|
The Oiling of America
by Mary Enig, PhD, and
Sally Fallon
In 1954 a young
researcher from Russia named David
Kritchevsky published a paper describing the
effects of feeding cholesterol to rabbits.1
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.2
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.3
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.4
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.5
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.6
A 1960 report noted that the severity of
atherosclerotic lesions in Japan approached
that of the United States.7
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.8
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.9
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.10
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.11
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.12
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.12a
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.13
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 60.14
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
Proceedings15
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.16
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.17
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.18
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.
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
research19
and five months later the same journal
printed a blistering letter from Edward
Hunter on behalf of the Institute of
Shortening and Edible Oils.20
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
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 1993.21
Final results of
Enig’s ground-breaking compilation were
published in the October 1983 edition of the
Journal of the American Oil Chemists
Society.22
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 1984,23
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.24
Her testimony was omitted from the final
report, although her name in the
bibliography created the impression that her
research supported the FASEB whitewash.25
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 Nutrition26,
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
finding 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.27
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
28—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.29
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.”30
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.31
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 Mattson32—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.33
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.34
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.35
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,36
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,37
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.38
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,39
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.”40
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.41
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.42
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.43
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.44
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.45
Koletzko, a German pediatric researcher
found that excess trans consumption
in pregnant mothers predisposed them to low
birth weight babies.46
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.47
George Mann confirmed that trans
consumption increases the incidence of heart
disease.48
In 1995, European researchers found a
positive correlation between breast cancer
rates and trans consumption.49
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.50
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.51
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.52
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,53
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,54
are necessary for healthy bones,55
provide energy and structural integrity to
the cells,56
protect the liver57
and enhance the body’s use of essential
fatty acids.58
Stearic acid, found in beef tallow and
butter, has cholesterol lowering properties
and is a preferred food for the heart.59
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.60
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.61
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,62
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.”63
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.64
“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.65
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.66
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
-
D
Kritchevsky, et al, “Effect of
Cholesterol Vehicle in Experimental
Atherosclerosis, Am J Physiol ,
July-September 1954, 178:30-32
-
“Notice of Supelco-AOC Award to
Kritchevsky,” Inform, 1996, 7:315
-
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
-
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
-
W
Laurie, et al, “Atherosclerosis and its
Cerebral Complications in the South
African Bantu,” Lancet , Feb 1958, pp
231-232
-
W B
Robertson, “Atherosclerosis and
Ischaemic Heart Disease,” Lancet, 1959,
1:444
-
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
-
H C
McGill, et al, “General Findings of the
International Atherosclerosis Project,”
Laboratory Investigations, 1968,
18:(5):498
-
R L
Smith and E R Pinckney, The Cholesterol
Conspiracy, 1991, Warren H Green, Inc.
St. Louis, MO. p 125
-
M
De Bakey, et al, “Serum Cholesterol
Values in Patients Treated Surgically
for Atherosclerosis,” JAMA, 1964,
189:9:655-59
-
A
Keys, “Diet and Development of Coronary
Heart Disease,” J Chron Dis, Oct 1956,
4(4):364-380
-
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.
-
“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
-
R L
Rizek, et al, “Fat in Today’s Food
Supply—Level of Use and Sources,” J Am
Oil Chem Soc, 1974, 51:244
-
M G
Enig, et al, “Dietary Fat and Cancer
Trends—A Critique,” Federation
Proceedings, July 1978, 37:(9):2215-2220
-
T H
Applewhite, “Statistical ‘Correlations’
Relating Trans-Fats to Cancer: A
Commentary,” Federation Proceedings, Oct
1979, 38:(11):2435-2439
-
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
-
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
-
“New Focus on Trans Fatty Acids,” Food
Processing, December 1982, pp 64-66
-
E J
Hunter, “More on Those Trans Fatty
Acids,” Food Processing, May 1983, pp
35-36
-
W M
N Ratnayake, et al, “Fatty Acids in Some
Common Food Items in Canada,” J Am Coll
Nutr, 1993, 12:(6):651-660
-
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
-
J E
Hunter, “Letter to the Editor,” Science,
1984, 224:659
-
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
-
F R
Senti, ed, Health Aspects of Dietary
Trans Fatty Acids, Bethesda, MD, Life
Sciences Research Office-Fed Am Soc Exp
Biol, 1985
-
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
-
Ace
Federal Reporter, Inc., Stenotype
Reporters, 444 North Capitol Street,
Suite 402, Washington, DC 20001 (202)
347-3700
-
Food Chemical News, January 25, 1988,
29:(47):52; Nutrition Week, Community
Nutrition Institute (CNI), June 16,
1988, p 6
-
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
-
Castelli, William, “Concerning the
Possibility of a Nut. . .” Archives of
Internal Medicine, Jul 1992,
152:(7):1371-1372
-
“Multiple Risk Factor Intervention
Trial; Risk Factor Changes and Mortality
Results,” JAMA, September 24, 1982,
248:(12):1465
-
F H
Mattson, et al, “Effect of Dietary
Cholesterol on Serum Cholesterol in
Men,” Am J Clin Nutr, 1972, 25:589
-
P
Addis, Food and Nutrition News,
March/April 1990, 62:(2):7-10
-
“The Lipid Research Clinics Coronary
Primary Prevention Trial Results. I.
Reduction in Incidence of Coronary Heart
Disease,” JAMA, 1984, 251:359
-
S M
Grundy, “Cholesterol and Coronary Heart
Disease: A New Era,” JAMA, Nov 28, 1986,
256:(20):2849-2858
-
“Letters to the Editor and Authors’
Responses,” J Am Coll Nutr, 1991,
10:5:510-521
-
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
-
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
-
Mann, G V, et al, “Atherosclerosis in
the Maasai,” Am J Epidemiol, 1972,
95:26-37
-
Coronary Heart Disease, The Dietary
Sense and Nonsense, George V Mann, ed,
1993, Veritas Society, London, p 1
-
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
-
C V
Felton, et al, “Dietary Polyunsaturated
Fatty Acids and Composition of Human
Aortic Plaques,” Lancet, 1994, 344:1195
-
D
Kritchevsky, Medical Counterpoint, March
1969
-
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
-
T
Hanis, et al, “Effects of Dietary Trans
Fatty Acids on Reproductive Perforamnce
of Wistar Rats,” British Journal of
Nutrition, 1989, 61:519-529
-
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
-
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
-
G V
Mann, “Metabolic Consequences of Dietary
Trans Fatty Acids,” The Lancet, 1994,
343:1268-1271
-
L
Kohlmeier, et al, “Stores of Trans Fatty
Acids and Breast Cancer Risk, “Am J Clin
Nutr, 1995, 61:896;A25
-
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
-
M G
Enig, et al, “Isomeric Trans Fatty Acids
in the U.S. Diet,” J Am Coll Nutr, 1990,
9:471-486
-
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
-
W C
Willett, et al, “Intake of Trans Fatty
Acids and Risk of Coronary Heart Disease
Among Women,” Lancet, 1993, 341:581-585
-
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
-
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
-
J F
Mead, et al, Lipids: Chemistry,
Biochemistry and Nutrition, Plenum
Press, 1986, New York
-
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
-
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
-
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
-
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
-
H
Engelberg, “Low Serum Cholesterol and
Suicide,” Lancet, March 21, 1992,
339:727-728
-
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
-
M
Gurr, “A Fresh Look at Dietary
Recommendations,” Inform, April 1996,
7:4:432-435
-
AIN/ASCN Task Force on Trans Fatty
Acids, “Position Paper on Trans Fatty
Acids,” Am J Clin Nutr, 1996, 63:663-670
-
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
-
R E
Olson, “Evolution of Ideas about the
Nutritional Value of Dietary Fat:
Introduction,” J Nutr, 1998
128:421S-425S
|