There is a variety of persuading evidence that the fatty acid content of modern human and domesticated animal diets should be altered. The ability of fish oils to affect cardiovascular disease has recently become widely known. However, this is not new. It originally came to light more than 35 years ago.1,2 Epidemiological studies of Greenland Eskimos demonstrated a low incidence of cardiovascular disease compared to Western nations. A component of fish oil has subsequently been linked to this preventive action by some investigators. Since Eskimos, on their native diets, are known to be afflicted with only one tenth the amount of myocardial infarction as is present in Danes and Americans, incorporating the preventive factors of the Eskimo diet in the Western diet might therefore have dramatic health consequences.3

ANIMAL EVIDENCE

Experimental evidence from animal studies demonstrates a like effect of improper lipid nutriture. For example, in vessel ligating studies measuring vascular necrosis in rats, cats, dogs, swine, and primates, it has been determined that increasing omega-3 fatty acids produces a protective effect.4-8

A comparison of the tissues of domestic animals to that of wild animals demonstrates the dramatic nutritional shift which has occurred with domestication and modern farming practices. (Fig. 30) If humans eat factory farmed animals, their tissues will mirror the changes which have occurred in the food animal. Humans, like domestic animals, will also therefore have fatty acid profile discordancy with their preindustrialized ancestors

[ Comparison Of Domestic An Wild Animal Meat Image ]

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PRE-MODERN POPULATION EVIDENCE

There are likely factors other than just the incorporation of high levels of fish oils in the diet which have protective effects against cardiovascular disease. Anthropological studies demonstrate that preindustrial civilizations and wild populations of animals do not fall victim to this disease as we do, yet they do not by and large consume fish. Consuming a natural, raw, whole food diet likely presents a wide range of health augmenting effects which help protect not only against cardiovascular disease but many other degenerative diseases as well. 9,10

A study of the nature of the modern processed diet as compared to natural diets demonstrates the wide gap that has occurred between the two. Not only have oils been stripped from their natural food context but, through various processing methods, they have been altered in ways that prevent their participation in essential fatty acid functions. These alterations may not only remove nutritional value but may turn them into metabolic toxins as previously discussed. Such changes have occurred within a very short time period, primarily within the last 50-75 years.

However, the genome was adapted over thousands of years to natural food sources containing natural ratios of natural fatty acids. Food changes, like environmental changes which are occurring at a rapid pace, can outstrip the ability of organisms to adapt. We are in a genetic time warp; our genes are adapted to a natural form of food and environment, yet we are now increasingly experiencing an entirely different context. By outlining this idea from the perspective of time our precarious position is dramatically demonstrated. Study and ponder Figure 31 well; it represents the most important concept in the book.

[ Time And Adaptation Image ]

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It is now estimated that 75-80% of all deaths occurring in Western cultures are a result of exposing our genes to the wrong environment and food. Chronic degenerative diseases are the symptoms of this genetic discordancy. These include cardiovascular disease, cancers, arthritis, autoimmune diseases, adult onset diabetes, and a wide range of other degenerative conditions.11, 12

The logical solution is to restore the diet to its more archetypal, natural form. This can be accomplished through fresh raw, natural products in the diet and the selection of specific foods which contain high levels of certain beneficial nutrients.

If processed foods are to be consumed, foods should be selected as close to their original form as possible with minimization of manipulation.

THE DYNAMICS OF TISSUE FATTY ACIDS

“We are what we eat” is particularly true in relation to lipid nutrition. Since lipids make up a large percentage of the substance of the body, and lipids undergo a continual turnover, our lipid composition is therefore a direct reflection of what we have been eating.

The composition of serum triglycerides reflects the composition of the last few meals: that of cholesterol esters (in LDL’s for example) and erythrocyte membranes reflects the intake of the preceding weeks or months: whereas the composition of adipose tissue is an index of the habitual diet over the past 23 years.13 Changing the dietary composition of fatty acids will therefore first change serum lipids, then LDL’s and erythrocytes, then adipose tissue. In other words, if we are eating high saturated fat burgers and french fries boiled in denatured oil, our membranes will reflect this composition and predispose us to degenerative disease over time. On the other hand, if our diet consists of a large proportion of fresh, raw vegetables, fruits and seeds minimally prepared, our membranes will reflect the composition of these ingredients with omega-3, -6, and -9 fatty acids more nearly matching our distant preindustrial ancestors, our genetic expectation. (Fig. 32)

COMPLEMENTARY NUTRIENTS

A variety of nutrient cofactors contributes to proper lipid nutrition. As fatty acids are enzymatically converted into energy, eicosanoids, and structural components, enzyme systems are at work. These systems require the presence of micronutrients found in whole natural foods such as the minerals zinc, copper, potassium, iron, and manganese, and vitamins such as B3′ B6′ B12′ C and folic acid. About two thirds of the 50 or more known essential nutrients are believed to be involved. Focusing only on fatty acids would be as erroneous

[ Tissue Fatty Acid Dynamics Image ]

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as omitting them. Nutrition is an unimaginably complex entanglement of elements that is best supported by balanced whole fresh foods and intelligent, balanced supplementation when necessary.

References available within book text, click the following link to view this article on wysong.net:

http://www.wysong.net/articles/lipid/10_article_lipid_chapter_ten_lipid_nutriture.shtml

For further reading, or for more information about, Dr Wysong and the Wysong Corporation please visit www.wysong.net or write to wysong@wysong.net. For resources on healthier foods for people including snacks, and breakfast cereals please visit www.cerealwysong.com.

PLATELETS

Platelets play a pivotal role in the relationship between lipids and atherogenesis. Blood platelets are powerful biochemical packages wrapped in a phospholipid membrane. When platelets in the circulation are exposed to broken endothelial tissue lining blood vessels and underlying collagen. they become activated to stimulate the healing of the injury.

The arachidonic acid within the platelet forms two different eicosanoids, which serve two opposing functions. If the platelet is next to another platelet, thromboxane (TXA2) is formed (500 million platelets can form as much as 2 mg of thromboxane) which stimulates the aggregation and clotting of platelets and other blood components.7 For those platelets near the endothelium, prostaglandin E2 (PGE2) is formed which stimulates hyperplasia in the exposed blood vessel tissue and inhibits further clotting adjacent to the injury. Prostaglandins also stimulate bone resorption bringing calcium to the site of the injury to decrease tissue pH and further stimulate hyperplasia.

These are normal mechanisms occurring continually and are essential to life. If they did not occur, minor vascular lesions could lead to runaway hemorrhage, and healing and repair would not happen. However, when there is an excess of omega-6 fatty acids in platelets which can generate excess amounts of arachidonic acid at blood vessel injury sites, the blood clotting, vessel constricting, bone resorbing, and hyperplastic effects can exceed the countering moderating effects of prostaglandins from fatty acids such as the omega-3’s.

PATHOGENESIS

High levels of dietary fat can result in high levels of low density lipoprotein (LDL). These protein-lipid complexes can contain large amounts of cholesterol, much of which can be oxidized as a result of the way modern foods are processed.8 LDL can migrate to areas of injury, be engulfed by monocytes and macrophages, and accumulate at the site of these injuries to provide more arachidonic acid and free radical generating oxidized cholesterol fuel for further endothelium damage.

This ongoing cycle, beginning with perhaps a small lesion which occurs as a matter of course in the endothelium, or induced injury as a result of high blood levels of oxidized fats, may turn out to be a self-perpetuating, out-of-control, cancerlike growth accumulating in vessels resulting in atheromas and eventual closure of coronary vessels leading to heart attacks. Additionally, hardening (sclerosis) of the arteries can result in hypertension and loss of vascular resiliency, potentially causing stroke, aneurysms, general loss of health and vigor, and predisposition to a range of other diseases.

In other words, if there is vascular injury, the normal clotting, vessel constricting, tissue regenerating mechanisms can run out of control as a result of an imbalance of moderating e1cosanoids which are ultimately derived from dietary lipids. In tissue with excess arachidonic cascade potential, vessel injury recruits excess platelets, which stimulate excess clotting, vessel constriction and vessel wall inflammation,

[ Atherosclerosis Sequence Image ]

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which in turn releases more arachidonic cascade eicosanoids, which stimulate further platelet aggregation, clotting and so on, leading to atheroma and vessel closure.

If there is no initial endothelial injury but it is being induced from high oxidized lipid blood levels, a similar cycle occurs. Oxidized LDL’s are scavenged by monocytes which become macrophages, which accumulate within the vessel wall causing free radical damage, foam cell formation, calcium deposition and inflammation. This produces arachidonic cascade metabolites, which further induce inflammation leading to progressive atheroma and vessel closure. (Fig. 26, 27)

PREVENTION RATIONALE

An alteration of the diet such that oxidized fats are decreased, saturated fats are decreased, omega-6 fats are decreased (in Western societies), and omega-3 and omega-9 rich foods are increased may potentially result in a restoration of health to the vessel wall. Prostaglandins created by omega-3 and omega-9 oils create opposite effects to the vessel constricting, clot-forming effects of the omega-6 oils since they compete for the same enzyme system. (Refer to Fig. 18) Therefore, if omega-3 and -9 fatty acids are increased in the diet, they use up the enzyme systems normally used byarachidonic acid to form the atherogenic promoting eicosanoids. This is the present explanation for the epidemiological evidence showing that humans and animals consuming higher levels of the omega-3 and omega-9 classes of fatty acids develop far less of the common cardiovascular problems than exist in Western society.

There is some evidence that the incidence of cardiovascular disease is proportional to the ratios of fatty acid classes in platelets, which is in turn related to diet. Eskimos, for example, have a higher omega-3 to omega-6 ratio in their tissues reflecting their high fish diet, which is in turn related to their low risk of cardiovascular disease compared to Western nations. (Fig. 28)

[ The Formation Of Atheroma Image ]

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This is not to say omega-6 fatty acids such as linoleic are harmful per se. Balance is key. Indeed if sufficient linoleic is not present, atherosclerosis can result as evidenced in a variety of species.9,10

ASPIRIN

By shifting the balance of these same eicosanoid enzyme systems, aspirin is also believed to exert its effect as an anticlotting agent in cardiovascular disease. Aspirin is a specific inhibitor (acetylator) of cyclooxygenase which normally is used to convert arachidonic acid into TXA2 and PGE2. Aspirin’s inhibition of clot forming TXA2 is several days longer than its effect on anticoagulating and vasodilating PGE2. Thus the net effect is clot inhibition. (Refer to Fig. 19)

[ Comparative Dietary Oil/Fat Composition Image ]

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However, aspirin is a bandage. It does not address the root cause, which is dietary impropriety. It is also not without its dangers since it can precipitate allergic reactions such as asthma by shunting arachidonic acid into the lipoxygenase leukotriene path and may actually increase platelet clotting if given in conjunction with fish oils.11

Excess consumption of oxidized fats and fatty acids of the omega-6 family will fuel the atherosclerotic system. Excess raw materials can exceed the ability of moderators. If the root cause is dietary, the ultimate solution must therefore also be dietary, not pharmacologic. It is ironic that the 80 million aspirin tablets taken daily by Americans may in large part be necessary to cancel the effects of 15 million pounds of omega-6-predominant processed polyunsaturated oils.

NUTRIENTS

Many nutrients found within foods have the ability to block or modulate prostaglandin synthesis. These include sulfur compounds found in garlic, onions and cruciferous vegetables, and various minerals, particularly the divalent cations zinc, copper, lithium, silver, selenium, and calcium.12 A variety of fresh whole foods, (raw if possible) grown on nutrient-rich soils (as opposed to modern agribusiness mined soils where only nitrogen, phosphorus and potassium — NPK fertilizers — are replaced) provides the body with raw materials which augment proper fatty acid nutrition and may lessen or obviate the need for potentially dangerous drugs.

Other nonpharmacologic factors which may help produce more “friendly” lipid profiles include decreased stress, increased exercise and the elimination of tobacco and perhaps caffeine.13 Highly refined carbohydrate and sugar diets increase cardiovascular disease risk perhaps through increased glycosylation reactions, increased lipoprotein (a) levels and decreasing HDL levels.14 Calcium at 800 mg per day can decrease cholestero1.15 Chromium deficiency can decrease glucose tolerance factor and thus affect sugar metabolism and adversely affect lipid proflies.16Legumes, soluble fiber, garlic and onions can decrease cholesterol levels.17 Vitamin C at 1000 mg per day and vitamin E at 200-400 I.U. per day are excellent antioxidants and can decrease glycosylation reactions, decrease cholesterol and increase HDL’S.18 Pantethine, a derivative of pantothenic acid at 300 mg. 3-4 times daily,19 and niacin from 1-4 grams daily can positively affect lipids. Niacin in fact is one of the few agents capable of lowering genetically controlled Lp(a) levels.20 L-carnitine, an amino acid, at 1000 mg per day can ameliorate hyperlipoproteinemia.21

These nutrients are supplied in a varied whole raw food diet. Some researchers argue, however, that therapeutic levels of some nutrients are not possible from simply consuming natural foods. An accumulated deficit from a lifetime of dietary indiscretion may indeed require a boost. Disease, an extraordinary event, may require extraordinary measures to effect a cure. But before consuming any isolated nutrient become well aware of its merits and demerits since some nutrients can present toxicities or imbalances at certain levels. Guidance by a well qualified nutritional health care professional would be advised for anyone with existing disease who desires to use isolated nutrients in therapy.

As mentioned in the previous chapter, the case for the link between diet and heart disease is not closed. Some argue that the diet-heart hypothesis began, remains, and grows because of the support of powerful institutions and personalities who subserve gigantic health-disease and food industries.22 Some have calculated that for persons aged 20-62 that a lifelong program of cholesterol reduction might increase life expectancy three days to thirty months.23 Even Sir William Osler, the most highly respected physician of his time, said in 1879 that arterial degeneration could occur even at a young age and was due to “the high pressure in which men live, and habit of working the machine to its maximum capacity,” not to excesses in eating and drinking. 24

There is little doubt that singular focus on diet or exercise, for example, misses the mark. It ignores equally important factors such as self esteem, affectionate relationships and feeling in control of one’s life.25 The controversy aside, living and eating in a more natural synergonic context can only help and is likely the greatest potential for life free from disease.

References available within book text, click the following link to view this article on wysong.net:

http://www.wysong.net/articles/lipid/08_article_lipid_chapter_eight_atherogenesis.shtml

For further reading, or for more information about, Dr Wysong and the Wysong Corporation please visit www.wysong.net or write to wysong@wysong.net. For resources on healthier foods for people including snacks, and breakfast cereals please visit www.cerealwysong.com.