Having gone from a weak and flabby 250
pounds to a strong and lean 175 pounds, I am often asked for the
details of how I did it. When I describe a diet moderate-to-high in
protein, high in saturated and mono-unsaturated fats, made of real
foods and excluding processed food-products, grains, added sugar
(which technically is a
processed food-product), and legumes, I almost invariably hear some
variation on, “Saturated fats? Won't that raise my cholesterol?”
This has to be the
most common stumbling block I encounter when I try to encourage my
clients to eat healthfully. Since at least the 1970's, science has
understood that total blood cholesterol levels are not a good
predictor of heart disease. In fact, many people with very high
cholesterol levels never develop heart disease, and many people who
have died of heart disease had cholesterol levels only slightly above
“normal”. Yet the medical establishment continues to push the
idea that high cholesterol kills, and eating saturated fat will turn
you into a cholesterol factory working overtime. Most men are so
afraid of heart disease that they have serious reservations about a
way of eating which can eliminate excess body fat, lower blood
pressure, reduce cancer and Alzheimer's risk, and practically
eliminate dozens of auto-immune diseases, but which might raise
cholesterol levels.
So
today I would like to take a closer look at cholesterol, and it's
role in our health. I know this has already been done by other
people,
but maybe I will reach the three or four internet-savvy people they
haven't, and besides, I understand things better when I write about
them, so here goes.
First, what
exactly is cholesterol? According to wikipedia.com, “Cholesterol
is a waxy steroid metabolite found in the cell membranes and
transported in the blood plasma of all animals.[2] It is an essential
structural component of mammalian cell membranes, where it is
required to establish proper membrane permeability and fluidity. In
addition, cholesterol is an important component for the manufacture
of bile acids, steroid hormones, and several fat-soluble vitamins.”
Well, I sure am glad I know that. I guess for my purposes,
cholesterol is something found in animal cell membranes and blood
plasma. Good enough.
What
is cholesterol for? Well, it is required to build and maintain cell
membranes, regulate membrane fluidity, intracellular transport, cell
signaling and nerve conduction, forms the myelin sheaths on neurons.
It forms bile, which is essential to intestinal absorption of fat
molecules as well as the fat-soluble vitamins, Vitamin A, Vitamin D,
Vitamin E, and Vitamin K, (ask me why I hate Olestra, sometime) and
it is a precursor molecule in several biochemical pathways. That all
sounds like it is pretty important to me. It seems that we humans
need cholesterol in
many, many ways to ensure our bodies actually function properly.
In fact, our
bodies make most of our cholesterol, and carefully regulate the
levels. If we increase or decrease our dietary levels of
cholesterol, our bodies respond by making less or more of it to
maintain balance. Today, it is fairly commonly known to doctors that
reducing cholesterol intake will not do much to reduce blood
cholesterol levels.
So
why is everyone afraid of what is not only an essential part of our
bodies, but also a product of those self-same bodies? The answer
lies in something called the Diet-Heart Hypothesis. The Diet-Heart
Hypothesis basically says that saturated fat elevates blood
cholesterol levels, and that elevated blood cholesterol causes blood
lipid accumulation in arterial walls (a.k.a. plaques or lesions), and
that this is at the root of coronary artery disease. The hypothesis
has been around in one form or another for over 100 years, but it
really came into the public's notice in the 1950's, when Ancel Keys
published his Seven Countries Study, which allegedly showed a direct
correlation between fat intake and heart disease. Keys made it onto
the cover of Time magazine, which failed to mention that he had
reliable data from twenty-two countries, but didn't publish it
because the data as a whole showed very little correlation between
fat intake and heart disease. Basically, he cherry-picked his data.
One
part of this and subsequent studies which really caught the public
eye was the super-low heart disease rate on the island of Crete. The
people of Crete had a low saturated fat intake, and ate a great deal
of fresh vegetables, and this is the basis of today's “Mediterranean
Diet”. What most people don't hear about is the fact that the
Cretans ate large amounts of meat, did not have a low total fat
intake (and in fact ate copious amounts of olive oil, some going so
far as to drink it straight up), had no electricity (an therefor
didn't stay up very long past dark, generally), walked everywhere,
worked hard in the physical sense... and so on. Their lifestyles
were, and probably are, entirely different than ours. Singling out
not just diet, but one small component of diet, and saying that
must be the difference which makes their heart disease rate so low is
just sheer idiocy.
These
ideas about cholesterol and heart disease have persisted to this day,
despite the fact that high-quality studies to back them up are pretty
hard to come by.
So what is really going on inside of us? Let's take a look.
Our bodies produce
molecules called “lipoproteins”. There are many kinds, but the
kinds which are important to us are high-density lipoprotein (HDL),
low-density lipoprotein (LDL), and very-low-density lipoproteins
(VLDL). Many of you have probably heard of these, or at least the
first two.
What
lipoproteins do, in simple terms, is shuttle cholesterol and
triglycerides (fat) around in our bloodstream. HDL's collect
cholesterol from the body's tissues, and bring it back to the liver.
LDL's carry cholesterol from the liver to cells of the body, and
VLDL's carry (newly synthesized) triglycerides from the liver to
adipose tissue. So when the tissues need cholesterol the LDL's take
it to them, when they are done with it the HDL's take it back to the
liver, and when the liver makes triglycerides the VLDL's take them to
the adipose tissue.
In the eyes of the general public and most General Practitioners,
HDL is the good, LDL is the bad, and VLDL might count as the ugly if
they have even heard of it. Yet each one of these has an important
role to play inside of us. LDL is demonized because it is often
found as part of arterial plaques (see, it isn't really the
cholesterol at all), yet it has long been known that LDL levels are
only marginal risk factors for heart disease, and a much more
reliable indicator is the ratio of the blood triglycerides to HDL
cholesterol. But why?
Not
all LDL particles are created equal. Some of them are large and
fluffy, sometimes called “buoyant”, and some of them are small
and dense. It is the small, dense ones which seem to be gathering in
the arterial lesions which are associated with coronary artery
disease; the large, fluffy ones are simply too big and buoyant to get
stuck in the pile-up. On a standard lipid profile, the small, dense
LDL and the large, fluffy LDL do not show up separately. This means
that the lipid profile is not telling you which you have or whether
you should be worried about them if your LDL actually is elevated.
And if it is not elevated?
You could still have the majority of your LDL as the small, dense
kind, and be at a higher risk of heart disease than someone with a
higher LDL level, but much lower small, dense particle levels. So
much for total LDL levels telling you anything.
What
increases the small, dense LDL particle levels? Is it really
saturated fat? Let's ask Gary Taubes: “This suggests that
saturated fat elevates LDL-cholesterol in part by increasing the
amount of cholesterol
in the LDL, and so making larger and fluffier LDL to begin with,
rather than by increasing the number of LDL particles or by
increasing the number of small, dense LDL particles.” So if it
isn't the cholesterol itself which is the problem, but the LDL
particle it is carried on, and it isn't just any LDL particles, but
the small, dense ones we need to worry about, then saturated
fat is not going to cause heart disease.
Nothing I have said leading up to that last statement is really
considered controversial science. It is commonly known and accepted
as fact, by both sides of the argument, that saturated fat raises
large, fluffy LDL and that it is the small, dense LDL which is very
strongly associated with heart
disease. It makes me wonder why the Diet-Heart Hypothesis lives on.
Still the question
remains, what increases the small, dense LDL particles? Taubes
again, “After we eat a carbohydrate rich meal, the bloodstream is
flooded with glucose, and the liver takes some of this glucose and
transforms it into fat—i.e., triglycerides—for temporary
storage... The triglycerides constitute the cargo that the
lipo-proteins drop off at tissues throughout the body... The
resulting lipo-protein has a very low density, and so is a VLDL
particle.” As these VLDL particles go about their business of
dropping the triglycerides off hither and yon, they slowly become the
small, dense LDL particles we should fear. The more triglycerides
which were originally packed into the VLDL particle, the smaller and
denser the resulting LDL particle will be.
What this means is
that eating a lot of carbohydrate, and in particular, highly refined
carbohydrates such as flour and sugar, will increase the amount of
small, dense LDL we produce. The more of it we eat, the more we
produce, while at the same time making them smaller and denser.
Sugar itself, and all things related to it (high-fructose corn syrup,
anyone?), go one step further. The fructose portion of sucrose is
processed exclusively in the liver. Unlike the glucose portion, none
of it is burned by the cells as energy. The liver deals with what is
effectively a toxin by converting it to triglycerides, and shipping
it out for storage. Comparing glucose to fructose (all carbohydrate
you eat, except fructose, becomes glucose in your body), you will get
a much, much higher elevation in blood triglycerides from the
fructose. The particles which carry the resulting triglycerides
around are those same VLDL mentioned above. That is why knowing your
ratio of blood triglycerides to HDL is a much better indicator of
heart disease risk than just your LDL levels, or LDL to HDL ratio.
What is the
take-away? We know that eating cholesterol will not affect our
cholesterol very much, and that our cholesterol levels are not really
the issue anyway. We understand that our bodies need lipoproteins to
function, that LDL has an important role in our bodies, and that we
cannot live without it. We have seen that it is the small, dense LDL
we don't want, and that the large, fluffy LDL is what we should be
making. We have also seen that it is carbohydrates, especially
refined carbohydrates, which result in the creation of the small,
dense particles, and that it is saturated fat which helps to raise
the levels of the large, fluffy LDL particles. Knowing all of this,
it sure seems clear to me that replacing the refined carbs in our
diets with fats, especially the saturated kind (and not those damned
trans-fats), will greatly reduce the risk of developing heart
disease. I would not be surprised to find that such a change could
actually reduce the symptoms of heart disease where it already
exists. The next time you start out making egg whites and oatmeal
with honey for breakfast, throw out the oatmeal and eat the yolks
instead.
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