Posts Tagged ‘Disease’
The Need to Change Lipid Nutriture
THE ESKIMO EVIDENCE
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.
Green Tea and Its Many Health Benefits
The Asian community has used different teas and herbal remedies since before the Great wall of China (over 3000 years ago) and green tea has stood out as one of its hallmark and most helpful constituents. Green tea has been used to treat everything from heart attacks, stroke to infections like sepsis (blood infection) and numerous other conditions and maladies. Many studies have been undertaken to research and extract the helpful and beneficial compounds in Green tea that exhibit these medicinal qualities.
Recent scientific studies listed in Chemical & Engineering News (produced by the American Chemical Society) show numerous benefits from the different compounds contained in green tea leaves (polyphenols like EGCG, a powerful antioxidant that inhibits the rapid growth of cancer cells without harming healthy cells). Studies done at Harvard and Cornell Universities on these polyphenols have shown a marked decline in carcinogen activity (up to 60% blocking reduction in oxidation capabilities) and even a biocide or antiseptic quality (hence the current research on green tea polyphenols and tooth and gum disease). Green tea has shown and evidenced antibacterial properties and more research in this area is needed.
Green tea polyphenols inhibit and retard cancer growth in every study and form of cancer from liver cancer to uterine and breast cancer. It is important to note, that although no cancer in these studies was completely cured, duration of survival and quality of life were increased in every circumstance. EGCG, due to its abilities to retard cancer with no known side effects is currently being researched to see if higher concentrations and / or more powerful synthetic derivatives could be used as a replacement for the current highly toxic chemotherapy.
Study after study shows a vast reduction in onset and risk of various cancers and disease. Other green tea findings included a study of smokers at the Arizona Cancer Center in Tucson showing that four cups of decaffeinated green tea every day for four months provided some protection against potentially carcinogenic damage to DNA, as measured by the amount of an enzyme in the urine.
Many studies have linked green tea to lower risk for breast, pancreatic, colon, esophageal, and lung cancers. University of Purdue researchers recently concluded that a compound in green tea inhibits the growth of cancer cells. There is also research indicating that drinking green tea lowers total cholesterol levels, as well as improving the ratio of good (HDL) cholesterol to bad (LDL) cholesterol. The polyphenols inhibit the absorption of cholesterol in the digestive tract, which actually helps lower the amount of LDL cholesterol in the bloodstream.
Basically, to sum this up, green tea has been proven to reduce the risk of cancer and retard the growth of cancer cells in every case and for this reason alone should be incorporated into every diet. Just 4 cups of green tea per day has been found to slow and retard breast cancer in women (Japanese scientists at the Saitama Cancer Research Institute). 4 cups of green tea daily gives the optimal amount of polyphenols for the best results.
Atherogenesis
The putative ability of fish oils to affect cardiovascular health has focused considerable attention on lipid nutriture. Investigations of societies consuming high levels of omega-3 and -9 oils as well as both prospective and retrospective scientific studies have demonstrated the increasing importance of dietary fats.1-6 Complex mechanisms have been theorized but ultimately hinge on eicosanoid synthesis pathways. Fatty acids and other lipid substances such as cholesterol found within the circulation and as a part of the endothelial lining of blood vessels and their smooth muscle coat, and within platelets, provide an important substrate for vascular health or disease.
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.
High Blood Cholesterol Candidate for Heart Attack
Cholesterol, a yellowish fatty substance, is one of the essential ingredients of the body. Although
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.
Lipid Transport
LIPOPROTEINS
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 ]
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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)
[ Lipid Transport Vehicles Image ]
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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)
[ Lipoprotein Metabolism Image ]
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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.
[ Blood Lipid Levels Image ]
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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.
[ The Cause Of Cardiovascular Disease Image ]
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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.
[ Cholesterol Forms Image ]
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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
[ Cholesterol Metabolism Image ]
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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.
References available within book text, click the following link to view this article on wysong.net:
http://www.wysong.net/articles/lipid/07_article_lipid_chapter_seven_lipid_transport.shtml
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