lifestyle in the rural Philippines, where most people can live off the food they grow themselves. People there are so much more connected to their communities where the food is grown, and the traditional knowledge of the plants and herbs are still commonplace.
I also miss growing our own upland rice, pineapples and other foods free of pesticides or other chemicals, or of picking wild berries and fruit that grew everywhere. We had guava and tiny little hot peppers that were literally weeds and would just pop up everywhere without being planted. The Philippines is seen as a poor country, but they actually have incredible wealth in the land where about 50 percent of the population are still family farmers.

Experience the Incredible Health & Weight Loss Benefits of the Premier Coconut Oil

Why should you be using coconut oil versus any other type of oil? Because it can:
  • Help you lose weight, or maintain your already good weight
  • Reduce the risk of heart disease
  • Lower your cholesterol
  • Improve conditions in those with diabetes and chronic fatigue
  • Improve Crohn?s, IBS, and other digestive disorders
  • Prevent other disease and routine illness with its powerful antibacterial, antiviral and antifungal agents
  • Increase metabolism and promotes healthy thyroid function
  • Boost your daily energy
  • Rejuvenate your skin and prevent wrinkles
In short, after unjustly getting lumped in the "no-fat" craze of past decades, coconut oil is now starting to get the respect it deserves as not only the healthiest oil you can consume, even superior to olive oil which contains trans-fat, but as one of the most nutritious of all foods.
Coconut oil?s benefits are finally reaching the mainstream. For example, the May 20, 2003 edition of Women?s World, a very popular and wide-reaching magazine, called coconut oil a "miracle food" and particularly touted its ability help the body burn unwanted fat, triple your energy, and greatly help those with thyroid problems.
You should be absolutely certain, however, of the quality and effectiveness of whatever coconut oil brand you choose. There is a very wide variance in terms of the types of coconuts, the manufacturing processes used to make the oil, and more, which will have a major impact on the healthiness and effectiveness your coconut oil.
Because there is so much uncertainty, my team and I here researched coconut oil extensively until we found the ideal source. I now highly recommend and offer you what is clearly the premier brand of virgin coconut oil in the U.S., Tropical Traditions.
What Makes Our Coconut Oil Superior to Other Brands?
Our oil meets all of the requirements in the chart below. Meeting such high standards is no small feat, but you should not settle for anything less if you want to experience all of the health benefits of coconut oil without exposing yourself to unnecessary health risks. (If you are considering another brand, I urge you to make sure it meets the requirements below.)
Requirements for Healthy and Safe Coconut Oil
Certified organic, USDA standards
No refining
No chemicals added
No bleaching
No deodorization
No hydrogenation
Non-GMO
Coconuts from traditional palms only -- no hybrid varieties
From fresh coconuts, not the dried "copra" used in most coconut oils
Low-level heated only -- does not damage nutrients
The fresh coconuts used to make the oil (not "copra" or dried coconuts like most oils) come from a rural region of the Philippines untainted by urban pollution. Philippine coconuts are considered the best in the world, in large part due to the fact that the Philippine Islands are made up of volcanoes that brought nutrient-rich soil beneath the sea up to form the islands.
Tropical Traditions closely inspects the groves and coconuts to ensure the highest quality, and oversees the entire process, from growing to final packaging. Unlike other coconut oils, in other words, there are no middlemen with potentially lower standards involved in the process.
What?s more, small families, not corporate conglomerates, grow the coconuts. Tropical Traditions works through local churches in the rural areas to organize communities for the production of the coconuts and oil, therefore providing a livelihood for these farmers.
What this means for you is a virgin coconut oil of unsurpassed quality, not mass processed like most others but created using traditional methods. And because this coconut oil is made from fresh coconuts within 24 hours of harvesting, there are no dangers of mycotoxins or afflatoxins that can form in coconut oils made from "copra" coconuts. Overall, this superior quality makes a huge difference, not only in terms of health and safety, but also in terms of taste, cooking quality, and other tangible results.
A Delicious Way to Prevent Disease, Lose Weight, & Increase Energy
During the "no-fat" craze of the past decades, all saturated fats were marked as bad, as something to be avoided. Knowledge was already in place to the contrary, but as often happens, perceptions -- pushed by industries like the corn oil companies who profited immensely from doing so -- overshadowed science. And coconut oil, far more nutritious and beneficial than corn, peanut, soy, safflower and the other oils out there, nonetheless got tossed into the "no saturated fat" overgeneralizations and lunacy.
What you didn?t hear is that some saturated fats A) are necessary to human health; B) are not the primary perpetrator of weight gain (grains and sugars are, as you?ll read in my New York Times bestseller, The No-Grain Diet; and C) come in three classes, of which the medium-chain can actually help you lose weight and increase metabolism.
Coconut oil?s saturated fat is of the medium-chain fatty acid variety. These MCFAs are digested more easily and utilized differently by the body than other fats. In short, whereas other fats are stored in the body?s cells, the MCFAs in coconut oil are sent directly to the liver where they are immediately converted into energy. So when you eat coconut oil, the body uses it immediately to make energy rather than store it as body fat. Because this quick and easy absorption puts less strain on the pancreas, liver and digestive system, coconut oil "heats up" the metabolic system and is outstanding for those with thyroid problems.
Since coconut oil will actually speed up metabolism, your body will burn more calories in a day -- this will contribute to weight loss, and you?ll have more energy. Meanwhile, studies have shown the opposite for unsaturated fats: they cause hypothyroidism and lower metabolic rate.
Perhaps even more important, virgin coconut oil is rich in lauric acid, a proven antiviral, antibacterial and antifungal agent that is very beneficial in attacking viruses, bacteria, and other pathogens, and that builds the body?s immune system.
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. Mary Enig, an internationally respected expert on fats and lipid biochemistry, and author of the "fat information bible" Know Your Fats, provides excellent detail on the ability of coconut oil to prevent illness and disease in her article, "A New Look at Coconut Oil."
Finally, coconut oil contains no dangerous trans-fats, which are found in vegetable oils (including olive oil), margarine, shortening and more. Trans-fats can raise LDLs or "bad" cholesterol levels and lead to clogged arteries, heart disease, type-II diabetes and more, and should be avoided.
Why Diabetics and those with Crohn?s and IBS Should Seriously Consider Coconut Oil
For those with diabetes, it?s almost a sin that coconut oil has been kept hidden from them. Not only does it not contribute to diabetes, but it also helps regulate blood sugar, thus lessening the effects of the disease.
Coconut oil also raises metabolic rate causing the body to burn up more calories and thus promoting weight loss. A faster metabolic rate stimulates increased production of needed insulin and increases absorption of glucose into cells, thus helping both Type I and Type II diabetics.
 For those with Crohn?s and IBS, the anti-inflammatory and healing effects of coconut oil have been shown to play a role in soothing inflammation and healing injury in the digestive tract. Interestingly, researchers have demonstrated the benefits of coconut oil on patients with digestive problems, including, Crohn's disease, at least since the 1980s. Its antimicrobial properties also promote intestinal health by killing troublesome microorganisms that may cause chronic inflammation.
Finally, for those with chronic fatigue syndrome, coconut oil may provide a vital solution. The fatty acids in coconut oil can kill herpes and Epstein-Barr viruses which are believed to be major causes. They kill Candida and giardia. They kill a variety of other infectious organisms, any of which could cause chronic fatigue. The key to overcoming CFS is strengthening the immune system. Coconut oil supports the immune system by ridding the body of harmful microorganisms, thus relieving stress on the body. With fewer harmful organisms taxing the body's energy, the immune system can function better.
The Many Uses of Coconut Oil -- Cooking & Eating, Skincare, Massage and More
To capture all of the benefits of coconut oil while avoiding the risks, I strongly advise you to consider the Tropical Traditions brand I offer here or another brand that meets all of the requirements defined in the chart above. Uses for this virgin coconut oil with both a pleasant scent and taste include:
  • In place of other oils, margarine, butter, shortening, etc. for all cooking needs, as it is a stable cooking oil
  • As an ingredient when juicing or making smoothies
  • It smells and tastes so pleasant and has such excellent nutritional properties that some also consume it straight, by the tablespoon, and use it in place of other oils on their salads
  • An excellent massage oil
  • As a skin lotion for healthier, younger skin, as explained below
For skincare, using the Virgin Coconut Oil as you would any lotion is ideal. It prevents destructive free-radical formation and provides protection against them. It can help to keep the skin from developing liver spots, and other blemishes caused by aging and over exposure to sunlight. It helps to prevent sagging and wrinkling by keeping connective tissues strong and supple. In some cases it might even restore damaged or diseased skin. The oil is absorbed into the skin and into the cell structure of the connective tissues, limiting the damage excessive sun exposure can cause.
Coconut oil will not only bring temporary relief to the skin, but it will aid in healing and repairing. It will have lasting benefits, unlike most lotions. It can help bring back a youthful appearance. The coconut oil will aid in removing the outer layer of dead skin cells, making the skin smoother. The skin will become more evenly textured with a healthy "shine". And the coconut oil will penetrate into the deeper layers of the skin and strengthen the underlying tissues.

The Truth About Coconut Oil:
Why it Got a Bad Rep When it?s Actually Good


Coconut oil is truly the healthiest oil you can consume. It is rich in lauric acid, which is known for being antiviral, antibacterial and antifungal, contains no trans fat (even olive oil has some trans fat), and boosts the immune system. You can even use it on your skin to help prevent wrinkles.
This may be surprising to hear, but coconut oil, in addition to tasting and smelling great, can:
  • Help you lose weight, or maintain your already healthy weight
  • Reduce your risk of heart disease
  • Lower your cholesterol
  • Improve conditions in those with diabetes and chronic fatigue
  • Improve Crohn?s, IBS, and other digestive disorders
  • Prevent other disease and routine illness with its powerful antibacterial, antiviral and antifungal agents
  • Increase metabolism and promote healthy thyroid function
  • Boost your daily energy
  • Rejuvenate your skin and prevent wrinkles
Unfortunately, there is a widespread misconception that coconut oil is bad for you because it contains saturated fat. To really understand the benefits of coconut oil, I suggest you read Dr. Mary Enig and Sally Fallon?s article "The Truth About Saturated Fat" to first dispel any lingering notions you may have that all saturated fats are dangerous.
Fats are categorized as either short-, medium-, or long-chain depending on how many carbon molecules they contain. Close to two-thirds of the saturated fat in coconut oil is made up of medium-chain fatty acids, which have antimicrobial properties, are easily digested by the body for quick energy, and are beneficial to the immune system. Far from being dangerous, the saturated fat in coconut oil is actually health promoting.
So how could an oil that is so good for you have gotten such a bad reputation? The answer comes down to simple economics and politics. Based on some flawed studies performed over four decades ago, some of which used primarily hydrogenated coconut oils, a powerful anti-saturated fat movement began. Remember--hydrogenated oils are oils with trans-fatty acids, which have been altered from their original chemical composition and have been shown to raise cholesterol levels and lead to heart disease and other health problems. You should not consume hydrogenated oils, whether it is coconut or another vegetable oil.
Around this time the edible oil industry began to denounce all saturated fats and heavily promote polyunsaturated fats such as canola, soybean, safflower, corn, and other seed and nut oils. However, these oils easily become rancid when exposed to oxygen and produce large amounts of damaging free radicals in the body. What is not commonly known is that these oils can actually cause aging, clotting, inflammation, cancer and weight gain. You can read the article " Secrets of the Edible Oil Industry" for more information.
Fortunately, coconut oil has begun to gain some positive media exposure as researchers realize its health-promoting qualities. However, coconut oil can vary widely in terms of the types of coconuts used, the manufacturing processes used to make the oil, and more, and all of these factors play a major role in the effectiveness of the oil.
Most commercial coconut oils are RBD (refined, bleached, and deodorized). RBD oils do contain the medium chain fatty acids, however they also contain chemicals used in processing. Because of these variations we have searched for quality coconut oil and found excellent quality product source. Compare this brand of virgin coconut oil with Tropical Traditions, the best quality products available. This virgin coconut oil met all requirements, including no GMO ingredients, bleaching, deodorizing, refining or hydrogenation. It is made from fresh coconuts (not "copra" or dried coconuts like most oils) in India. Try the virgin coconut oil and experience the health benefits for yourself.
http://www.life-enthusiast.com/index/Articles/Mercola/Truth_About_Coconut_Oil

Thyroid Health and Virgin Coconut Oil
Óleo de coco e tireóide
http://www.coconutoil.com/thyroid_health.htm

Many Americans experience cold hands and feet, low body
temperature, sensitivity to cold, a feeling of always being chilled,
headaches, insomnia, dry skin, puffy eyes, hair loss, brittle nails,
joint aches, constipation, mental dullness, fatigue, frequent
infections, hoarse voice, ringing in the ears, dizziness, loss of
libido, and weight gain, which is sometimes uncontrollable.
Approximately 65 percent of the U. S. population is overweight; 30
percent is clinically obese. Research is pointing to the fact that
an insufficiently nourished thyroid might be the number one cause of
weight problems, especially among women, in the US today.

Virgin Coconut Oil offers great hope for those suffering from
hypothyroidism (low thyroid function) today. I didn't even realize
how much hypothyroidism was affecting my life till I started on the
Virgin Coconut Oil and suddenly had energy like the Energizer Bunny!
I also gave up the white toxins (wheat flour, refined sugar,
potatoes, and other high-glycemic index foods) and that, in
combination with my Virgin Coconut Oil consumption has made a
tremendous difference in my hormonal balance, mood stability,
stamina and overall energy. And, I'm slowly but steadily losing a
little bit of weight without effort. Ya gotta love that! Julia
(Coconut Diet Forums)

I began taking coconut oil to address a hypothyroid issue. Recently,
especially over the last month, thyroid activity plunged and my
temperatures would top out for the day somewhere between 97.2 and
97.8. Definitely hypothyroid territory. Now in just a couple of days
the coconut oil has boosted my metabolism back toward the normal
range (still subnormal but getting there) and my sleep has been
incredible. From past experience with thyroid management, I know
that--in my case--greatly improved sleep and feelings of
rejuvenation after sleep are related to more normal thyroid
activity. Whatever the precise mechanism, it's a welcome
development. Mike (Coconut Diet Forums)

We have received literally hundreds of comments such as these from
those with hypothyroidism using Virgin Coconut Oil.

Hypothyroidism Reaching Epidemic Proportions

In 1995, researchers studied 25,862 participants at the Colorado
statewide health fair.  They discovered that among patients not
taking thyroid medication, 8.9 percent were hypothyroid (under-
active thyroid) and 1.1 percent were hyperthyroid (over-active
thyroid). This indicates 9.9 percent of the population had a thyroid
problem that had most likely gone unrecognized. These figures
suggest that nationally, there may be as many as 13 million
Americans with an undiagnosed thyroid problem.1

In her book Living Well With Hypothyroidism: What Your Doctor
Doesn't Tell You. . . That You Need to Know, Mary Shomon quotes
endocrinologist Kenneth Blanchard, M.D., of Lower Newton Falls,
Massachusetts as saying, "The key thing is . . . doctors are always
told that TSH is the test that gives us a yes or no answer. And, in
fact, I think that's fundamentally wrong. The pituitary TSH is
controlled not just by how much T4 and T3 is in circulation, but T4
is getting converted to T3 at the pituitary level. Excess T3
generated at the pituitary level can falsely suppress TSH."2  Hence,
many people who are simply tested for TSH levels and are found to be
within "normal" range are, in fact, suffering from "sub-clinical"
thyroid problems that are going undetected.

Ridha Arem, MD, Associate Professor of Medicine in the Division of
Endocrinology and Metabolism at Baylor College of Medicine, agrees.
He says that hypothyroidism may exist despite "normal range" TSH
levels.  In his book The Thyroid Solution he says:

Many people may be suffering from minute imbalances that have not
yet resulted in abnormal blood tests. If we included people with low-
grade hypothyroidism whose blood tests are normal, the frequency of
hypothyroidism would no doubt exceed 10 percent of the population.
What is of special concern, though, is that many people whose test
results are dismissed as normal could continue to have symptoms of
an under active thyroid. Their moods, emotions, and overall well-
being are affected by this imbalance, yet they are not receiving the
care they need to get to the root of their problems.  Even if the
TSH level is in the lower segment of normal range, a person may
still be suffering from low-grade hypothyroidism.3 

Thus, if we were to include those who may be suffering from "low-
grade hypothyroidism," the number could well be double the 13
million estimate from the Colorado study.

What is Causing This Epidemic?

While more research needs to be done, it is generally accepted that
diet plays a major role in thyroid health.  For decades we have
known that low iodine intake leads to low thyroid function and
eventually to goiter.  Iodized salt was intended to solve this
problem, but it has not been the answer.  There are a number of
foods known as goitrogens that block iodine. Two goitrogens are
quite prevalent in the American diet—peanuts and peanut butter and
soybeans used most often in prepared foods as textured vegetable
protein (a refined soy food) and soybean oil.

The rise of industrialization, corporate farming, and mass
production of food has drastically changed our food supply from what
our ancestors ate. Many studies show the detrimental effects of
refined sugars and grains on our health. These foods are very taxing
on the thyroid gland, and we consume them in large quantities.

Environmental stress such as chemical pollutants, pesticides,
mercury, and fluoride are also tough on the thyroid.  A growing body
of evidence suggests that fluoride, which is prevalent in toothpaste
and water treatment, may inhibit the functioning of the thyroid
gland.  Additionally, mercury may diminish thyroid function because
it displaces the trace mineral selenium, and selenium is involved in
conversion of thyroid hormones T4 to T3.

The Truth About Fats and Oils

Many dietary oils can negatively affect thyroid health. We cook with
them almost every day and they are plentiful in commercially
prepared foods. Expeller-pressed or solvent-extracted oils only
became a major part of the American diet in the last century.  It is
possible they are among the worst offenders when it comes to the
thyroid.  They are known as vegetable oils or polyunsaturated oils.
The most common source of these oils used in commercially prepared
foods is the soybean.

Large-scale cultivation of soybeans in the United States began after
World War II and quickly increased to 140 billion pounds per year. 
Most of the crops are produced for animal feed and soy oil for
hydrogenated fats such as margarine and shortening. Today, it is
nearly impossible to eat at restaurants or buy packaged foods that
don't have soy oil in the ingredients.  Often labels simply
state "vegetable oil."

Ray Peat Ph.D., a physiologist who has worked with progesterone and
related hormones since 1968, says that the sudden surge of
polyunsaturated oils into the food chain post World War II has
caused many changes in hormones. He writes:

Their [polyunsaturated oils] best understood effect is their
interference with the function of the thyroid gland.  Unsaturated
oils block thyroid hormone secretion, its movement in the
circulatory system, and the response of tissues to the hormone. 
When the thyroid hormone is deficient, the body is generally exposed
to increased levels of estrogen.  The thyroid hormone is essential
for making the `protective hormones' progesterone and pregnenolone,
so these hormones are lowered when anything interferes with the
function of the thyroid.  The thyroid hormone is required for using
and eliminating cholesterol, so cholesterol is likely to be raised
by anything which blocks the thyroid function.4

There is a growing body of research concerning soy's detrimental
affect on the thyroid gland. Much of this research centers on the
phytoestrogens ("phyto" means plant) that are found in soy.  In the
1960s when soy was introduced into infant formulas, it was shown
that soy was goitrogenic and caused goiters in babies. When iodine
was supplemented, the incidence of goiter reduced dramatically.
However, a retrospective epidemiological study by Fort, et al.
showed that teenaged children with a diagnosis of autoimmune thyroid
disease were significantly more likely to have received soy formula
as infants (18 out of 59 children; 31 percent) when compared to
healthy siblings (nine out of 76, 12 percent) or control group
children (seven out of 54; 13 percent).5 

When healthy individuals without any previous thyroid disease were
fed 30 grams of pickled soybeans per day for one month, Ishizuki, et
al. reported goiter and elevated individual thyroid stimulating
hormone (TSH) levels (although still within the normal range) in
thirty-seven healthy, iodine-sufficient adults.  One month after
stopping soybean consumption, individual TSH values decreased to the
original levels and goiters were reduced in size.6

Traditionally, polyunsaturated oils such as soybean oil have been
used for livestock feed because they cause the animals to gain
weight.  These oils are made up of what is known as long chain fatty
acids—the kind of fatty acids that promote weight gain. In the North
Carolina State University's Extension Swine Husbandry 1998-2000
Departmental report, for example, was a study entitled "EFFECT OF
DIETARY FAT SOURCE, LEVEL, AND FEEDING INTERVAL ON PORK FATTY ACID
COMPOSITION" by M.T. See and J. Odle. Ironically, since the market
in its low-fat dogma of recent years is demanding leaner meats, this
study showed that one could produce leaner meat and reduce the
weight on swine by reducing their intake of soy oil and substituting
it with saturated animal fat!7

According to Dr. Ray Peat, the fattening effect of polyunsaturated
oils (primarily soy and corn) is due to the presence of Linoleic and
linolenic acids, long-chain fatty acids, which have an anti-thyroid
effect. Peat says:

Linoleic and linolenic acids, the "essential fatty acids," and other
polyunsaturated fatty acids, which are now fed to pigs to fatten
them, in the form of corn and soy beans, cause the animals' fat to
be chemically equivalent to vegetable oil.  In the late 1940s,
chemical toxins were used to suppress the thyroid function of pigs,
to make them get fatter while consuming less food.  When that was
found to be carcinogenic, it was then found that corn and soy beans
had the same antithyroid effect, causing the animals to be fattened
at low cost.  The animals' fat becomes chemically similar to the
fats in their food, causing it to be equally toxic, and equally
fattening.8

Of course in the 1940s the fat from pigs (lard) was highly
desirable, as were most saturated fats. Today, saturated fats are
fed to pigs to keep them lean, while most people buy polyunsaturated
soy and corn oils in the grocery stores as their primary cooking
oil! So we have a population now characterized by lean pigs and
obese people…

Coconut Oil: A-Healthy Choice for the Thyroid

Coconut oil, on the other hand, is a saturated fat made up primarily
of medium chain fatty acids. Also known as medium chain
triglycerides (MCTs), medium chain fatty acids are known to increase
metabolism and promote weight loss.  Coconut oil can also raise
basal body temperatures while increasing metabolism. This is good
nutritional news for people with low thyroid function. We have seen
many testimonies to this effect.

The "proof is in the pudding". Try it yourself and then you be the
judge. All these people certainly can't "be wrong". Everyone will
experience different benefits, some more than others, but definitely
something. In my own personal experience, I was suffering with
hypothyroidism that even prescription medications couldn't help.
After a few short weeks of taking Virgin Coconut Oil, my reading was
normal for the first time in a year. I use it on my skin after a
shower and no longer struggle with the incredibly dry skin that
often goes along with hypothyroidism, and I have used it on my hair
as a conditioner. All I can say that the phrase "The world's perfect
food" is quite accurate. Try it and see for yourself. Warmly,
Melanie (Coconut Diet Forums)

I am just now jumping on the coconut oil bandwagon (about three
weeks now) and I'm really starting to feel GREAT! I have suffered
from severe migraines for the past 25 years, the last 15 becoming
increasingly severe, coinciding with the addition of soy and
the "low-fat mentality" to my diet. Nothing helped! I should be
experiencing my pre-menstrual migraine by now and instead I feel
like I could climb Mt. Everest! Also I wondered if it decreased the
waist to hip ratio because mine has gone from 7.2 all my life to 7
(or something like that).  I think I had the sluggish thyroid too,
with a low body temperature of between 96 and 96.8. Now it's
starting to climb for the first time in years.
Thank you... Sincerely, V. Potter (Coconut Diet Forums)

For more information on how Virgin Coconut Oil works to promote
weight loss, see our article on Weight Loss.

Coconut Oil and Oxidative Stress
One of the reasons the long chain fatty acids in vegetable oils are
so damaging to the thyroid is that they oxidize quickly and become
rancid.  Food manufacturers know about this propensity towards
rancidity and, therefore, highly refine their vegetable oils.
Considerable research has shown that trans fatty acids, present when
vegetable oils are highly refined (hydrogenated or partially
hydrogenated), are especially damaging to cell tissue and can have a
negative affect on the thyroid as well as health in general. 
Because the longer chain fatty acids are deposited in cells more
often as rancid and oxidizing fat, impairment of the conversion of
thyroid hormone T4 to T3 occurs, which is symptomatic of
hypothyroidism. To create the enzymes needed to convert fats to
energy, T4 must be converted to T3.

Dr. Ray Peat says:

When the oils are stored in our tissues, they are much warmer, and
more directly exposed to oxygen than they would be in the seeds, and
so their tendency to oxidize is very great. These oxidative
processes can damage enzymes and other parts of cells, and
especially their ability to produce energy. The enzymes which break
down proteins are inhibited by unsaturated fats; these enzymes are
needed not only for digestion, but also for production of thyroid
hormones, clot removal, immunity, and the general adaptability of
cells. The risks of abnormal blood clotting, inflammation, immune
deficiency, shock, aging, obesity, and cancer are increased. Thyroid
[hormones] and progesterone are decreased.



Since the unsaturated oils block protein digestion in the stomach,
we can be malnourished even while "eating well." There are many
changes in hormones caused by unsaturated fats. Their best
understood effect is their interference with the function of the
thyroid gland. Unsaturated oils block thyroid hormone secretion, its
movement in the circulatory system, and the response of tissues to
the hormone. Coconut oil is unique in its ability to prevent weight-
gain or cure obesity, by stimulating metabolism. It is quickly
metabolized, and functions in some ways as an antioxidant.9

Because coconut oil is saturated and very stable (unrefined coconut
oil has a shelf life of about three to five years at room
temperature), the body is not burdened with oxidative stress as it
is with the vegetable oils. Coconut oil does not require the enzyme
stress that vegetable oils do, preventing T4 to T3 hormone
conversion, not only because it is a stable oil, but also because it
is processed differently in the body and does not need to be broken
down by enzyme dependent processes as do long chain fatty acids.
Also, since the liver is the main place where damage occurs from
oxidized and rancid oils that cause cell membrane damage, and since
the liver is where much of the conversion of T4 to T3 takes place,
eliminating long chain fatty acids from the diet and replacing them
with medium chain fatty acids found in coconut oil can, in time,
help in rebuilding cell membranes and increasing enzyme production
that will assist in promoting the conversion of T4 to T3 hormones.

More research in this area is necessary. In the meantime, those
switching from polyunsaturated oils to coconut oil are reporting
many positive results.  For example, Donna has experienced
encouraging improvements in her thyroid health.  She writes:

I've been on coconut oil since September, 2002 and, although, that
doesn't seem like long, it has changed my life and the lives of my
family and friends. My weight actually went UP when I started on
coconut oil but I felt so GREAT!   Being hypothyroid, I was on
Synthroid and Cytomel and had been for years, but with inconsistent
results and feeling worse. Other changes besides the addition of
coconut oil were the complete removal of soy (and that is a major
challenge in itself!), all trans fatty acids, no refined sugar, and
organ cleanses seasonally. My thyroid meds were discontinued with my
doctor's knowledge as I was getting too energetic and having trouble
sleeping!  [Imagine], from being a "sleepaholic" couch potato that
was cold!  My weight stayed steady until the last three weeks and it
has now started the downward move. My goal was health and just
believed the weight would come off when I found the right diet and
exercise routine that my life was comfortable with. I've tried
removing the coconut oil but my energy drops and I don't feel as
good. Donna (Coconut Diet Forums)

Another coconut oil user writes:

I have experienced thyroid problems . . .  body temperature not
going above 97 degrees, cold hands and feet, can't lose weight,
fatigued, slow heart rate, can't sleep some nights, dry skin,
etc..... My doctor did the thyroid test and it came back normal.  I
am 46 and peri-menopausal. My Naturopath symptomatically diagnosed
me with hypothyroidism.  She explained the blood tests currently
used by allopathic medicine are not sensitive enough.  I started on
the coconut oil 5 weeks ago. In the first week I noticed my body
temperature had risen and my resting heart rate had gone from 49 to
88 beats per minute.  This has since settled to 66. My energy is now
really high and I am slowly losing the weight - 3 lbs. in the past 5
weeks. I also had been taking flaxseed oil and gamma linoleic acid
oil but have stopped eating every other oil but what Dr. Raymond
Peat recommends, which is coconut oil, olive oil and butter… I take
3 tablespoons of coconut oil daily.  Cindy (Coconut Diet Forums)

Increasing Metabolism and Losing Weight

Many people with hypothyroidism also struggle with weight gain that
is difficult to lose even on strict diets, due to a sluggish
thyroid. Coconut oil is nature's richest source of medium chain
fatty acids which are known to increase metabolism and help lose
weight. For more information on weight loss and coconut oil, go here.
 
Saturated fat prevents coronary artery disease? An American
paradox1,2
Robert H Knopp and Barbara M Retzlaff
1 From the Northwest Lipid Research Clinic, University of Washington
School of Medicine, Seattle

2 Address reprint requests to RH Knopp, Northwest Lipid Research
Clinic, University of Washington, School of Medicine, 325 9th
Avenue, Seattle, WA 98104. E-mail: rhknopp@u.washington.edu.

See corresponding article on page 1175.


It is an article of faith that saturated fat raises LDL cholesterol
and accelerates coronary artery disease, whereas unsaturated fatty
acids have the opposite effect (1, 2). One of the earliest and most
convincing studies of the better efficacy of unsaturated than of
saturated fat in reducing cholesterol and heart disease is the
Finnish Mental Hospital Study conducted in the 12 y between 1959 and
1971. In this study, the usual high-saturated-fat institutional diet
was compared with an equally high-fat diet in which the saturated
fat in dairy products was replaced with soybean oil and soft
margarine and polyunsaturated fats were used in cooking. Each diet
was provided for 6 y and then the alternate diet was provided for
the next 6 y (3). After a comparison of the effects of the 2 diets
in both men and women, the incidence of coronary artery disease was
lower by 50% and 65% after the consumption of polyunsaturated fat in
the 2 hospitals.

In this issue of the Journal, Mozaffarian et al (4) report the
opposite association. They found that a higher saturated fat intake
is associated with less progression of coronary artery disease
according to quantitative angiography. How can this paradox be
explained? In food-frequency questionnaires, saturated fat intake is
more precisely estimated than is total fat. If saturated fat is more
precisely estimated, it will associate more strongly in statistical
analyses with the outcome variable, even though other variables—such
as total fat or carbohydrate—could be more relevant physiologically.
We believe that these possibilities deserve a closer look.

Unlike the diet used in the Finnish Mental Hospital Study, the diet
described by Mozaffarian et al was low in fat, averaging 25% of
energy. The study subjects were women with coronary artery disease:
most were hypertensive, many had diabetes (19–31%), their body mass
index (kg/m2) ranged from 29 to 30, and their lipid profile
indicated combined hyperlipidemia (triacylglycerol concentration:
200 mg/dL; HDL-cholesterol concentration: 40–50 mg/dL; above-average
LDL concentration: 135–141 mg/dL); these characteristics are
consistent with the metabolic syndrome. In addition, two-thirds of
these women were taking sex hormones. The importance of each of
these points is addressed below.

What are the effects of a low-fat, high-carbohydrate diet in
comparison with those of a higher-fat, lower-carbohydrate diet? The
response differs by the 2 main types of hyperlipidemia: simple
hypercholesterolemia and combined hyperlipidemia. In our studies of
simple hypercholesterolemia in men, a fat intake <25% of energy and
a carbohydrate intake >60% of energy was associated with a sustained
increase in triacylglycerol of 40%, a decrease in HDL cholesterol of
3.5%, and no further decrease in LDL in comparison with higher fat
intakes (5). In contrast, a low-fat diet in persons with combined
hyperlipidemia caused no worsening of triacylglycerol or HDL, but
intakes of fat >40% of energy and of carbohydrate <45% of energy for
2 y were associated with a lower triacylglycerol concentration at a
stable weight (6). In the subjects of Mozaffarian et al, a greater
saturated fat intake paralleled a total fat intake, which ranged
from 18% to 32% of energy in the first to fourth quartiles. Modest
favorable trends in triacylglycerol and HDL-cholesterol
concentrations were observed with higher fat intakes.

Triacylglycerol and HDL-cholesterol concentrations are stronger
predictors of coronary artery disease in women, whereas the LDL-
cholesterol concentration is a stronger predictor in men (7).
Because VLDL triacylglycerol secretion and removal rates in healthy
women are double those of men (8), conditions impairing lipoprotein
removal would be expected to exaggerate the hyperlipidemic response
in women as compared with that in men (9). This sex difference is
seen with the development of diabetes. The increment in lipids is
greater in women than in men and is associated with a greater
increment in coronary artery disease risk in women than in men (9).
Similarly, the development of insulin resistance and obesity is
associated with a greater lipoprotein increment in women than in men
(10). The exaggerated decreases in HDL- and HDL2-cholesterol
concentrations observed with the consumption of a low-fat Step II
diet in women but not in men appear to be another facet of this
effect (11).

The failure of female sex hormones to prevent coronary artery
disease has been a great disappointment (9). This effect might also
be due to an estrogen-induced increase in lipoprotein entry against
a fixed or impaired rate of lipoprotein removal, as might be
expected in women with the metabolic syndrome and coronary artery
disease.

Would saturated fat still be bad for anyone? Not necessarily. The
effect of saturated fat and cholesterol ingestion in the form of 4
eggs/d for 1 mo in obese, insulin-resistant subjects is 33% of that
seen in lean, insulin-sensitive subjects, likely because of
diminished cholesterol absorption (12). Thus, the classic effects of
saturated fat as compared with those of unsaturated fat seen in the
Finnish Mental Hospital Study are likely blunted in the subjects of
Mozaffarian et al, whereas the effects of low fat and high
carbohydrate intakes on triacylglycerol and HDL-cholesterol
concentrations appear to be exaggerated by the interactions of
female sex, exogenous sex hormones, and the metabolic syndrome. A
major effect on cardiovascular disease risk would be the result of
hypertriglyceridemia and low HDL-cholesterol concentrations, which
are attenuated by an increase in saturated fat intake itself or in
total fat intake, for which saturated fat is a more statistically
stable surrogate (4).

In conclusion, the hypothesis-generating report of Mozaffarian et al
draws attention to the different effects of diet on lipoprotein
physiology and cardiovascular disease risk. These effects include
the paradox that a high-fat, high–saturated fat diet is associated
with diminished coronary artery disease progression in women with
the metabolic syndrome, a condition that is epidemic in the United
States. This paradox presents a challenge to differentiate the
effects of dietary fat on lipoproteins and cardiovascular disease
risk in men and women, in the different lipid disorders, and in the
metabolic syndrome.

REFERENCES


Kinsell LW, Michaels GD, Cochrane GC, Partridge JW, Jahn JP, Balch
HE. Effect of vegetable fat on hypercholesterolemia and
hyperphospholipidemia: observations on diabetic and nondiabetic
subjects given diets high in vegetable fat and protein. Diabetes
1954;3:113-9.[Medline]
Grundy SM, Denke MA. Dietary influences on serum lipids and
lipoproteins. J Lipid Res 1990;31:1149-72.[Abstract]
Miettinen M, Turpeinen O, Karvonen MJ, Elosuo R, Paavilainen E.
Effect of cholesterol-lowering diet on mortality from coronary heart-
disease and other causes. A twelve-year clinical trial in men and
women. Lancet 1972;2:835-8.[Medline]
Mozaffarian D, Rimm EB, Herrington DM. Dietary fats, carbohydrate,
and progression of coronary atherosclerosis in postmenopausal women.
Am J Clin Nutr 2004;80:1175-84.[Abstract/Free Full Text]
Knopp RH, Walden CE, Retzlaff BM, et al. Long-term cholesterol-
lowering effects of 4 fat-restricted diets in hypercholesterolemic
and combined hyperlipidemic men. The Dietary Alternatives Study.
JAMA 1997;278:1509-15.[Abstract]
Retzlaff BM, Walden CE, Dowdy AA, McCann BS, Anderson KV, Knopp RH.
Changes in plasma triacylglycerol concentrations among free-living
hyperlipidemic men adopting different carbohydrate intakes over 2 y:
the Dietary Alternatives Study. Am J Clin Nutr 1995;62:988-95.
[Abstract]
Knopp RH, Zhu X, Bonet B. Effects of estrogens on lipoprotein
metabolism and cardiovascular disease in women. Atherosclerosis
1994;110(suppl):S83-91.[Medline]
Mittendorfer B, Patterson BW, Klein S. Effect of sex and obesity on
basal VLDL-triacylglycerol kinetics. Am J Clin Nutr 2003;77:573-9.
[Abstract/Free Full Text]
Barrett-Connor E, Giardina EG, Gitt AK, Gudat U, Steinberg HO,
Tschoepe D. Women and heart disease: the role of diabetes and
hyperglycemia. Arch Intern Med 2004;164:934-42.[Abstract/Free Full
Text]
Aikawa K, Retzlaff B, Fish B, et al. Dyslipidemia of insulin
resistance and obesity: gender differences. Circulation 2002;106
(suppl 2):II-75 (abstr 377).
Walden CE, Retzlaff BM, Buck BL, Wallick S, McCann BS, Knopp RH.
Differential effect of the National Cholesterol Education Program
(NCEP) Step II diet on HDL cholesterol, its subfractions, and
apoprotein A-I levels in hypercholesterolemic women and men after 1
year: the beFIT Study. Arterioscler Thromb Vasc Biol 2000;20:1580-7.
[Abstract/Free Full Text]
Knopp RH, Retzlaff B, Fish B, et al. Effects of insulin resistance
and obesity on lipoproteins and sensitivity to egg feeding.
Arterioscler Thromb Vasc Biol 2003;23:1437-43.[Abstract/Free Full
Text]


Related articles in AJCN:


Dietary fats, carbohydrate, and progression of coronary
atherosclerosis in postmenopausal women
Dariush Mozaffarian, Eric B Rimm, and David M Herrington
AJCN 2004 80: 1175-1184. [Abstract] [Full Text]  

Another sources:
http://www.biblelife.org/bowel.htm




*As matérias foram mantidas propositalmente no original.
Alessandro Luiz Freire
Coodenador Geral Equipe Harmônica Medicinas Integradas

1. Issacs, C.E. et al. Inactivation of enveloped viruses in human bodily fluids by purified lipids. Annals of the New York Academy of Sciences 1994;724:457-464.



2. Kabara, J.J. Antimicrobial agents derived from fatty acids. Journal of the American Oil Chemists Society 1984;61:397-403.

3. Hierholzer, J.C. and Kabara J.J. In vitro effects on Monolaurin compounds on enveloped RNA and DNA viruses. Journal of Food Safety 1982;4:1-12.

4. Wang, L.L. And Johnson, E.A. Inhibition of Listeria monocytogenes by fatty acids and monoglycerides. Appli Environ Microbiol 1992; 58:624-629.

5. Issacs, CE et al. Membrane-disruptive effect of human milk: inactivation of enveloped viruses. Journal of Infectious Diseases 1986;154:966-971.

6. Anti-viral effects of monolaruin. JAQA 1987;2:4-6 7. Issacs CE et al. Antiviral and antibacterial lipids in human milk and infant formula feeds. Archives of Disease in Childhood 1990;65:861-864.

TEXTO EXTRA DE: http://www.westonaprice.org


A New Look at Coconut Oil
(Um novo olhar sobre o óleo de coco)
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
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.

Eraly MG. IV. Coconut oil and heart attack. Coconut and Coconut Oil
in Human Nutrition, Proceedings. Symposium on Coconut and Coconut
Oil in Human Nutrition. 27 March 1994. Coconut Development Board,
Kochi, India, 1995, pp 63-64.

Enig MG. Diet, serum cholesterol and coronary heart disease, in Mann
GV (ed): Coronary Heart Disease: The Dietary Sense and Nonsense.
Janus Publishing, London, 1993, pp 36-60.

Felton CV, Crook D, Davies MJ, Oliver MF. Dietary polyunsaturated
fatty acids and composition of human aortic plaques. Lancet,
344:1195-1196;1994.

Fletcher RD, Albers AC, Albertson JN, Kabara JJ. Effects of
monoglycerides on mycoplasma pneumoniae growth, in The
Pharmacological Effect of Lipids II (JJ Kabara, ed) American Oil
Chemists' Society, Champaign IL, 1985, pp.59-63.

Florentino RF, Aquinaldo AR. Diet and cardiovascular disease in the
Philippines. The Philippine Journal of Coconut Studies 12:56-
70;1987.

Halden VW, Lieb H. Influence of biologically improved coconut oil
products on the blood cholesterol levels of human volunteers. Nutr
Dieta 3:75-88;1961.

Hashim SA, Clancy RE, Hegsted DM, Stare FJ. Effect of mixed fat
formula feeding on serum cholesterol level in man. American Journal
of Clinical Nutrition. 7:30-34;1959.

Hegsted DM, McGandy RB, Myer ML, Stare FJ. Quantitative effects of
dietary fat on serum cholesterol in man. American Journal of
Clinical Nutrition. 17:281-295;1965.

Hierholzer, J.C. and Kabara, J.J. In vitro effects of monolaurin
compounds on enveloped RNA and DNA viruses. Journal of Food Safety
4:1-12;1982.

Hostmark AT, Spydevold O, Eilertsen E. Plasma lipid concentration
and liver output of lipoproteins in rats fed coconut fat or
sunflower oil. Artery 7:367-383, 1980.

Isaacs CE, Thormar H. Membrane-disruptive effect of human milk:
inactivation of enveloped viruses. Journal of Infectious Diseases
154:966-971;1986.

Isaacs CE, Thormar H. Human milk lipids inactivated enveloped
viruses. in Breastfeeding, Nutrition, Infection and Infant Growth in
Developed and Emerging Countries (Atkinson SA, Hanson LA, Chandra
RK, eds) Arts Biomedical Publishers and Distributors, St. John's NF,
Canada, 1990.

Isaacs CE, Thormar H. The role of milk-derived antimicrobial lipids
as antiviral and antibacterial agents in Immunology of Milk and the
Neonate (Mestecky J, et al, eds) Plenum Press, New York, 1991.

Isaacs CE, Schneidman K. Enveloped Viruses in Human and Bovine Milk
are Inactivated by Added Fatty Acids(FAs) and Monoglycerides(MGs).
FASEB Journal. Abstract 5325, p.A1288, 1991.

Isaacs CE, Kashyap S, Heird WC, Thormar H. Antiviral and
antibacterial lipids in human milk and infant formula feeds.
Archives of Disease in Childhood 65:861-864;1990.

Isaacs CE, Litov RE, Marie P, Thormar H. Addition of lipases to
infant formulas produces antiviral and antibacterial activity.
Journal of Nutritional Biochemistry 3:304-308;1992.

Kabara JJ. Fatty acids and derivatives as antimicrobial agents -- A
review, in The Pharmacological Effect of Lipids (JJ Kabara, ed)
American Oil Chemists' Society, Champaign IL, 1978,

Kabara JJ. Inhibition of staphylococcus aureaus in The
Pharmacological Effect of Lipids II (JJ Kabara, ed) American Oil
Chemists' Society, Champaign IL, 1985, pp.71-75.

Kaunitz H, Dayrit CS. Coconut oil consumption and coronary heart
disease. Philippine Journal of Internal Medicine 30:165-171;1992.

Keys A, Anderson JT, Grande F. Prediction of serum-cholesterol
responses of man to changes in the diet. Lancet, 959;1957.

Kurup PA, Rajmohan T. II. Consumption of coconut oil and coconut
kernel and the incidence of atherosclerosis. Coconut and Coconut Oil
in Human Nutrition, Proceedings. Symposium on Coconut and Coconut
Oil in Human Nutrition. 27 March 1994. Coconut Development Board,
Kochi, India, 1995, pp 35-59.

Lim-Sylianco CY. Anticarcinogenic effect of coconut oil. The
Philippine Journal of Coconut Studies 12:89-102;1987.

Macallan DC, Noble C, Baldwin C, Foskett M, McManus T, Griffin GE.
Prospective analysis of patterns of weight change in stage IV hulman
immunodeficiency virus infection. American Journal of Clinical
Nutrition 58:417-24;1993.

Mann GV. A short history of the diet/heart hypothesis, in Mann GV
(ed): Coronary Heart Disease: The Dietary Sense and Nonsense. Janus
Publishing, London, 1993, pp 1-17.

Mendis S, Wissler RW, Bridenstine RT, Podbielski FJ. The effects of
replacing coconut oil with corn oil on human serum lipid profiles
and platelet derived factors active in atherogenesis. Nutrition
Reports International 40:No.4;Oct.1989.

New York Times, Medical Science, Tuesday, January 29, 1991. Common
virus seen as having early role in arteries' clogging (byline Sandra
Blakeslee).

Ng TKW, Hassan K, Lim JB, Lye MS, Ishak R. Nonhypercholesterolemic
effects of a palm-oil diet in Malaysian volunteers. American Journal
of Clinical Nutrition, 53:1015S-1020S;1991.

Prior IA, Davidson F, Salmond CE, Czochanska Z. Cholesterol,
coconuts, and diet on Polynesian atolls: a natural experiment: the
Pukapuka and Tokelau Island studies. American Journal of Clinical
Nutrition 34:1552-1561;1981.

Projan SJ, Brown-Skrobot S, Schlievert PM, Vandenesch F, Novick RP.
Glycerol monolaurate inhibits the production of beta-lactamase,
toxic shock toxin-1, and other staphylococcal exoproteins by
interefering with signal transduction. Journal of Bacteriology.
176:4204-4209;1994.

Ravnskov U. Quotation bias in reviews of the diet-heart idea.
Journal of Clinical Epidemiology 48:713-719;1995.

Reddy BS, Maeura Y. Tumor promotion of dietary fat in azoxymethane-
induced colon carcinogenesis in female F 344 rats. Journal of the
National Cancer Institute 72:745- 750;1984.

Sands JA, Auperin DD, Landin PD, Reinhardt A, Cadden SP. Antiviral
effects of fatty acids and derivatives: lipid-containing
bacteriophages as a model system in The Pharmacological Effect of
Lipids (JJ Kabara, ed) American Oil Chemists' Society, Champaign IL,
1978, pp 75-95.

Smith RL. The Cholesterol Conspiracy. Warren H Green Inc. St. Louis,
Missouri, 1991.

Sundram K, Hayes KC, Siru OH. Dietary palmitic acid results in lower
serum cholesterol than does a lauric-myristic acid combination in
normolipemic humans. American Journal of Clinical Nutrition 59:841-
846;1994.

Tholstrup T, Marckmann P, Jespersen J, Sandstrom B. Fat high in
stearic acid favorably affects blood lipids and factor VII coagulant
activity in comparison with fats high in palmitic acid or high in
myristic and lauric acids. American Journal of Clinical Nutrition
59:371-377;1994.

Thormar H, Isaacs EC, Brown HR, Barshatzky MR, Pessolano T.
Inactivation of enveloped viruses and killing of cells by fatty
acids and monoglycerides. Antimicrobial agents and chemotherapy
1987;31:27-31.

Willett W. Editorial: Challenges for public health nutrition in the
1990s. American Journal of Public Health. 80:1295-1298;1990.

The Health Benefits of Coconuts & Coconut Oil

by Mary G. Enig, PhD, FACN
Director, Nutritional Sciences Division, Enig Associates, Inc.
Coconuts and coconut oil contain health-promoting saturated fatty acids and derivative compounds which have powerful antimicrobial properties.
The following is the text of a talk and paper, "Coconuts: In Support of Good Health in the 21st Century", presented by Dr Mary Enig at the Asian Pacific Coconut Community (APCC) meeting held in Pohnpei in the Federated States of Micronesia in 1999.

Abstract

Coconuts play a unique role in the diets of mankind because they are the source of important physiologically functional components. These physiologically functional components are found in the fat part of whole coconut, in the fat part of desiccated coconut and in the extracted coconut oil.
Lauric acid, the major fatty acid from the fat of the coconut, has long been recognised for the unique properties that it lends to nonfood uses in the soaps and cosmetics industry. More recently, lauric acid has been recognised for its unique properties in food use, which are related to its antiviral, antibacterial and antiprotozoal functions. Now, capric acid, another of coconut's fatty acids, has been added to the list of coconut's antimicrobial components. These fatty acids are found in the largest amounts only in traditional lauric fats, especially from coconut. Also, recently published research has shown that natural coconut fat in the diet leads to a normalisation of body lipids, protects against alcohol damage to the liver and improves the immune system's anti-inflammatory response.
Clearly, there has been increasing recognition of the health-supporting functions of the fatty acids found in coconut. Recent reports from the US Food and Drug Administration about required labelling of the trans fatty acids will put coconut oil in a more competitive position and may help its return to use by the baking and snack-food industry, where it has continued to be recognised for its functionality. Now it can be recognised for another kind of functionality: the improvement of the health of mankind.

I. INTRODUCTION: BENEFITS OF COCONUT OIL SATURATES

Mr Chairman and members of the Asian Pacific Coconut Community: I would like to thank you for inviting me once again to speak to this gathering of delegates on the occasion of your 36th session as you celebrate the 30th anniversary of APCC.
When I addressed the 32nd Cocotech meeting in Cochin, India, I covered two areas of interest to the coconut community. In the first part, I reviewed the major health challenge facing coconut oil at that time, which was based on a supposed negative role played by saturated fat in heart disease. I hope that my talk was able to dispel any acceptance of that notion. In the second part of my talk, I suggested that there were some new, positive health benefits from coconut which should be recognised. These benefits stemmed from coconut's use as a food with major functional properties for antimicrobial and anti-cancer effects.
In my presentation today, I will bring you up to date about the new recognition of "functional foods" as important components in the diet. Additionally, I would like to review briefly the state of the anti - saturated fat situation and bring you up to date on some of the research that compares the beneficial effects of saturated fats with those of omega-6 polyunsaturates, as well as the beneficial effects of the saturated fats relative to the detrimental effects of the partially hydrogenated fats and the trans fatty acids. In particular, I will review some of the surprising beneficial effects of the special saturates found in coconut oil as they compare with those of the unsaturates found in some of the other food oils. Components of coconut oil are increasingly being shown to be beneficial. Increasingly, lauric acid and even capric acid have been the subject of favourable scientific reports on health parameters.

II. FUNCTIONAL PROPERTIES OF LAURIC FATS AS ANTIMICROBIALS

Earlier this year, at a special conference entitled "Functional Foods For Health Promotion: Physiologic Considerations" (Experimental Biology '99, Renaissance Washington Hotel, Washington, DC, April 17, 1999), which was sponsored by the International Life Sciences Institute (ILSI) North America, Technical Committee on Food Components for Health Promotion, it was defined that "a functional food provides a health benefit over and beyond the basic nutrients".
This is exactly what coconut and its edible products such as desiccated coconut and coconut oil do. As a functional food, coconut has fatty acids that provide both energy (nutrients) and raw material for antimicrobial fatty acids and monoglycerides (functional components) when it is eaten. Desiccated coconut is about 69% coconut fat, as is creamed coconut. Full coconut milk is approximately 24% fat.
Approximately 50% of the fatty acids in coconut fat are lauric acid. Lauric acid is a medium-chain fatty acid which has the additional beneficial function of being formed into monolaurin in the human or animal body. Monolaurin is the antiviral, antibacterial and antiprotozoal monoglyceride used by the human (and animal) to destroy lipid-coated viruses such as HIV, herpes, cytomegalovirus, influenza, various pathogenic bacteria including Listeria monocytogenes and Helicobacter pylori, and protozoa such as Giardia lamblia. Some studies have also shown some antimicrobial effects of the free lauric acid.
Also, approximately 6 - 7% of the fatty acids in coconut fat are capric acid. Capric acid is another medium-chain fatty acid which has a similar beneficial function when it is formed into monocaprin in the human or animal body. Monocaprin has also been shown to have antiviral effects against HIV and is being tested for antiviral effects against herpes simplex and for antibacterial effects against Chlamydia and other sexually transmitted bacteria (Reuters, London, June 29, 1999).
The food industry has, of course, long been aware that the functional properties of the lauric oils, and especially coconut oil, are unsurpassed by other available commercial oils. Unfortunately in the United States, during the late 1930s and again during the 1980s and 1990s, the commercial interests of the domestic fats and oils industry were successful in driving down usage of coconut oil. As a result, in the US and in other countries where the influence from the US is strong, the manufacturer has lost the benefit of the lauric oils in its food products.
As we will see from the data I will present in this talk, it is the consumer who has lost the many health benefits that can result from regular consumption of coconut products.
The antiviral, antibacterial and antiprotozoal properties of lauric acid and monolaurin have been recognised by a small number of researchers for nearly four decades. This knowledge has resulted in more than 20 research papers and several US patents, and last year it resulted in a comprehensive book chapter which reviewed the important aspects of lauric oils as antimicrobial agents (Enig, 1998). In the past, the larger group of clinicians and food and nutrition scientists has been unaware of the potential benefits of consuming foods containing coconut and coconut oil, but this is now starting to change.
Kabara (1978) and others have reported that certain fatty acids (FAs) (e.g., medium-chain saturates) and their derivatives (e.g., monoglycerides, MGs) can have adverse effects on various micro-organisms. Those micro-organisms that are inactivated include bacteria, yeast, fungi and enveloped viruses. Additionally, it is reported that the antimicrobial effects of the FAs and MGs are additive, and total concentration is critical for inactivating 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 caprylic acid (C-8), capric acid (C-10) or myristic acid (C-14).
In general, it is reported that the fatty acids and monoglycerides produce their killing/inactivating effect by lysing the plasma membrane lipid bilayer. The antiviral action attributed to monolaurin is that of solubilising the lipids and phospholipids in the envelope of the virus, causing the disintegration of the virus envelope. However, there is evidence from recent studies that one antimicrobial effect in bacteria is related to monolaurin's interference with signal transduction (Projan et al., 1994), and another antimicrobial effect in viruses is due to lauric acid's interference with virus assembly and viral maturation (Hornung et al., 1994).
Recognition of the antiviral aspects of the antimicrobial activity of the monoglyceride of lauric acid (monolaurin) has been reported since 1966. Some of the early work by Hierholzer and Kabara (1982), which showed virucidal effects of monolaurin on enveloped RNA and DNA viruses, was done in conjunction with the Centers for Disease Control of the US Public Health Service. These studies were done with selected virus prototypes or recognised representative strains of enveloped human viruses. The envelope of these viruses is a lipid membrane, and the presence of a lipid membrane on viruses makes them especially vulnerable to lauric acid and its derivative, monolaurin.
The medium-chain saturated fatty acids and their derivatives act by disrupting the lipid membranes of the viruses (Isaacs and Thormar, 1991; Isaacs et al., 1992). Research has shown that enveloped viruses are inactivated in both human and bovine milk by added fatty acids and monoglycerides (Isaacs et al., 1991) and also by endogenous fatty acids and monoglycerides of the appropriate length (Isaacs et al., 1986, 1990, 1991, 1992; Thormar et al., 1987).
Some of the viruses inactivated by these lipids, in addition to HIV, are the measles virus, herpes simplex virus-1 (HSV-1), vesicular stomatitis virus (VSV), visna virus and cytomegalovirus (CMV). Many of the pathogenic organisms reported to be inactivated by these antimicrobial lipids are those known to be responsible for opportunistic infections in HIV-positive individuals. For example, concurrent infection with cytomegalovirus is recognised as a serious complication for HIV-positive individuals (Macallan et al., 1993).
Thus, it would appear to be important to investigate the practical aspects and the potential benefits of an adjunct nutritional support regimen for HIV-infected individuals, which will utilise those dietary fats that are sources of known antiviral, antimicrobial and antiprotozoal monoglycerides and fatty acids such as monolaurin and its precursor, lauric acid.
Until now, no one in the mainstream nutrition community seems to have recognised the added potential of antimicrobial lipids in the treatment of HIV-infected or AIDS patients. These antimicrobial fatty acids and their derivatives are essentially nontoxic to man; they are produced in vivo by humans when they ingest those commonly available foods that contain adequate levels of medium-chain fatty acids such as lauric acid. According to the published research, lauric acid is one of the best "inactivating" fatty acids, and its monoglyceride is even more effective than the fatty acid alone (Kabara, 1978; Sands et al., 1978; Fletcher et al., 1985; Kabara, 1985).
The lipid-coated (enveloped) viruses are dependent on host lipids for their lipid constituents. The variability of fatty acids in the foods of individuals, as well as the variability from de novo synthesis, accounts for the variability of fatty acids in the virus envelope and also explains the variability of glycoprotein expression - a variability that makes vaccine development more difficult.
Monolaurin does not appear to have an adverse effect on desirable gut bacteria but, rather, only on potentially pathogenic micro-organisms. For example, Isaacs et al. (1991) reported no inactivation of the common Escherichia coli or Salmonella enteritidis by monolaurin, but major inactivation of Hemophilus influenzae, Staphylococcus epidermidis and group B gram-positive Streptococcus.
The potentially pathogenic bacteria inactivated by monolaurin include Listeria monocytogenes, Staphylococcus aureus, Streptococcus agalactiae, groups A, F and G streptococci, gram-positive organisms, and some gram-negative organisms if pretreated with a chelator (Boddie and Nickerson, 1992; Kabara, 1978, 1984; Isaacs et al., 1990, 1992, 1994; Isaacs and Schneidman, 1991; Isaacs and Thormar, 1986, 1990, 1991; Thormar et al., 1987; Wang and Johnson, 1992).
Decreased growth of Staphylococcus aureus and decreased production of toxic shock syndrome toxin-1 was shown with 150 mg monolaurin per litre (Holland et al., 1994). Monolaurin was shown to be 5,000 times more inhibitory against Listeria monocytogenes than is ethanol (Oh and Marshall, 1993). Helicobacter pylori was rapidly inactivated by medium-chain monoglycerides and lauric acid, and there appeared to be very little development of resistance of the organism to the bactericidal effects of these natural antimicrobials (Petschow et al., 1996).
A number of fungi, yeast and protozoa have been found to be inactivated or killed by lauric acid or monolaurin. The fungi include several species of ringworm (Isaacs et al., 1991). The yeast reported is Candida albicans (Isaacs et al., 1991). The protozoan parasite Giardia lamblia is killed by free fatty acids and monoglycerides from hydrolysed human milk (Hernell et al., 1986; Reiner et al., 1986; Crouch et al., 1991; Isaacs et al., 1991). Numerous other protozoa were studied with similar findings, but these have not yet been published (Jon J. Kabara, private communication, 1997).
Research continues in measuring the effects of the monoglyceride derivative of capric acid, monocaprin, as well as the effects of lauric acid. Chlamydia trachomatis is inactivated by lauric acid, capric acid and monocaprin (Bergsson et al., 1998). Hydrogels containing monocaprin are potent in vitro inactivators of sexually transmitted viruses such as HSV-2 and HIV-1 and bacteria such as Neisseria gonorrhoeae (Thormar, 1999).

III. ORIGINS OF THE ANTI - SATURATED FAT, ANTI - TROPICAL OILS AGENDA

The coconut industry has suffered more than three decades of abusive rhetoric from the consumer activist group Centers for Science in the Public Interest (CSPI), from the American Soybean Association (ASA) and other members of the edible oil industry, and from those in the medical and scientific community who learned their misinformation from groups like CSPI and ASA. I would like to review briefly the origins of the anti - saturated fat, anti - tropical oil campaigns and hopefully give you some useful insight into the issues.
When and how did the anti - saturated fat story begin? It really began in part in the late 1950s, when a researcher in Minnesota announced that the heart disease epidemic was being caused by hydrogenated vegetable fats. The edible oil industry's response at that time was to claim it was only the saturated fat in the hydrogenated oils that was causing the problem. The industry then announced that it would be changing to partially hydrogenated fats and that this would solve the problem.
In actual fact, there was no change because the oils were already being partially hydrogenated and the levels of saturated fatty acids remained similar, as did the levels of the trans fatty acids. The only thing that really changed was the term for "hydrogenation" or "hardening" listed on the food label.
During this same period, a researcher in Philadelphia reported that consuming polyunsaturated fatty acids lowered serum cholesterol. This researcher neglected, however, to include the information that the lowering was due to the cholesterol going into the tissues such as the liver and the arteries. As a result of this research report and the acceptance of this new agenda by the domestic edible oils industry, there was a gradual increase in the emphasis on replacing "saturated fats" in the diet and on consuming larger amounts of the "polyunsaturated fats".
As many of you probably know, this strong emphasis on consuming polyunsaturates has backfired in many ways. The current adjustments, being recommended in the US by groups such as the National Academy of Sciences, replace the saturates with mono-unsaturates instead of with polyunsaturates and replace polyunsaturates with mono-unsaturates.
Early promoters of the anti - saturated fat ideas included companies such as Corn Products Company (CPC International), through a book written by Jeremiah Stamler in 1963, with the professional edition published in 1966 by CPC. This book took some of the earliest pejorative stabs at the tropical oils. In 1963, the only tropical fat or oil singled out as high in saturated fats was coconut oil. Palm oil had not entered the US food supply to any extent, had not become a commercial threat to the domestic oils and was not recognised in any of the early texts.
The editorial staff of Consumer Reports noted that "...in 1962...one writer observed, the average American now fears fat [saturated fat, that is] 'as he once feared witches"'.
In 1965, a representative of Procter & Gamble Pharmaceuticals told the American Heart Association to change its diet/heart statement to remove any reference to the trans fatty acids. This altered official document encouraged the consumption of partially hydrogenated fats. In the 1970s, this same Procter & Gamble employee served as nutrition chairman in two controlling positions for the National Heart, Lung, and Blood Institute's Lipid Research Clinic (LRC) trials and as director of one of the LRC centres. These LRC trials were the basis for the 1984 NIH Cholesterol Consensus Conference, which in turn spawned the National Cholesterol Education Program (NCEP). This program encourages consumption of margarine and partially hydrogenated fats, while admitting that trans should not be consumed in excess. The official NCEP document states that "coconut oil, palm oil, and palm kernel oil...should be avoided".
In 1966, the US Department of Agriculture documents on fats and oils talked about how unstable the unsaturated fats and oils were. There was no criticism of the saturated fats. That criticism of saturated fats was to come later to this agency when it came under the influence of the domestic edible fats and oils industry and when it developed the US Dietary Guidelines. These Dietary Guidelines became very anti - saturated fat and remain so to this day. Nevertheless, as we will learn later in my talk, there started some reversal of the anti - saturated fat stance in the works of this agency in 1998.
In the early 1970s, although a number of researchers were voicing concerns about the trans fats, the edible oil industry and the US Food and Drug Administration (FDA) were engaging in a revolving-door exchange that would promote the increasing consumption of partially hydrogenated vegetable oils, condemn the saturated fats and hide the trans issue. As an example of this "oily" exchange, in 1971 the FDA's general counsel became president of the edible oil trade association, the Institute of Shortening and Edible Oils (ISEO), and he in turn was replaced at the FDA by a food lawyer who had represented the edible oil industry.
From that point on, the truth about any real effects of the dietary fats had to play catch-up. The American edible oil industry sponsored "information" to educate the public, and the natural dairy and animal fats industries were inept at countering any of that misinformation. Not being domestically grown in the US, coconut oil, palm oil and palm kernel oil were not around to defend themselves at that time. The government agencies responsible for disseminating information ignored those protesting "lone voices", and by the mid-1980s American food manufacturers and consumers had made major changes in their fats and oils usage - away from the safe, saturated fats and headlong into the problematic trans fats.
Enig and Fallon (1998 - 99) have reviewed the above history in "The Oiling of America", published in Nexus Magazine [see 6/01 - 2].

IV. THE DAMAGING ROLE OF THE US CONSUMER ACTIVIST GROUP CSPI

Some of the food oil industry members - especially those connected with the American Soybean Association and some of the consumer activists (particularly the Centers for Science in the Public Interest and also the American Heart Savers Association) further eroded the status of natural fats when they sponsored the major anti - saturated fat, anti - tropical oils campaign in the late 1980s.
Actually, an active anti - saturated fat bias started as far back as 1972 at the CSPI. But beginning in 1984, this very vocal consumer activist group started its anti - saturated fat campaign in earnest. In particular at this time, the campaign was against the "saturated" frying fats, especially those being used by fast-food restaurants. Most of these so-called saturated frying fats were tallow-based, but also included was palm oil in at least one of the hotel/restaurant chains.
Then, in a critical "News Release" in August 1986 - "Deceptive Vegetable Oil Labeling: Saturated Fat Without The Facts" - CSPI referred to "palm, coconut and palm kernel oil" as "rich in artery-clogging saturated fat". CSPI further announced that it had petitioned the Food and Drug Administration to stop allowing labelling of foods as having "100% vegetable shortening" if they contained any of the "tropical oils". CSPI also asked for the mandatory addition of the qualifier, "a saturated fat", when coconut, palm or palm kernel oil was named on the food label.
In 1988, CSPI published a booklet called "Saturated Fat Attack". This booklet contains lists of processed foods "surveyed" in Washington, DC, supermarkets. The lists were used for developing information about the saturated fat in the products. Section III is entitled "Those Troublesome Tropical Oils" and it contains statements encouraging pejorative labelling. There were lots of substantive mistakes in the booklet, including errors in the description of the biochemistry of fats and oils and completely erroneous statements about the fat and oil composition of many of the products.
At the same time that CSPI was conducting its campaign in 1986, the American Soybean Association began its anti - tropical oils campaign by sending inflammatory letters, etc., to soybean farmers. The ASA took out advertisements to promote a "[tropical] Fat Fighter Kit". The ASA hired a Washington, DC, "nutritionist" to survey supermarkets to detect the presence of tropical oils in foods.
Then, early in 1987, the ASA petitioned the FDA to require labelling of "tropical fats". In mid-1987 the Soybean Digest was continuing an active and increasing anti - tropical oils campaign.
At about the same time, the New York Times (June 3, 1987) published an editorial, "The Truth About Vegetable Oil", in which it called palm, palm kernel and coconut oils "the cheaper, artery-clogging oils from Malaysia and Indonesia" and claimed that US federal dietary guidelines opposed tropical oils, although it is not clear that this was so. The "artery-clogging" terminology was right out of CSPI.
Two years later, in 1989, the ASA held a press conference with the help of the CSPI in Washington, DC, in an attempt to counter a press conference held on March 6 by the palm oil group. The ASA "Media Alert" stated that the National Heart, Lung, and Blood Institute and National Research Council "recommend consumers avoid palm, palm kernel and coconut oils".
Only months before these press conferences, millionaire Phil Sokolof, the head of the National Heart Savers Association (NHSA), purchased the first of a series of anti - saturated fats and anti - tropical fats advertisements in major newspapers. No one has found an overt connection between Sokolof (and his NHSA) and the ASA, but the CSPI bragged about being his adviser.

V. USE OF COCONUT OIL IN THE PREVENTION AND TREATMENT OF HEART DISEASE

The research over four decades concerning coconut oil in the diet and heart disease is quite clear: coconut oil has been shown to be beneficial in combatting/reducing the risk factors in heart disease. This research leads us to ask the question, "Should coconut oil be used both to prevent and treat coronary heart disease?" This is based on several reviews of the scientific literature concerning the feeding of coconut oil to humans.
Blackburn et al. (1988) reviewed the published literature of "coconut oil's effect on serum cholesterol and atherogenesis" and concluded that when "fed physiologically with other fats or adequately supplemented with linoleic acid, coconut oil is a neutral fat in terms of atherogenicity".
After reviewing this same literature, Kurup and Rajmohan (1995) conducted a study on 64 volunteers and found "no statistically significant alteration in the serum total cholesterol, HDL cholesterol, LDL cholesterol, HDL cholesterol/total cholesterol ratio and LDL cholesterol/HDL cholesterol ratio of triglycerides from the baseline values". A beneficial effect of adding the coconut kernel to the diet was noted by these researchers.
Kaunitz and Dayrit (1992) reviewed some of the epidemiological and experimental data regarding coconut-eating groups and noted that the "available population studies show that dietary coconut oil does not lead to high serum cholesterol nor to high coronary heart disease mortality or morbidity".
They noted that, in 1989, Mendis et al. reported undesirable lipid changes when young adult Sri Lankan males were changed from their normal diets by the substitution of corn oil for their customary coconut oil. Although the total serum cholesterol decreased 18.7% from 179.6 to 146.0 mg/dL and the LDL cholesterol decreased 23.8% from 131.6 to 100.3 mg/dL, the HDL cholesterol decreased 41.4% from 43.4 to 25.4 mg/dL (putting the HDL values very much below the acceptable lower limit of 35 mg/dL) and the LDL/HDL ratio increased 30% from 3.0 to 3.9. These latter two changes are considered quite undesirable.
Mendis and Kumarasunderam (1990) also compared the effect of coconut oil and soy oil in normolipidemic young males, and again the coconut oil resulted in an increase in the HDL cholesterol, whereas the soy oil reduced this desirable lipoprotein.
As noted above, Kurup and Rajmohan (1995), who studied the addition of coconut oil alone to previously mixed fat diets, had reported no significant difference from baseline.
Previously, Prior et al. (1981) had shown that islanders with high intakes of coconut oil showed "no evidence of the high saturated fat intake having a harmful effect in these populations". When these groups migrated to New Zealand, however, and lowered their intake of coconut oil, their total cholesterol and LDL cholesterol increased and their HDL cholesterol decreased. Statements that any saturated fat is a dietary problem is not supported by evidence (Enig, 1993).
Studies that allegedly showed a "hypercholesterolemic" effect of coconut oil feeding usually only showed that coconut oil was not as effective at lowering the serum cholesterol as was the more unsaturated fat to which coconut oil was being compared. This appears to be in part because coconut oil does not "drive" cholesterol into the tissues as do the more polyunsaturated fats. The chemical analysis of the atheroma showed that the fatty acids from the cholesterol esters are 74% unsaturated (41% of the total fatty acids is polyunsaturated) and only 24% are saturated. None of the saturated fatty acids was reported to be lauric acid or myristic acid (Felton et al., 1994).
There is another aspect to the coronary heart disease picture. This is related to the initiation of the atheromas that are reported to be blocking arteries. Recent research shows that there is a causative role for the herpes virus and cytomegalovirus in the initial formation of atherosclerotic plaques and the reclogging of arteries after angioplasty (New York Times, January 29, 1991). What is so interesting is that the herpes virus and cytomegalovirus are both inhibited by the antimicrobial lipid monolaurin, but monolaurin is not formed in the body unless there is a source of lauric acid in the diet.
Thus, ironically enough, one could consider the recommendations to avoid coconut and other lauric oils as contributing to the increased incidence of coronary heart disease.
Chlamydia pneumoniae, a gram-negative bacterium, is another of the micro-organisms suspected of playing a role in atherosclerosis by provoking an inflammatory process that would result in the oxidation of lipoproteins with induction of cytokines and production of proteolystic enzymes - a typical phenomenon in atherosclerosis (Saikku, 1997). Some of the pathogenic gram-negative bacteria with an appropriate chelator have been reported to be inactivated or killed by lauric acid and monolaurin as well as capric acid and monocaprin (Bergsson et al., 1997; Thormar et al., 1999).
However, the micro-organisms which are most frequently identified as probable causative infecting agents are in the herpes virus family and include cytomegalovirus, type 2 herpes simplex (HSV-2) and Coxsackie B4 virus.
The evidence for a causative role for cytomegalovirus is the strongest (Ellis, 1997; Visseren et al., 1997; Zhou et al., 1996; Melnick et al., 1996; Epstein et al., 1996; Chen and Yang, 1995), but a role for HSV-2 is also shown (Raza-Ahmad et al., 1995).
All members of the herpes virus family are reported to be killed by the fatty acids and monoglycerides from saturated fatty acids ranging from C-6 to C-14 (Isaacs et al., 1991), which include approximately 80% of the fatty acids in coconut oil.
In spite of what has been said over the past four or more decades about the culpability of the saturated fatty acids in heart disease, they are ultimately going to be held blameless. More and more research is showing the problem to be related to oxidised products. The naturally saturated fats such as coconut oil are one protection we have against oxidised products.

VI. THE LATEST ON THE TRANS FATTY ACIDS

Both the United States and Canada will soon require labelling of the trans fatty acids, which will put coconut oil in a more competitive position than it has been in the past decade. (In 2001, Canada published examples of the labels it plans to use, while the US is still to finalise its labels.)
A fear of the vegetable oil manufacturers has always been that they would have to label trans fatty acids. The producers of trans fatty acids have relied on the anti-saturated fat crusade to protect their markets. However, the latest research on saturated fatty acids and trans fatty acids shows the saturated fatty acids coming out ahead in the health race.
It has taken a decade, from 1988 to 1998, to see changes in perception. During this period, the trans fatty acids have taken a deserved drubbing. Research reports from Europe have been emerging since the seminal report by Mensink and Katan in 1990 that the trans fatty acids raised the low-density lipoprotein (LDL) cholesterol and lowered the high-density lipoprotein (HDL) cholesterol in serum. This has been confirmed by studies in the US (Judd et al., 1994; Khosla and Hayes, 1996; Clevidence, 1997).
In 1990, the Lipids Research Group at the University of Maryland published a paper (Enig et al., 1990) correcting some of the erroneous data sponsored by the food industry in the 1985 review of the trans fatty acids by the Life Sciences Research Office of the Federation of American Societies for Experimental Biology (LSRO-FASEB) (Senti, 1985).
In 1993, a group of researchers at Harvard University, led by Professor Walter Willett, reported a positive relationship between the dietary intake of the trans fatty acids and coronary heart disease in a greater than 80,000 cohort of nurses who had been followed by the School of Public Health at Harvard University for more than a decade.
Pietinen and colleagues (1997) evaluated the findings from the large cohort of Finnish men who were followed in a cancer prevention study. After controlling for the appropriate variables including several coronary risk factors, the authors observed a significant positive association between the intake of trans fatty acids and the risk of death from coronary disease. There was no association between the intake of saturated fatty acids or dietary cholesterol and the risk of coronary death. This is another example of the differences between the effects of the trans fatty acids and the saturated fatty acids, and a further challenge to the dietary cholesterol hypothesis.
The issue of the trans fatty acids as a causative factor in cancer remains underexplored, but recent reports have found a connection. Bakker and colleagues (1997) studied the data for the association between breast cancer incidence and linoleic acid status across European countries, since animal and ecological studies had suggested a relationship. They found that the mean fatty acid composition of adipose did not show an association with omega-6 linoleic acid and breast, colon or prostate cancer. However, cancers of the breast and colon were positively associated with the trans fatty acids. Kohlmeier and colleagues (1997) also reported that data from the EURAMIC study showed adipose tissue concentration of trans fatty acids having a positive association with postmenopausal breast cancer in European women.
In 1995, a British documentary on the trans fatty acids was aired on a major television station in the UK. This documentary included an exposé of the battle between the edible oil industry and some of the major researchers of the trans fatty acids. Just this year [1999], this same documentary was aired on television in France, where it had been requested by a major television station. Several of the early researchers into the trans problems, including Professor Fred Kummerow and Dr George Mann, have continued their research and/or writing (Kummerow, 1999, 2000; Mann, 1994, 2000). The popular media have continued to press the issue of the amounts of trans in foods, for which there are still no comprehensive government databases.
A recently published paper from a US Department of Agriculture researcher states: "Because trans fatty acids have no known health benefits and strong presumptive evidence suggests that they contribute markedly to the risk of developing CHD, the results published to date suggest that it would be prudent to lower the intake of trans fatty acids in the US diet" (Nelson, 1998).
Professor Meir Stampfer from Harvard University refers to trans fats as "one of the major nutritional issues of the nation", contending that "they have a large impact" and that "we should completely eliminate hydrogenated fats from the diet" (Gottesman, 1998).
Lowering the trans fatty acids in foods in the US can only be done by returning to the use of the natural, unhydrogenated and more saturated fats and oils.
Predictions can be made regarding the future of trans fatty acids. Our ability to predict has been pretty good; for example, when Enig Associates started producing the marketing newsletter Market Insights, written by Eric Enig, we predicted that trans fatty acids would eventually be swept out of the market. It appears that this prediction may be close to coming true.
Also in the early 1990s, Market Insights predicted that the Center for Science in the Public Interest (CSPI) would change its mind about the trans fatty acids, which it had spent years defending. CSPI did change its mind, and in fact went on the attack regarding the trans, but CSPI never admitted that it had originally been promoting trans or that the high levels of trans fatty acids found in the fried foods in fast food and other restaurants and in many other foods are directly due to CSPI lobbying. While its change was welcome, CSPI's revisionist version of its own history of support of partially hydrogenated oils and trans fatty acids would have fitted perfectly into George Orwell's Nineteen Eighty-Four.

VII. COMPARISON OF SATURATED FATS WITH THE TRANS FATS

The statement that trans fatty acids are like saturated fatty acids is not correct for biological systems. A listing of the biological effects of saturated fatty acids in the diet versus the biological effects of trans fatty acids in the diet is in actuality a listing of the good (saturated) versus the bad (trans).
When one compares the saturated fatty acids and the trans fatty acids, we see that:
1) saturated fatty acids raise HDL cholesterol, the so-called "good cholesterol", whereas the trans fatty acids lower HDL cholesterol (Mensink and Katan, 1990; Judd et al., 1994);
2) saturated fatty acids lower the blood levels of the atherogenic lipoprotein (a), whereas trans fatty acids raise the blood levels of lipoprotein (a) (Khosla and Hayes, 1996; Hornstra et al., 1991; Clevidence et al., 1997);
3) saturated fatty acids conserve the elongated omega-3 fatty acids (Gerster, 1998), whereas trans fatty acids cause the tissues to lose these omega-3 fatty acids (Sugano and Ikeda, 1996);
4) saturated fatty acids do not inhibit insulin binding, whereas trans fatty acids do inhibit insulin binding;
5) saturated fatty acids are the normal fatty acids made by the body and they do not interfere with enzyme functions such as the delta-6-desaturase, whereas trans fatty acids are not made by the body and they interfere with many enzyme functions such as delta-6-desaturase; and
6) some saturated fatty acids are used by the body to fight viruses, bacteria and protozoa and they support the immune system, whereas trans fatty acids interfere with the function of the immune system.

VIII. WHAT ABOUT THE UNSATURATED FATS?

The arteries of the heart are also compromised by the unsaturated fatty acids. When the fatty acid composition of the plaques (atheromas) in the arteries has been analysed, the level of saturated fatty acids in the cholesterol esters is only 26% compared to that in the unsaturated fatty acids, which is 74%. When the unsaturated fatty acids in the cholesterol esters in these plaques are analysed, it is shown that 38% are polyunsaturated and 36% are mono-unsaturated. Clearly, the problem is not with the saturated fatty acids.
As an aside, you need to understand that the major role of cholesterol in heart disease and cancer is as the body's repair substance and that cholesterol is a major support molecule for the immune system, an important antioxidant and a necessary component of neurotransmitter receptors. Our brains do not work very well without adequate cholesterol. It should be apparent to scientists that the current approach to cholesterol has been wrong.
The pathway to cholesterol synthesis starts with a molecule of acetyl CoA [coenzyme A] that comes from the metabolism of excess protein-forming ketogenic amino acids and from the metabolism of excess carbohydrates as well as from the oxidation of excess fatty acids. Grundy in 1978 reported that the degree of saturation of the fat in the diet did not affect the rate of synthesis of cholesterol. However, research reported by Jones in 1997 showed that the polyunsaturated fatty acids in the diet increase the rate of cholesterol synthesis relative to other fatty acids. Furthermore, research reported in 1993 (Hodgsons et al.) showed that dietary intake of the omega-6 polyunsaturated fatty acid, linoleic acid, was positively related to coronary artery disease.
Thus, those statements made by the consumer activists in the United States, to the effect that the saturated fatty acids increase cholesterol synthesis, are without any foundation.
What happens when there is an increase or a decrease of cholesterol in the serum is more like a shift from one compartment to another as the body tries to rectify the potential damage from the excess polyunsaturated fatty acids. Research by Dr Hans Kaunitz (1978) clearly showed the potential problems with excess polyunsaturated fatty acids.

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

One major concern expressed by the nutrition community is related to whether or not people are getting enough elongated omega-3 fatty acids in their diets. The elongated omega-3 fatty acids of concern are eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Some research has shown that the basic omega-3 fatty acid, linolenic acid, is not readily converted to the elongated forms in humans or animals, especially when there is ingestion of the trans fatty acids and the consequent inhibition of the delta-6-desaturase enzyme. One recent study (Gerster, 1998), which used radioisotope-labelled linolenic acid to measure this conversion in adult humans, showed that if the background fat in the diet was high in saturated fat, the conversion was approximately 6% for EPA and 3.8% for DHA; whereas, if the background fat in the diet was high in omega-6 polyunsaturated fatty acids (PUFA), the conversion was reduced 40-50%.
Nanji and colleagues (1995) reported that a diet enriched with saturated but not unsaturated fatty acids reversed the alcoholic liver injury in their animals which was caused by dietary linoleic acid. These researchers concluded that this effect may be explained by the down-regulation of lipid peroxidation. This is another example of the need for adequate saturated fat in the diet.
Cha and Sachan (1994) studied the effects of saturated fatty acid and unsaturated fatty acid diets on ethanol pharmacokinetics. The hepatic enzyme alcohol dehydrogenase and plasma carnitines were also evaluated. The researchers concluded that dietary saturated fatty acids protect the liver from alcohol injury by retarding ethanol metabolism, and that carnitine may be involved.
Hargrove and colleagues (1999) noted the work of Nanji et al. and postulated that they would find that diets rich in linoleic acid would also cause acute liver injury after acetaminophen injection. In the first experiment, two levels of fat (15g/100g protein and 20g/100g protein), using corn oil or beef tallow, were fed. Liver enzymes indicating damage were significantly elevated in all the animals except for those animals fed the higher level of beef tallow. These researchers concluded that "diets with high [linoleic acid] may promote acetaminophen-induced liver injury compared to diets with more saturated and mono-unsaturated fatty acids".

X. RESEARCH SHOWING GENERAL BENEFICIAL EFFECTS FROM CONSUMING COCONUT OIL

Research that compares the feeding of coconut oil with other oils to answer a variety of biological questions is increasingly finding beneficial results from the coconut oil.
Obesity is a major health problem in the United States and the subject of much research. Several lines of research dealing with metabolic effects of high-fat diets have been followed. One study used coconut oil to enrich a high-fat diet and the results reported were that the "coconut oil-enriched diet is effective in...[producing]...a decrease in white fat stores" (Portillo et al., 1998).
Cleary et al. (1999) fed genetically obese animals high-fat diets of either safflower oil or coconut oil. Animals fed safflower oil had higher hepatic lipogenic enzyme activities than did animals fed coconut oil. When the number of fat cells was measured, the safflower oil fed also had more fat cells than the coconut oil fed.
Many of the feeding studies produce results at variance with the popular conception. High-fat diets have been used to study the effects of different types of fatty acids on membrane phospholipid fatty acid profiles. When such a study was performed on mice, the phospholipid profiles were similar for diets high in linoleic acid from high-linoleate sunflower oil relative to diets high in saturated fatty acids from coconut oil. However, those animals fed diets high in oleic acid (from the high-oleate sunflower oil) or high in elongated omega-3 fatty acids (from menhaden fish oil) were not only different from the other two diets, but they also resulted in enlarged spleens in the animals (Huang and Frische, 1992).
Oliart-Ros and colleagues (1998) at the Instituto Tecnológico de Veracruz, Mexico, reported on effects of different dietary fats on sucrose-induced cardiovascular syndrome in rats. The most significant reduction in parameters of the syndrome was obtained by the n-3 PUFA-rich diet. These researchers reported that the diet thought to be PUFA-deficient presented a tissue lipid pattern similar to the n-3 PUFA-rich diet (fish oil), which surprised and puzzled them. When the researchers were questioned, it turned out that the diet was not really PUFA-deficient, but rather just a normal coconut oil (nonhydrogenated) which conserved the elongated omega-3 and normalised the omega-6 to omega-3 balance.
A recent study measured the effect of high-fat diets, fed for more than three months to neonatal pigs, on the HMG-CoA reductase enzyme's function and gave some surprises. There were two feeding protocols: one with the added cholesterol and one without added cholesterol, but both with coconut oil. The hepatic reductase activity, which was the same in all groups at the beginning of the feeding on the third day and similar on the 42nd day, was increased with and without added cholesterol on the 13th day and then decreased on the 25th day. The data were said to suggest that dietary cholesterol suppressed hepatic reductase activity in the young pigs regardless of their genetic background, that the stage of development was a dominant factor in its regulation, and that both dietary and endogenously synthesised cholesterol were used primarily for tissue building in very young pigs (McWhinney et al., 1996). The feeding of coconut oil did not in any way compromise the normal development of these animals.
When compared with feeding coconut oil, feeding two different soybean oils to young females caused a significant decrease in HDL cholesterol. Both soybean oils, one of which was extracted from a new mutant soybean thought to be more oxidatively stable, were not protective of the HDL levels (Lu et al., 1997).
Trautwein et al. (1997) studied cholesterol-fed hamsters on different oil supplements for plasma, hepatic and biliary lipids. The dietary oils included butter, palm stearin, coconut oil, rapeseed oil, olive oil and sunflowerseed oil. Plasma cholesterol concentrations were higher (9.2 millimoles/litre) for olive oil than for coconut oil (8.5 mmol/L), hepatic cholesterol was highest in the olive oil group, and none of the diet groups differed for biliary lipids. Even in this cholesterol-sensitive animal model, coconut oil performed better than olive oil.
Smit and colleagues (1994) had also studied the effect of feeding coconut oil compared with feeding corn oil and olive oil in rats, and measured the effect on biliary cholesterol. Bile flow was not different between the three diets, but the hepatic plasma membranes showed more cholesterol and less phospholipid from corn and olive oil feeding relative to coconut oil feeding.
Several studies (Kramer et al., 1998) have pointed out problems with canola oil feeding in newborn piglets, which results in a reduction in the number of platelets and alteration in their size. There is concern for similar effects in human infants. These undesirable effects can be reversed when coconut oil or other saturated fat is added to the feeding regimen (Kramer et al., 1998).
Research has shown that coconut oil is needed for good absorption of fat and calcium from infant formulas. The soy oil (47%) and palm olein (53%) formula gave 90.6% absorption of fat and 39% absorption of calcium, whereas the soy oil (60%) and coconut oil (40%) gave 95.2% absorption of fat and 48.4% absorption of calcium (Nelson et al., 1996). Both fat and calcium are needed by the infant for proper growth. These results clearly show the folly of removing or lowering the coconut oil content in infant formulas.

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

Coconut oil appears to help the immune system response in a beneficial manner. Feeding coconut oil in the diet completely abolished the expected immune factor responses to endotoxin that were seen with corn oil feeding. This inhibitory effect on interleukin-1 production was interpreted by the authors of the study as being largely due to a reduced prostaglandin and leukotriene production (Wan and Grimble, 1987). However, the damping may be due to the fact that effects from high omega-6 oils tend to be normalised by coconut oil feeding.
Another report from this group (Bibby and Grimble, 1990) compared the effects of corn oil and coconut oil diets on tumour necrosis factor-alpha and endotoxin induction of the inflammatory prostaglandin E2 (PGE2) production. The animals fed coconut oil did not produce an increase in PGE2, and the researchers again interpreted this as a modulatory effect that brought about a reduction of phospholipid arachidonic acid content.
Another study from the same research group (Tappia and Grimble, 1994) showed that omega-6 oil enhanced inflammatory stimuli, but that coconut oil, along with fish oil and olive oil, suppressed the production of interleukin-1.
Several recent studies are showing additional helpful effects of consuming coconut oil on a regular basis, thus supplying the body with the lauric acid derivative, monolaurin. Monolaurin and the ether analogue of monolaurin have been shown to have the potential for damping adverse reactions to toxic forms of glutamic acid (Dave et al., 1997). Lauric acid and capric acid have been reported to have very potent effects on insulin secretion (Garfinkel et al., 1992). Using a model system of murine splenocytes, Witcher et al. (1996) showed that monolaurin induced proliferation of T-cells and inhibited the toxic shock syndrome toxin-1 mitogenic effects on T-cells.
Monserrat and colleagues (1995) showed that a diet rich in coconut oil could protect animals against the renal necrosis and renal failure produced by a diet deficient in choline (a methyl donor group). The animals had less or no mortality and increased survival time as well as decreased incidence or severity of the renal lesions when 20% coconut oil was added to the deficient diet. A mixture of hydrogenated vegetable oil and corn oil did not show the same benefits.
The immune system is complex and has many feedback mechanisms to protect it, but the wrong fat and oils can compromise these important mechanisms. The data from the several studies show the helpful effects of coconut fat. Additionally, there are anecdotal reports that consumption of coconut is beneficial for individuals with the chronic fatigue and immune dysfunction syndrome known as CFIDS.

XII. US PATENTS FOR MEDICAL USES OF LAURIC OILS, MEDIUM-CHAIN FATTY ACIDS AND THEIR DERIVATIVES SUCH AS MONOLAURIN

A number of patents have been granted in the United States for medical uses of lauric oils, lauric acid and monolaurin. Although one earlier patent was granted to Professor Kabara more than three decades ago, the rest of these patents have been granted within the past decade.
In 1989 a patent was issued to the New England Deaconess Hospital (Bistrian et al., 1989) for the invention titled "Kernel Oils and Disease Treatment". This treatment requires lauric acid as the primary fatty acid source, with lauric oils constituting up to 80% of the fat in the diet "using naturally occurring kernel oils".
In 1991 and 1995, two patents were issued to the group of researchers whose work has been reviewed above.
The first invention (Isaacs et al., 1991) was directed to antiviral and antibacterial activity of both fatty acids and monoglycerides, primarily against enveloped viruses. The claims are for "a method of killing enveloped viruses in a host human...wherein the enveloped viruses are AIDS viruses...[or]...herpes viruses...[and the]...compounds selected from the group consisting of fatty acids having from 6 to 14 carbon atoms and monoglycerides of said fatty acids...[and]...wherein the fatty acids are saturated fatty acids".
The second patent (Isaacs et al., 1995) was a further extension of the earlier one. This patent also includes discussion of the inactivation of enveloped viruses, and it specifically cites monoglycerides of caproic, caprylic, capric, lauric and myristic acids. These fatty acids make up more than 80% of coconut oil. Also included in this patent is a listing of susceptible viruses and some bacteria and protozoa.
Although these latter patents may provide the owners of the patents with the ability to extract royalties from commercial manufacturers of monoglycerides and fatty acids, they cannot require royalties from the human gastrointestinal tract when it is the "factory" that is doing the manufacturing of the monoglycerides and fatty acids.
Clearly, though, these patents serve to illustrate to us that the health-giving properties of monolaurin and lauric acid are well recognised by some individuals in the research arena, and they lend credence to our appropriate choice of lauric oils for promoting health and as an adjunct treatment of viral diseases.

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

I would like to review for you my perception of the status regarding the coconut and coconut products markets in the United States and Canada at the end of the 20th century and the beginning of the 21st century.
Coconut products are trying to regain their former place in several small markets. The extraction of oil from fresh coconut has been reported in the past decade and my impression is that this is being considered as a desirable source of minimally processed oil with desirable characteristics for the natural foods market.
There have been some niche markets for coconut products developing during the past half-decade. These are represented primarily by the natural foods and health foods producers. Some examples are the new coconut butters produced in the US and Canada by Omega Nutrition and Carotec, Inc. And this is no longer as small a market as it has been in past years. Desiccated coconut products, coconut milk and even coconut oil are appearing on the shelves of many of these markets. After years of packaging coconut oil for skin use only, one of the large suppliers of oils to the natural foods and health foods stores has introduced coconut oil for food use, and it has appeared within the last few months on shelves in the Washington, DC, metropolitan area, along with other oils. I believe I indirectly had something to do with this turn of events.

XIV. CONCLUSIONS AND RECOMMENDATIONS

There is much to be gained from pursuing the functional properties of coconut for improving the health of humanity.
On the occasion of the 30th anniversary of the Asian Pacific Coconut Community, at this 36th meeting of APCC, I wanted to bring you a message that I hope will encourage you to continue your endeavours on behalf of all parts of the coconut industry. Coconut products for inedible and especially edible uses are of the greatest importance for the health of the entire world.
Some of what I have been telling you, most of you already know. But in saying these things for the record, it is my intention to tell those who did not know all the details until they heard or read this paper about the positive properties of coconut.
Coconut oil is a most important oil because it is a lauric oil. The lauric fats possess unique characteristics for both food industry uses and also for the uses of the soaps and cosmetics industries. Because of the unique properties of coconut oil, the fats and oils industry has spent untold millions to formulate replacements from those seed oils so widely grown in the world outside the tropics. While it has been impossible to truly duplicate coconut oil for some of its applications, many food manufacturers have been willing to settle for lesser quality in their products. Consumers have also been willing to settle for a lesser quality, in part because they have been fed so much misinformation about fats and oils.
Desiccated coconut, on the other hand, has been impossible to duplicate, and the markets for desiccated coconut have continued. The powdered form of desiccated coconut now being sold in Europe and Asia has yet to find a market in the United States, but I predict that it will become an indispensable product in the natural foods industry. Creamed coconut, which is desiccated coconut very finely ground, could be used as a nut butter.
APCC needs to promote the edible uses of coconut, and it needs to promote the re-education of the consumer, the clinician and the scientist. The researcher H. Thormar (Thormar et al., 1999) concluded his abstract with the statement that monocaprin "is a natural compound found in certain foodstuffs such as milk and is therefore unlikely to cause harmful side effects in the concentrations used". It is not monocaprin that is found in milk, but capric acid. It is likely safe at most any level found in food. However, the level in milk fat is at most 2%, whereas the level in coconut fat is 7%.
One last reference for the record. Sircar and Kansra (1998) have reviewed the increasing trend of atherosclerotic disease and type-2 diabetes mellitus in the Indians from both the subcontinent of India and abroad. They note that over the time when there has been an alarming increase in the prevalence of these diseases, there has been a replacement of traditional cooking fats with refined vegetable oils that are promoted as heart-friendly, but which are being found to be detrimental to health. These astute researchers suggest that it is time to return to the traditional cooking fats like ghee, coconut oil and mustard oil.
There are a number of areas of encouragement. The nutrition community in the United States is slowly starting to recognise the difference between medium-chain saturated fatty acids and other saturated fatty acids. We predict now that the qualities of coconut, both for health and food function, will ultimately win out.

About the Author:

Dr Mary G. Enig holds an MS and PhD in Nutritional Sciences from the University of Maryland in the USA. She is a consulting nutritionist and biochemist of international renown and an expert in fats/oils analysis and metabolism, food chemistry and composition and nutrition and dietetics.
Dr Enig is Director of the Nutritional Sciences Division of Enig Associates, Inc., President of the Maryland Nutritionists Association and a Fellow of the American College of Nutrition. She is also Vice President of the Weston A. Price Foundation and Science Editor of the Foundation's publication. Dr Enig has many years of experience as a lecturer and has taught graduate-level courses for the Nutritional Sciences Program at the University of Maryland, where she was a Faculty Research Associate in the Lipids Research Group, Department of Chemistry and Biochemistry, University of Maryland. She also maintains a limited clinical practice for patients needing nutritional assessment and consultation.
Dr Enig has extensive experience consulting and lecturing on nutrition to individuals, medical and allied health groups, the food processing industry and state and federal governments in the US. She also lectures and acts as a consultant to the international health and food processing communities. Since 1995 she has been invited to make presentations at scientific meetings in Europe, India, Japan, Vietnam, Indonesia, the Philippines and Micronesia.
Dr Enig is the author of numerous journal publications, mainly on fats and oils research and nutrient/drug interactions. She also wrote the book Know Your Fats (Bethesda Press, Silver Spring, MD, May 2000). She is a popular media spokesperson and was an early critic speaking out about the use of trans fatty acids and advocating their inclusion in nutritional labelling.
One of Dr Enig's recent research topics dealt with the development of a nutritional protocol for proposed clinical trials of a non-drug treatment for HIV/AIDS patients. Her articles, "The Oiling of America" and "Tragedy and Hype: The Third International Soy Symposium", written with nutritionist/ researcher Sally Fallon, were published in NEXUS 6/01 - 2 and 7/03 respectively.

References:

  • a.. Aveywardena MY and Charnock JS. Dietary lipid modification of myocardial eicosanoids following ischemia and reperfusion in the rat. Lipids 1995;30:1151-1156.
  • b.. Awad AB. Effect of dietary lipids on composition and glucose utilization by rat adipose tissue. Journal of Nutrition 1981;111:34-39.
  • c.. Bakker N, Van't Veer P, Zock PL. Adipose fatty acids and cancers of the breast, prostate and colon: an ecological study. EURAMIC Study Group. International Journal of Cancer 1997;72:587-591.
  • d.. Bergsson G, Arnfinnsson J, Karlsson SM, Steingrimsson O, Thormar H. In vitro inactivation of Chlamydia trachomatis by fatty acids and monoglycerides. Antimicrobial Agents and Chemotherapy 1998;42:2290-2294.
  • e.. Bibby DC, Grimble RF. Tumour necrosis factor-alpha and endotoxin induce less prostaglandin E2 production from hypothalami of rats fed coconut oil than from hypothalami of rats fed maize oil. Clinical Science (Colch) 1990;79:657-62.
  • f.. 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 1967;202:1119-1123.
  • g.. Blackburn GL, Kater G, Mascioli EA, Kowalchuk M, Babayan VK, Bistrian BR. A reevaluation of coconut oil's effect on serum cholesterol and atherogenesis. The Journal of the Philippine Medical Association 1989;65:144-152.
  • h.. Boddie, RL and Nickerson, SC. Evaluation of postmilking teat germicides containing Lauricidin, saturated fatty acids, and lactic acid. Journal of Dairy Science 1992;75:1725-1730.
  • i.. Castelli WP. Editorial: Concerning the possibility of a nut. Archives of Internal Medicine 1992;152:1371-2.
  • j.. Cha YS, Sachan DS. Opposite effects of dietary saturated and unsaturated fatty acids on ethanol-pharmacokinetics, triglycerides and carnitines. Journal of the American College of Nutrition 1994;13:338-343.
  • k.. Chen A, Li W, Yang Y. [Detection of human cytomegalovirus DNA in vascular plaques of atherosclerosis by in situ hybridization] (translation from Chinese). Chung Hua I Hsueh Tsa Chih 1995;10:592-593, 638.
  • l.. Cleary MP, Phillips FC, Morton RA. Genotype and diet effects in lean and obese Zucker rats fed either safflower or coconut oil diets. Proceedings of the Society for Experimental Biology and Medicine 1999;220:153-161.
  • m.. Clevidence BA, Judd JT, Schaefer EJ, Jenner JL, Lichtenstein AH, Muesing RA, Wittes J, Sunkin ME. Plasma lipoprotein (a) levels in men and women consuming diets enriched in saturated, cis-, or trans-mono-unsaturated fatty acids. Arterioscler Thromb Vasc Biol 1997;17:1657-1661.
  • n.. 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 1986;77:33.
  • o.. Cohen LA, Thompson DO, Choi K, Blank M, Rose DP. Dietary fat and mammary cancer. II. Modulation of serum and tumour lipid composition and tumour prostaglandins by different dietary fats: Association with tumour incidence patterns. Journal of the National Cancer Institute 1986;77:43.
  • p.. Crouch AA, Seow WK, Whitman LM, Thong YH. Effect of human milk and infant milk formulae on adherence of Giardia intestinalis. Transactions of the Royal Society of Tropical Medicine and Hygiene 1991;85:617-619.
  • q.. Dave JR, Koenig ML, Tortella FC, Pieringer RA, Doctor BP, Ved HS. Dodecylglycerol provides partial protection against glutamate toxicity in neuronal cultures derived from different regions of embryonic rat brain. Molecular Chemistry and Neuropathology 1997;30:1-13.
  • r.. Dodge JA and Sagher FA. Antiviral and antibacterial lipids in human milk and infant formula. Archives of Disease in Childhood 1991;66:272-273.
  • s.. Ellis RW. Infection and coronary heart disease. Journal of Medical Microbiology 1997;46:535-539.
  • t.. Enig MG. Diet, serum cholesterol and coronary heart disease, in Mann GV (ed): Coronary Heart Disease: The Dietary Sense and Nonsense. Janus Publishing, London, 1993, pp 36-60.
  • u.. Enig, MG. Lauric oils as antimicrobial agents: theory of effect, scientific rationale, and dietary applications as adjunct nutritional support for HIV-infected individuals. In Nutrients and Foods in AIDS (RR Watson, ed), CRC Press, Boca Raton, 1998, pp 81-97.
  • v.. Enig MG, Atal S, Sampugna J and Keeney M. Isomeric Trans Fatty Acids in the US Diet. Journal of the American College of Nutrition 1990;9:471-486.
  • w.. Epstein SE, Speir E, Zhou YF, Guetta E, Leon M, Finkel T. The role of infection in restenosis and atherosclerosis: focus on cytomegalovirus. Lancet 1996;348 Supplement 1:S13-17.
  • x.. Eraly MG. IV. Coconut oil and heart attack. Coconut and Coconut Oil in Human Nutrition, Proceedings. Symposium on Coconut and Coconut Oil in Human Nutrition, 27 March 1994. Coconut Development Board, Kochi, India, 1995, pp 63-64.
  • y.. Felton CV, Crook D, Davies MJ, Oliver MF. Dietary polyunsaturated fatty acids and composition of human aortic plaques. Lancet 1994;344:1195-1196.
  • z.. Fletcher RD, Albers AC, Albertson JN, Kabara JJ. Effects of monoglycerides on Mycoplasma pneumoniae growth. In The Pharmacological Effect of Lipids II (JJ Kabara, ed), American Oil Chemists' Society, Champaign, IL, 1985, pp 59-63.
  • aa.. Florentino RF, Aquinaldo AR. Diet and cardiovascular disease in the Philippines. The Philippine Journal of Coconut Studies 1987;12:56-70.
  • ab.. Garfinkel M, Lee S, Opara EC, Akkwari OE. Insulinotropic potency of lauric acid: a metabolic rational for medium chain fatty acids (MCF) in TPN formulation. Journal of Surgical Research 1992;52:328-333.
  • ac.. Gerster H. Can adults adequately convert alpha-linolenic acid (18:3n-3) to eicosapentaenoic acid (20:5n-3) and docosahexaenoic acid (22:6n-3)? International Journal of Vitamin and Nutrition Research 1998;68:159-173.
  • ad.. Gottesman S. Making Sense of Shortenings. Baking Buyer August 1998, pp 45-49.
  • ae.. Grundy SM. Cholesterol metabolism in man, Western Journal of Medicine 128:13;1978.
  • af.. Halden VW, Lieb H. Influence of biologically improved coconut oil products on the blood cholesterol levels of human volunteers. Nutr Dieta 1961;3:75-88.
  • ag.. Hargrove JL, Hwang J, Wickwire K, Liu J. Diets with corn oil or soybean oil increase acute acetaminophen hepatotoxicity compared to diets with beef tallow. The FASEB Journal 1999;13:A222, Abstract 204.1.
  • ah.. Hashim SA, Clancy RE, Hegsted DM, Stare FJ. Effect of mixed fat formula feeding on serum cholesterol level in man. American Journal of Clinical Nutrition 1959;7:30-34.
  • ai.. Hegsted DM, McGandy RB, Myer ML, Stare FJ. Quantitative effects of dietary fat on serum cholesterol in man. American Journal of Clinical Nutrition 1965;17:281-295.
  • aj.. Hernell O, Ward H, Blackberg L, Pereira ME. Killing of Giardia lamblia by human milk lipases: an effect mediated by lipolysis of milk lipids. Journal of Infectious Diseases 1986;153:715-720.
  • ak.. Hierholzer, J.C. and Kabara, J.J. In vitro effects of monolaurin compounds on enveloped RNA and DNA viruses. Journal of Food Safety 1982;4:1-12.
  • al.. Hodgson JM, Wahlqvist ML, Boxall JA, and Balazs ND. Can linoleic acid contribute to coronary artery disease? American Journal of Clinical Nutrition 1993;58:228-234.
  • am.. Holland KT, Taylor D, Farrell AM. The effect of glycerol monolaurate on growth of, and production of toxic shock syndrome toxin-1 and lipase by Staphylococcus aureus. Journal of Anti-microbial Chemotherapy 1994;33:41-55.
  • an.. Hornstra G, van Houwelingen AC, Kester AD, and Sundram K. A palm oil-enriched diet lowers serum lipoprotein(a) in normocholesterolemic volunteers. Atherosclerosis 1991;90:91-93.
  • ao.. Hornung B, Amtmann E, Sauer G. Lauric acid inhibits the maturation of vesicular stomatitis virus. Journal of General Virology 1994;75:353-361.
  • ap.. Hostmark AT, Spydevold O, Eilertsen E. Plasma lipid concentration and liver output of lipoproteins in rats fed coconut fat or sunflower oil. Artery 1980;7:367-383.
  • aq.. Huang SC, Frische KL. Alteration in mouse splenic phospholipid fatty acid composition and lymphoid cell populations by dietary fat. Lipids 1992;27:25-32.
  • ar.. Isaacs CE, Thormar H. Membrane-disruptive effect of human milk: inactivation of enveloped viruses. Journal of Infectious Diseases 1986;154:966-971.
  • as.. Isaacs CE, Thormar H. Human milk lipids inactivated enveloped viruses. in Breastfeeding, Nutrition, Infection and Infant Growth in Developed and Emerging Countries (Atkinson SA, Hanson LA, Chandra RK, eds) Arts Biomedical Publishers and Distributors, St John's, NF, Canada, 1990.
  • at.. Isaacs CE, Thormar H. The role of milk-derived antimicrobial lipids as antiviral and antibacterial agents. In Immunology of Milk and the Neonate (Mestecky J, et al., eds), Plenum Press, New York, 1991.
  • au.. Isaacs CE, Schneidman K. Enveloped Viruses in Human and Bovine Milk are Inactivated by Added Fatty Acids (FAs) and Monoglycerides (MGs). FASEB Journal 1991;5, Abstract 5325, p A1288.
  • av.. Isaacs CE, Kashyap S, Heird WC, Thormar H. Antiviral and antibacterial lipids in human milk and infant formula feeds. Archives of Disease in Childhood 1990;65:861-864.
  • aw.. Isaacs CE, Litov RE, Marie P, Thormar H. Addition of lipases to infant formulas produces antiviral and antibacterial activity. Journal of Nutritional Biochemistry 1992;3:304-308.
  • ax.. Isaacs CE, Kim KS, Thormar H. Inactivation of enveloped viruses in human bodily fluids by purified lipids. Annals of the New York Academy of Sciences 1994;724:457-464.
  • ay.. Jones PJH. Regulation of cholesterol biosynthesis by diet in humans. American Journal of Clinical Nutrition 1997;66:438-446.
  • az.. Judd JT, Clevidence BA, Muesing RA, Wittes J, Sunkin ME, and Podczasy JJ. Dietary Trans Fatty Acids: Effects on Plasma Lipids and Lipoproteins of Healthy Men and Women. American Journal of Clinical Nutrition 1994;59:861-868.
  • ba.. Kabara JJ. Fatty acids and derivatives as antimicrobial agents: A review. In The Pharmacological Effect of Lipids (JJ Kabara, ed), American Oil Chemists' Society, Champaign IL, 1978.
  • bb.. Kabara JJ. Inhibition of Staphylococcus aureus. In The Pharmacological Effect of Lipids II (JJ Kabara, ed), American Oil Chemists' Society, Champaign IL, 1985, pp.71-75.
  • bc.. Kaunitz H. Toxic effects of polyunsaturated vegetable oils. In Symposium on the Pharmacological Effect of Lipids (JJ Kabara, ed), American Oil Chemists' Society, Champaign, IL, 1978, pp 203-210.
  • bd.. Kaunitz H, Dayrit CS. Coconut oil consumption and coronary heart disease. Philippine Journal of Internal Medicine 1992;30:165-171.
  • be.. Keys A, Anderson JT, Grande F. Prediction of serum-cholesterol responses of man to changes in the diet. Lancet 959;1957.
  • bf.. Khosla P and Hayes KC. Dietary trans-mono-unsaturated fatty acids negatively impact plasma lipids in humans: critical review of the evidence. Journal of the American College of Nutrition 1996;15:325-339.
  • bg.. Kohlmeier L, Simonsen N, van't Veer P, Strain JJ, Martin-Moreno JM, Margolin B, Huttunen JK, Fernandez-Crehuet Navajas J, Martin BC, Thamm M, Kardinaal AF, Kok FJ. Adipose tissue trans fatty acids and breast cancer in the European Community Multicenter Study on Antioxidants, Myocardial Infarction, and Breast Cancer. Cancer Epidemiology and Biomarkers Prev 1997;6:705-10.
  • bh.. Kramer JK, Sauer FD, Farnworth ER, Stevenson D, Rock GA. Hematological and lipid changes in newborn piglets fed milk-replacer diets containing erucic acid. Lipids 1998;33:1-10.
  • bi.. Kurup PA, Rajmohan T. II. Consumption of coconut oil and coconut kernel and the incidence of atherosclerosis. Coconut and Coconut Oil in Human Nutrition, Proceedings. Symposium on Coconut and Coconut Oil in Human Nutrition, 27 March 1994. Coconut Development Board, Kochi, India, 1995, pp 35-59.
  • bj.. Lim-Sylianco CY. Anticarcinogenic effect of coconut oil. The Philippine Journal of Coconut Studies 1987;12:89-102.
  • bk.. Lu Z, Hendrich S, Shen N, White PJ, Cook LR. Low linolenate and commercial soybean oils diminish serum HDL cholesterol in young free-living adult females. Journal of the American College of Nutrition 1997;16:562-569.
  • bl.. Macallan DC, Noble C, Baldwin C, Foskett M, McManus T, Griffin GE. Prospective analysis of patterns of weight change in stage IV hulman immunodeficiency virus infection. American Journal of Clinical Nutrition 1993;58:417-24.
  • bm.. Mann GV. A short history of the diet/heart hypothesis. In Mann GV (ed), Coronary Heart Disease: The Dietary Sense and Nonsense. Janus Publishing, London, 1993, pp 1-17.
  • bn.. McWhinney VJ, Pond WG, Mersmann HJ. Ontogeny and dietary modulation of 3-hydroxy-3-methylglutaryl-CoA reductase activities in neonatal pigs. Journal of Animal Science 1996;74:2203-10.
  • bo.. Melnick JL, Adam E, DeBakey ME. Cytomegalovirus and atherosclerosis. Archivum Immunologiae et Therapiae Experimentalis (Wroclaw) 1996;44:297-302.
  • bp.. Mendis S, Kumarasunderam R. The effect of daily consumption of coconut fat and soyabean fat on plasma lipids and lipoproteins of young normolipidaemic men. British Journal of Nutrition 1990;63:547-52.
  • bq.. Mendis S, Wissler RW, Bridenstine RT, Podbielski FJ. The effects of replacing coconut oil with corn oil on human serum lipid profiles and platelet derived factors active in atherogenesis. Nutrition Reports International 40:4, Oct 1989.
  • br.. Mensink RP and Katan MB. Effect of Dietary Trans Fatty Acids on High-Density and Low-Density Lipoprotein Cholesterol Levels in Healthy Subjects. The New England Journal of Medicine 1990;323:439-445.
  • bs.. Monserrat AJ, Romero M, Lago N, Aristi C. Protective effect of coconut oil on renal necrosis occurring in rats fed a methyl-deficient diet. Renal Failure 1995;17:525-537.
  • bt.. Nanji AA, Sadrzadeh SM, Yang EK, Fogt F, Maydani M, Dannenberg AJ. Dietary saturated fatty acids: a novel treatment for alcoholic liver disease. Gastroenterology 1995;109:547-554.
  • bu.. Nelson GJ. Dietary fat, trans fatty acids, and risk of coronary heart disease. Nutrition Reviews 1998;56:250-252.
  • bv.. Nelson SE, Rogers RR, Frantz JA, Ziegler EE. Palm olein in infant formula: absorption of fat and minerals by normal infants. American Journal of Clinical Nutrition 1996;64:291-296.
  • bw.. New York Times, Medical Science, Tuesday, January 29, 1991. Common virus seen as having early role in arteries' clogging (byline Sandra Blakeslee).
  • bx.. Ng TKW, Hassan K, Lim JB, Lye MS, Ishak R. Nonhypercholesterolemic effects of a palm-oil diet in Malaysian volunteers. American Journal of Clinical Nutrition 1991;53:1015S-1020S.
  • by.. Oh DH and Marshall DL. Antimicrobial activity of ethanol, glycerol monolaurate or lactic acid against Listeria monocytogenes. International Journal of Food and Microbiology 1993;20:239-246.
  • bz.. Oliart-Ros RM, Torres-Marquez ME, Badillo A, Guerrero OA. Effects of dietary polyunsaturated fatty acids on sucrose-induced cardiovascular syndrome in rats. 89th AOCS Annual Meeting Abstracts, H&N 5: General Health and Nutrition II, p 76, Chicago, IL, May 10-13, 1998.
  • ca.. Petschow BW, Batema RP, Ford LL. Susceptibility of Helicobacter pylori to bactericidal properties of medium-chain monoglycerides and free fatty acids. Antimicrobial Agents and Chemotherapy 1996;40:302-306.
  • cb.. Pietinen P, Ascherio A, Korhonen P, Hartman AM, Willett WC, Albanes D, Virtamo J. Intake of fatty acids and risk of coronary heart disease in a cohort of Finnish men. The Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. American Journal of Epidemiology 1997;145:876-887.
  • cc.. Portillo MP, Serra F, Simon E, del Barrio AS, Palou A. Energy restriction with high-fat diet enriched with coconut oil gives higher UCP1 and lower white fat in rats. International Journal of Obesity and Related Metabolic Disorders 1998;22:974-9.
  • cd.. Prior IA, Davidson F, Salmond CE, Czochanska Z. Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapuka and Tokelau Island studies. American Journal of Clinical Nutrition 1981;34:1552-1561.
  • ce.. Projan SJ, Brown-Skrobot S, Schlievert PM, Vandenesch F, Novick RP. Glycerol monolaurate inhibits the production of beta-lactamase, toxic shock toxin-1, and other staphylococcal exoproteins by interfering with signal transduction. Journal of Bacteriology 1994;176:4204-4209.
  • cf.. Ravnskov U. Quotation bias in reviews of the diet-heart idea. Journal of Clinical Epidemiology 1995;48:713-719.
  • cg.. Raza-Ahmad A, Klassen GA, Murphy DA, Sullivan JA, Kinley CE, Landymore RW, Wood JR. Evidence of type-2 herpes simplex infection in human coronary arteries at the time of coronary artery bypass surgery. Canadian Journal of Cardiology 1995;11:1025-1029.
  • ch.. Reddy BS, Maeura Y. Tumour promotion of dietary fat in azoxymethane-induced colon carcinogenesis in female F 344 rats. Journal of the National Cancer Institute 1984;72:745-750.
  • ci.. Reiner DS, Wang CS, Gillin FD. Human milk kills Giardia lamblia by generating toxic lipolytic products. Journal of Infectious Diseases 1986;154:825-832.
  • cj.. Saikku P. Chlamydia pneumoniae and atherosclerosis - an update. Scandinavian Journal of Infectious Diseases Supplement 1997;104:53-56.
  • ck.. Sircar S, Kansra U. Choice of cooking oils - myths and realities. Journal of the Indian Medical Association 1998;96:304-307.
  • cl.. Sands JA, Auperin DD, Landin PD, Reinhardt A, Cadden SP. Antiviral effects of fatty acids and derivatives: lipid-containing bacteriophages as a model system. In The Pharmacological Effect of Lipids (JJ Kabara, ed), American Oil Chemists' Society, Champaign, IL, 1978, pp 75-95.
  • cm.. Smit MJ, Wolters H, Temmerman AM, Kuipers F, Beynen AC, Vonk RJ. Effects of dietary corn and olive oil versus coconut fat on biliary cholesterol secretion in rats. International Journal of Vitamin and Nutrition Research 1994;64:75-80.
  • cn.. Smith RL. The Cholesterol Conspiracy. Warren H Green Inc., St Louis, Missouri, 1991.
  • co.. Sugano M, Ikeda I. Metabolic interactions between essential and trans-fatty acids. Current Opinions in Lipidology 1996;7:38-42.
  • cp.. Sundram K, Hayes KC, Siru OH. Dietary palmitic acid results in lower serum cholesterol than does a lauric-myristic acid combination in normolipemic humans. American Journal of Clinical Nutrition 1994;59:841-846.
  • cq.. Tappia PS, Grimble RF. Complex modulation of cytokine induction by endotoxin and tumour necrosis factor from peritoneal macrophages of rats by diets containing fats of different saturated, mono-unsaturated and polyunsaturated fatty acid composition. Clinical Science (Colch) 1994;87:173-178.
  • cr.. Tholstrup T, Marckmann P, Jespersen J, Sandstrom B. Fat high in stearic acid favorably affects blood lipids and factor VII coagulant activity in comparison with fats high in palmitic acid or high in myristic and lauric acids. American Journal of Clinical Nutrition 1994;59:371-377.
  • cs.. Thormar H, Isaacs EC, Brown HR, Barshatzky MR, Pessolano T. Inactivation of enveloped viruses and killing of cells by fatty acids and monoglycerides. Antimicrobial Agents and Chemotherapy 1987;31:27-31.
  • ct.. Trautwein EA, Kunath-Rau A, Dietrich J, Drusch S, Erberdobler HF. Effect of dietary fats rich in lauric, myristic, palmitic, oleic or linoleic acid on plasma, hepatic and biliary lipids in cholesterol-fed hampsters. British Journal of Nutrition 1997;77:605-620.
  • cu.. Visseren FL, Bouter KP, Pon MJ, Hoekstra JB, Erkelens DV, Diepersloot RJ. Patients with diabetes mellitus and atherosclerosis; a role for cytomegaloviorus? Diabetes Research and Clinical Practice (Limerick) 1997;36:49-55.
  • cv.. Wan JM, Grimble RF. Effect of dietary linoleate content on the metabolic response of rats to Escherichia coli endotoxin. Clinical Science (Colch) 1987;72:383-385.
  • cw.. Wang LL and Johnson EA. Inhibition of Listeria monocytogenes by fatty acids and monoglycerides. Applied and Environmental Microbiology 1992; 58:624-629.
  • cx.. Willett W. Editorial: Challenges for public health nutrition in the 1990s. American Journal of Public Health 1990;80:1295-1298.
  • cy.. Witcher KJ, Novick RP, Schlievert PM. Modulation of immune cell proliferation by glycerol monolaurate. Clinical and Diagnostic Laboratory Immunology 1996;3:10-13.
  • cz.. Zhou YF, Buetta E, Yu ZX, Finkel T, Epstein SE. Human cytomegalovirus increases modified low-density lipoprotein uptake and scavenger receptor mRNA expression in vascular smooth muscle cells. Journal of Clinical Investigation 1996;98:2129-

Estudos mostram que o
óleo de côco é um PODEROSO IMUNOESTIMULANTE
Por Frank Cimatu


Cidade de Baguio
Inquirer News Service
PDI Northern Luzon Bureau


            A Fundação Filipina para Pesquisa e Desenvolvimento do Coco juntamente com o Hospital São Lázaro e os Laboratórios United, conduziram em 1999 os primeiros testes de HIV / AIDS efetuados nas Filipinas. Os testes envolveram 15 pacientes do Hospital São Lázaro portadores de HIV, nos primeiros estágios de desenvolvimento do vírus.

            Os testes basicamente procuravam determinar se a monolaurina, um derivado do ácido laurico seria responsável pelo aumento de células CD4 e a redução da carga viral nos pacientes num estágio ainda não detectável. As células CD4 são a primeira linha de defesa do corpo contra doenças e infecções, mas também são as primeiras a serem atacadas pelo HIV. A carga viral é a quantidade de vírus no sangue.                           

            O Dr. Conrado Dayrit, Presidente da Academia Nacional de Ciências e Tecnologia e membro do Conselho do PCRDF, num pronunciamento anterior, afirmou que o HIV, o vírus que causa a AIDS, está envolvido por uma membrana gordurosa que a monolaurina pode penetrar e mutilar rapidamente após ingerido. A monolaurina destrói a membrana que envolve o vírus por um processo de amaciamento. “Se isso acontece, o vírus morre” disse o Dr Dayrit.

            Romulo Conde, Supervisor Técnico do PCRDF, disse que os resultados foram promissores, mas a fim de satisfazer a comunidade cientifica, precisam de conclusões mais concretas. Não é bom tirar conclusões pela metade, acrescentou. Disse ainda que os testes continuarão no próximo ano.

            De acordo com a edição de Novembro da “Discover Magazine”, um grupo de cientistas canadenses desenvolveram o que eles chamaram de “camisinha invisível”, que nada mais é do que uma gelatina anti-microbiana atuando na prevenção do HIV.  A equipe liderada pelo Dr Michael Bergeron disse que o gel, incolor e inodoro, não é um preventivo para gravidez, mas pode bloquear o vírus da AIDS e de outras doenças sexualmente transmissíveis.

            “O preparado do Dr Bergeron, que ele chama de “camisinha invisível” consiste de dois componentes. O primeiro é um polímero gelatinoso, que é liquido na temperatura ambiente, mas torna-se um gel quando na temperatura do corpo.

            Quando introduzido, o liquido se dissemina por toda a parede vaginal, tornando-se em seguida uma gelatina e criando uma barreira semi-sólida contra agentes infecciosos”,  reportou a  Discover Magazine. O segundo ingrediente é um anti-germe como o lauril sulfato de sódio, uma substância saponácea que dissolve as membranas dos vírus, eliminando-os. O lauril sulfato de sódio é um elemento químico derivado do ácido laurico e do leite materno, conhecido como um eliminador de micróbios. A gelatina, quando testada em ratos, foi 90 a 100 por cento eficaz na eliminação do vírus da herpes genital.

            Em outro artigo publicado no “Indian Coconut Journal em Setembro de 1995, a Dra. Enig afirmou :


            Os testes basicamente procuravam determinar se a monolaurina, um derivado do ácido laurico seria responsável pelo aumento de células CD4 e a redução da carga viral nos pacientes num estágio ainda não detectável. As células CD4 são a primeira linha de defesa do corpo contra doenças e infecções, mas também são as primeiras a serem atacadas pelo HIV. A carga viral é a quantidade de vírus no sangue.                           

            O Dr. Conrado Dayrit, Presidente da Academia Nacional de Ciências e Tecnologia e membro do Conselho do PCRDF, num pronunciamento anterior, afirmou que o HIV, o vírus que causa a AIDS, está envolvido por uma membrana gordurosa que a monolaurina pode penetrar e mutilar rapidamente após ingerido. A monolaurina destrói a membrana que envolve o vírus por um processo de amaciamento. “Se isso acontece, o vírus morre” disse o Dr Dayrit.
            
 

"O reconhecimento da atividade anti-microbiana  da monolaurina tem sido registrada desde 1966. O trabalho embrionário pode ser creditado a Jon Kabara. Essa pesquisa anterior foi direcionada para os efeitos virucidais por causa dos possíveis problemas relacionados com a preservação de alimentos. Alguns dos antigos trabalhos de Hierholzer e Kabara (1982), que mostravam os efeitos virucidais da monolaurina sobre vírus envolvidos em RNA e DNA, foram elaborados em conjunto com o Centro de Controle de Doenças do Serviço Publico de Saúde Americano, com protótipos selecionados ou reconhecidos como envolvidos em membranas de lipídios de grande rigidez.“
 


            A Dra. Enig afirmou em seu artigo, que a monolaurina, cujo precursor é o ácido láurico, destrói a membrana de lipídios que envolve o vírus bem como torna inativas bactérias, leveduras e fungos.

            Ela escreveu: “Dos ácidos graxos saturados, o ácido láurico tem uma atividade antiviral maior do que os ácidos caprílico(C10) e mirístico (C14). A ação atribuída ao monolauril é a de que ele solubiliza os lipídios contidos no envoltório do vírus, causando a destruição desse envoltório.”  Na Índia, o óleo de côco é ministrado a bezerros no tratamento de Cryptosporidium conforme reportado por Lark Lands Ph.D no seu livro a ser lançado, “Positivamente Bem”.

            Apesar de não ter sido mencionado por Enig, o HHV-6A é um vírus que tem uma capa envolvente cuja expectativa é que se desintegre na presença de ácido láurico e/ou monolaurina

            Segundo Dra. Enig, HIV, sarampo, Vírus da Estomatite Vesicular (VSV), Herpes Simplex Virus (HSV-1), Visna, Cytomegalovirus (CMV), Influenza vírus, Pneumonovirus, Syncytial vírus e Rubéola, são algumas das doenças que tem suas atividades inibidas pela monolaurina. Algumas bactérias, que incluem Listeria, Staphylococus aureus, Streptococus agalactiae, Streptococci dos Grupos A, B, F e G, Organismos Gran-positivos e Gran-negativos tornaram-se inativas pelo ação da monolaurina.




            Em 19 de Julho de 1995 a Dra. Enig falava para um artigo publicado no jornal “THE HINDU”, O Jornal Nacional da Índia, quando afirmava que o óleo de côco é convertido pelo organismo em “monolaurina”, um ácido graxo com propriedades anti-virais, que pode ser útil no tratamento da AIDS. Um repórter do “THE HINDU” escreveu o seguinte a respeito da apresentação Dra. Enig durante uma conferência em Kochi:

“Houve um momento nos Estados Unidos em que uma criança comprovadamente diagnosticada positiva, tornou-se HIV Negativa. Essa criança havia sido alimentada com uma fórmula com alto teor de óleo de côco. A experiência foi significativa e os esforços estão voltados para se encontrar as causas da redução da carga viral da criança com HIV quando alimentada com uma dieta que ajuda na geração de monolaurina no organismo”.

            O repórter comenta também a observação feita pela Dra. Enig de que a monolaurina ajuda também na inibição de outros vírus como o sarampo, herpes, estomatite vesicular e citomegalovirus e que pelo avançado das pesquisas, há também uma indicação de que o óleo de côco oferece certas medidas de proteção contra substâncias cancerígenas.

            Estudos divulgados pelo Dr. Conrado S. Dayrit, MD em 25 de julho de 2000 em Chennai na Índia, no 37º Encontro Cocotécnico, mostraram um grande potencial terapêutico para os óleos láuricos (com alto teor de ácido láurico, como o babaçu, tucumã e côco da bahia). A experiência da administração de 50ml de óleo de côco diária em 15 pacientes (10 mulheres e 5 homens) portadores do HIV (o vírus da AIDS) e que nunca haviam recebido nenhum tipo de tratamento anti-HIV, no Hospital de São Lázaro, nas Filipinas, sob a responsabilidade do Dr. Eric Tayan, M.D, mostraram um aumento do linfócitos de defesa do corpo, CD4 e CD8 de 248 para 1.065 e 570 para 1671 respectivamente. Um homem que possuía uma carga viral muito baixa (<0.4X103) e que não sofreu mudanças, não foi incluído no resultado final da pesquisa. As estatísticas finais incluíram resultados para 4 homens e 10 mulheres e mostram que 7 (2h, 5m) de 14 pacientes tiveram uma redução em 3 meses de uso diário do óleo, enquanto 8 (3h, 5m) sofreram redução em 6 meses. Os níveis de CD4 e CD8 aumentaram em 5 pacientes, mas não mantiveram relação com a diminuição da contagem viral.

           A adição de óleos láuricos na alimentação de pacientes portadores do HIV pode trazer como benefício a diminuição do nível da carga viral em indivíduos HIV positivos, diminuição do antígeno P24 e o aumento do CD4 e/ou CD4/CD8. Com bases nas pesquisas acima, o uso de óleos láuricos na alimentação de pessoas com baixa imunológica, que possuem grande facilidade em gripar, pessoas com doenças bacterianas e viróticas como tuberculose, pneumonia, herpes, doenças venéreas, auto-imunes como o lúpus e a psoríase, câncer, Crohn entre outras, seria de extrema valia. Da mesma maneira, o emprego destes óleos na massagem se mostra eficaz para o tratamento dos mesmos problemas, dada sua penetração pela pele ser muito fácil. Óleos láuricos são os óleos mais finos e de melhor penetração pelos poros, sendo também os melhores veículos carreadores para óleos essenciais. Na alimentação podem ser utilizados para cozinhar e fritar alimentos, substituindo os óleos de soja, girassol e milho. O refino não interfere nas suas propriedades terapêuticas, apesar de ser melhor o óleo in natura, porém a hidrogenação da parte insaturada do óleo pode levar à formação de gordura trans capaz de causar câncer, aumento do colesterol, entre outros desequilíbrios. O uso local destes óleos ainda pode ser uma fonte interessante para tratamento de escaras, feridas infeccionadas e inflamações.


A DOSE TERAPÊUTICA

                Baseada nos seus cálculos, e na quantidade de acido láurico encontrado no leite materno humano, a Dra. Enig sugere para adultos, uma dieta rica de 24 gramas de ácido láurico  diariamente. Essa quantidade corresponde a aproximadamente 3,5 colheres de sopa de óleo de coco ou 10 onças de Puro Leite de Côco. Aproximadamente 7 onças de côco bruto devem conter 24 gramas de ácido láurico. Essa é a dose terapêutica diária sugerida pela Dra. Enig, baseada nas suas pesquisas de ácido láurico contidos no leite humano materno.


ÓLEO DE CÔCO E CÂNCER

            Em um estudo de Reddy e al (1984) com animais, puro óleo de côco exerceu efeito inibitório mais forte que o óleo MCT quando empregado em tumores do cólon induzidos pelo uso de azoximetano. Outras pesquisas de Cohen e al (1986) mostraram que os efeitos não promotores do cãncer do óleo de côco foram também observados no câncer dos seios induzido quimicamente. Neste modelo, a pequena elevação do colesterol nos animais comendo óleo de côco funcionou como protetora enquanto os animais comendo mais óleo poliinsaturado (milho, girassol, etc) tiveram redução do colesterol, mas contudo mais tumores. Os autores notaram que “...uma tendência inversa geral tem sido observada entre os tipos de lipídeos no organismo e a incidência de tumores para os 4 maiores grupos de gorduras.”  

OS EFEITOS DO OLEO DE CÔCO NOS NIVEIS DE COLESTEROL E HDL

                A Dra. Mary Enig MS (Cientista Nutricional) desenvolveu uma pesquisa original onde mostra a correlação positiva entre o óleo vegetal e o câncer e a negativa entre este e a gordura animal.  Ela elaborou uma análise clara dos componentes das gorduras “trans” em 200 alimentos.

 As gorduras “trans” são formadas quando os óleos vegetais são hidrogenados ou aquecidos a altas temperaturas. Com altas temperaturas, fica alterada a sua forma original “cis” transformando a gordura em gordura “trans”.

            Ela estudou o efeito dessas gorduras trans, originárias de alimentos, sobre a função mista do sistema oxidativo do fígado que metaboliza no organismo drogas e poluentes ambientais. Um importante achado desses estudos foi que animais de laboratórios submetidos a uma dieta especial contendo gorduras trans, sofreram alterações nas atividades desse  sistema de enzimas. Esses resultados foram em parte responsáveis pela revisão no Health Aspects of Dietary Trans Fatty Acids, mantidas pela Federação das Sociedades de Biologia Experimental, Life Sciences Research Office por solicitação do FDA (Food and Drug Administration)

            Dra. Mary Enig tem 17 artigos publicados em jornais científicos desde 1976. Em 1986 foi nomeada pelo Governador de Maryland para o Conselho Estadual de Aconselhamento Nutricional. Foi editora colaboradora da revista  Clinical Nutrition” e consultora editorial do jornal do Colégio Americano de Nutrição. Desde 1979 já proferiu mais de 50 palestras em seminários sobre alimentos e nutrição.

            Num artigo publicado no “Indian Coconut Journal,” em 1995, a Dra. Enig afirmou que Ancel Keys tem uma grande responsabilidade pelo início da campanha contra a gordura saturada nos Estados Unidos. Ela questionou Keys afirmando que “toda gordura aumenta o colesterol; gorduras saturadas aumentam e as polinsaturadas reduzem o colesterol ; as gorduras hidrogenadas são problemas; as gorduras animal são problemas. E a Dra Enig conclui: “Como pode ser visto, seus achados não têm consistência”.

            A Dra. Enig também declarou : “Os problemas com o óleo de côco começaram há quatro décadas quando pesquisadores alimentaram animais com óleo de côco hidrogenado propositadamente alterado, para torná-lo completamente destituído de qualquer ácido graxo essencial. Os animais alimentados com óleo de coco hidrogenado (sendo a única fonte de gordura) apresentaram naturalmente uma deficiência em ácidos graxos essenciais. Houve um aumento do colesterol no sangue. Dietas que causam uma deficiência dos ácidos graxos essenciais provocam um aumento nos níveis de colesterol assim como nos índices arteroscleróticos. Os mesmos efeitos foram verificados com outros óleos hidrogenados como e de semente de algodão, soja e milho. Fica portanto claro que trata-se de uma função dos produtos hidrogenados, tanto por causa de uma deficiência dos ácidos graxos essenciais, como por causa das gorduras trans.

                Uma questão que se coloca é: O que acontece quando animais são alimentados com óleo de côco não processado?  A Dra. Enig escreveu :Hostmark at al...” (1980) comparou os efeitos das dietas contendo 10% de óleo de côco e 10% de óleo de girassol em proteínas distribuídas em ratos fêmeas da raça Wistar. Em relação ao óleo de girassol, o óleo de côco produziu níveis significativamente mais baixos  (p=0,05) de beta-pre lipoproteinas (VLDL) e significativamente mais altos (p=0,01) de alfa-lipoproteinas (HDL).  “(Nota do Editor : HDL é considerado o bom colesterol prevenindo os depósitos do colesterol LDL  nas paredes arteriais.)”. Enig cita também um estudo elaborado por Awad (1981) onde ratos da raça Wistar foram alimentados com 14% de óleo de côco natural e 14% de óleo de girassol. Ela afirmou:”  O óleo de girassol provocou nos tecidos dos animais um acúmulo de colesterol  seis vezes maior do que os animais alimentados com óleo de côco (não hidrogenados)”. A conclusão que se pode tirar é que alimentar animais com óleo de côco hidrogenado destrói a formação de ácidos graxos essenciais potencializando a formação de arteriosclerose. É importante frisar que animais alimentados com óleo de côco regular tiveram um índice mais baixo de colesterol no fígado e em outros órgãos do corpo.

            Enig também se referiu a um estudo epidemiológico elaborado por Kaunitz e Davrit (1992) em sociedades que se utilizavam do coco como alimento, onde se confirmou por um estudo da população, que uma dieta rica em óleo de côco não leva a um aumento dos índices de colesterol,  nem  das doenças coronarianas. Vale ressaltar que nessa sociedade não houve qualquer consumo de óleos hidrogenados. Apenas óleo de côco natural.

            Em 1989, Kaunitz e Davrit chamaram atenção para um relatório de Mendis et al onde mostrava que mulheres do Sri Lanka que tiveram suas dietas alteradas de óleo de côco natural para óleo de milho, apresentaram uma redução no Colesterol LDL de23.8%, o que é uma boa noticia, porem o colesterol HDL também apresentou uma redução de 41,4% o que é uma má noticia. Isso criou uma relação LDL/HDL desfavorável, significando que numa dieta de óleo de milho haverá um maior depósito de colesterol nas artérias em relação ao óleo de côco natural. Em suma, a dieta com óleo de milho líquido acelera o depósito de colesterol, em comparação com aquela de óleo de côco natural. 

            O óleo de côco natural, ao provocar um aumento no HDL (bom colesterol), ajuda na prevenção de arteriosclerose e de doenças do coração. Enig cita também a pesquisa de Tholstrup et al (1994) com óleo de palmeira (não hidrogenado) rico em acido láurico contendo também ácido mirístico. Tholstrup encontrou também um aumento significativo nos níveis de colesterol HDL
No seu artigo, Enig registrou que os efeitos do óleo de côco em pessoas com baixo nível de colesterol é justamente o contrário daqueles com um alto nível. As pessoas com uma baixa contagem de colesterol, deverão apresentar um aumento de colesterol sanguíneo, do colesterol LDL e especialmente do colesterol HDL. Já as pessoas com alto nível de colesterol apresentarão uma redução dos níveis de colesterol total e colesterol LDL.

            Os estudos que ela menciona mostra que em ambos os grupos a relação HDL/LDL se move numa direção favorável. Para pessoas com AIDS ou com comprometimento da imunidade para outras doenças, as conclusões desse pesquisa são profundas. Isto significa que tudo que tem sido informado ao público pela televisão no últimos 15 anos a respeito dos óleos vegetais têm sido meias-verdades, levando esse público a conclusões errôneas. O público tem sido levado a acreditar que óleos tropicais provocarão bloqueio nas artérias levando a doenças cardíacas. O que ocorre na verdade é justamente o contrário. Óleos tropicais naturais ajudam na preservação das artérias enquanto que ocorre o oposto com a maioria dos outros óleos vegetais, principalmente as gorduras hidrogenadas tão utilizadas hoje em pastelarias, biscoitos, pães, margarinas e produtos industrializados em geral.

Esta política contra o coco, babaçu e o dendê (palma), tem sido mantida por grandes multinacionais americanas que, sendo os maiores produtores mundiais de óleos vegetais poliinsaturados (soja, milho, canola e girassol), não querem sofrer perdas financeiras que estas alternativas trariam a eles, pois óleos extraídos de plantas tropicais como os coqueiros custariam muito mais baratos e seriam mais acessíveis às populações de baixa renda.

            A Dr, Enig também informa que o óleo de canola é o pior para ser utilizado em qualquer circunstância. Quando utilizado na cozinha ele produz um elevado nível de gorduras trans.

ÓLEO DE CÔCO E MASSAGEM

            Óleos láuricos como o de coco da Bahia, palmiste e babaçu, são extremamente finos, de baixa viscosidade, sendo por isso excelentes veículos carreadores para óleos essenciais, dada à sua fácil e rápida penetração pelos poros da pele. São excelentes fontes alternativas para substituição do óleo mineral, hoje considerado dentro de alguns estudos científicos como cancerígeno. A vantagem é que são baratos e competitivos como produtos naturais.

            São emolientes naturais, que podem ser empregados refinados ou não, possuindo normalmente uma longa durabilidade. Agem na pele hidratando suavemente, refrescando e devido ao seu teor em ácido láurico, como moderados anti-sépticos, além de terem efeito imunoestimulantes.  

            Como coco, são compreendidas várias alternativas da família das palmeiras, que contém óleos vegetais extraídos por prensagem, fervura ou artesanalmente por exposição ao sol de seus frutos e com alto teor de ácido láurico (acima de 40%) e que podem ser utilizadas para tudo o que foi descrito anteriormente por gerarem monolaurina no corpo. Entre estas alternativas disponíveis atualmente no mercado para uso tanto alimentar quanto para massagens temos:

Coco da Bahia
Babaçu
Palmiste
Tucumã (tucum)
Murumuru
Coquinho
Macaúba (macaúva)


Textos organizados, selecionados e complementados pelos Profs. Fábián László e Alessandro Luiz Freire


Onde comprar óleo (coco da bahia, babaçu, palmiste, tucumã)  produzidos no Brasil, para uso na alimentação e como veículo carreador em massagens, ou em formulações cosméticas (como base de cremes, shampoos, cremes dentais, etc...):

Bio Orgânicos Brasil:
+55 (12) 82035180
bioorganicosbrasil@yahoo.com.br












Mary Enig cita 24 referências científicas na página 7 de seu artigo “Lauric Acid for HIV-infected Individuals,":
Para Aquisição do produto - óleo de coco extra-virgem:

bioorganicosbrasil@yahoo.com.br

(12) 82035180
Maiores informações, consultorias, assessorias a spas, clínicas e empresas ou atendimentos pessoais:
Alessandro Luiz Freire
Contatos: (12) 82035180
 
Atendimentos online!  - à distância para todo o Brasil e exterior 

Marcadores: , , ,

3 Comentários:

Às 3 de novembro de 2015 11:25 , Blogger Poli Bell disse...

Herpes is one of the most common type of sextually transmitted disease. There are two type of herpes simplex virus. One is HSV-1 and another is HSV-2.what is herpes?

 
Às 7 de novembro de 2015 14:04 , Blogger Jone Jaksan disse...

Herpes is a simplex virus it is an infection that called HSV. HSV-1 can spread from eating with someone from the same utensils, using the same lip balm and kissing. what is herpes?HSV-2 spread through sex with a person who is suffering from HSV-2. The HSV-2 infection are caused by touch with a person who is in contact with herpes sore.

 
Às 28 de maio de 2016 04:47 , Blogger koyal khanna disse...


There are many women are suffering from Bacterial Vaginitis in the world. Are you also faces this problem. Don't worry. We provide you the best Home Remedies For Bacterial Vaginitis which is work effectively in all circumstances. Bacuse it is natural and there is no side effects. We are here to assist you.

 

Postar um comentário

Assinar Postar comentários [Atom]

<< Página inicial