Lipid Transport

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)

[ Lipoproteins Image ]

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)

[ Lipid Transport Vehicles Image ]

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

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)

[ Lipoprotein Metabolism Image ]

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

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.

[ Blood Lipid Levels Image ]

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

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.

[ The Cause Of Cardiovascular Disease Image ]

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.

[ Cholesterol Forms Image ]

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.

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

[ Cholesterol Metabolism Image ]

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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