CHOLESTEROL
compiled by Nelson Brunton
What
is Cholesterol? Cholesterol, from the Ancient Greek chole- and
stereos followed by the chemical suffix -ol for an alcohol, is an
organic molecule.A waxy fat like substance.
Where
does it come from? Your body makes all the cholesterol it needs.
Between 75-80% cholesterol is produced by the Liver and the remaining
comes from the food you eat.
What
are the different types? HDL, LDL, TG. These are the types that are
generally addressed by the Medics. But you must realise that there is
another type of cholesterol that the average person does not know,
neither is it addressed. It is known as VLDL of Very Low Density
Lipids.
Why
does the body produce Cholesterol?
What
does Cholesterol do? Cholesterol has major functions in the body. Its
a component of cell membranes which is composed of Proteins,
Cholesterol and Phospholipids. First major function of cholesterol is
It Enables cells not to meet a cell and help maintain integrity and
fluidity and cause free movement. The second major function is to
help produce vitamin D. Vitamin D is produced when we consume fats
and attacks upon the ultraviolet light of the sun to produce the
hormone D3 Cholecalciferol The next function of cholesterol is that
it helps the liver to make bile Since bile increases the
absorption of fats, it is an important part of the absorption of the
fat-soluble substances, such as the vitamins A, D, E, and K. Besides
its digestive function, bile serves also as the route of excretion
for bilirubin, a byproduct of red blood cells recycled by the liver.
After
the brain, the organs hungriest for cholesterol are our endocrine
glands: adrenals and sex glands. They produce steroid hormones.
Steroid hormones in the body are made from cholesterol: testosterone,
progesterone, pregnenolone, androsterone, estrone, estradiol,
corticosterone, aldosterone and others.
LDL
particles are sometimes referred to as "bad" lipoprotein
because concentrations, dose related, correlate with atherosclerosis
progression. High-density lipoproteins(HDL) collect fat molecules
(phospholipids, cholesterol, triglycerides, etc.) from the body's
cells/tissues, and take it back to the liver to be reused..
Triglycerides Tg is an ester derived from glycerol and three
fatty acids. Triglycerides are the main constituents of body fat in
humans and other animals, as well as vegetable fat. Triglycerides
provide your body with energy, but their main function is to store
energy for later use. The food you eat contains calories in the form
of carbohydrates, protein and fat. When you consume more calories
than your body can use, it stores those calories in the form of
triglycerides.
Conventional
Cholesterol test. Test your cholesterol
Your
risk of heart disease can be assessed with a blood- cholesterol test.
According to expert guidelines:
Total
cholesterol should be 5.0 mmol/L or less.
LDL
should be 3.0mmol/L or less after an overnight fast.
HDL
should be 1.0mmol/L or more.
Total
cholesterol/HDL ratio should be less than 4.0.
VLDL:
(very low-density lipoprotein) contains very little protein. The main
purpose of VLDL is to distribute the triglyceride produced by your
liver. A high VLDL cholesterol level can cause the buildup of
cholesterol in your arteries and increases your risk of heart disease
and stroke.
Your
Total Cholesterol reading will be calculated according to you
HDL+LDL+20% of your Tg.
Taken
from: Doc's Opinion Blog About Heart Disease, LDL Cholesterol,
Particle Number and Particle Size Made Easy
By
Axel F. Sigurdsson MD
Recently
measurements of atherogenic lipoprotein particles, such as LDL-P (LDL
particle number), apolipoprotein B (apoB) and lipoprotein(a) have
been found to be very useful to assess risk.
LDL-P
measures the actual number of LDL particles (particle concentration).
LDL-P may be a stronger predictor of cardiovascular events than
LDL-C. Low LDL-P is a much stronger predictor of low risk than low
LDL-C. In fact, about 30 – 40% of those with low LDL-C may have
elevated LDL-P. Therefore you can have low LDL-C but still be at risk
for heart disease, particularly if your LDL-P is elevated.
Discordance is considered present if LDL-C differs from LDL-P.
LDL-C
is a measure of the cholesterol mass within LDL-particles. LDL-C only
indirectly reflects the atherogenic potential of LDL particles. ApoB
and LDL-P on the other hand reflect the number of atherogenic
particles, with no mention of cholesterol mass. ApoB and LDL-P are
believed to be better risk predictors than LDL-C.
Many
recent studies have looked into the importance of LDL-particle size.
Studies show that people whose LDL particles are predominantly small
and dense, have a threefold greater risk of coronary heart disease.
Furthermore, the large and fluffy type of LDL may be protective.
Sometimes
it is difficult to understand the difference between LDL-C and LDL-P
and how particle size comes into the picture. It is quite likely that
LDL particle number and size will be used more often in the future to
assess risk.
How
did the Myth on Cholesterol come about? Taken from, THE TRUTH ABOUT
ANCEL KEYS: WE’VE ALL GOT IT WRONG by Denise Minger. Once upon a
time, a scientist named Ancel Keys did an awful thing. He published a
study about different countries that made it look like heart disease
was associated with fat intake. But the truth was that he started out
with 22 countries and just tossed out the ones that didn’t fit his
hypothesis! When other researchers analyzed his data using all the
original countries, the link between fat and heart disease totally
vanished. Keys was a fraud, and he’s the reason my mom made me eat
skim milk and Corn Chex for breakfast instead of delicious bacon and
eggs.
The
study began with a great many more countries … but Keys deleted the
countries whose results did not match his pre-conceived conclusions,
leaving him with only Japan, Italy, Great Britain, Australia, Canada
and the US. Full disclosure would have made a great deal of
difference.
Keys
published this graph in 1953 in a paper called called
“Atherosclerosis: A problem in newer public health” (which is
apparently so brilliant that neither the abstract nor full text is
allowed to exist online). It was simple, really: he graphed fat
consumption alongside heart disease mortality in men from six
different countries—and voila! The data points landed in a tidy
little line. Keys first unveiled his Wonder Curve to a handful of
people at Mt. Sinai Hospital in New York, but his most famous
presentation was at that WHO conference a few years later.
It
is well known that the indirect method merely suggests that there is
an association between the characteristics studied and mortality
rates and, further, that no matter how plausible such an association
may appear, it is not in itself proof of a cause-effect relationship.
But quotation and repetition of the suggestive association soon
creates the impression that the relationship is truly valid, and
ultimately it acquires status as a supporting link in a chain of
presumed proof.
What
is the truth? The evidence—both from experiments and from field
surveys—indicates that the cholesterol content, per se, of all
natural diets has no significant effect on either the serum
cholesterol level or the development of atherosclerosis in man.
You
decide.
