Myth over Cholesterol

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.