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Why Coconut Oil, or
Any Saturated Fat, Cannot Raise Cholesterol Levels (LDL levels)
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by Brian Shilhavy
Editor, Health Impact News
Editor, Health Impact News
Scottish medical doctor, Malcolm Kendrick, has just written a
brilliant expose on
his blog explaining,
scientifically, why it is impossible for saturated fats to raise LDL
cholesterol levels.
As I have written many times over the years,
this is the kind of information that can save your life and help you make wise
dietary choices, but it is information that the U.S. government, Big Pharma,
and the corporate-sponsored “mainstream” media cannot afford to publish.
Because to do so would be to admit guilt in
one of the biggest medical scams of all time: the lipid theory of heart
disease.
This theory, which has been proven
scientifically to be false, has been an economic success for
cholesterol-lowering statin medical drugs, the most profitable class of medical
drugs all time. This theory also promotes the low-fat diet which encourages
consumption of carbohydrates from U.S. subsidized crops, as well as
polyunsaturated oil, also derived from U.S. subsidized crops.
This theory of heart disease, which condemns
cholesterol and saturated fat, has probably been responsible for many millions
of people’s early deaths and the life-long suffering of autoimmune diseases for
an entire generation.
Why
saturated fat cannot raise cholesterol levels (LDL levels)
“Explanations exist; they have existed for
all time; there is always a well-known solution to every human problem — neat,
plausible, and wrong.”
H.L. Mencken.
Of all the flaws of the human mind, the
number one must be the overwhelming desire to find simple, easy to understand
answers – to everything. I think this is why my favourite film of all time is
Twelve Angry Men. It was a stage play first.
A black youth is accused of killing his
father. The evidence that is presented by the prosecution seems utterly
overwhelming. A unique knife is used for the murder, one that the youth was
known to carry. He was seen leaving the apartment after shouting ‘I’ll kill
you’ and suchlike. Most importantly, however, he was a young black youth, and
young black youths are widely considered to be the sort of person who do such
things.
In the film, prejudice presses down heavily
on most of the jurors. Some of them, it is hinted, would have found him guilty
no matter if there had been any evidence, or not. Here we have all the worst
aspects of human decision making on show. Confirmation bias, prejudice,
gathering together only the evidence that supports a case, the desire to ‘get
on with it’ and not hang about listening to people who just want to make things
complicated.
In my mind, for many years, I have changed
‘black youth’, into the word ‘cholesterol’ as I watch the ‘heart disease
jurors’ in action. A suspect was found, fitted up, put on trial and found
guilty by people who were just desperate to get on with it. At the very first
congressional meetings on dietary guidelines, any attempts to wait until there
was sufficient evidence, were railroaded.
When the US government
introduced “Dietary Goals for the United States”, they did not have unanimous
support. The guidelines, which urged the public to cut saturated fat from their
diet, were challenged by a number of scientists in a Congressional hearing. The
findings were not based on sufficient evidence, they argued.
They were ignored. Dr. Robert Olson recounts an
exchange he had with Senator George McGovern, in which he said: “I plead in my
report and will plead again orally here for more research on the problem before
we make announcements to the American public.” McGovern replied: “Senators
don’t have the luxury that the research scientist does of waiting until every
last shred of evidence is in.’
Senator McGovern might as well have said. ‘Listen son, we know that saturated fat
raises cholesterol and causes heart disease, we don’t need any damned
evidence.’ Of course, they didn’t have any evidence at all.
None. But they still managed to find saturated fat and cholesterol guilty. Some
people would call this proper leadership. Make a decision and go with it.
I would call it monumental stupidity.
As you can see I am stepping back in this
blog to look at saturated fat – again. Because I am going to share some
thinking with you, which I have not really shared before. Some of you will know
that I am a ‘first principles’ kind of guy. I take very little at face value,
and I am certainly highly critical of accepted wisdom: I usually translate it,
in my mind, into accepted stupidity.
So, I am going to try and explain to you that
saturated fat cannot raise blood cholesterol levels. By which I mean low
density lipoprotein levels (LDLs) as this is the substance which someone or
another ended up calling ‘bad’ cholesterol. It is the lipoprotein that is
thought to cause CVD.
However, LDL is not cholesterol, it never was.
We do not have a blood cholesterol level – but we are seemingly stuck with this
hopelessly inaccurate terminology for all time.
Anyway, the idea that saturated fat raised
cholesterol was driven by Ancel Keys in the late nineteen forties. The first
point to make here is that, when Keys first started his anti-fat crusade,
no-one knew that there was such a thing as LDL. You took a blood test, gathered
together all the lipoproteins you could find (good, bad, and indifferent) and
measured them all. Quite what they were measuring is a good question.
Despite this rather important gap in his
knowledge, Ancel Keys was able to create an equation to exactly predict the
effect of saturated and polyunsaturated fatty acids in the diet on serum
cholesterol levels.
Change in serum cholesterol concentration
(mmol/l) = 0.031(2Dsf −
Dpuf) + 1.5√Dch
[Where Dsf is the change in percentage
of dietary energy from saturated fats, Dpuf is the change in percentage of
dietary energy from polyunsaturated fats, and Dch is the change in intake
of dietary cholesterol].
This became the accepted wisdom. You could
believe, given the apparent precision of this equation, that he did some proper
research to prove it was true. Frankly, it seems bloody unlikely, as the
equation contains the ‘change
in dietary cholesterol’ as a key factor in raised blood
cholesterol levels. It is now accepted that cholesterol in the diet has no
significant impact on blood cholesterol levels. Keys even knew this himself.
To quote him 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 human diets.’
In
1997 Keys wrote this:
“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.
More
recently, the fact that cholesterol in the diet has no impact on ‘cholesterol
levels’ or CVD was reaffirmed. In 2015, the Dietary Guidelines Advisory
Committee in the US, having reviewed all the evidence made this statement:
“Cholesterol
is not considered a nutrient of concern for overconsumption.” 2
This
was even supported by the likes of Walter Willet and Steven Nissen:
‘Nutrition
experts like Dr. Walter C. Willett, chair of the Department of Nutrition at
Harvard School of Public Health, called the plan a reasonable move. Dr. Steven
Nissen, chair of cardiovascular medicine at the Cleveland Clinic, told USA
Today “It’s the right decision. We got the dietary guidelines wrong.’3
Anyway, Keys had started out with a hypothesis
that cholesterol in the diet raised cholesterol levels in the blood but
discarded it after feeding eggs to volunteers (eggs contain more cholesterol
than any other food) and finding that their cholesterol level remained
stubbornly unchanged.
Undaunted, he did what no scientist should
ever do. He simply changed the hypothesis. The nutrient of concern was no
longer cholesterol, it was saturated fat. So, what is it about saturated fat
that can raise LDL? I wanted to know the exact, proven, mechanism.
We start with the certain knowledge that the
body is exceptionally good at keeping all substances in the blood under strict
control. If the level of something rises too high, mechanisms are triggered to
bring them back under down, and vice-versa. The entire system is known as
homeostasis.
Thus, if saturated fat intake really does
cause LDL levels to reach damaging levels, it must be overcoming homeostasis,
and breaking metabolic and physiological systems. How does it do this?
To try to answer this question we should look
at what happens to saturated fat when we eat it. The first step is that it
binds to bile salts in the bowel. Bile salts are a form of mildly adapted
cholesterol, synthesized in the liver and released from the gall bladder.
Without bile, fat cannot be absorbed well, if at all, and simply passes through
the guts and out the other end.
The absorbed saturated fat is then packed
into a very large lipoprotein (known as a chylomicron). Once a chylomicron is
formed it travels up a special tube, called the thoracic duct, and is released
directly into the blood stream. It does not, and this is important, pass
through the liver.
Chylomicrons then travel around the body and
are stripped of their fat, shrinking down until they become about the size of
an LDL. At which point they are called chylomicron remnants. These are absorbed
back into the liver – using LDL receptors – and are then broken down into their
constituent parts
Therefore, a small amount of fat that you eat
will end up in the liver. However, the vast, vast, majority will go straight
from the guts to fat cells (adipose tissue). Whereupon they are stored away for
later use.
In fact, this is the fate of all types of
fat: saturated, polyunsaturated, or monounsaturated. There is nothing unique
about saturated fat in the way that it is absorbed and transported around the
body. Anyway, as you may have noticed, none of this has anything to do with LDL
whatsoever. Nothing. Ergo the consumption of saturated fat, or any fat, can
have no direct impact on LDL levels.
I suppose the next question to ask is simple.
Where does LDL come from? LDL is created when VLDLs (very low-density
lipoproteins) shrink down in size. VLDLs are the type of lipoproteins that are
synthesized in the liver, then released into the bloodstream. They contain fat
and cholesterol and, as they travel around the body, they lose fat and become
smaller and smaller, until they become an LDL -which contains proportionately
more cholesterol.
Almost all LDL molecules are removed from the
circulation by LDL receptors in the liver. They are then broken down and the
contents used again. Some LDL continues to circulate in the blood, and cells
that need more cholesterol synthesize an LDL receptor to bind
to LDL molecules and bring the entire LDL/LDL receptor complex into the cells.
Just to re-cap. Saturated fat (any fat) is
absorbed from the gut and packed into chylomicrons. These travel around the
body, losing fat, and shrink down to a chylomicron remnant – which is then
absorbed by the liver. There is no connection between chylomicrons and LDL.
Instead LDL comes from VLDL. VLDLs are made
in the liver, they contain fat and cholesterol. VLDLs leave the liver, travel
around the body and lose fat, shrinking down to become an LDL.
As the only source of LDL is VLDL, this leads
to the next obvious question. What makes VLDL levels rise? Well, it sure as
hell isn’t fat in the diet. What causes VLDL levels to rise is eating
carbohydrates. The next quote is a bit jargon heavy but worth including.
‘De
novo lipogenesis is the biological process by which the precursors of
acetyl-CoA are synthesized into fatty acids [fats]. In human subjects consuming
diets higher in fat (> 30 % energy), lipogenesis is down regulated and
extremely low; typically < 10 % of the fatty acids secreted by the
liver. This
percentage will increase when dietary fat is reduced and replaced by
carbohydrate.’4
To simplify this as much as possible. If you
eat more carbohydrates than your body needs, or can store, the liver converts the
excess (primarily fructose and glucose) into fat in the liver. This process is
called de novo lipogenesis (DNL) The fats that are synthesized are saturated
fats, and only saturated fats. Once synthesized they are then packed into VLDLs
and sent out of the liver.
In short, if you eat fat, the VLDL level
falls. If you eat carbohydrates the VLDL level rises. Which is pretty much what
you would expect to see.
Moving the discussion on, as VLDLs are the
only source of LDL. you now have a conundrum to solve. How can you connect
saturated fat intake to a rise in LDL levels, when saturated fat consumption
reduces VLDL synthesis? What is the mechanism? The mechanism does not exist!
You could counter by saying, what of the many
studies that have shown a fall in LDL when saturated fats are replaced by
polyunsaturated fats? Well, this seems to have been shown often enough for me
to believe it may even be true.
The explanation for this finding is most
likely the fact that, in these studies, saturated fats were replaced by
polyunsaturated fats, from plant oils. Plant oils contains stanols (the plant
equivalent of cholesterol).
Stanols are known to lower LDL levels, see
under Benecol and other suchlike ‘low fat’ spreads. Because stanols compete
with cholesterol for absorption there is an impact on the ‘measured’ LDL
levels. What this means, in turn, is that the studies that demonstrate a lower
LDL, with a reduction in saturated fat consumption, fall foul of the two
variables problem.
Namely, if you change two variables in an
experiment at the same time, you cannot say which of the variables was
responsible for the effect you have seen. Was it the reduction in saturated
fats, or the increase in plant stanols, that lowers LDL?
This is all tacitly accepted in this Medscape
article – again heavy on jargon: ‘Saturated
Fat and Coronary Artery Disease (CAD): It’s Complicated.’
‘In a meta-analysis of over 60 trials, higher intakes
of saturated fat were associated with increases in both LDL-C and high-density
lipoprotein cholesterol (HDL-C) and decreases in triglyceride levels
[VLDL}, for a net neutral effect on the ratio of total cholesterol
to HDL cholesterol.
Although saturated fats increase LDL-C, they reduce
the LDL particle number. Total
LDL particle number quantifies the concentration of LDL particles in various
lipid subfractions and is considered a stronger indicator of CV risk than
traditional lipoprotein measures.
As for stearic acid, the allegedly
non-cholesterol-raising fat, while it appears to lower LDL-C relative to other
SFAs, one analysis concluded that it raised LDL-C, lowered HDL-C, and increased
the ratio of total to HDL cholesterol in comparison with unsaturated fatty
acids. And this is one of the confounders of much nutrition
research—observations about a given nutrient are highly dependent on what you
compare it to.’5
Which is a long-winded way of saying that
everything we have been told about saturated fat, its impact on LDL, and its
impact on CVD is – frankly – complete bollocks. And if it is complete bollocks,
the Keys equation – which has driven all research in this area for seventy
years – is also bollocks.
In truth, all possible combinations of LDL
going up, down, and staying the same have been found in dietary studies. But I
would like to focus on the most recent study. It formed the basis of an episode
of a programme called ‘Trust me I’m a doctor’, on the BBC. Researchers studied
the impact of different types of saturated fat on LDL and HDL levels.
For the experiment, the
team recruited nearly one hundred volunteers, all aged over fifty. They were
split into three groups and every day for four weeks each ate fifty grams of
coconut oil (about two tablespoons), or fifty grams of olive oil – an
unsaturated fat already known to lower bad LDL cholesterol – of fifty grams of
butter.
This amount of coconut
oil contains more than forty grams of saturated fat, twice the maximum
recommended daily amount for women, according to Public Health England, but is
the level previous research has revealed is necessary to show measurable
changes in blood cholesterol over a four-week period.
Before the experiment,
all the volunteers had their bad LDL and good HDL cholesterol measured, as well
as their height, waist, blood pressure, weight and body fat percentage. Four
weeks later, these tests were repeated.
The group who ate butter
saw their bad LDL levels rise by about ten per cent, as expected. But the olive
oil and coconut oil saw no rise in bad LDL – despite coconut oil having more
saturated fat than butter.’
Even more surprisingly, while butter and olive oil
both raised good HDL cholesterol by five per cent, coconut oil raised it by a
staggering fifteen percent, meaning that it seemed to have a more positive
effect on cholesterol related health than olive oil.’ 6
It is worth pointing out that this was the
largest study of the kind ever to have been done. This may surprise you, but in
many nutritional studies the number of subjects is often in single digits. In
case you are thinking we can simply ignore a study done by the BBC, it was
carried out to high standards, and has since been published in the BMJ. Equally
I can see no reason why the BBC would have any desire to bias the conclusions
in any direction.7
What they found was that coconut oil,
containing the highest percentage of saturated fat, had absolutely no impact on
LDL. But it did raise HDL (so-called ‘good’ cholesterol) by 15%. Which is no
surprise. If VLDL goes down, HDL goes up. And in this experiment they kept
everything else the same, but just added saturated fat. A single variable.
Anyway, the thing that interests me most, and
the reason for writing this particular blog is that I have come to the
realisation that the best way to find the answer to a scientific question is to
immerse yourself in the science. I would like to believe the published
research, because it would be lovely if you could look at a study and believe
it to be correct/true/unbiased. But that is no longer possible, most especially
in the connected fields of heart disease, and nutrition.
‘It is simply no longer possible to believe much of
the clinical research that is published, or to rely on the judgement of trusted
physicians or authoritative medical guidelines.” Marcia Angell – long-time editor of the NEJM.
‘The case against science is straightforward: much of
the scientific literature, perhaps half, may simply be untrue…science has taken
a turn towards darkness.’ Richard
Horton – editor of The Lancet.
‘The poor quality of medical research is widely
acknowledged, yet disturbingly the leaders of the medical profession seem only
minimally concerned about the problems and make no apparent efforts to find a
solution.’ Richard Smith – long time
editor of the BMJ.
It is always, of course, risky to base your
thinking and conclusions on what is known about the basic science. New facts
can come along to upend your thinking at any time. However, with mainstream
medical research in such a corrupt mess, I do not know how else to do it. The
basic research tells us that there is no mechanism whereby saturated fat can
raise LDL levels, and the research, such as it can be disentangled, appears to
fully support this.
I looked at this blog again, and again, and I
thought: Why did I write it…for sure? I wrote it because I wanted to make you
aware of three things. First, how powerful a thought can be. Saturated fat
raises the LDL level, and how difficult this is to shift. The power of a simple
idea.
Secondly, so that you can see that the truth
is out there. It is not to be found amongst the experts in the field. It cannot
be found by reading the research, or the guidelines. But it is out there, if
you look hard enough.
Third, the mainstream just will not change
its mind. A recent conference in Switzerland, organised by the BMJ, and others,
tried to discuss the dietary guidelines and the role of Saturated fat. I was
invited, but did not go, as I was working. Zoe Harcombe went, and wrote a blog
about it.8 As she wrote about the conclusion of the
conference:
‘At the recent Swiss
Re/The BMJ Food for Thought conference, the closing speakers tried to find some
agreement on dietary fat guidelines…
Fiona (Fiona Godlee,
editor of the BMJ) started with: “The point about saturated fat is: the
evidence is now looking pretty good, but the guidance hasn’t shifted… there doesn’t
seem to have been an enormous ‘mea culpa’ from the scientific community that we
got it so wrong. That does surprise me.”
Salim replied: “We got
brainwashed by a very questionable study, called The Seven Countries Study,
many years ago and it was ingrained in our DNA and generations of us were
brought up with that… Somebody said that you need to wait for guidelines
committees to die before you can change the guidelines committees”!
Fiona then said: “Maybe
one outcome of this meeting would be for this meeting to say ‘that’s gone now’,
the science has changed. Am I right Salim? Am I right Dariush? It seems to be
that should be an outcome of some sort from this meeting.”
Alas, the UK guidelines committee shows no signs of
such change, let alone the ‘mea culpa’ that Fiona suggests might be in order.’
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