a long-term study showing that a high cholesterol or saturated fat diet has
any impact on blood cholesterol levels in a normal healthy population - or any
effect whatsoever on the rate of death from coronary heart disease
is a much maligned substance, the ‘cause’ of heart disease. If it is, it
must have killed billions of people. Far more than the plague, every war
ever fought, and all plane, train and car crashes ever - all added together,
then multiplied by three.
if it does cause heart disease, how does it do it? The simple ‘answer’
is that, if you eat too much cholesterol, the level in your blood rises, the
cholesterol then travels through the artery wall causing cholesterol-laden
plaques to develop which then rupture and kill you. That’s the initial
cholesterol hypothesis. Dead simple, couldn’t be more simple.
little problem - dietary intake of cholesterol has no impact on the level of
cholesterol in your blood. If we look at two major long-term studies,
Framingham and Tecumseh, it is clear that those who ate the most cholesterol
had exactly the same level of cholesterol in their blood as those who ate
the least cholesterol.
is hardly news. The man, who, more than any other, is responsible for the
creation of the diet heart hypothesis fully agrees. To quote Ancel Keys,
from a paper in 1956:
‘In the adult man the serum cholesterol level is
essentially independent of the cholesterol intake over the whole range of
did Ancel Keys think, more recently, about the connection between
cholesterol in the diet, and cholesterol in the blood?
"There's no connection whatsoever between
cholesterol in food and cholesterol in blood. And we've known that all along.
Cholesterol in the diet doesn't matter at all unless you happen to be a
chicken or a rabbit." Ancel Keys, Ph.D., professor emeritus at the
University of Minnesota 1997.
this come as a surprise?
it doesn’t matter one jot how much cholesterol you eat, it has no impact
whatsoever on blood cholesterol levels. Which just blows up a fairly
important part of the cholesterol hypothesis.
hold on, that doesn’t matter,’ (the sound of goalposts being desperately
moved fills the air) ‘It is not cholesterol in the diet that causes the
cholesterol level to rise, it is the consumption of saturated fat?’
again at the Tecumseh study.
explain that table in a little more detail. Basically, it divides people
into thirds with high, average or low blood cholesterol levels. The absolute
values are not important.
done this we can examine the level of saturated fat consumed by these three
groups. As can be seen:
Those in the lowest third of cholesterol levels consumed 52g/day of
Those in the mid-range consumed 54g/day of saturated fat
Those with the highest levels consumed 54g/day of saturated fat
lead to the conclusion, from the authors that:
‘Serum cholesterol and triglyceride values were not
positively correlated with selection of dietary constituents.’
shall translate those weasel words into plain English. ‘You can eat as
much saturated fat as you like and it makes no difference whatsoever to your
blood cholesterol levels.’
what of Framingham and saturated fat. Let us quote William Castelli,
director of the Framingham study for many years.
"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." Dr William Castelli 1992 (Director
of the Framingham study)
you may think that I am just quoting studies that support my ideas. However,
a special prize to the man, or woman, who can find a long-term study showing
that a high cholesterol, or high saturated fat diet, has any impact on blood
cholesterol levels (in a normal, healthy population). Or, indeed, has any
effect whatsoever on the rate of death from CHD.
time to move those goalposts again.
not saturated fat in the diet, it’s the ratio of polyunsaturated to
saturated fat ratio….. the P/S ratio. Hey, can’t you people just give up
and admit that fat, of whatever sort, in the diet and cholesterol levels
just are not related?
how could they be? For, in the next episode I shall make it clear that there
is no way you can link fat intake with cholesterol levels in the blood. The
two substances are completely unrelated chemically, and only ever meet when
they are, coincidentally, rammed together inside a lipoprotein.
then I will show why a high blood cholesterol level cannot cause heart
disease. Ladies and gentlemen, roll up, roll up and gasp in amazement as the
fearsome cholesterol hypothesis disintegrates in front of your very eyes.
studies have shown that a high saturated fat intake raises cholesterol
levels; others have shown the exact opposite. The longest, most prestigious
and widely quoted long-term study on CHD, the Framingham study, clearly
shows that those who eat the most saturated fat have the lowest cholesterol
own belief is that in healthy people, dietary intake, of anything, has no
effect on cholesterol levels - beyond a few percentage points of
my belief is not an act of personal faith with no foundation on fact. For
the science of fat metabolism confirms that there cannot be any
connection whatsoever between saturated fat consumption and cholesterol
levels. And I am wondering how best to explain this without getting too
first point to make is that you do not have a cholesterol level in your
blood. Cholesterol is insoluble in blood, and therefore has to be carried
around the body inside a small sphere known as a lipoprotein. There are many
different types of lipoprotein, ranging from the monster chlyomicron to the
teeny, weeny, High Density Lipoprotein (HDL).
do not just carry cholesterol. They also carry all sorts of other fats,
saturated, monounsaturated and polyunsaturated. These fats are all attached
to a glycerol molecule, in sets of three, and the resulting substance is
therefore called a triglyceride.
= three fats attached to a backbone glycerol molecule. (Just in case
you’re wondering, a fat is a fatty acid, and a fatty acid is a fat).
when you eat cholesterol and saturated fat, they are both absorbed into the
intenstinal wall, where the saturated fats are all stuck onto a glycerol
molecule, to make triglycerides, the cholesterol remains unchanged. Then,
within the intestinal wall both are rammed into a chylomicron before being
expelled into the portal circulation system to be moved around the body.
chylomicrons go directly to the liver where they are absorbed, broken down,
and reconstructed into a smaller type of lipoprotein known as a Very Low
Density Lipoprotein VLDL. These VLDLs then go out into the general
circulation and gradually lose triglyceride. As they do so, they get smaller,
transforming from VLDL to Intermediate Density Lipoproteins (IDLs), then Low
Density Lipoproteins (LDLs).
LDL is either absorbed back into the liver, to be reused to create more
VLDLs, or they are absorbed into other tissues where the contents are used
by the cell.
at what point does saturated fat get turned into cholesterol?
it doesn’t. You don’t make cholesterol out of saturated fat. Cholesterol,
when it is made in the liver, starts out as a substance called Acteyl-co A.
This is not a fat; it is nothing like a fat. It has several nitrogen atoms
in it, and nitrogen comes from protein.
A SATURATED FAT* CHOLESTEROL
one, therefore, is that saturated fat and cholesterol and completely
unrelated chemically, and you don’t make cholesterol from fats. So why
would eating saturated fat increase cholesterol production in the
liver?….. It can’t and it doesn’t.
of course, the substance we are interested in nowadays is LDL. Which is not
the same thing as cholesterol at all. So why do we called a raised LDL level
a raised cholesterol level?
fact, the nomenclature in this whole area is just designed to make things
almost impossible to understand. For example, a raised VLDL level is known
as hypertriglycerideamia. Why? Goodness only knows. Perhaps if researchers
in this area were to use a clear form of nomenclature, the weakness of the
diet/heart hypothesis would be more easily exposed.
for a little review
Cholesterol and saturated fats are unrelated substances and you don’t
make cholesterol from saturated fat, or any other type of fat
A raised cholesterol level is, in reality, a raised LDL level
A raised VLDL level is called hypertriglyceridaemia
The only connection between saturated fats and cholesterol is that,
because they are insoluble in water, they sit inside lipoproteins in order
that they can be carried around the body
The liver doesn’t make LDL - LDL is the metabolic residue of VLDL.
the whole concept of saturated fat intake raising cholesterol levels
doesn’t seem so simple anymore, does it? But, if the substance in the
blood that causes CHD is actually LDL, maybe we just need to move the
goalposts….again, and ask a different question.
a high saturated fat intake increase LDL levels?
to review some of the facts. The liver doesn’t make LDL, it makes VLDL,
and when VLDL loses triglyceride it turns into LDL.
if you eat more saturated fat (or any other kind of fat), the liver will
churn our more VLDL. NOT because there is more cholesterol around, but
because there are more triglycerides around to deal with.
presumably, after all the VLDLs have shrunk in size, there will be more LDLs
left. Which means that a high fat consumption could lead to a higher level
of LDL, via VLDL metabolism - although we have to abandon the whole
cholesterol argument at this point, as cholesterol has nothing whatsoever to
do with this process, it just gets carried around as an innocent bystander.
even if you move the discussion onto LDLs rather than cholesterol, there is
a further huge and insurmountable problem here. After a meal VLDL levels go
up, as you would expect, but the LDL level remains absolutely constant.
Absolutely constant….(and there is no delayed response either).
the amount of VLDL in the blood is totally unrelated to the level of LDL in
the blood. Despite the fact that you ‘make’ one from the other.
this proves, beyond any doubt, is that the metabolic system tightly controls
the level of LDL in the blood. It doesn’t matter how many VLDLs are
converted to LDL, the system takes the excess LDL out of play - instantly.
It pulls excess LDLs into the liver where it recycles them.
although fat intake can increase VLDL production, it has no effect on the
level of LDL. Which means that, not only does saturated fat have no effect
on cholesterol production in the liver, it also has no effect on LDL levels.
In reality, it has no effect at all. And why should it? If you eat too much
protein, your blood protein level doesn’t rise. If you eat too much sugar
your ‘fasting’ blood sugar level doesn’t rise. Why should fat or
cholesterol be any different?
will not read this type of information anywhere, but here. However, every
single fact I have used has been demonstrated many, many times. These are
facts beyond dispute. It’s just that no-one chooses to highlight what all
of these facts, when brought together, actually mean.
one: The liver does not use fats, saturated or otherwise to make cholesterol
A Raised LDL Level Has No Impact On Heart Disease
previously demonstrated that neither cholesterol, nor saturated fat
consumption, can have any impact on LDL levels. I now intend to make it
clear that a raised LDL level has no impact on heart disease (CHD).
most of you probably know, current thinking in CHD is that when the level of
Low Density Lipoprotein (LDL) is raised, LDLs travel through the artery wall
and form a big lumpy cholesterol deposit (‘plaques’) that narrow the
arteries. Cholesterol is found in plaques because LDL contains lots of
these plaques get bigger they narrow the artery so much that blood flow is
obstructed - causing symptoms such as angina. Finally a plaque may burst,
causing a blood clot to form over the ruptured area. This blocks the artery
completely. A myocardial infarction results, which may or may not kill you.
agree with this basic mechanism underlying CHD, but there are about eight
million problems with the idea that a raised LDL is the cause. Let’s just
concentrate on three:
People with normal and even low LDL levels develop plaques and die of CHD.
means that we have a disease process on our hands that can occur when the
LDL is level is high, average or low. The first ever example in medical
history whereby a normal level of a normal (and vital) substance in the
blood can cause a disease.
LDL is so terrible that any level at all can kill you. The only good LDL is
a dead LDL - or words to that effect. This concept, that a normal level of
substance in the blood can cause disease, is absolutely nuts and runs
contrary to all of biological science, or any other type of science. ‘My
goodness you have a NORMAL LDL level, it must be lowered.’
that aside, for the moment, let’s move to problem number two.
LDL can’t get through the lining of the artery wall
endothelium - single cell lining of the artery wall - is impermeable to LDL
- unless you get the level to about three times normal, which is 15mmol/l,
rather than 5.0mmol/l. So how does LDL get through in the first place?
Considering that 99% of the population has an LDL level below 10.
you can’t get it through. And even if it could, you run into problem
are discreet ‘lesions’ in the artery wall, they are not present
everywhere in all artery walls. So, if LDL ‘leaks’ through the arteries
when the concentration is raised, then it should leak through all artery
walls everywhere, and what we should see, therefore, is thickened artery
walls full of LDL everywhere, which is exactly what we don’t see.
use an analogy, if you lie in the sun for too long, all of your body will
become sunburned, not just a few bits here and there. But we are expected to
believe that, if you bathe the artery wall in a high level of LDL, it will
only leak through in a few discreet areas. Hmmmmm? Again, quite frankly,
know what you are thinking at this point, I think. Aha, you are thinking,
obviously you need to damage the artery wall, in discreet areas, to get LDL
through…… Exactly. And this could hardly be more obvious. So, the
underlying process that starts a plaque is damage to the endothelium. Of
course it is; there is no other possible explanation.
to admit this, is to admit that LDL has nothing whatsoever to do with
causing atherosclerotic plaques, because LDL doesn’t damage the
with this major, and I would say insurmountable problem, what has the
cholesterol/LDL brotherhood chosen to do? Discard the diet-heart/cholesterol/LDL
(whatever it is now called) hypothesis. Or keep trying to find ways to
explain the causal role of LDL in plaque formation.
surprise to find that no-one was remotely willing to discard the hypothesis.
This square peg of orthodoxy had to be rammed into the circular hole of CHD
causation at all costs. Otherwise the entire diet-heart/cholesterol/LDL
hypothesis collapses into a little heap of dust.
where are we now? How exactly does LDL cause CHD?
it is oxidised.
may faintly detect the sound of me beating my head against a wall in the
distance, somewhere just south of Manchester UK.
dear reader, LDL is oxidised! You have probably heard of anti-oxidants, and
their magical protection against CHD. But how are they thought to provide
this protection? Mainly because oxidised LDL can be absorbed by the
endothelium, as there are receptors for oxidised LDL on endothelial cells (called
Lox-1 receptors, if you are interested).
the thinking goes, once oxidised, the LDL binds to the Lox-I receptor it is
then transported into - then through - the endothelium and into the artery
wall behind. At which point, white blood cells, designed to get rid of all
nasty substances in the body, attack, engulf and try to clear away all of
the oxidised LDL molecules.
these white cells have no means to tell them to stop engulfing oxidised LDL,
allegedly, so they just get bigger and bigger until they explode, releasing
a horrible goo of dead white blood cells, bits of LDL, cholesterol and
triglyerides etc. into the artery wall. Once you have enough exploding white
blood cells, the lump of goo becomes big enough to start an atherosclerotic
plaque. And that is why oxidised LDL is such a bad thing, and why
anti-oxidants are protective.
are so many problems with this proposed mechanism of action that it is
almost impossible to know where to start. Perhaps the best place to start is
with a previous example.
there are receptors for oxidised LDL on endothelial cells, then oxidised LDL
will be absorbed through all artery walls everywhere, and therefore we would
not see discrete plaques forming, just general thickening of all artery wall
as they fill up with the residual goo from exploding white blood cells. But
we do see discreet plaques, and therefore? Therefore the hypothesis is wrong
as it does not match the observed disease process.
other problem is just as serious, although a little more difficult to
plaques are created by oxidised LDL, then the ‘cause’ of CHD must be
excess oxidisation of LDL in the bloodstream. If this is true, then the
level of LDL is completely irrelevant, it is only the amount of oxidised LDL
that counts. Therefore, if you believe in this hypothesis, then the
‘raised LDL causes CHD’ hypothesis has to be discarded.
essence, you can’t have this argument both ways. You can claim a raised
LDL causes CHD - in which case how can people with a low level get CHD? Or
you can claim that excess oxidised LDL causes CHD. In which case CHD has
nothing to do with LDL levels.
the oxidised LDL hypothesis - which was supposed to protect the LDL
hypothesis - actually destroys the LDL hypothesis. But by throwing up so
much jargon and incomprehensible mechanisms of actions into the air, it
appears that you are keeping both hypotheses going. But you can’t, it’s
one or the other, you can’t have both.
by the way, in the Heart Protection Study (HPS), which lasted five years,
ten thousand patients received the anti-oxidants and ten thousand patients
did not. And the results?
‘’’There was no evidence of any benefit at all’
from antioxidant vitamins. On the other hand, there was no evidence of any
harm.’’’ Dr Rory Collins BMJ Nov 2001
bang goes the anti-oxidant hypothesis. Please spare me the claim that they
used the ‘wrong’ anti-oxidants.
again, as with almost every part of the diet-heart/cholesterol hypothesis,
when you start to examine the facts objectively, the whole thing starts to
disintegrate in front of your very eyes. There is no way that LDL, oxidised
or otherwise, can ‘cause’ CHD, and here are a few more facts to back
There is a direct association between falling cholesterol levels over the first 14 years and mortality over the following 18 years (11% overall and 14% CVD death rate increase per 1 mg/dL per year drop in cholesterol levels). Anderson KM JAMA 1987
Framingham therefore, as LDL/cholesterol levels fell, CHD rates went up.
‘Our data accord with previous findings of increased
mortality in elderly people with low serum cholesterol, and show that
long-term persistence of low cholesterol concentration actually increases
the risk of death. Thus, the earlier that patients start to have lower
cholesterol concentrations, the greater the risk of death.’ Lancet Aug
Honolulu, the lower the LDL/cholesterol, the greater the risk of dying - of
everything, including CHD.
main author of the report on this study was Shestov, of the Institute of
Experimental Medicine, Russian Academy of Medical Sciences, St. Petersburg.
And the main conclusion of this study was as follows:
‘The results disclose a sizeable subset of
hypocholesterolemics in this population at increased risk of cardiac death
associated with lifestyle characteristics.’ Russian Lipid Research Clinics
Prevalence Follow-up Study Shestov
Russian, a greater risk of death from heart disease in those with low blood
Between 1980 and 1989, age-adjusted total serum
cholesterol levels increased from 4.84 to 5.22 for men and from 4.91 to 5.24
mmol/l for women. Prevalence of age-adjusted hypercholesterolaemia of >
or = 5.68 mmol/l increased from 15.8% to 29.4% for men and from 18.4% to
30.6% for women…. Considerable increases in total serum cholesterol
levels do not offer an explanation of the recent decline in mortality from
coronary heart disease in Japan.’ Okayama A, Marmot MG Int J Epidemiol
Japan, as cholesterol/LDL levels went up, death rates from CHD went down.
much more evidence would you like? Perhaps another study from the USA?
‘Kummerow and colleagues from the UI and Carle
Foundation Hospital in Urbana, Ill., studied 1,200 patients who were
cardiac-catheterized. Sixty-three percent had at least 70 percent of their
arteries blocked -- enough to warrant bypass surgery. Of the 506 men who had
a bypass, only 71 (14 percent) had plasma cholesterol levels above 240
(6.2mmol/l); 50 percent had levels below 200 (5.2mmol/l). Thirty-two percent
of the 244 women who had bypass surgery had levels above 240 (6.2mmol/l); 34
percent were below 200 (5.2mmol/l)…
… a 3-to-1 ratio of LDL (bad cholesterol) to HDL (good
cholesterol) is a low heart-disease risk? with a total cholesterol of less
than 200 (5.2mmol/l) being the most desirable. However, in this study,
Kummerow noted, 51 percent of the catheterized men had levels below 200
(5.2mmol/l) but needed a bypass.’ Paper by Kummerow Atherosclerosis March
this study, the majority of men who needed a bypass had cholesterol levels
were not, I will add, small studies, with surrogate end-points. These were
great big studies done on thousands and thousands of people, and they
measured death rates and blockages in coronary arteries, which are
‘hard’ end-points. They include Framingham - the study that is used to
set the CHD prevention guidelines! And they all demonstrate very clearly
that the rate of CHD has nothing whatever to do with the level of LDL/cholesterol
in your bloodstream.
studies were also published in journals as prestigious as the Lancet,
Atherosclerosis and JAMA. This is not wacky, fringe research, carried out by
people with a distrust of mainstream medicine. This is as mainstream and
conventional as it gets, and all of this research utterly and completely
contradicts the current cholesterol/LDL theory of CHD. And I will bet that
you have never, ever, come across these facts before. For some strange
reasons this research doesn’t get a lot of publicity.
but, you might say, statins reduce LDL levels and protect against CHD.
Surely that proves - despite your clever arguments, and all of the evidence
- that a raised LDL truly is the cause of CHD, even if it is biologically
for those of you who are interested, I can easily prove that the LDL
lowering effects of statins have nothing whatsoever to do with their impact