it is essential to life, it has a bad reputation, being a major villain in heart disease. Every person

with a high blood cholesterol is regarded as a potential candidate for heart attack, a stroke or

high blood pressure.

Cholesterol is a building block of the outer membrane of cells. It is the principal ingredient in the

digestive juice bile, in the fatty sheaths that insulate nerves and in sex hormones, namely,

estrogen and androgen. It performs several functions such as transportation of fat, providing

defense mechanism, protecting red blood cells and muscular membrane of the body.

Most of the cholesterol found in the body is produced in the liver. However, about 20 to 30

percent generally comes from the foods we eat. Some cholesterol is also secreted into the

intestinal tract in bile and becomes mixed with the dietary cholesterol. The percentage of

ingested cholesterol absorbed seemed to average 40 to 50 percent of the intake. The body

excretes extra cholesterol from the system through bowels and kidneys.

The amount of cholesterol is measured in milligrams per 100 millimeters of blood. Normal level

of cholesterol varies between 150- 250 mg. per 100 ml. Persons with atherosclerosis have

uniformly high blood cholesterol usually above 250 mg. per 100 ml.

In blood, cholesterol is bound to certain proteins – lipoproteins which have an affinity for blood

fats, known as lipids. There are two main types of lipoproteins : a low density one (LDL) and a

high density one (HDL). The low density lipoprotein is the one which is considered harmful and

is associated with cholesterol deposits in blood vessels. The higher the ratio of LDL to the total

cholesterol, the greater the risk of arterial damage and heart disease. The HDL on the other

hand plays a salutary role by helping remove cholesterol from circulation and thereby reduce the

risk of heart disease.

Cholesterol has been the subject of extensive study by researchers since 1769, when French

chemist, Polutier de La Salle purified the soapy-looking yellowish substance. The results of the

most comprehensive research study, commissioned by the National Heart and Lung Institute of

the U.S.A. were announced about four years ago. The 10-year study, considered most elaborate

and most expensive research project in medical history, indicates that heart disease is directly

linked to the level of cholesterol in the blood and that lowering cholesterol significantly reduces

the incidence of heart attacks. It has been estimated that for every one per cent reduction in

cholesterol, there is a decrease in the risk of heart attack by two per cent.

Causes

Hyperchjolsterolaemia or increase in cholestrol is mainly a digestive problem caused by rich

foods such as fried foods, excessive consumption of milk and its products like ghee,butter and

cream,white flour, sugar, cakes, pastries, biscuits, cheese, ice cream as well as non-vegetarian

foods like meat, fish and eggs. Other causes of increase in cholesterol are irregularity in habits,

smoking and drinking alcohol.

Stress has been found to be a major cause of increased level of cholesterol. Adrenaline and

cortison are both released in the body under stress. This, in turn, produces a fat metabolising

reaction. Adrenal glands of executive type aggressive persons produce more adrenaline than

the easy going men. Consequently they suffer six to eight times more heart attacks than the

relaxed men.

The Cure

To reduce the risk of heart disease, it is essential to lower the level of LDL and increase the level

of HDL. This can be achieved by improving the diet and changing the life style. Diet is the most

important factor. As a first step, foods rich in cholesterol and saturated fats, which lead to

increase in LDL level, should be reduced to the minimum. Cholesterol -rich foods are eggs,

organ meats and most cheese, butter, bacon, beef, whole milk, virtually all foods of animal origin

as well as two vegetable oils, namely coconut and palm, are high in saturated fats and these

should be replaced by polyunsaturated fats such as corn, safflower, sobayeans and sesame oils

which tend to lower the level of LDL. There are monosaturated fats such as olive and peanut oils

which have more or less neutral effect on the LDL level.

The American Heart Association recommends that men should restrict themselves to 300 mg. of

cholesterol a day and women to 275 mg. It also prescribes that fat should not make up more

than 30 per cent of the diet and not more than one third of this should be saturated. The

Association, however, urges a somewhat strict regimen for those who already have elevated

levels of cholesterol.

The amount of fibre in the diet also influences the cholesterol levels and LDL cholesterol can be

lowered by taking diets rich in fibres. The most significant sources of dietary fibre are

unprocessed wheat bran, whole cereals such as wheat , rice, barley, rye; legumes such as

potato, carrot, beet and turnips; fruits like mango and guava and green vegetables such as

cabbage, lady’s finger, lettuce and celery. Oat bran is especially beneficial in lowering LDL

cholesterol.

Lecithin, also a fatty food substance and the most abundant of the phospholipids, is highly

beneficial in case of increase in cholesterol level. It has the ability to break up cholesterol into

small particles which can be easily handled by the system. With sufficient intake of lecithin,

cholesterol cannot build up against the walls of the arteries and veins. It also increases the

production of bile acids made from cholesterol, thereby reducing its amount in the blood. Egg

yolk, vegetable oils, whole grain cereals, soyabeans and unpasteurised milk are rich sources of

lecithin. The cells of the body are also capable of synthesizing it as needed, if several of the B

vitamins are present.

Diets high in vitamin B6, cholin and inositol supplied by wheat germ, yeast, or B vitamins

extracted from bran have been particularly effective in reducing blood cholesterol. Sometimes

vitamin E elevates blood lecithin and reduces cholesterol presumably by preventing the essential

fatty acids from being destroyed by oxygen.

Persons with high blood cholesterol level should drink at least eight to 10 glasses of water every

day as regular drinking of water stimulates the excretory activity of the skin and kidneys. This in

turn facilitates elimination of excessive cholesterol from the system. Regularly drinking of

coriander (dhania) water also helps lower blood cholesterol as it is a good diuretic and

stimulates the kidneys. It is prepared by boiling dry seeds of coriander and straining the

decoction after cooling.

Regular exercise also plays an important role in lowering LDL cholesterol and in raising the level

of protective HDL. It also promotes circulation and helps maintain the blood flow to every part of

the body. Jogging or brisk walking, swimming, bicycling and playing badminton are excellent

forms of exercise.

Yogasnas are highly beneficial as they help increase perspiratory activity and stimulate

sebaceous glands to effectively secrete accumulated or excess cholesterol from the muscular

tissue. Asanas like ardhamatsyaendrasana, shalabhasana, padmasanaand vajrasana are useful

in lowering blood cholesterol by increasing systemic activity.

Hydrotherapy can be successfully employed in reducing excess cholesterol. Cold hip baths for

10 minutes taken twice every day have proved beneficial. Steam baths are also helpful except in

patients suffering from hypertension and other circulatory disorders. Mud packs, applied over the

abdomen improve digestion and assimilation. They improve the functioning of the liver and other

digestive organs and activate kidneys and the intestines to promote better excretion.

Once lipids are disassembled in the intestinal lumen and mucosal cell (enterocyte) they are reassembled in the mucosal cell as chylomicrons (CM’s) and very low density lipoproteins (VLDL’s). These vehicles contain primarily nonpolar cholesterol esters and triglycerides in the core and polar cholesterol, protein, and phospholipids in their membranes. (Fig. 20)

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They are transported via the lymph and blood circulation to the liver, fat depots, and muscles. There the endothelial enzyme lipoprotein lipase removes the lipid contents.

Lipid carrying vehicles are also made by the liver primarily as very low density lipoproteins (VLDL) and these function to move lipids made by the body itself into tissues. On the other hand, high density lipoproteins (HDL), which are made in the intestines and liver, function primarily to reverse this process and transport lipids from tissue to liver hepatocytes.1 HDL’s are of two types: HDL3 and HDL2. HDL3 is an empty package composed of a bilayer lipid membrane plus proteins. Lysolecithin cholesterol acyl transferase (LCAT) and apoprotein A associated with HDL3 remove free cholesterol from the blood, esterify it and fill the HDL3 package.

The LCAT enzyme uses the fatty acid in the number two position of lecithin to esterify to cholesterol. If this fatty acid is saturated, the process is inhibited: if it is unsaturated, the process is enhanced. Thus, cholesterol blood clearing by HDL3 is linked to dietary intake of saturated and unsaturated fatty acids. High saturated triglycerides are often clinically associated with high blood cholesterol levels.

As HDL3 swells with cholesterol ester, it becomes HDL2, which in the liver releases its cholesterol through the action of hepatic lipase. Released cholesterol is conjugated with the amino acids glycine (predominantly in most species) and taurine (predominantly in cats) to form bile salts which are then excreted in the bile into the small intestine.2,3 Some cholesterol is then reabsorbed via the enterohepatic circulation and some passes with the feces. The less reabsorbed, the lower the blood levels of cholesterol. A variety of complex factors influences the reuptake of bile cholesterol. For example, some of the beneficial effects of fiber and certain bowel microorganisms can be related to decreasing cholesterol uptake.4,5

Characterization of lipid transport vehicles is based on physical density, size and ratios of constituents. Chylomicrons are the largest particles, the very low density lipoprotein (VLDL) is the next largest, the intermediate density lipoprotein (IDL) is the next largest, the low density lipoprotein (IDL) is the next largest, and then high density lipoproteins (HDL) are the smallest. In terms of their constituents, as the particle becomes smaller as it is hydrolyzed by lipoprotein lipase on capillary endothelial cells, its protein and cholesterol content becomes greater, triglyceride content becomes smaller and its density increases.6 Thus chylomicrons are laden with lipid but lean of protein, whereas high density lipoproteins contain smaller amounts of lipid and larger measures of protein. (Fig. 21)

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Diagnostically the measure of these lipid carriers in the blood is important as indicators of risk particularly to cardiovascular disease. If there are high levels of LDL’s, this would be unfavorable whereas high levels of HDL’s would be favorable. High levels of LDL’s mean that there is a large amount of circulating cholesterol which may have atherogenic potential. On the other hand, a high level of HDL’s would mean that lipid stores are being mobilized from tissue and metabolized in the liver to be excreted in the bile.7

APOPROTEINS

The proteins associated with lipid carriers help solubilize the lipids, and identify them for enzymatic action. There are a host of these apoproteins. Some of those believed to be most important diagnostically are B, found on LDL’s and VLDL’s, E, found on IDL’s, and A. found on HDL’s. Apoprotein B on LDL’s and VLDL’s tags lipids for uptake by liver cells or scavenger cells in blood vessel walls. Apoprotein A tags HDL’s for liver uptake. Another apoprotein, C-2, serves as a cofactor for lipoprotein lipase which hydrolyzes the contents of low density lipid carriers on the endothelial wall. (Fig 22)

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This is a very brief overview of some increasingly complex biochemistry coming to light.8-l0 Diagnostically, identifying apoproteins may be most revealing since they are more specific than simply measuring cholesterol or lipoproteins. High apoprotein A, for example, indicates high levels of HDL’s whereas high levels of B indicate high levels of LDL’s.

Lipoprotein (a) (different than A) may be one of the best independent markers for both cardiovascular risk and severity of existing disease. It is comprised of LDL and apoproteins B-100 and (a). Lp(a) is genetically controlled and due to the homology between apo (a) and plasminogen, a blood clot lysing factor, it interferes with clot lysis and adheres LDL to the endothelial surface where it can initiate atherosclerosis. Lp(a) levels greater than 50 mg/ell, plus high LDL levels can increase cardiovascular disease risk six fold. 11-14

TARGET BLOOD LEVELS

Blood cholesterol is increasingly used as a screening tool for cardiovascular risk. One third of all adults in the U.S. now know their blood cholesterol level. How much is the right amount? Looking at just LDL cholesterol, it is argued that since newborns have levels of approximately 30 mg/dl and that 25 mg/dl is sufficient to nourish the body’s tissue with cholesterol, and that species which do not experience cholesterol-related cardiovascular disease consistently have LDL cholesterol levels of less than 80 mg/dl, a recommended level of 25-80 mg/dl is considered to be in the healthy range. This is 1/5 the level normally seen in Western societies.15 Other tests measuring HDL, total cholesterol, triglycerides, apoproteins and cholesterol/HDL and Apo A/Apo B ratios are also used to determine cardiovascular risk.

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By measuring various lipid factors it is possible to compile a composite lipid risk score.16 Diagnostic values, however, are subject to error both in testing and interpretation. We are far from being able to accurately quantitate health. A false “positive” risk could create anxiety and disease (convert a normal person to a patient) where none was present, and a false “negative” risk could lead to complacency and exacerbation of existing disease. Therefore, laboratory results and “normal” values should always be viewed with suspicion and used only as leads for further diagnostic evaluation.17-20

CHOLESTEROL

The level of various lipids in the blood, including cholesterol, is dependent upon cholesterol ingested and the amount of cholesterol being synthesized within the body. Cholesterol is an extremely important compound that makes up part of cellular membranes, is a substrate for the synthesis of a variety of hormones and vitamin D, and also is a component of bile acids which permit the digestion of lipids.

If cholesterol is a normal and healthy physiological compound, why such an uncomplimentary reputation? Government, through the National Cholesterol Education Program (NCEP) seeks to decrease the nation’s blood cholesterol levels. This is the largest medical intervention in the history of the U.S.A. It has not been done without cause. Heart disease takes the life of one of every two in this country. Cholesterol is an integral part of the atherosclerotic plaque and major studies such as the federally supported Framingham (Mass.) Heart Study following thousands of subjects since 1948 show significant correlations between cholesterol and heart disease.

Simply lowering blood cholesterol is not a panacea, however. If the diet were totally depleted of cholesterol, the body would be forced to produce that which is necessary to sustain life. If blood cholesterol is unusually low (less than 160 mg/dl) the risk of stroke increases three fold and the risk of cancer increases two fold.21, 22 Thus dietary cholesterol, although perhaps a contributing factor to disease, is not likely a “poison” in its natural food form. The body has elaborate biochemical systems designed to synthesize approximately 80% of the cholesterol found within normal tissue. The body evidently thinks cholesterol is important. Cholesterol synthesis uses foods such as sugar, alcohol and starch to form the precursor acetate. A host of enzymes specifically designed to assure cholesterol availability then builds the complex molecule from acetate.

Cholesterol has been a part of the diet since the beginning of life yet cholesterol-linked disease is recent, reportedly being of significant consequence only since about the 1930’s. The Masai in Tanzania consume up to 2,000 mg of cholesterol per day yet their serum levels remain low, 115-145 mg/dl.23 A study of South African egg farm workers who consume large numbers of eggs resulting in a cholesterol intake of 1,200 mg per day have serum cholesterol levels of 180 mg/dl.

So why would cholesterol cause cardiovascular disease, the number one killer in many developed nations, when:

1. Cholesterol has been a part of the natural diet of humans and animals for millennia:

2. Cardiovascular disease is not significant in many so societies consuming high levels of cholesterol:

3. As cardiovascular disease increased, cholesterol and saturated fat levels have remained relatively constant: (Fig. 24) and,

4. As deaths from heart attacks decreased by 42% from 1963 to 1986, average cholesterol levels decreased only 3%.24

Some argue that the apparent paradox of increased cardiovascular disease is a result of increased life span creating an older population naturally more given to degenerative diseases. But contrary to popular belief, life span (the length of life one can expect to live, life potential) has not increased significantly since actuarial data has been reliably tabulated. Life expectancy (the average length of life of a population), on the other hand, has increased (47 years in 1900, 73 years today) due to decreased infant mortality resulting from better public hygiene and food distribution. Thus although at birth our chance of survival to a natural old-age death is increased, our age at the time of a natural death has not increased over that of our distant ancestors.25 Increased cardiovascular disease rates are therefore not simply a function of the increasing average age of our population.

The evidence is, however, quite convincing that cardiovascular disease is linked to diet in some way. Additionally, atherosclerotic plaques in vessel walls (particularly carotid and coronary) do indeed contain cholesterol although it may be difficult to prove that cholesterol’s presence is a cause rather than a result of atherosclerosis. The issue is not closed. There is evidence that cardiovascular disease is ancient and that genetics and the stresses of modern living. particularly. may be more important than diet.26

It is likely that atherosclerosis is a consequence of the influence of a variety of modern factors. These include but are not limited to sedentary living, stress, environmental pollution and diet. Looking only at diet, correlations between cardiovascular disease and increased consumption of proinflammatory omega-6 oils, processed (hydrogenated, oxidized) polyunsaturated fatty acids found in manufactured margarines and a wide range of other commercial processed products and oxidized cholesterol are far more logically convincing as etiologic factors than natural cholesterol or saturated fats.

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The early 1900’s, marking a seemingly rapid rise in cardiovascular disease, also marked the rise in the consumption of the fabricated, fractionated processed diet.27-30 (Fig. 23) Cholesterol as a part of raw, whole, natural foods (natural here would also mean food animals in the wild, not factory farmed) has not been demonstrated to be linked to any disease conditions. The putative relationship between cholesterol and disease confuses definitions. The cholesterol referred to and shown through metanalysis, retrospective studies and prospective controlled clinical trials to be positively associated with atherosclerosis is not “natural” cholesterol. For example, in animal studies which induce atherosclerosis, an oxidized (“activated”) cholesterol is used.31,32 Additionally, human studies measure the effects of processed fats and oils as they occur in processed foods, not lipids as they occur in raw, natural, whole, fresh foods. Cholesterol in a homogenized, pasteurized butter, scrambled egg, fastfood burger or a grilled steak is a whole different creature than the cholesterol found in the living tissue of a wild antelope. (Fig.24)

Not only is the form of the cholesterol different (there are over 60 different cholesterol oxide species alone) but its context is totally different. The value of food is not only determined by its individual components, but by the company kept, the kind and relative amounts of neighbors — its synergonic nature. Processed foods are made from fractionated ingredients which are modified and then reassembled to create taste, shelf life and profit. Afresh, raw, natural food is entirely different, it is a complex milieu of interrelationships. It is a whole more than an assemblage of parts. A real food is no more X% protein, fat, minerals, vitamins and carbohydrates than a novel is X% ink, cellulose and glue.

Although experiments have yet to be devised to measure the effects of natural cholesterol by means of an all raw diet, the results are predictable. The grandest experiment of all, that of the development and sustenance of life on the planet prior to the roller mill, extruder, solvent extractor and hydrogenator, has already given the answer. Life owes its very existence to the presence of whole raw natural food. Such food is not the cause of disease, it is the cause of life.

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Natural food was the only food available until the technological era. The new food, the new cholesterol, hydrogenated and oxidized fatty acids and their new artificial combinations, were born out of technology. Also, it is argued, born at that time was the plaque of atherosclerosis. Thus the relationship of “cholesterol” and “saturated fats” to atherosclerosis is an indictment of food processing and not true food cholesterol as a part of whole, raw, natural foods.

REGULATING BLOOD LIPIDS

The level of cholesterol in the blood is regulated by a wide array of feedback mechanisms. If there is an excessive amount of LDL cholesterol in the bloodstream, receptors in the liver responsible for taking up these transport units will become saturated. When high blood levels of LDL are reached, the liver cells decrease the number of LDL receptors thus decreasing the liver’s ability to clear the blood of cholesterol. Thus when the liver is saturated with cholesterol and it needs no more, it simply shuts down the production of LDL receptors. At the same time, cholesterol excretion of bile acids would be increased to capacity. If the diet is low in fiber, or digestive tract microflora are out of balance, much of this cholesterol would be reabsorbed thus contributing to escalating blood levels of cholesterol. The cycle perpetuates itself continuing to build higher and higher blood levels of cholesterol. A familial hyperlipidemic condition whereby receptors for taking up LDL are defective can also contribute to exaggerated blood levels of cholesterol in some individuals.33 (Fig. 25)

High blood cholesterol and saturated fat levels and unfavorable lipoprotein ratios are a reality for many individuals and may place them at risk of life threatening disease. Improvements in lifestyle can decrease the absorption of cholesterol, increase its excretion, and change the ratio of LDL’s to HDL’s resulting in blood levels which are more conducive to

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the healthy state. Such improvements include: (1) increasing the consumption of fresh fruits and vegetables, and: (2) consuming a variety of high fiber foods containing various sterols which compete for uptake of cholesterol in the intestinal tract combined with: (3) a lower consumption level of processed cholesterol combined with: (4) increased exercise: (5) and perhaps increased consumption of omega-3 and omega-9 fatty acid containing foods. Omega-3’s are extremely effective in mixed hyperlipidemias, and omega-9’s are reported to have the ability to decrease LDL’s while increasing HDL’s.34-37 Decreasing saturated fat consumption also may help since saturated triglycerides are hydrophobic and encourage the formation of the higher fat and cholesterol carrying LDL’s and VLDL’s and retard cholesterol uptake by HDL’s.

Additionally, certain drugs (Probucol, Cholestyramine, Colestipol, Clofibrate, Gemfibrozil, Lovastatin and others) have been devised to decrease the hepatic synthesis of cholesterol and decrease the amount of cholesterol that is intestinally absorbed or reabsorbed from bile into the enterohepatic circulation which may be required if more natural modifications are not effective. (These are not without significant dangers, however.) 38-42

Diet modification and lifestyle changes are sensible tools to improve health and will offer the greatest chance of optimizing health and preventing disease. Careless hedonistic living based on the presumption that early diagnosis and heroic invasive procedures, such as transplants, angioplasty, bypasses, or drugs will provide forgiveness is a poor second to thoughtful preventive practices.

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