Cholesterol gets a bad press from those who know little about it, and really it does not deserve to be so abused. Perhaps the persons who abuse cholesterol might deserve the bad press.
Origin and excretion of cholesterol.
The cholesterol in the human body is 50% ingested with the average diet (exogenous cholesterol), the remainder is manufactured in the body (endogenous cholesterol), 10% in the liver, 10% in the intestine and the remaining 30% from virtually all of the body’s tissues
Bile acids are formed in the liver largely from cholesterol, excreted through the gall bladder and duct into the duodenum, the bile acids (salts) play a role in digestion, in particular in relation to making fat absorbable by the membrane of the intestine. Some of the bile is reabsorbed and returns to the liver. The principal sterol of the feces is coprostanol formed from cholesterol under the influence of the intestine’s own bacteria.
Functions of cholesterol
Cholesterol is an essential structure in the formation of cell membranes, it is the precursor of all other steroids, including the sex hormones, corticosteroids, and Vitamin D. If it wasn’t for cholesterol there’d be no babies! It is also deposited in the skin and helps to make us waterproof.
Transport of cholesterol
The numerous fat-protein combinations (lipoproteins) are grouped by density – fat is lighter than water so low density means more fat, high density means more protein in the make-up of the lipoprotein. The least heavy are chylomicrons, next in weight are the Very Low Density (VLD) lipoproteins, then Lxow Density (LDL) and High Density (HDL) lipoproteins.
The liver, factory of the body, makes the VLD lipoproteins which serve as transport agents of the lipids to be deposited in the fat cells or to be metabolized into energy. Cholesterol is carried by the LDL lipoproteins; excessive cholesterol intake, combined with LDL as LDL-cholesterol may be deposited on the inner surface of blood vessels, blocking them as in coronary infarction, and this is where LDL-cholesterol gets its unsavory reputation.
By contrast HDL lipoproteins are the good guys of the cholesterol scenario – they carry excess cholesterol back to the “factory” where the liver cells break it down and excrete the products in the bile.
The lipid targets set for good health are:
LDL cholesterol: less than 100 mgs/dl (< 2.6 mmol/l)
Triglycerides: less than 150 mgs/dl (< 1.7 mmol/l)
HDL cholesterol: more than 40 mgs/dl (> 1.1 mmol/l)
A full laboratory analysis requires a fasting sample However, after the first visit an annual “lipid panel” is recommended. Total cholesterol and High Density Lipoprotein (HDL) assays do not require fasting and may be sufficient in some circumstances.
Lipoproteins: US National Library of Medicine
Cholesterol and Coronary Artery Disease
The coronary arteries arise from the aorta, close to the point where it leaves the left ventricle, they then curve back, spread over the heart and are essential for its blood supply and the life of the heart which is in fact very specialized muscle. The artery is composed of three recognizable layers, an outer coat of fibrous tissue (adventitia), a middle layer of finer structured fibers (media), and the innermost single cell thick layer (intima or endothelium). The cells of this innermost layer are far from inert; they produce hormones that participate in regulating the functioning diameter of the artery and preventing formation of clot on its surface.
Deterioration starts early
It is incorrectly supposed by many that arterial degeneration is a middle-age phenomenon, in fact the process begins in childhood and by the age of 20 most persons have developed fatty streaks of lipoproteins in the media layer of their coronary arteries. These streaks contain not only the lipoprotein, but also the cells characteristic of the immune reaction (T-lymphocytes) and the body’s scavenger cells (macrophages).
Formation of plaque
There follows a highly complex sequence involving numerous hormones and enzymes, some known and surely many yet to be discovered, the process is far from a simple deposition of unwanted cholesterol crystals. But the active process does in fact result in deposition of the LDL cholesterol-bearing lipoprotein together with cells and scar fibers to form a mass, designated a plaque. This plaque occupies space and may cause the coronary artery either to bulge out or to close in on its lumen (the space inside a tube).
If the artery bulges out, not until the plaque takes up 40% of the cross section of the artery is there any significant reduction in the lumen width, and not until it takes up 70% of the cross section is there any significant interference in blood flow. Fortunately less common, but if the artery bulges inwards, symptoms of angina (chest pain with effort) will occur much earlier.
Rupture of the Plaque
There comes a point with expansion of the plaque that it bursts its inner coat. It’s easy to think of this as the plaque growing passively and then just getting too big for its container, the wall of the coronary artery, and although that is partially true there are also very complex biochemical and physiologic processes actively involved. On this ruptured surface there will be clot formation with obstruction of the artery (thrombus), or a portion of the plaque may break loose, obstructing the artery (embolus), in both instances a portion of the heart loses its blood supply, setting up a condition known as an infarct and described as AMI, or Acute Myocardial Infarct.
Risk factors of AMI
Although risk factor assessment is a popular pastime, they predict only half the cases of AMI. The most important predictor is family history, if your predecessors had an AMI, your chances are right up there. Then uncontrolled diabetes and excessive LDL levels come next.
The factors that can be modified are the level of LDL, smoking, air pollution and diabetes; the factors that can’t be modified are genetics, age and sex.
Epidemiology of AMI
Symptoms of Coronary Artery Disease (CAD) are annually experienced by 14 million persons in the USA, where it is responsible for 20% of the deaths. Each year 1.5 million persons have a heart attack, and a third of them die, the number one cause of death in that country.
The French Paradox is the name given to the observation that although in France there is a high dietary intake of foods likely to raise LDL levels, there is a lower rate of coronary artery disease – a not altogether believable explanation is related to alcohol intake.
Inuit (Esquimaux) have a high fat intake in their diet, but a supposition that they are genetically tolerant of this is used to explain their low rate of CAD.
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