Upon completion of this 5 unit course, the learner will be able to:
1. Describe the main points and history of the Lipid Hypothesis of heart disease.
2. Describe the distinctions among the different types of fatty acids and their
3. List the main objectives of the Lipid Hypothesis.
4. Describe the role of the high and low density lipoproteins in heart disease.
5. Describe the clinical implications and health benefits of saturated fats and
the dangers of low fat/low cholesterol diets.
Note to the student: Key points of this course are in italics and
are preceeded by **.
The Lipid Hypothesis
As most health professionals know, heart disease is the Western world's number
one killer. The Lipid Hypothesis is the current theory offered to explain how heart disease has risen to become
the Western world's number one killer. Basically, this theory states that saturated fats and cholesterol clog the
arteries, leading to atherosclerosis, heart disease, and an ever-increasing assortment of serious illnesses, most
notably cancer. According to this theory, the main reason why heart disease and cancer rates have skyrocketed in
this century is because people have been eating an increasing amount of saturated fat and cholesterol-rich foods.
The solution to heart disease (and cancer) is to simply reduce our consumption of such foods, replacing them with
more complex carbohydrates, fruits, vegetables, legumes, and unsaturated fats, especially polyunsaturated fats,
which have been shown to reduce serum cholesterol levels.
Traditional foods like butter, cream, lard, meats, and eggs have been blamed for
horrible diseases, especially heart disease. Eliminate them, say the experts, and your risk for heart disease will
drop drastically. Diets low in fat are also urged by some health professionals for people with current heart conditions
or high blood cholesterol levels. A brief scan of nutrition books, both for the professional and the lay person,
illustrates the basic tenets underlying the Lipid Hypothesis:
While most people are aware that cholesterol is a culprit in heart disease, the average American continues to consume
about 175 pounds of meat, 234 eggs, about 15 pounds of margarine and butter, and almost 18 pounds of ice cream
annually, while the heart struggles to pump blood through arteries accumulating cholesterol deposits at a rate
of 1 to 2 percent per year... . Year after year, study after study, cholesterol's role as a promoter of cardiovascular
disease (CVD) has been, and continues to be, confirmed.
The risk of developing cardiovascular disease is directly related to serum cholesterol
levels. As cholesterol rises above 200 mg/dl, CVD rates climb proportionately. A direct correlation exists between
the incidence of CVD in a particular group, blood cholesterol levels, and the amount of fatty foods of animal origin
in the diet... . The link between dietary fat and cardiovascular disease is well-documented (1).
We have gradually increased our intake of butter, milk, other dairy
products and eggs. The proportion of calories from fat has increased from a national figure of 30 percent in 1910
to over 40 percent - with a corresponding increase in heart disease (2).
Coronary heart disease is a twentieth-century phenomenon and so is
the emphasis on animal products in our diet. In the early 1900's,
coronary heart disease was a comparatively rare illness... . The rise
of coronary heart disease in the United States (and other Western countries) paralleled the changes in the U.S.
As the consumption of animal fat and cholesterol began to rise during this century,
so did the incidence of coronary heart disease. People in most of the world... have never increased their consumption
of animal products. In these countries, coronary heart disease is still a rare illness (3).
It is very common in nutritional medicine books to see low fat diet/low cholesterol diets recommended for hypertension
and CVD. Such diets are also urged for "cancer prevention" and improved vitality and well being. All
of the major health and nutritional organizations in the Western world embrace and promote the Lipid Hypothesis
and its twin, the Cholesterol Hypothesis. A third theory goes along with the Lipid and Cholesterol hypotheses -
a theory about high and low density lipoproteins (or HDL and LDL, respectively).
While we'll look at the HDL/LDL theory by itself later in this course, what you
need to know now is that, according to this theory, higher levels of HDL translate to a decreased rate and risk
for heart disease, while higher levels of LDL translate to the exact opposite. It is routine for people having
a general check-up to have their serum cholesterol levels checked, as well as their ratio of HDL to LDL. A cholesterol
reading over 200 mg/dl is viewed as a risk for CVD.
Boon for Industry
The Lipid Hypothesis has been a boon for many industries, especially the pharmaceutical
and food processing industries, which make a brisk dollar on cholesterol-lowering drugs and low-fat/cholesterol
processed foods. The other major benefactor of the Lipid Hypothesis has been the vegetable oil and shortening industry.
Since most vegetable oils are high in polyunsaturated fatty acids (PUFA) and since
PUFAs lower serum cholesterol levels, corn, safflower, soybean, and in some countries, canola oils have been heavily
marketed to the public. For example, a popular brand of corn oil in America was advertised for years in popular
and professional magazines as "good for your heart" and labeled a "cholesterol depressant"
(4). A margarine derived from pine tree sterols is about to hit the market - the plant sterols lower cholesterol
Since margarine is manufactured from vegetable oils, it was also heavily promoted
to the public and medical profession as being more "heart healthy" than butter or lard. To this day,
companies will conspicuously label a product as "Low In Fat," "Fat-Free," or "Cholesterol-Free"
to enhance sales. In the mind of the public, the words "cholesterol" and "fat" have become
synonymous with disease, while "low fat, low cholesterol" have become synonymous with health.
An indirect result of the Lipid Hypothesis has been an increasing number of people
embracing vegetarianism. Since saturated fat is found primarily in animal foods, and since cholesterol is only
found in animal foods, many have eliminated animal products from their diets in the belief that it is healthier.
Health food companies that manufacture vegetable replacement foods, such as soy milk, imitation chicken, beef,
or cheese made from soybeans or other vegetable proteins, have benefited as well.
As a matter of fact, a whole industry of processed "health" foods has
mushroomed in the last twenty years. Products include eggless mayonnaise made from assorted vegetable oils, egg
replacer products made from vegetable proteins and oils, and an array of foods manufactured from organically raised
plant foods. Proponents of vegetarianism never fail to inform their readers of the benefits of a vegetarian diet
that is "low in artery-clogging cholesterol and saturated fats."
Lipid Hypothesis Never Proven
Of course, a bevy of scientific studies have supposedly proven the Lipid Hypothesis
theory - that eliminating saturated fats is a good idea. Unfortunately, the Lipid Hypothesis has never been proven.
There have always been scientific detractors from the Lipid Hypothesis, some very vocal in fact, but their minority
views never seem to get much attention, either from the medical or journalistic communities. Nevertheless, there
is ample evidence against the Lipid Hypothesis, as well as the cholesterol and HDL/LDL theories that deserves our
attention. Before we get into this, however, we need to clarify a few things about lipids, or fats, so we'll all
know what we're talking about.
Lots of Lipids
As you might have noticed in reading the excerpt from Garrison and Somer above,
there is a tendency for some nutrition writers to mix different kinds of fats together, treating them as if they
were all the same. Garrison and Somer list meat, milk, eggs, butter, margarine, and ice cream in the same category.
This creates the impression to the reader that one fat is the same as another. This is false.
The error is repeated time and time again by researchers who hold to the Lipid
Hypothesis. At the onset, you must remember that there are different types of fat, each with a mode of action different
from the other. Lipid biochemistry is a complicated field, but anyone can understand the basics. Let's define our
Fatty acids are chains of carbon and hydrogen atoms - short and some long depending
on the one in question. They are placed into three groups:
Saturated fatty acids (SFA),
Monounsaturated fatty acids (MUFA), and
Polyunsaturated fatty acids (PUFA).
The number of available carbon bonds in the fatty acid molecule is what determines
its degree of saturation. If all of the carbon bonds in a fatty acid are full and occupied by hydrogen atoms, it
is saturated. If two carbon atoms
are double-bonded to each other, therefore lacking two hydrogen atoms, it is monounsaturated. And if more than two carbon bonds are available, it is polyunsaturated. All fats, whether of animal or vegetable origin, are blends of these three types of fatty
acids, but with one type usually predominating, depending on the fat in question.
|Degree of Saturation
||# of carbon bonds linked to hydrogen
||Mostly found in:
||Carbon bonds fully occupied by hydrogen
||Animal fats, palm and coconut oils
||1-2 carbon bonds unavailable to hydrogen
||Nuts, avacados, olive oil, some animal fats (especially lard)
||>2 carbon bonds unavailable to hydrogen
||Vegetable fats, fish oils, chicken skin (except commercially-raised animals that
are fed a high vegetable diet)
Saturated fats predominate principally in animal fats, though palm and coconut oils are noted plant sources. Monounsaturated
fats abound in nuts, avocados, olive oil, and some animal fats (especially lard). Vegetable fat is mostly made
up of polyunsaturated fats, but appreciable amounts are found in fish oils and chicken skin. Important exceptions
to this are commercially-raised animals that have been fed a high vegetable diet.
The best example of this is a commercially-raised turkey. This meat source usually
has dry flesh and goes bad quickly in the refrigerator; the result of too many polyunsaturates in its body. It
should be noted here that
**the more a fat is saturated, the more stable it is chemically.
Saturated and monounsaturated fats do not go rancid easily if stored properly.
Likewise, these fats are more stable under heat, making them ideal for cooking.Polyunsaturated fats, however, especially
those of vegetable origin, are not as stable and go rancid more quickly, even in the body.
Rancid oils breed cancer-causing and tissue damaging free radicals. While some
polyunsaturated fats are needed by the body, they should not exceed 4% of your total caloric intake due to this
problem. Ironically, it is the polyunsaturates that have been urged by health experts for the last 50 years. And
as people have consumed more of them, certain health problems, like heart disease, have escalated.
Essential Fatty Acids
There are two groups of fatty acids that are vital for our health: omega 3's and
omega 6's. These are also known as the essential fatty acids (EFAs) and, like vitamins and minerals, must be gotten
from our food. The body manufactures chemicals called prostaglandins from certain EFAs. Prostaglandins are localized
tissue hormones that appear to regulate numerous chemical activities in our cells. In times past, humans consumed
a balance of omega 3's - found in fish, walnuts, eggs, flax oil, dark green leafy vegetables, and some whole grains
and omega 6's - found principally in vegetables. This is as it should be as both are equally important.
When there is an overabundance of omega 6's in the diet, however, our body's ability
to absorb and utilize the omega 3's is inhibited. This causes a host of undesirable reactions including sexual
and immune dysfunction, and increased cancer risk (5). This is something that most modern lipid researchers, especially those wedded to the
Lipid Hypothesis, either overlook or do not know.
There is another type of "fat" that is produced during chemical processing
called a trans-fatty acid (TFA). The major way that trans-fats are produced is by forcing hydrogen atoms into a
vegetable oil by adding a nickel catalyst. In other words, hydrogenation makes a liquid lipid (vegetable oil) solid
through chemical tampering. Although the finished product looks like a saturated fat (also solid), its chemical
structure is very different. These are unnatural fats that our bodies cannot utilize properly because of their
These fake fats are found in margarine, "vegetable oil spreads," shortening,
processed vegetable oils, and canola oil, as well as any foods made with them. As we shall see,
**it is mostly trans-fatty acid consumption, and not saturated fat consumption,
that is strongly correlated with increased cancer and cardiovascular disease, not saturated fat or cholesterol.
Cholesterol is a heavy weight molecule, actually an alcohol or sterol. It is a
slippery substance that moves at a high rate of speed through the body. It is found in every cell membrane. It
is also the substrate used by the body to manufacture several hormones (e.g., adrenalin and progesterone). It is
also an antioxidant that the body uses to repair damaged tissues, including damaged or weakened arteries (6). Although
the foregoing discussion is by no means complete, it is enough to give you some basic knowledge in lipids. This
should help you to understand this course more.
The History of the Lipid Hypothesis
Mortality data from the turn of the century indicate that heart disease and deaths from myocardial infarction (MI),
a massive blood clot leading to death of the heart muscle, were extremely rare, usually less than 6% of total deaths
This rarity continued up until the late 1920s. Then, things started to change for the worse. Doctors who had never
even seen a heart attack patient their entire careers, now began seeing them with increased frequency. By the 1950s,
heart disease and MI's accounted for about 30% of all deaths in Western countries. That figure has risen steadily
and now holds at about 45%.
In just five or six decades, a once rare condition grew to become our number one
killer. Scientists and doctors in the 1950s were grappling with this problem, trying to figure out what had caused
the dramatic rise. In 1954 a young Russian researcher named David Kritchevsky published a paper describing the
effects of feeding cholesterol to rabbits by mixing the substance with rabbit chow. He noted that the rabbits developed
arterial plaque, i.e., atherosclerosis (8). The studies were actually repeats of experiments carried out decades before, also in
Russia, in which cholesterol and saturated fat fed to rabbits resulted in clogged arteries and heart problems.
Later in 1954, Kritchevsky published another paper demonstrating that PUFAs in
the diet could lower blood cholesterol levels (9). These two studies attracted immediate attention because they lent support to a theory
that had developed to explain the rise of CVD, namely that saturated fats and cholesterol from animal products
raise cholesterol levels in the blood, leading to fatty deposits in the arteries. It was as a result of this research
that the Lipid Hypothesis was born.
In 1956, the American Heart Association (AHA) held a nationally-televised fundraiser
to officially present the Lipid Hypothesis to the public and to kick-off the AHA's "Prudent Diet" campaign.
The Prudent Diet called for the replacement of butter with margarine, skinless chicken for beef, cold cereal and
toast for bacon and eggs, low-fat or skim milk for whole milk and cream, and corn oil for tallow and lard. During
the televised event, the Master of Ceremonies interviewed doctors who endorsed the Lipid Hypothesis, including
Irving Page, Jeremiah Stamler and Dr. Paul Dudley White. When pressed to endorse the Lipid Hypothesis and the Prudent
Diet, White surprisingly retorted:
See here, I began my practice as a cardiologist in 1921 and I never saw an MI patient 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 (4).
Despite this glitch, the televised campaign was a success in terms of public acceptance. On the surface, it appeared
that the theory was true because it was so simple - if you eat more fat and cholesterol, then more will clog your
arteries. A number of researchers appeared in support of the Lipid Hypothesis. One of the most famous was Ancel
Keys. Keys headed up the massive Seven Countries Study where he and his colleagues analyzed the diets of 12,000
men in seven countries that were hand-picked by Keys.
Keys and his researchers concluded that the men who ate the most fat had the highest
rates of CVD, while the men who ate the least had the lowest rates of CVD. This was odd as Keys had, in 1956, suggested
in a published paper that the increasing use of hydrogenated vegetable oils might be the underlying cause of CVD
Other studies in later years were undertaken to prove the Lipid Hypothesis. One
of the more interesting studies was orchestrated by Dr. Norman Jolliffe, Director of the Nutrition Bureau of the
New York Health Department. He organized the Anti-Coronary Club in 1957 in which selected businessmen, ranging
in age from 40-59 years were placed on the AHA's Prudent Diet. Club members followed the Prudent Diet religiously.
They were compared to another group of businessmen who ate eggs and bacon for breakfast, used butter, and ate meat
three times a day. Jolliffe, an overweight diabetic confined to a wheelchair, was confident, along with the other
Lipid Hypothesis supporters, that the "Prudent Diet" group would fare much better than the "non-Prudent"
In 1966 the results of the study were published in the Journal of the American
Medical Association (11). Although the Prudent Diet men had slightly lower serum cholesterol levels than the non-Prudent
group (220 vs. 250), there were eight deaths from heart disease in the Prudent group and none in the non-Prudent
group! Despite this negative study, the Lipid Hypothesis kept marching on. Oh, and Dr. Jolliffe? He died of a vascular
thrombosis in 1961. Apparently, the Prudent Diet was not able to save him either (4).
Other supporters of the Lipid Hypothesis such as Dr. Irving Page, on the AHA panel
in the 1956 broadcast wanted to organize a more extensive trial to prove the Prudent Diet's effectiveness after
the dismal results of Jolliffe's "Anti-Coronary Club" experiment, but the planned dietary experiment
was abandoned in silence.
Nevertheless, the Lipid Hypothesis, despite the initial resistance from the American
Medical Association, took off and entrenched itself in the minds of Western researchers. Things were helped along
by slick advertising campaigns carried out by vegetable oil and margarine companies in which doctors such as Frederick
Stare of Harvard University endorsed new products and belittled traditional animal fats and cholesterol-containing
By the 1970s, the American Medical Association, the American Dietetics Association,
the National Academy of Sciences (USA), and the National Heart, Lung, and Blood Institute (USA) had endorsed the
Lipid Hypothesis and called for Americans, and by extension all Westerners, to throw away butter, cream, lard,
and fatty meats and sausages, and embrace corn oil, margarine, imitation eggs, skim milk, lean meats, and more
plant foods. A dietary committee in America headed by Senator George McGovern in the 1970s, urged PUFA consumption
and elimination of animal fats. American doctors received a "Cholesterol Education Kit" in the 1980s
in which cholesterol screening was encouraged, as well as the use of cholesterol-lowering drugs and margarine.
Dr. Dudley White's pleas in 1956 went unheard at the time, but he had brought up a telling point - how could the
Lipid Hypothesis possibly be true if,
**in times when heart disease and MI's were rare, people consumed plenty of
animal fats, namely, butter and lard?
One would expect to see the same high rates of CVD in those who ate a lot of animal
fats, like the Masai of East Africa or the Inuit of the Arctic Circle, but such was not the case. Several nutrition
researchers noted the same thing and began to publish their objections.
Dr. Fred Kummerow of the University of Illinois at Urbana had conducted studies
in the early 1970s showing that the consumption of trans-fatty acids in margarine and processed vegetable oils
caused increased rates of heart disease in pigs (12). Kummerow also authored the paper showing that imitation eggs could not support life (13).
Kummerow also wrote a moving and impassioned letter against the Lipid Hypothesis and submitted it to the US Senate
Committee on Nutrition and Human Needs in the early 1970s.
Kummerow specifically urged a return to traditional foods and fats, the very ones
demonized by the Lipid Hypothesis (and the Senate Committee): butter, cream, eggs, milk, lard, and tallow. Kummerow's
papers, rat pictures, and letter were summarily ignored and buried. Kummerow also discovered the result of holding
an unpopular minority opinion - his subsequent applications for research funding in nutritional biochemistry were
all turned down. Had it not been for a private endowment, he would have been unable to continue his work.
I recently interviewed the venerable Kummerow, who is still doing research at
the University of Illinois. He told me an interesting story about his damning paper on imitation eggs. "I
originally submitted it to the Journal of the American Medical Association (JAMA), but the assistant editor at
the time rejected it and advised me to submit it instead to Pediatrics, a lesser journal also owned by the American
Medical Association. Pediatrics published the paper and the photos. I think I know why the editor turned the article
down: the following issue of JAMA contained a full page ad for those imitation eggs."
Dr. Mary Enig and her associates at the University of Maryland published a series
of papers severely damaging to the vegetable oil and margarine industries and the American government agencies
urging a low-fat/cholesterol diet, specifically noting that the trans-fatty acids in such products produced dangerous
changes in cells. One of the main findings Enig and her colleagues determined was that trans-fatty acids interfered
with cellular enzyme systems that neutralised carcinogens, but increased enzymes that potentiated them, hence the
high correlation between trans fat consumption and various cancers (14).
Dr. Enig became suspicious of the validity of the Lipid Hypothesis when she realized
that animal fat consumption had declined steadily since the turn of the century. For example, a report in the Journal
of American Oil Chemists 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 low 21 grams to almost 60 grams. Total
fat consumption had increased, as the proponents of the Lipid Hypothesis argued, but this increase was due mostly
to vegetable oils with 50 percent coming from liquid oils and another 41 percent from margarine made from vegetable
Enig and her colleagues wrote up a detailed paper criticizing one of the assertions
of the Lipid Hypothesis - that there is a strong correlation between dietary fat intake and the incidence of colon
and breast cancer. The paper also demonstrated that the positive correlations between fat intake and cancer rates
came from vegetable and trans fats, not the saturated fats of animals or coconuts. Indeed, Enig concluded that
saturated fats seemed to protect against cancer! The paper was published in an American journal, Federation Proceedings,
in July 1978 to the dismay of the vegetable oil industry.
After the publication of this paper, Enig and her colleagues lost all their funding
for research. The paper was subsequently viciously attacked by proponents of the Lipid Hypothesis and scientists
employed by food companies, but Enig and her colleagues defended themselves well, at least in the scientific journals
that printed their response letters; several journals refused to print her rebuttals to criticisms (4).
Enig also began investigating the trans fat levels in a wide variety of foods
on the market. Despite pressures from the food industry and the University of Maryland to halt the research, Enig
and her colleagues discovered disturbing things about the amount of trans fat consumption, as well as its effects
on the body.
Another well-known detractor was Dr. John Yudkin of Great Britain. In the 1950s,
at the same time that Ancel Keys was promoting the Lipid Hypothesis, Yudkin and his colleagues published conclusive
findings that excessive refined sugar intake was associated with elevated blood cholesterol, elevated triglycerides
(blood fats), enlargement of the liver, increased corticosteroid levels in the blood, hypertrophy of the adrenal
glands, and shrinkage of the pancreas (16). Other researchers, following Yudkin's lead, also looked into the role of refined sugar
in disease and discovered that
**increased sugar intake was one of the main causes of heart disease (17).
Yudkin's studies were ignored, too.
Dr. George Mann did independent studies on the Masai of East Africa (discussed
below) that convinced him that the diet/heart hypothesis was a "scam." He called the Lipid Hypothesis,
"the public health diversion of this century . . . the greatest scam in the history of medicine" (18).
Mann organised an "Anti-Lipid Hypothesis" conference, out of his own pocket, of course, as the food industry
and major government agencies refused to fund it. Mann invited several scientists and researchers, many of whom
initially confirmed their attendance, and then backed out. Mann noted in his initial speech at the November 1991
conference, attended by a whopping seven participants, that:
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 jeopardise my perks and funding.' For me, that kind
of hypocritical response separates the scientists from the operators, the men from the boys (4).
So, as is often the case in science, to dissent from the majority opinion is dangerous business, especially when
research dollars are at stake. If you disagree, or if you show support or interest in those that do, you either
lose your funding or are in danger of losing it. It is time now to look at the evidence brought forward to support
the Lipid Hypothesis, as well as the considerable evidence against it. It will be seen that the connection between
diet and heart disease is not what most of you think.
The Validity of the Lipid Hypothesis
The main points of the Lipid Hypothesis are as follows:
- Saturated fat and cholesterol consumption has increased through the 20th century,
with a corresponding increase in heart disease;
- Dietary intake of cholesterol through cholesterol-containing foods raises blood
- Increased blood cholesterol levels correlate with an increased risk and occurrence
- Saturated fats and cholesterol clog arteries in the form of arterial plaque;
- A high intake of saturated fat and cholesterol increases the risk for CVD and
that increased rates of CVD are seen in those who eat high fat/cholesterol diets;
- Reducing intake of saturated fat and cholesterol, and increasing intake of unsaturated
fats, translates to a decreased risk for CVD;
- Numerous studies prove that increased dietary saturated fat/cholesterol intake
strongly correlates with higher rates of atherosclerosis and heart disease.
Let's take a close look at each of these points.
The Points Analyzed
fat and cholesterol consumption has increased through the 20th century, with a corresponding increase in heart
The quotations from Stamler and Ornish at the beginning of this chapter clearly stated this. Unfortunately, these
claims are absolutely false. Anthropological data confirm that humans have always eaten meat and animal fat and,
unless constrained by environmental or economical factors, preferred them as food sources over vegetable foods
Paleolithic peoples apparently hunted certain species to extinction and the expansion of humanity across and around
the globe was due to its quest for more animal foods (19).
Societies only turn to a diet of predominantly plant stuffs when absolutely necessary,
and when they do, the effects are deleterious. For example, Abrams, citing Wells, notes that, "The dependence
on high carbohydrate foods such as grain crops and other plant foods have resulted in undermining the health adaptations
of food-producing populations unless they have been able to provide and maintain a balance between meat animals
and their low protein crops" (19). A cursory survey of dietary habits of native peoples from around the world flatly contradicts
claims that humans ate less animal products than 20th century people.
As noted above, all cultures show a preference for animal protein and animal fat
and there is no such thing as a totally vegetarian culture anywhere in the world--veganism is primarily a 20th
century phenomenon. For example, the Masai of East Africa, before modernization, consumed a diet of almost 100%
animal products. The Inuit, before they adopted civilized foods, also were almost 100% carnivorous. Australian
Aborigines traditionally consume an array of animal products, including insects, supplemented by plant foods.
When it comes to Americans, and other Western peoples, a survey of any cookbook
from the last century will quickly reveal what people were eating lots of saturated fat from butter, cream, eggs,
and lard (21).
For example, the Baptist Ladies Cookbook contains recipes for such dishes as lamb croquettes, scalloped fish, creamed
liver, creamed sweetbreads, creamed onions, and salmon with cheese sauce (22).
An entire chapter of the cookbook is devoted to oysters, with recipes such as
oysters wrapped in bacon, scalloped oysters, and deviled oysters (made with eggs). A recipe for oyster pie calls
for a quart of cream and a dozen egg yolks. The vegetable chapter reveals that creamed vegetable dishes were quite
popular. There are recipes for creamed cabbage, creamed cucumbers, and parsnips fried in bacon fat. Even sugary
desserts contained substantial amounts of saturated fats. A recipe for German waffles, for example, calls for an
entire pound of butter and 12 eggs.
Recipes from the Boston Cooking School Cookbook (23) are similar to those of the
Baptists with meal suggestions that go like this:
Breakfast: Oatmeal with sugar
and cream; creamed fish; baked potatoes; corncakes; coffee with cream.
Lunch: Lamb croquettes fried in lard;
"dressed" lettuce; biscuits with butter; gingerbread; cheese.
Dinner: Soup with cream or whole milk;
meat or fish with scalloped potatoes; two other vegetable dishes, usually creamed; vegetable salad; crackers, cheese,
and coffee with cream.
A caloric analysis of some of these menus reveals up to 43% of calories coming from fat, with a slightly higher
ratio of saturated to unsaturated fats (21). Recipes from a Jewish housewives cookbook published in London, England, in 1846 reveal
similar recipes with tallow being substituted for lard. The Searchlight Recipe Book (24), also has similar recipes
for creamed fish and organ meats, along with dessert recipes with lots of butter and eggs, and vegetable dishes
with a cream or cheese sauce.
One thing very noticeable in this later cookbook, however, is the option in some
recipes of using butter or a "butter substitute," i.e., margarine. Some recipes also call for "vegetable
oil." This cookbook clearly shows the substitution of vegetable fats for animal. By the 1950's, heart disease
On a more scientific level, food data from the United States Department of Agriculture
(USDA) shows that animal fat consumption, especially of butter, has steadily declined in this century, but that
vegetable oil and margarine consumption, i.e., polyunsaturated fats, has gone up tremendously (USDA- HNI). A report
published in the Journal of the American Oil Chemist's Society demonstrated that animal fat consumption was substantially
higher at the beginning of this century compared to now (15).
While it is true that meat consumption has risen in the last few decades, the
rise has mostly been from increased chicken consumption, specifically recommended by the Prudent Diet. Chicken, however, is lower in saturated fat than
beef or pork. Even chicken skin, recommended not to be eaten, contains significant levels of PUFAs. Beef and pork
consumption, the high saturated fat meats, has risen only slightly. Some try to use these data to prove that animal
food/fat intake therefore correlates with higher CVD rates, but what is not mentioned is that intake of margarine,
trans-fats, refined sugar, and processed foods has also risen, quite astronomically in fact. Laying the blame on
meat products and saturated fat is very bad reasoning indeed.
The first claim of the Lipid Hypothesis cannot be supported by any factual data.
If anything, the data supports the opposite
of the Lipid Hypothesis:
**as animal fat consumption has decreased
and vegetable fat consumption has increased, heart disease and cancer have increased!
B. Dietary intake of cholesterol through cholesterol-containing
foods raises blood cholesterol levels.
It is claimed by supporters of the Lipid Hypothesis that cholesterol-rich foods like whole milk, cheese, meat,
eggs, liver, and shellfish raise blood cholesterol levels when eaten. There is a mountain of evidence to demonstrate
that this is not true. When Dr. George Mann of Vanderbilt University studied the Masai, a people whose diet mostly
consists of beef, whole milk, and blood, he found they had serum cholesterol levels well within the "normal"
range (180-200 mg/dl). He also discovered that they had very little, if any, CVD (25).
A study conducted by Hitchcock and Bracey in Busselton, Australia studied three
groups of mothers and children - one with high, one with medium, and one with low cholesterol levels. The researchers
studied the diet patterns of each group and found no significant difference among their daily food intakes. In
other words, their diet had no bearing on their cholesterol levels (26).
A group of New Guinea natives whose diets were very low in cholesterol were given
eggs in an experiment designed to measure how the eggs would affect cholesterol levels. Their cholesterol levels
remained the same; the eggs had no effect on their cholesterol levels (27).
**Studies conducted on diet and cholesterol
levels by other researchers found no significant difference in plasma cholesterol levels in egg eaters and non-egg
The liver manufactures most of the cholesterol the body needs for an assortment
of biochemical processes - about 2 grams a day. Only a small amount is absorbed from food in the small intestines,
but this quantity is needed by the body to give it the substrates necessary to manufacture enough cholesterol (4).
Eliminating cholesterol foods from one's diet is therefore ill advised.
Abrams and Rowland rightly point out that eggs are an incredibly healthy, and
inexpensive food, containing every nutrient known by man for healthly living (except for vitamin C). Citing Kummerow's
research, they conclude that cholesterol-free egg substitutes cannot support life and that eliminating eggs from
the diet in an effort to lower cholesterol levels simply deprives the body of "an excellent source of nutrients"
C. Increased blood cholesterol
levels correlate with an increased risk and occurrence of CVD.
Despite what the public, and supporters of the Lipid Hypothesis think,
**most people - over 80%, do NOT have
elevated cholesterol levels prior to experiencing a heart attack (31).
Abrams concurs, "There is no positive or direct proof that high cholesterol
levels results in heart disease.(19) Dr. Michael DeBakey, a world renowned heart surgeon from Houston, has done
extensive research on the Lipid Hypothesis - specifically the dietary cholesterol aspect. He found that only 30
or 40% of people with atherosclerosis or CVD actually have elevated cholesterol levels (28).
He stated, "If you say cholesterol is the cause, how do you explain the other
60% to 70% with heart disease who don't have high cholesterol?"(22-28) DeBakey did an analysis of 1,700 patients
with CVD from hospital records and found no definitive relationship or correlation between serum cholesterol and
the extent of CVD (32). Reiser cites a study in which men from Crete and Crevalcore, Italy, with similar cholesterol
levels, nevertheless had different rates of CVD (28).
It would appear from the preceeding research that serum cholesterol levels are
neither an indicator nor a risk factor for heart disease. There are, however, small numbers of people who posess
a genetic defect that interferes with their ability to metabolize cholesterol - a condition called hypercholesterolemia.
People with this genetic condition DO have to watch their blood cholesterol levels.
As Dr. Uffe Ravnskov points out in his excellent book The Cholesterol Myths, most
of the studies done demonstrating positive correlations between cholesterol levels and heart disease have been
performed on people with this condition, but one cannot apply data from a group of people with a metabolic defect
to the general population. Ravnskov's book is available through New Trends Publishing, (877) 707-1776; see also
D. Saturated fats and cholesterol clog arteries in the
form of arterial plaque.
Studies using rabbits done by Kritchevsky are offered as proof that saturated fats and cholesterol cause the formation
of arterial plaques. Unfortunately, the basis of the experiment is flawed - rabbits are herbivorous creatures and
lack the physiological traits required to assimilate and metabolize cholesterol, which is only found in animal
products. It is no wonder that Kritchevsky's rabbits developed problems. One cannot apply the results of an experiment
done on herbivores to an omnivorous species like humans (31).
A study in the medical journal Lancet (33) demonstrated that the fatty acids in
arterial plaque are mostly unsaturated (74%), of which 41% are polyunsaturated. This finding flatly contradicts
the Lipid Hypothesis. It is consistent, however, with what we know about excessive PUFAs, they are bad news. The
studies that Kritchevsky did with his rabbits were actually done with powdered cholesterol mixed with corn oil,
a predominantly PUFA (4).
The evidence for saturated fat clogging arteries is so flimsy that the eminent
biochemist Dr. Michael Gurr stated in a recent article, "Whatever is the cause of heart disease, it is not
primarily the consumption of saturated fats." Gurr went on to criticize "the degree of self delusion
in research workers wedded to a particular hypothesis despite the contrary evidence!" (34)
As Rowland points out, cholesterol is a slippery, waxy substance that moves through
the blood at a high rate of speed (31). It is, therefore, impossible that it could "stick" to arterial walls, which
are very smooth. He also points out that, "There is just as much cholesterol in our veins as in our arteries;
but plaque is always found only in arteries and never in veins. If cholesterol were the cause of circulatory disease,
then surely it would damage veins as much as arteries. But it does not."
Then why is cholesterol found in arterial plaque? Because the arteries have been
damaged by something else and the body uses cholesterol as a repair substance (35). Furthermore, cholesterol is
one of the last substances to be laid down in arterial plaque, not the first (31). It is, therefore, impossible
that it could be the cause of arterial clogs.
What is the cause? In answering this question, one must realize first that all
peoples, no matter what their diet, experience some atherosclerosis as a consequence of aging. The 1968 International
Atherosclerosis Project, in which over 22,000 corpses in 14 countries were autopsied for arterial plaque, showed
arterial degeneration in all subjects - in populations that suffered from a great deal of heart disease, and in
populations that did not (36).
What the difference is, though, is the degree of blockage. Having a fatty-streaked
artery is quite different from having a totally occluded one. As we shall see in the following chapter, the primary
culprits in arterial clogs are processed vegetable oils, refined sugars, and oxidized cholesterol (the kind used
by Kritchevsky in his experiments).
E. A high intake of saturated fats and cholesterol increases
the risk of CVD and increased rates of CVD are seen in those who eat high fat/cholesterol diets.
Native peoples the world over consume high amounts of animal fats with no incidence of heart disease. For example,
the Masai and related tribes of East Africa subsist largely on beef, whole milk, and blood. Yemenite Jews eat a
diet containing fats solely of animal origin, yet have an almost zero incidence of heart disease and hypertension.
Peoples living in northern India consume 17 times more animal fat, but have an incidence of CVD seven times LOWER
than in southern India.
Eskimos eat liberal amounts of animal fats, both from fish and marine mammals,
yet, as long as they stay on their native diet, enjoy freedom from CVD, obesity, osteoporosis, diabetes, and cancer.
Several Mediterranean societies are free of CVD, even though fat consumption accounts for up to 70% of their diet.
A study of Puerto Ricans revealed that, in spite of a high animal fat intake, they have low rates of colon and
breast cancer (5).
Ancel Keys claimed that the Japanese had the lowest incidence of CVD because of
their low fat diet in his Seven Countries study, but this is not altogether true. The Japanese consume moderate
amounts of fat and substantial amounts of cholesterol from their diet of seafoods and shellfish. Additionally,
the Swiss, the second longest lived people in the world right behind the Japanese, eat a diet loaded with saturated
fat from dairy products (37).
With all of this contrary evidence, how could anyone possibly hold the Lipid Hypothesis
to be true? The problem is that researchers fail to properly isolate specific dietary factors in their subjects.
We saw this at the beginning of this chapter - Garrison and Somer lumped together ice cream and margarine right
along with butter and beef. Yet any person with common sense knows that these foods are not identical. The fats
in these foods are vastly different.
Another good example of this is a "Dietary Questionnaire" developed
by dieticians at the Northwest Lipid Research Clinic in Seattle, Washington. One question, designed to determine
saturated fat intake asks, "How many ounces of meat, fish, or poultry do you usually eat?" As meat contains
primarily SFAs, but fish and poultry contain mostly UFAs, the answers given will not provide accurate information
as to the subject's saturated fat intake.
Another question asks, "How many commercial baked goods and how much regular
ice cream do you usually eat?" (Examples: cake, cookies, coffee cake, sweet rolls, donuts, etc. Do not count
low fat versions). Here commercial baked goods, always made with hydrogenated vegetable oils and shortenings, are
lumped together with full fat ice cream made with milk.
Question number seven asks: "What is the main type of fat you cook with?"
and provides four answers:
(1) non-stick spray or nothing at all,
(2) liquid vegetable oils,
(4) butter, shortening, bacon drippings, or lard.
Here we have trans-fatty acids mixed in with PUFAs, MUFAs, and SFAs. How in the
world can anyone accurately measure saturated fat intake with such a poor questionnaire (38)?! Hopefully, you're getting
**Modern researchers fail to properly isolate dietary factors in people with
CVD or cancer.
As a result, the harmful effects of trans fat (and sugar) consumption get mixed
up with SFA consumption (39). The result is that SFAs get blamed for the evils of trans fats, excessive PUFAs, and
refined sugars. This is actually how the Lipid Hypothesis got its start - in the 1940s, American researchers found
a strong correlation between cancer and fat consumption and the fats used were hydrogenated fats, not naturally
saturated fats (40).
The error has been repeated ever since despite a number of studies clearly exonerating
animal fats as causes of either heart disease or cancer. A good example of this is the result of a long term study
of 60,000 Scandinavian women reported in the Archives of Internal Medicine. The authors noted that animal fat consumption,
even when high, did not translate into an increased risk for cancer, unlike vegetable oils and other polyunsaturates
Other US studies, such as the Veterans Clinical Trial, the Minnesota State Hospital Trial, the Honolulu Heart Program,
and the Puerto Rico Heart Health Study, found no correlation between a diet high in saturated fats and cholesterol
with CVD (7).
Rowland, lamenting the sad state of exacting research among supporters of the
Lipid Hypothesis, stated: "I believe many of the ill effects attributed to eating meat (and fat) are misplaced.
Western diets that are high in meat also tend to be low in dietary fibre and high in refined sugar and adulterated
fats. Is it only one dietary culprit that is to blame or the combination of all?"(42)
F. Reducing one's intake of saturated fat and cholesterol,
and increasing one's intake of unsaturated fats, translates to a decreased risk for CVD.
Since we have already seen that dietary cholesterol has little effect on serum cholesterol levels, and that a high
intake of SFAs does not correlate with greater risk for cancer or heart disease, the first part of this contention
is wrong. The second, however, deserves our attention.
Kritchevsky's studies did show that PUFAs reduced serum cholesterol levels. The
likely explanation for this is that as PUFAs are increasingly incorporated into our cell membranes, they become
more weak. The body then sequesters cholesterol from the blood to add "stiffness" to the cellular membrane
The result is a reduction of serum cholesterol levels. But remember - there is no proof that such a reduction translates
into a reduced risk for CVD.
While small amounts of PUFAs are needed by the body, excessive consumption is
extremely deleterious. How tragic that, for the past 50 years, Westerners have been urged to consume more PUFAs
in the form of vegetable oils. This advice has translated into nothing but death and suffering.
Finally, early in 1998 a symposium entitled Evolution of Ideas about the Nutritional
Value of Dietary Fat reviewed the flaws of the Lipid Hypothesis, as well as studies that showed that mice fed whole
milk lived several months longer than mice on fat-free milk. One of the participants noted that low fat diets and
cholesterol-lowering drugs in study trials "did not affect overall CHD (coronary heart disease) mortality."
This person also went on to say, "Research continues apace and, as new findings appear, it may be necessary
to re-evaluate our conclusions and preventive medicine policies" (43). Who made such statements? David Kritchevsky,
the father of the Lipid Hypothesis!
G. Numerous studies prove that increased dietary saturated
fat/cholesterol intake strongly correlate with higher rates of atherosclerosis and heart disease.
There have been a number of studies completed that supposedly prove the Lipid Hypothesis of heart disease. As we
shall see from the following analysis, these studies have actually proven little and in fact, present data that
confounds the Lipid Hypothesis. Let us go through the major studies one by one.
1. The Framingham Heart Study is often brought up to prove the Lipid Hypothesis. This study began in 1948 and involved
about 6,000 people from a small town in Massachusetts. Two groups were compared at five year intervals - one group
ate lots of saturated fat and cholesterol, and another group ate little.
One major finding of the study was that those who weighed more and had higher
blood cholesterol levels were more at risk for CVD. Weight gain and cholesterol levels, however, had an INVERSE
correlation with dietary intake of fat and cholesterol. In other words, there was no correlation whatsoever. Dr.
William Castelli, MD, headed the study and had to admit in 1992:
In Framingham, Massachusetts, 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 (44).
2. In a multi-year British study involving several thousand men, half were asked to reduce saturated fat and cholesterol,
to stop smoking, and to increase their intakes of margarine and vegetable oils. After a year, those on the "good"
diet had 100% more deaths than those on the "bad" one, even though these men continued to smoke!
In describing the study, however, the lead researcher ignored these results and
urged that the British public to follow the "good" diet designed by the study's authors (45).
3. The US Multiple Risk Factor Intervention Trial compared mortality rates and
eating habits of 12,000+ men. Those with "good" dietary habits, i.e., low saturated fat, reduced smoking,
etc., showed a slight reduction in total CVD rates, but their all-cause death rate was higher than the "bad"
This result has been repeated many times in other similar studies, but it is never
revealed to the public. The few studies that indicate a correlation between fat reduction and a decrease in CVD
mortality also clearly document a sizeable increase in deaths from cancer, suicide, and violence (46).
4. The Lipid Research Clinics Coronary Primary Prevention Trial is, like the Framingham study, often brought forward
to support the Lipid Hypothesis. But this study did not actually test for dietary cholesterol and saturated fat
intake as all the subjects involved were already on a low fat diet. Instead, the study tested the effects of a
cholesterol-lowering drug. Statistical analysis of the results indicated a 24% reduction in the rate of CVD in
the drug-taking group compared to the other who took no drug at all.
Deaths, however, from cancer, stroke, violence, and suicide rose considerably
in the drug-taking group. The 24% reduction claim was challenged later by independent researchers. They found NO
statistical difference in the CVD rates between both groups. Despite these disturbing data, the press and medical
communities hailed the study as proof that animal fats kill people and that lowering cholesterol is good (47, 48).
5. Another popular study was the Leiden Intervention Trial conducted in the Netherlands.
Over 10 years ago, the elderly people of this small town had their cholesterol levels measured and were placed
on a low cholesterol/saturated fat diet. A decade later, investigators made the shocking discovery that those who
had higher serum cholesterol levels lived longer than those with lower levels. Those with a cholesterol level of
251+ had a 44% lower mortality rate than those whose readings were 194 or less (49).
6. Even Keys' famous "Seven Countries" study, thought to establish the Lipid Hypothesis by showing that
high rates of CVD correlated with high intakes of saturated fat (10), was severely flawed.
His evidence for contending that animal fat causes heart disease was
based on two kinds of data - a comparison of the cause of death from widely differing groups as listed on death
certificates, data on the diet of the nation (not the individual) and levels of serum cholesterol. From these rather
unreliable types of data, he concluded that a high intake of animal fats causes a high level of serum cholesterol,
which in turn leads to coronary heart disease (19).
Keys also neglected to account for lifestyle factors that contribute to heart disease. For example, Keys claimed
that Finland had the highest level of animal fat intake and the highest incidence of CVD and then concluded that
there was a cause and effect relationship. But the Finns are also heavy smokers, something overlooked by Keys.
Years later, when health professionals tried to change the Finn's dietary habits by encouraging more low-fat foods,
heart disease rates did drop.
But at the same time the "diet reeducation" was going on, an aggressive
and successful stop smoking campaign was carried out - this was the likely reason for the reduction in heart disease
Yudkin also demonstrated that Keys ignored refined sugar intakes of his study subjects. Yudkin determined that
in the same countries that Keys studied in a 1953 paper, the correlation between refined sugar intake and CVD was
much higher than between fat and CVD.
Yudkin specifically criticised Keys saying, "No one has ever shown any difference
in fat consumption between people with and people without coronary diseases, but this has in way deterred Dr. Keys
and his followers" (51).
7. Dean Ornish, MD, is a popular American doctor who claimed to have statistically proven that a low fat, low cholesterol
diet could reverse and prevent CVD. "The Ornish Plan" is well-known and heavily advocated as a treatment
for CVD. Unfortunately, it appears that the dietary component of Ornish's plan has little effect on CVD.
Ornish not only takes a dietary approach to CVD, but also encourages lifestyle
changes such as daily meditation, stress reduction techniques, exercise, and smoking cessation. In a recent advertisement
for Ornish's products, it was revealed that for the first time,
"Dr, Ornish's research offers strong scientific evidence that lifestyle changes
alone (emphasis added) can actually
begin to reverse even severe coronary artery disease after only one year without the use of cholesterol-lowering
drugs". (Claude Lenfant, M.D., Director, National Heart, Lung, and Blood Institute, National Institutes of
Patients reported a 91% reduction in the frequency of chest pains, and for most
of them, the progression of arterial clogging reversed after only one year. In contrast, heart disease worsened for the majority of patients in the control
group, who exercised moderately and followed a conventional 'low fat' diet.(emphasis added)
In commenting on Ornish's studies, Dr. Russell Smith wrote "the amount of [arterial] regression did not correlate
with the amount of cholesterol reduction. This was a most significant finding that was not discussed in Ornish's
paper when all subjects had completed the 1-year program" (52). Dr. Smith, Ph.D., authored a massive analysis (52) of all studies done that supposedly prove
the Lipid Hypothesis and showed in painstaking detail how study results were manipulated to prove the theory.
In one revealing section of his book, he shows that, in some study groups, death
rates decreased as people consumed more saturated fat and cholesterol! Smith also constantly points out how all
studies showing the Lipid Hypothesis to be true are sponsored, either all or in part, by various companies who
manufacture cholesterol-lowering drugs, or who make low fat foods.
A dietary approach to CVD and hypertension that does not receive much attention
from the medical world is the program of popular diet writer Dr. Robert Atkins, MD, of New York. Atkins treats
his CVD patients with a high protein, high fat, high cholesterol, but low carbohydrate, diet with much success
Such clinical evidence is an embarrassment to the Lipid Hypothesis. But it demonstrates the point of this course
- saturated fat and cholesterol do not cause heart disease.
In closing this section, let us turn to the review paper authored by Dr. Laura
Corr, M.D. Corr, one of Great Britain's leading cardiologists, wrote in her startling paper "The Low-fat Diet
The commonly-held belief that the best diet for prevention of coronary
heart disease is a low saturated fat, low cholesterol diet is not supported by the available evidence from clinical
trials. In primary preventions, such diets do not reduce the risk of myocardial infarction or coronary or all-cause
mortality. Cost-benefit analyses of extensive primary prevention programmes, which are at present vigorously supported
by governments, health departments, and health educationalists, are urgently required... .
Similarly, diets focused exclusively on reduction of saturated fats and cholesterol
are relatively ineffective for secondary prevention and should be abandoned. There may be other effective diets
for secondary prevention of coronary heart disease but these are not yet sufficiently well-defined or adequately
A number of studies seem to indicate that low levels of High Density Lipoproteins
(HDL) and high levels of Low Density Lipoproteins (LDL) translate into an increased risk for heart disease. HDL
is often referred to as "good cholesterol," and LDL as "bad" cholesterol. Some studies show
that a reduction of saturated fat intake raises HDL levels (but others show the opposite - see references to Dr.
Mary Enig's work in the Works Cited). In short, HDLs carry cholesterol in the blood back to the liver for breakdown,
while LDLs carry cholesterol from the liver out to tissues (1).
It is routine for people to have their ratios of HDL to LDL checked when going
for a medical exam or blood work. It appears, however, that the HDL-LDL theory is unfounded. Smith cites numerous
studies showing no significant relationship between HDL or LDL levels and heart disease (52). He quotes Lipid Hypothesis
supporters Grundy, Rifkin, and Cleeman as saying:
Often, populations with a high prevalence of CHD (coronary heart disease) have relatively HIGH [emphasis added]
HDL concentrations... . Moreover, there are populations... in which low HDL cholesterol concentrations seemingly
do not convey increased risk for CHD. Finally, certain genetic causes of severely reduced HDL apparently are not accompanied by a markedly
increased coronary risk (52). (emphasis added)
Smith then cites research from Knuiman, et al, demonstrating that among different populations from different countries,
there is no significant relationship between HDL levels and heart disease. Smith also cites research from Lewis,
et al, who reported that HDL levels were almost identical in large samples of men and women from Italy, Switzerland,
England, and Sweden, but that deaths from heart disease differed among these countries. If the HDL-LDL theory were
true, then there should have been a consistent death rate from heart disease since all of the subjects had similar
HDL levels, but such was not the case.
One Lipoprotein to Worry About Is Lipoprotein (a)
Even the conservative Garrison and Somer warn against Lp(a): "Evidence implicates
elevated levels of Lp(a) as an independent risk factor for CVD. Some researchers suggest that Lp(a) promotes atherosclerosis..."
Dr. Joseph Mercola, an osteopath, writes in his online newsletter, "Elevated lipoprotein A levels are a serious
risk factor for cardiovascular disease. We screen all of our chelation patients for this" (55). Dr. Mary Enig describes Lp(a)
as "atherogenic" (56). Though research is still continuing on this substance,
**it is recommended that you request your
Lp(a) levels be measured at your next checkup.
Acceptable levels per dl of blood would be <10 mg. 11-24 md/dl are borderline
high; >25 are very high. If your Lp (a) levels are over 10, you need to take action at once. What raises Lp(a)
levels? Trans-fatty acids. What lowers them? Saturated fats (56)! Mercola states that he uses a combination of vitamin C, niacin, and the amino acids lysine
and proline to lower Lp(a) levels (55). This is similar to the protocol advocated by Dr. Mathias Rath, former research colleague
of Dr. Linus Pauling.
Saturated Fats: What You Haven't Been Told
Many people, because of the anti-fat propaganda of the last 50 years, think there
is nothing nutritious about saturated fats, but there are many vital nutrients and substances found in saturated
fats not found in other foods. Butter, for example, is rich in trace minerals, particularly selenium, all the fat-soluble
vitamins, as well as two fatty acids: butyric and lauric. Both of these are antifungal, antibacterial, and antineoplastic
(against cancer) substances.
Additionally, butter provides the fatty material needed by the intestines to convert
plant carotenes into active vitamin A. Due to the unjustified saturated fat and cholesterol scare of the past few
decades, most people have eliminated butter from their diets. These people would probably reconsider this decision
if they knew of butter's healthful qualities.
Coconut oil is another good example. Formerly used widely in baked goods, this
oil is very rich in lauric acid. This fatty acid converts in the intestines into monolaurin, a powerful antifungal
and antibacterial substance. Coconut oil also contains caprylic acid, also a powerful antifungal. Yet these properties
are lost amidst a plethora of unwarranted warnings about "the dangers of saturated fat". Tropical peoples
have had coconut as an integral part of their diet for thousands of years, yet suffer from no CVD, as long as they
remain on their native diet (57,58).
The body needs saturated fats in order to properly utilize essential fatty acids.
Saturated fats also lower the blood levels of the artery-damaging lipoprotein (a), elevate HDL levels, are needed
for proper calcium utilization in the bones, and provide a good energy source for the vital organs. They stimulate
the immune system, protect the liver, do not initiate free radical formation, and are non-irritating to the arterial
walls. Omitting them from one's diet, then, is poor advice indeed (6, 57, 59-65)!
The Dangers of the Prudent Diet
You should have noticed that:
**subjects placed on low fat/cholesterol
diets suffered from serious health problems.
This is not difficult to understand. Cholesterol is needed by the body to manufacture
an array of hormones, as well as contribute to the structural integrity of the cell membrane. Cholesterol is also
needed for the proper function of serotonin receptors in the brain. Serotonin is what makes us "feel"
good - this is why low cholesterol levels are associated with higher rates of depression, suicide, and aggressive
Dietary cholesterol plays an important role in maintaining the health of the intestinal
wall. People on low cholesterol diets tend to suffer from gastrointestinal problems, including "Leaky Gut
Syndrome." As a practitioner who has dealt with several former "low fat folk," I can clinically
attest to this. Cholesterol is also needed for the proper development of the brain and nervous system. This is
one of the reasons why human breast milk contains high amounts of saturated fat and cholesterol.
Despite this, and the fact that low fat diets cause learning disabilities, stunted
growth, and failure to thrive, major public health organizations recommend low fat/cholesterol diets for all children
over the age of two! One can only lament the fate of these unfortunate innocents (4).
Since fat provides a reliable energy source to the body,
**low fat diets are associated with depression,
low energy, and fatigue.
Additionally, since saturated animal fats are carriers of the fat-soluble vitamins
(A, D, E, and K), and since the body needs such nutrients to properly assimilate protein, omitting them from one's
diet is ill-advised. Dr. Weston Price, a researcher who studied native peoples and their diets in the 1930s, concluded
that diets of healthy robust peoples contained 10 times the amount of fat-soluble vitamins than modern diets at
that time. Obviously, it is impossible to stay healthy on a low-fat diet as fats are the principal carriers of
the fat-soluble vitamins.
Not only are low-fat, high carbohydrate diets deleterious to our health in general,
they actually increase risk for heart disease, breast cancer, diabetes, hyperinsulinism (a major risk factor for
heart disease), high triglycerides, and aggravation of schizophrenia (66). Some people have reservations about
adding more butter, cream, and coconut into their diets for they fear they will put on weight from consuming more
fat. This is not altogether true. The fatty acids the body stores as fat tissue are the long and very long ones,
the kind found more in olive and vegetable oils; the short and medium length ones are used for energy and not stored.
Most of the fatty acids in butter and coconut are of the short and medium chain variety - weight gain is unlikely.
Points to Remember
** The more a fat is saturated, the more stable it is chemically.
** It is mostly trans-fatty acid consumption, and not saturated fat consumption,
that is strongly correlated with increased cancer and cardiovascular disease.
** In times when heart disease and MIs were rare, people consumed plenty of animal
fats, namely, butter, lard, cream, eggs, and tallow.
** Increased sugar intake is one of the main causes of heart disease.
** As animal fat consumption has decreased and vegetable fat consumption has increased,
heart disease and cancer have increased.
** Studies conducted on diet and cholesterol levels found no significant difference
in plasma cholesterol levels in egg eaters and non-egg eaters.
** Most people do NOT have elevated cholesterol levels prior to experiencing a
* * Native peoples the world over consume high amounts of animal fats with no
incidence of heart disease.
** Modern researchers fail to properly isolate dietary factors in people with
CVD or cancer.
** It is recommended that you request your Lp(a) levels be measured at your next
** Subjects placed on low fat/cholesterol diets suffered from serious health problems.
** Low fat diets are associated with depression, low energy, and fatigue.
APPENDIX A: GOOD FATS & BAD
GOOD: Butter, beef and lamb tallow, lard, sesame seed oil, olive oil, peanut oil, cold (expeller) pressed nut oils
(almond, macadamia, walnut, etc.), coconut oil, fish oils (e.g., cod liver oil), poultry fats (chicken, duck, and
goose), cream, ghee, flax oil, palm oil, palm kernel oil, high oleic safflower or sunflower oils.
NOTE: Do not cook or heat flax or walnut oils.
BAD: Margarine, partially hydrogenated oils of any type, vegetable oil, commercial corn oil, canola oil, hemp seed
oil, soybean oil, cottonseed oil, vegetable shortening, safflower oil, all fats and oils heated to extremely high
APPENDIX B: FATTY ACID BREAKDOWN
OF SOME FATS AND OILS
|Lauric acid (1)
|Linoleic acid (2)
|Palmitoleic acid (3)
|Stearic acid (4)
|See Appendix C
|Oleic acid (5)
|Palmitoleic acid (3)
|Lauric acid (1), Betacarotene (7)
|Oleic acid (5)
|Oleic acid (5)
|Linoleic acid (6)
|Oleic acid (5)
|Human milk fat
|Lauric acid (1)
NOTES TO APPENDIX B
1. Lauric acid: This medium chain saturated fatty acid is a 12-carbon fatty acid with potent antimicrobial properties.
The major fatty acid in human breast milk, it is lauric acid that protects the babies' intestines from microbial
invasions until its immune system is more competent. Lauric acid converts into the monoglyceride monolaurin in
the small intestines.
2. Linoleic acid: This fatty acid is an omega-6 polyunsaturated essential fatty acid. Linoleic acid is mostly found
in vegetable fats and converts in the body to such fatty acids as gamma linoleic acid (GLA) and arachidonic acid
(AA), both needed as precursors to hormone-like substances called prostaglandins. In this century, there has been
a major increase in the amount of linoleic acid consumed by Westerners due to the increasing use of vegetable oils.
High intake of linoleic acid inhibits our cells' ability to utilize omega-3 fatty acids, as well as increases one's
risks for cancer, immune dysfunction, and cancer.
3. Palmitoleic acid: This 16-carbon monounsaturated fatty acid is found in marine oils, chicken fat, lamb tallow,
lard, butter, macadamia nuts, and olive oil. Palmitoleic acid, like lauric acid, has considerable antimicrobial
4. Stearic acid: This 18 carbon chain saturated fatty acid is found in beef tallow, cocoa butter, lard, chicken
fat, butter, and seed oils. Stearic acid has been shown to be the preferred fuel of the heart muscle.
5. Oleic acid: The most prevalent monounsaturated fatty acid found in food, oleic acid is an 18-carbon chain omega-9
fatty acid that predominates in olive oil and lard.
6. Linolenic acid: An 18-carbon chain omega-3 polyunsaturated essential fatty acid, alpha linolenic acid converts
in the body to such fatty acids as eicosapentanoic acid (EPA) and docosahexaenoic acid (DHA), both found in fish
oils such as salmon and sardines. Linolenic acid is found in small amounts in animal fats and larger amounts in
flax, walnut, and soybean oils. Due to its triple bonds, it is more fragile chemically and very heat and light
sensitive. Oils with a high amount of linolenic acid are unsuitable, therefore, for cooking.
7. Betacarotene: Betacarotene is a metabolic precursor to vitamin A and is found in all orange, yellow, and dark
green vegetables and fruits. It is betacarotene that gives palm oil its orange color. Betacarotene is a potent
antioxidant that helps neutralize free radicals within the body.
Sources: Know Your Fats by Mary Enig, Ph.D., Bethesda Press; 2000; Nourishing Traditions by Sally Fallon and Mary
Enig, Ph.D., New Trends Publishing; 2000.
APPENDIX C: GOOD THINGS IN BUTTER
Fat soluble vitamins (A, D, E, K)
Essential fatty acids (small amounts of linoleic and linolenic acids)
Butyric acid (1)
Conjugated Linoleic Acid (from grass-fed cows only) (3)
Trace minerals (5)
NOTES TO APPENDIX C:
1. Butyric acid is a short-chain saturated fatty acid that has demonstrated anti-tumorigenic activity. It is also
the major fuel source for the large intestine.
2. Glycosphingolipids: These are a special class of lipids that help protect against intestinal infections, especially
in the young and elderly.
3. Conjugated Linoleic Acid (CLA) has strong anti-cancer properties. It also encourages the build up of muscle
and prevents weight gain. CLA is ONLY found in butter from pasture-fed cows.
4. Lecithin is a phospholipid that assists in the proper assimilation and metabolism of cholesterol and other fat
5. Trace minerals like manganese, zinc, chromium, and iodine are found in the fat globule membrane of butterfat.
6. Selenium is an essential trace mineral that is a powerful antioxidant. Its activity is synergistic with vitamin
E (also found in butter). Selenium is key in cancer prevention and, ounce for ounce, butter has more selenium than
any other food.
7. Cholesterol is found in the membrane of every cell membrane. It is also the precursor to vitamin D and steroid
hormones. Cholesterol is also an antioxidant and the body's repair substance. Dietary cholesterol contributes to
the health of the intestinal wall.
Sources: Know Your Fats by Mary Enig, Ph.D., Bethesda Press; 2000; Nourishing Traditions by Sally Fallon and Mary
Enig, Ph.D., New Trends Publishing; 2000.
Copyright © Stephen Byrnes, 2000-2001. Reprinted with permission.
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