Why Cholesterol?                                

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Get Your Cholesterol Up!

Adapted From Dr. Ray Pete, Ph.D, Endocrine Physiologist; Karp's Cell & Molecular Biology Text Book Series, and other Text of interest.

Cholesterol is not a fat! It is an alcohol. We look upon it as a fat, and doctors are now having to come to grips with the fact that, "Everything doctors know about cholesterol is wrong!"

The newest information about it is creating groundbreaking issues in pathology and physiology.

However, if you read medical journals and listen to television shows, the idea is continuously generated that cholesterol is a four-letter word – a bad thing. This idea has been promulgated all over America: "The lower the serum cholesterol is, the better for the patient’s health."

Most people know that heart disease is not caused by cholesterol. That is only a theory that has gone through numerous developmental stages and died out, but statin drugs and other cholesterol-lowering drugs brought it back to the forefront of most people’s brains and now they believe it is so.

For the last 50 or more years, people have been told to avoid red meat, eggs, butter and other saturated fats and to eat polyunsaturated fats to lower their cholesterol.

One doctor, writing years ago in M.D. Magazine, pointed out that cholesterol is the last thing to come along and get stuck in an atheroma. Doctors have focused mostly on the types of fats present in the atheroma of a diseased artery rather than in the process of the whole disease.

That process includes spasms of the vasculature, the thickness of the blood and iron and calcium deposition in those blood vessels, as well as heart rhythm, and including the whole inflammatory process, in which a major part of those reactions generating atherosclerosis is the bowl’s ability to absorb endotoxins secreted by the bacteria of the colon as they live, die and multiply. One thing for these bowel toxins is cascara sagrada, which contains emodin. The permeability of blood vessels and their tendency to leak, "leaky capillaries" and the bowel tissue is enhanced with unsaturated fats and endotoxins.

Dr. "B" feels, and there is enough scientific data to back up his followingt statement, that a person with varicose veins has leaky capillaries, which shows them with varicose veins, which can possibly be an indication and more so to the fact that they are absorbing larger amounts of bowel endotoxins, especially as they age. Unsaturated fats plays a major role in this too. With the capillaries in such a state in one’s legs, it would be wise to change one’s diet, as these people may be getting set up to generate a cancer because of this and other changes promulgated during this time. Inaddition to Cancer, one may first go into Diabetes; then, 'the Cancer!

There are chemical reasons for this, such as the By–Stander Effect; or, Aerobic Glycolysis, generating too much Lactate!

Simultaneously, while heart disease and cancer are/will be more prevalent than ever as Stress reaches heaven, the media says we are licking cancer and heart diseas – we aren’t – according to Dr. Stephen Sinatra, America is undergoing an epidemic of hypothyroidism. Broda Barnes decades ago, said the cure for heart disease is thyroid hormone!

Now consider, when rabbits were fed a diet of something not in a rabbit’s diet – cholesterol – it caused them to develop atherosclerosis. It was shown that rabbits do not respond this way to cholesterol which is generated not in their diet. But if they were fed cholesterol and they were also given T3 thyroid hormone, they did not develop atherosclerosis (Friedland, 1933). It was known by 1936 that in humans who had hypothyroidism, as well as in other animals, they developed hypercholesterolemia. Here is the big rub – and Sinatra seems to be in on this thinking too – that low thyroid generates development of many diseases and included in this is Cancer and Cardiovascular Disease. It was discovered during that time that increased cholesterol was not a danger but a means of protective adaptation against other things happening in an organism.

In the 1950s this cliche about cholesterol causing atherosclerosis became revived again when the vegetable oil industry learned that the polyunsaturated fats (PUFAs) reduce the cholesterol in the blood serum. However, they failed to mention that many other toxins do likewise, that is, lower cholesterol.

The edible oil industry was suffering after World War II because new chemicals had been discovered such that their oils were no longer needed in paint formulas. These new chemicals replaced the edible oil industry’s oils. They needed a new whipping boy and started advertising PUFAs as "heart protective." They got the American Dietetic Association, the U.S. Department of Agriculture, the American Medical Association, the FDA, and the American Heart Association to back them up in their advertising.

The early rabbit case researchers never made a claim against cholesterol, but what most people were unaware of: vegetable oils were used as a solvent for the cholesterol feedings of those rabbits! The PUFAs caused atherosclerosis in those rabbits! But the edible oil industry generated and promoted a large amount of unscientific and outright fraudulent work to support their claims. Hell ain’t half full, folks!

Because the PUFAs make the cells of tissues lose structurability, cholesterol left the bloodstream and rushed to the millions of cells in the tissues of the body in an attempt to restore the structure. This cholesterol leaving the bloodstream, when measured, showed a lowering, but nobody tells you about all the damage the PUFAs are doing throughout the body (Mary G. Enig, lipids chemist, writing for Wise Traditions).

In the 20th century, deaths from heart disease had been increasing and reached its peak in 1950 - 1975, after which it began to decline. During this time, in which there was a rise in the death rate, a parallelism exists. That is, animal fat (saturated fat) use was decreasing and the use of vegetable oils was continually on the rise. In those European countries that were said to have shown that eating very little animal fat prevents heart disease, the trend after World War II showed the opposite. People were eating more animal fat (saturated fat), but there was no increase in heart disease.

There is a relationship between saturated fat ingestion, heart disease and cholesterol that is nothing more than advertising copy. If you are looking for heart disease’s actual causes, you would need to consider other factors that changed in the United States during the time when heart disease was on the rise. Both increases of harmful factors and decreases in protective factors would need to be looked into.

It appears that one of the decreases in heart disease was correlated with eating saturated fat in red meat.

Other things that increased rapidly after World War II in the United States were lead in gasoline, cigarette smoking, increased use of drugs and other medications, and stresses of socioeconomic and psychosocial levels. Also, another thing that happened during the war was that radiation came into military, industrial, and medical usage. These things are not obvious to the regular citizens of the world, and there has been also during this time a decrease in certain nutrients, like magnesium, selenium, and vitamins to protect against this new thing called radiation. Many of these harmful factors have very well organized and powerful lobbies to defend them in Washington, D.C. The "30 Pieces of Silver" goes on and on.

Many doctors discovered selenium was very important for colon, lung and prostate cancers, which yielded to their treatments when nothing else would help.

Radiation, along with seed oils and foods with less nutrients (degraded foods) have well organized and specific lobbies to defend them. This is why radiation is a big thing in the cancer field as well as chemotherapy, but 50% of the people with cancer die from the chemo and not from the cancer. Even though there is increasing knowledge about PUFA dangers, medical journals still advocate "the official heart-protective diet." That is, avoid as much as possible the saturated fats and ingest more unsaturated fats as the primary fat in one’s diet (Hu and Willet, 2002).

It has been known for a long time that death from cancer and heart disease has a strong relationship to one’s exposure to (1) medical services and (2) medical radiation, when heart disease reached its peak mortality for some years, medical x-rays were being given in large doses with each exposure and those exposed were also exposed to (3) all the radioactive fallout from all the atomic bomb testing that went on from 1945 - 1963, and that fallout continued into the 1960s and 1970s.

Remember, that peak heart disease was not caused by saturate fats, as you just read.

In 1971, it was noted that the cholesterol that was used in various experiments to prove cholesterol caused heart disease wasn’t cholesterol! It was something totally different. It was oxidized cholesterol, which is NOT the same thing as cholesterol, and most doctors never noticed the difference between the two.

Vine and others, in 1998, found that dietary cholesterol, real cholesterol, wasn’t very atherogenic. It was only oxidized cholesterol, which is not really cholesterol at all, that was atherogenic, and that was what was used in the tests, but real cholesterol became the scapegoat.

Now, Folks...Get This!

This is what is going to kill the fishing business, especially salmon. All physicians now recommend poached salmon rather than eating what God ate when He came down to check out Sodom and Gomorrah – Red Meat – to lower cholesterol.

Numerous experiments have illustrated that poisonous oxidized cholesterol prepared in various ways in different foods have shown that steamed salmon generates many times more oxidized cholesterol than frying the salmon! This is because of the longer cooking time, which allows the PUFAs in the salmon to break down, causing poisons such as acrolein and free radicals, which, in turn, cause the cholesterol to become oxidized, along with other components contained within the fish. This poisonous cholesterol (oxidized) from steamed salmon is much higher than beef cooked at an even higher temperature.

When PUFAs are oxidized, such as linoleic acid, corn oil, etc., and are added to the food, you find these oxidized lipids in the blood, where they increase the formation in the arteries of cholesterol deposits (Straprans, et. al., 1994. 1996).

With what is now occurring throughout the world, with a nuclear war staring us in the face, Stress will become even more rampant than it is now!. There are various things Dr. "B" recommends to control stress and to help normalize the mood. They are Cortisol Control and Lithium Orotate, among others.

PUFAs in an organism undergo oxidation as stress increases, so anyone eating vegetable oil and fish will have some oxidized cholesterol throughout bodily tissues. But, if cholesterol is being fed to the body, this constant turnover of this substance tends to lower the toxic breakdown products of cholesterol. Hence, eat cholesterol in the form of whole eggs – the yolk too!

However, as we said earlier, hypothyroidism is also now rampant in America, which means the use of cholesterol by the body is much slower, allowing toxic forms to accumulate; that is, rise high. Therefore, thyroid hormone in its active form, T3, lowers cholesterol by allowing it to be used as it should be.

In 1934, it was discovered that many antioxidant constituents of the diet serve as a thyroid supplement that prevented atherosclerosis even though the rabbits were given toxic cholesterol. One such supplement was Selenium. Researchers found that the more selenium in the diet, the more it served as a protective nutrient, stopping atherosclerosis in animals as with the rabbits of the experiment that were fed toxic cholesterol. Toxic cholesterol is oxidized cholesterol.

In addition to Selenium, Vitamin E has been used for treating, and in many cases, preventing, heart disease, and now many doctors take Vitamin E because they have found this to be so. In free radical chemistry, we learned that PUFAs are easily oxidized and that saturated fats, like coconut oil or butter, tend to slow the PUFAs’ degradation into toxic forms. These saturated fats act in some measure as an antioxidant. Yet, many have bought into the cliche that "Cholesterol causes heart disease" ... like the old cliche, "Sugar causes diabetes."

It has been shown by various observers and many experiments that cholesterol can definitely do two things:

  1. It can protect against toxic oxidation of PUFAs.

  2. It protects DNA and other necessary organelles of the cell.

A program that has been proposed but that you will never hear of because there isn’t much money in it as compared to the cholesterol drugs, is that one should include all the minerals and all the vitamins involved in an antioxidant program and avoidance of substances in the diet that worsen the destructive oxidations and to normalize the hormones, including such factors as carbon dioxide that has protective effects against oxidation forming free radicals.

Having low cholesterol might increase one’s tendency toward oxidation which yields a greater likelihood to succumb to disease.

Dr. "B" recommends:
  1. Bioflavonoids,

  2. Beta Carotene,

  3. NAC,

  4. L-Glutathione,

  5. Vitamin C,

  6. Vitamin E,

  7. Selenium,

  8. Progesterone,

  9. Testosterone and DHEA, especially the latter for women.

These are part of the antioxidant defense system. Whether cholesterol is produced by the body or taken in through the bloodstream via diet, it is the progenitor, inside the body, for all steroid hormones.

A number of major steroid hormones are antiinflammatory, of which cholesterol itself is antiinflammatory.

With this war looming over us, if it hasn’t happened by the time this is published, cholesterol will help protect against radiation damage and a number of other toxic items, such as cobra venom, chloroform, and saponins (See W.G. MacCallum, A Text-book of Pathology, 1937, Saunders Co.). Later studies have shown that blood cells are protected by cholesterol from breakdown, hemolysis, caused by heat and various other agents.

Dr. "B" learned this when he was stung by a scorpion while crossing The Great Sahara Desert, and he knew the scorpion had a similar venom to cobra venom. In this case, Dr. "B" used saturated fat in the form of unrefined coconut oil and also poured coconut oil on the scorpion sting. He saturated his insides with saturated fat, also.

Dr. "B" recommends antioxidants that facilitate structural integrity of the cells. Such as Vitamin D, Vitamin E, progesterone and cholesterol. These substances support structure and they help prevent oxidation to a tissue or a cell by strengthening the molecular structures therein.

A basic function of cholesterol seems to be the stabilization of the mitochondria which drive our metabolic machinery. It also prevents the mitochondria from destruction by stress. When hard stress hits, it lowers the ATP, the energy currency of the cell, including magnesium and carbon dioxide of the stressed organism. When magnesium intracellularly and ATP are decreased, we see increases in cholesterol synthesis. That is how important this substance is for staying alive.

When we undergo serious stress, the tissues release free fatty acids to circulate in the blood. They are then highly prone to lose electrons, generating a toxic condition – a free radical – commonly called rancidity. A rancid fat in your bloodstream is no damn good, folks!

This oxidation generates lipofuscin formation, which is known as the "age pigment." This pigment wastes oxygen and is found in atheroma plaque throughout a diseased body’s blood vessels. Then what happens is that calcium and iron accumulate, adding to damaged tissue. PUFAs and an imbalance of oxidation and antioxidants cause hemolysis to occur inside the body, and this situation causes the formation of more iron and heme released into the bloodstream from the tissues. Atherosclerosis increases as body iron stores are high, and iron plays a role in lipid peroxidation and age pigment formation, which is a sign that one is aging (Kiechl, et al., 1997).

As the blood vessel lining becomes too permeable because of increased PUFAs, estrogen, and prostaglandins, and included would be nitric oxide, serotonin, and histamine formation. Iron, along with heme will then go into the endothelium of the blood vessels. Iron will cause the formation of free radicals (toxic!) and heme will break down by the enzyme heme oxygenase into iron, carbon monoxide and biliverdin. All these contribute to what is called oxidative stress, or reactive oxygen species (ROS) within cells of the body.

Carbon monoxide goes a step further. It makes the blood vessel lining even more open, allowing fibrinogen and fats to enter the integrity of the cell. In addition, this adds, most likely, to "leaky gut syndrome," including leaky capillaries causing edema.

Cholesterol protects against cytolytic damage, and all damage, including oxidative damage. The free radicals that are being released will oxidize the cholesterol, generating toxic cholesterol. Although cholesterol is protective against all this, if there is a chronicity of PUFAs, then free radicals will be present and oxidize the cholesterol. When cholesterol turnover is low, one can almost look for hypothyroidism. Various cholesterol oxidized substances accumulate and cholesterol itself loses its protective functions.

When an organism is healthy, cholesterol is being formed continuously and converted into hormones, steroids, and in the liver, to bile salts, which are necessary to emulsify fats in the intestines. Vitamin A and thyroid hormone are used in cholesterol conversion into pregnenolone, the mother of all hormones, which goes into protesterone and DHEA. Anything stopping or interfering with this process is dangerous for a body. Vitamin A, thyroid hormone and the cholesterol supply must be kept adequate for the production of steroid hormones and bile salts.

Stress, as we have said, suppresses thyroid activity. Then increased cholesterol by the body or organism compensates a certain amount by allowing more progesterone to be generated. Progesterone and DHEA often keep cholesterol low in the bloodstream. In the 1930s, the rise in cholesterol concentration was considered a very reliable way to diagnose hypothyroidism (See 1936 Yearbook of Neurology, Psychiatry, and Endocrinology, E.L. Sevringhaus, editor, Chicago, p. 533).

As one ages, the rate of metabolism slows and gets less, and the increase of cholesterol with aging is a regulatory spontaneous process supporting the generation of protective steroids, especially those called neurosteroids in the retina of the eye and in the brain. This is probably why we are seeing so many elderly on low cholesterol medications experiencing dementia.

Cholesterol is necessary for Structural Membrane (plasma membrane) support, however, not often do you hear this. Cholesterol is one of the primary ingredients in the chromosome nucleus, bound to DNA and the nuclear matrix, and looks over the activation of genes and the mitotic spindle, and this regulates separation of the chromosomes in cell division.

If cholesterol is not in sufficient amounts, your cells divide irregularly, producing aneuploid daughter cells, which have an abnormal number of chromosomes. This condition, due to low cholesterol, is a basic, essential feature of cancer cells! When cholesterol occurs in significant amounts, it was also bound to hemoglobin, and this will be found connected with many other types of proteins, if anyone looks for this.

Cell division has something which is closely involved with it, osmotic regulation and other functions. This seems to require proper cholesterol generation. What are people on? Medicines to lower cholesterol! We are not seeing the "War on Cancer" being won.

Note this, folks: A huge study around 1985 done in Hungary illustrated that when cholesterol is lowered with drugs, this causes a large increase in the cancer death rate. This Hungarian study generate publications by the hundreds in America, voicing that this is not possible because "Low cholesterol is good. The lower the better." Still, an increase of extreme nature in cancer deaths in the Hungarian study was probably the result of a drug commonly used at that time to lower cholesterol. However, the pattern in that group is the same as the pattern in other groups with very low cholesterol. Within the past 20 years or so, numerous studies show that the lower the cholesterol, the greater the death rate, especially from cancer and suicide, and that people with low cholesterol naturally are more apt to die from trauma, infections, suicide and cancer than those with higher than average cholesterol.

This increased mortality from accidents and suicides with low cholesterol takes us back to the problems seen in progesterone deficiency, and it is probably something to do with the neurosteroids, as they are low when cholesterol is low. When progesterone is deficient, other neurosteroids generate a mood depression as well as an impaired ability to learn. There are other neurological conditions that change, also.

In this case, with cancer, Big Pharma denies that the low cholesterol drugs cause cancer, depression and suicide, but there is a prevalence of evidence with animal and human studies, demonstrating that mood and intelligence are lowered when cholesterol is lowered.

The counter to this was that someone simply injected animals with cholesterol, and their learning improved. This was shown in the Framingham Heart Study of 1,894 persons that extended over twenty years. When the cholesterol was within the desirable range (less than 200 mg/%), these people scored lower in "verbal fluency, attention/concentration, abstract reasoning and a composite study measuring cognitive domains as opposed to those with higher cholesterols (Elias, et al., 2005). This is generally not well known among lay people.

When one reaches the age of 50 and beyond with low cholesterol, there is an association with an increased risk of death from a variety of causes. Women, old women who had a cholesterol of more than 200 mg/100 ml had the best longevity, and mortality was at its lowest at 270.6 mg%.

When one takes an active form of thyroid (T3) plus cholesterol, this increases their longevity, it has been shown. Cholesterol often rises with aging because it is not compensated for by the declining thyroid hormone. If we optimize various protective factors in aging, we will possibly see a change in the process of aging.

With the big radiation storms that are coming to the world, and possibly the planet getting hotter, with the heat stress, thymus cells are sensitive to various stressors, especially radiation. Thymus cells increase when cholesterol stops lipid peroxidation there and stops death of the thymus cells by radiation. This was discovered by Posokhov, et al., in 1992.

So what have we been telling you? Help your health out for the coming extreme earth changes, radiation storms, and the extreme stress from whatever sources with ingesting progesterone tablets (20 to 60 mg daily; divided doses), thyroid hormone (T3) 20 to 25 mcg daily, split into 4 parts taking 1/4 morning; 2 pm; evening; and before bed—empty stomach one hour before and after), and increase your cholesterol, plus take the vitamins and minerals we have proffered.

It has been a dogma for some time that the death rate from cancer and heart disease would increase at high altitudes. That is not true. Oxygen at lower pressure displaces less carbon dioxide from the blood at high altitude. The body then retains more carbon dioxide at higher altitudes, which protects against free radicals and helps to deliver oxygen to the tissues. It helps maintain energy production at a sufficient level and prevents cellular stress. It has been found that high blood pressure exists in low elevations more than in high altitudes. These principles have been applied in treating degenerative diseases at high altitude health resorts.

A short period of low oxygen can improve the body’s ability to eliminate atherogenic lipid peroxides, possibly by improving the stress-resistant functions of the liver.

Concerning LDL:

It has been shown that the size of an LDL particle is a major force in the development of atherosclerosis. As smaller lipoprotein particles have greater surface area exposed to oxidative forces in the blood serum; they are rapidly broken down into toxic substances. However, when a person has a large LDL particle size, those persons are more resistant to heart disease.

The answer to, How do you get larger LDL particles? The drug companies are even now trying to find some way to create these larger LDL particles into products to sell. But God, in His wisdom, already has it out there for them – Eat Real Butter! When one eats butter, the LDL particles become bigger on the butter diet (Mauger, et al., 2003).

And it was show that the diet of 414 people who had large LDL particles corresponded with a large increase in the amount of animal fat (saturated fat), protein and trans fatty acids (Kim and Campos, 2003).

In another study, 52 people ate an egg diet with 640 mg of extra cholesterol daily. After 30 days, those who ate the most cholesterol had the largest LDL particles (Heron, et al, 2004). Their study showed the following conclusion: "These data indicate that the consumption of a high cholesterol diet does not negatively influence the atherogenicity of the LDL particles."

In Mexico it was found that, "Intake of two eggs per day results in the maintenance of LDL:HDL and in the generation of less atherogenic LDL in this population of Mexican children." (Ballesteros, et al., 2004).

The estrogen promoters tried to get into the heart disease business several times within the last 50 years and they have not given up yet, but attention is now being given to the fact that estrogen decreases the size of LDL particles. Beware if you are on so–called 'BioIdentical Hormone Therapy!" Remember, what you want is a large-sized LDL particle (Campos, et al., 1997).

In menopause, the size of the LDL particles gets smaller, as well as in polycystic ovary syndrome, including preeclamptic pregnancy, and all of this involves a low ratio of progesterone to estrogen.

But various journals still promote claims that you can protect against heart disease with estrogen. It has been argued that estrogen is the protective factor against heart disease, while androgens incline men to the disease. One of their false arguments is that androgens lower HDL, but many studies show that testosterone and DHEA protect against atherosclerosis (Arad, et al., 1989).

It appears to this author that man has supplanted God when it comes to diet, and man knows more than the Creator of the universe. The fact is that androgens increase the size of the LDL particle, which is what you want, and androgens decrease after-meal triglyceridemia (Hislop, et al., 2001).

In the 1930s, various studies illustrated that thyroid hormone protects against heart disease and atherosclerosis. Some have interpreted this to mean the thyroid protects because it lowers cholesterol. Actually, it causes the body to use cholesterol better and to form a whole cascade of products. But cholesterol is protective and not harmful. There is something else that is protective against the inflammatory problem of atherosclerosis.

This protection arises when one keeps endotoxin down from being absorbed into the body in the intestines. Endotoxin is an inflammatory substance. However, a healthy liver normally keeps endotoxin from reaching the general circulation. The liver produces a variety of protective substances. This is why this author recommends NAC and Vitamin C. The NAC, through enzymatic systems in the liver, is converted into glutathione, a powerful detoxer of toxic substances throughout the body. NAC also works in other parts of the body to make active glutathione in various cells and tissues. The Vitamin C keeps the cysteine of NAC from forming kidney stones by making it more water soluble.

Another cancer killer, it appears, is the selenium metal. It has a major role in the thyroid gland, but selenium is required to produce the powerful antioxidant, glutathione. With selenium, glutathione peroxidase is made. This enzyme protects an organism from dangerous cancer-causing chemicals and toxins by neutralizing them. Selenium is said to be able to literally starve a tumor to its death by stopping angiogenesis of the tumor (blood vessel spread). It starves a Cancer To Death! Some studies have shown this strong antioxidant has reduced death rates from lung, colon, rectal and prostate cancers; that is, death rates are lower among people with a higher selenium intake.

To help protect the liver, Dr. "B" also recommends Alpha-Lipoic Acid. Another good thing one can use to reduce endotoxin in the colon is the laxative cascara sagrada, because it contains emodin. Use cascara sagrada periodically.

Another thing that has been found is that the antibiotic, Tetracycline, reduces endotoxin. Tetracycline is the only antibiotic known to also reduce inflammation.

We close this article by saying: Get your cholesterol up to reduce the exacerbating stress response coming to your land – to the world – soon.

Dr. "B" has had a number of physicians call on him with certain health problems of their own. When he changed their diets and advocated certain nutrients, it appears that the low cholesterol cult is beginning to fade away and more people are taking to heart what God ate when He came down to earth to check out Sodom and Gomorrah. Dr. "B" says, "If it’s good enough for God, it’s certainly good enough for me!"



As Given By Dr. Ray Peat, Endocrine Physiologist

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BMC Immunology 2002, 3:13. Decreased inducibility of TNF expression in lipid-loaded macrophages, Ares MP, Stollenwerk M, Olsson A, Kallin B, Jovinge S, Nilsson J. Am J Med. 2000 May;108(7):538-46. Effects of lovastatin on cognitive function and psychological well-being. Muldoon MF, Barger SD, Ryan CM, Flory JD, Lehoczky JP, Matthews KA, Manuck SB.

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Arterioscler Thromb Vasc Biol. 1996 Apr;16(4):533-8. Oxidized lipids in the diet accelerate the development of fatty streaks in cholesterol-fed rabbits. Staprans I, Rapp JH, Pan XM, Hardman DA, Feingold KR.

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Lancet. 2005 Jan 1;365(9453):53-9. Protection of hepatocyte mitochondrial ultrastructure and function by strict blood glucose control with insulin in critically ill patients. Vanhorebeek I, De Vos R, Mesotten D, Wouters PJ, De Wolf-Peeters C, Van den Berghe G.

Gastroenterology. 1991 Aug;101(2):457-64. Cell type-dependent effect of phospholipid and cholesterol on bile salt cytotoxicity. Velardi AL, Groen AK, Elferink RP, van der Meer R, Palasciano G, Tytgat GN.

J Lipid Res. 1998 Oct;39(10):1995-2004. Dietary oxysterols are incorporated in plasma triglyceride-rich lipoproteins, increase their susceptibility to oxidation and increase aortic cholesterol concentration of rabbits. Vine DF, Mamo CL, Beilin LJ, Mori TA, Croft KD.

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Obstet Gynecol. 1998 Feb;91(2):234-40. Estrogen-induced small low-density lipoprotein particles in postmenopausal women. Wakatsuki A, Ikenoue N, Sagara Y.

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Also, Include In Your Regimen, Aspirin: Which We Repeated Here In Reduced Form, From What You Read Last Time On

'Why Aspirin?'

     Aspirin is an antioxidant. This is very important, because, Pryor in Free Radicals In Biology, points out antioxidants are very important in protecting and/or helping in diminishing Radiation Damage!

    Rancidity, or lipid peroxidation, is protected against with aspirin. ATP formation, the making of the energy currency of an organism in man and lower animals, is known as mitochondrial respiration. Cell division that becomes abnormal can be inhibited by aspirin. And, what does radiation damage do to a cell? It destroys the normal electrical function, such that rancidity occurs on polyunsaturated fats, generating autoxidation—a domino effect destroying more susceptible cells making up tissues and into organs. Aspirin promotes normal cellular reactions, including division of cells. Generally not known, it helps in learning and prevents injury of nerves from excitotoxicity, a process whereby nerves are so stimulated, they are excited to death!

    Everyone has heard about inflammation. Aspirin inactivates the enzyme that generates prostaglandins.It is the second portion of aspirin (salicylic acid)—not the acetyl portion for the extremely important antiinflammatory response.

    The prostaglandins are made by the cyclooxygenase (COX) enzymes. With what is happening throughout the world today, and the coming World–War III; The global financial crash; Extreme Earth Changes, and more, this is all Stress Generating!

    When the going gets tough, as it will shortly, nitric oxide, serotonin, and chemical messengers between cells, the cytokines, are formed in excess and continue to wreak havoc instead of doing what they should do, then, drop to normal levels without causing more continued damage to you and allow repair to take place. Also, include in this array of dangerous chemicals out of control is the aromatase enzyme that makes estrogen; histamine is also made including the hormones induced by Stress from the adrenal glands; but, first, those of the pituitary gland. All of these are turned on when the threat or threats are present; but, have to be turned off when the threat is over.

    Mitochondrial Respiration, the energy production, is the major basis for overcoming all threats. And this must be there in conservation for when threats come again. Thyroid Hormone, T3 is necessary for this. Selenium, Se–Methyl L–Selenocysteine, 200 mcg, is most helpful, in this form.

    Aspirin keeps all these above reactions of Stress under control. And, combined with a little table sugar, controls the Stress Response considerably from Cortisol generation!

Life  Extension Olive Oil!     Now, with all this unbelievable stress coming,there is another thing to get. Real Dark Green Olive Oil because it has oleic acid in high amounts, and oleic acid goes to form a Mead Acid, which is extremely good for the Stress Response, as the Mead Acid is an antiinflammatory substance and some it acts on the Cannibinoid Receptor, commonly known as the 'Bliss Receptor' in the Brain! If one ate no unsaturated fats, the body would build large amounds of Mead Acids! These acids and their derivatives have a large number of reactions against the Stress Response.

    Most reading this document are totally unaware, especially those in the Medical Profession, that the so–called 'Essential Fatty Acids' are toxic universally and they suppress Black & Green Olives! the Mead Acids, as the PUFAs (Poly Unsaturated Fatty Acids) accumulate in the body. It has been shown that animals in the wild who live deficient of 'Essential' Fatty Acids, the Mead Acids are factors of necessity that keep their tissues stable. It probably has something to do with the positive electrical nature of a cell's regeneration.

    Extra Virgin Olive Oil, the kind we're talking about in this document, helps with memory, as does Aspirin, which helps in learning!

    The second portion of Aspirin, Salicylate, and other antiinflamatories, including antihistamines and muscle relaxants, act a substitute when the Mead Acid and its derivatives are absent. These then act as defensive substances for all the negative and toxic results of the PUFAs. This action explains how the hormone, estrogen, goes awry as it immitates PUFA's toxicity of those fats that are unstable.

Here's More About The 'Real' Stuff That You Do Not Know!

    In The Phenolic Compounds of olive oil: structure, biological activity and beneficial effects on human health, Institute of Physiology and Human Nutrition, Faculty of Pharmacy, University of Palermo, Via Augusto Elia 3, 90 127, Palermo, Italy

Writes, Under: The Antioxidant Activity of The Poloyphenolic Compounds

The 'reactive oxygen species' (ROS), which are continuously formed as a result of normal metabolic processes, can oxidise and damage cellular macromolecules, possibly leading to the development of degenerative diseases (for example, atherosclerosis, cancer, diabetes, rheumastoid arthritis and inflammatory diseases). Exogenous antioxidants are important because they have a twofold function, preventing food oxidation – and in particular lipid oxidation [Commentary By Kong: That's Rancidity, Rancid Fat In Your Body!] and at the same time increasing the amount of antioxidant agents present in the organism, protecting against degenerative diseases. The most important dietary antioxidants are certain vitamins (ascorbic acid, tocopherols, carotenes) and phenolic compounds, which are present in various foods of vegetable origin characteristic of the Mediterran diet, such as olivera (Berra et al. 1995).

[ Commentary–2 By Kong: Folks, Keep This Question In Mind, 'They Discovered Something Really Big, But probably Not Knowing Radiation Physics, They Did Not Recognize This Great Discovery, That We Will Tell What It Is, Shortly, That Your Are Reading Right Now! ]

Phenolic compounds can act as antioxidants in various ways. In oxidative systems using transition metals such as Cu and Fe, they can chelate metallic ions, which can prevent their involvement in Fenton reactions that can generate high concentrations of hydroxyl radicals (Halliwell & Gutterige, 1990; Halliwell et al. 1995). However, the most important antioxidant activity is related to the free radical-scavenging ability, by breaking the chain of reactions triggered by free radicals. The antioxidant properties of the o-diphenols are associated with their ability to form intramolecular hydrogen bonds between the hydroxyl group and the phenoxylic radicals (Visioli & Galli, 1998b) .... As similar studies on the flavonoids have already shown, the degree of antioxidant activity is correlated with the number of hydroxyl groups (Rice-Evans et al. 1996; Cao et al. 1997).

The number of –OH groups and their positions on the ring are important for both flavonoids and phenols. From the study of the resonance structures formed during the oxidation processes, it can be observed that the ortho- and para-substitutes of the radicals are more stable than the meta-substitute (Finotti & Di Majo, 2003). In particular, ortho-diphenolic substitution gives high antioxidant ability, while a single hydroxyl substitution, as in tyrosol, does not confer any activity, since tyrosol does not protect LDL from chemically induced oxidation.

Although olive oil contains a relatively low concentration of a-tocopherol, it is known to be highly resistant to oxidative degradation. This is due, in part, to the relatively low content of PUFA and also to the high concentration of polyphenolic antioxidants, particularly in extra-virgin olive oil.

The antioxidant activity of olive oil phenolic compounds, and in particular of oleuropein and its byproduct hydroxytyrosol, has been studied in many experimental models: with the use of transition metals; the Phenolic compounds of olive oil chemically induced oxidation of LDL; ROS formation, forexample the radicals superoxide and trichlormethylperoxylic, and hypochlorous acid (Aeschbach et al. 1994;Salami et al. 1995; Visioli et al. 1995a, 1998; Aruoma et al.1998).

By estimating the antioxidant activity of these polyphenolic compounds on the basis of their ability to inhibit the formation of peroxides, it has been shown that hydroxytyrosol and caffeic and protocatechuic acids have a higher protective activity (Papadopoulos & Boskou, 1991).

The antioxidant activity of oleuropein and hydroxytyrosol has also been demonstrated in cellular models and animals (Manna et al. 1997; Speroni et al. 1998). Some polyphenols can contribute to the regeneration of vitamin E, as has been demonstrated by treating human lipoproteins in vitro with peroxides. In a recent study, the antioxidant activity of a-tocopherol and phenolic extracts from olives and olive oil was compared over time. It was demonstrated that in the first 15 min the scavenger activity of a-tocopherol was higher but soon terminated. The extract from stoned olives and oil contained compounds that continued to reduce the concentration of these radicals more slowly; when on the other hand the reaction time was delayed to 60 min, all the extracts of the olives were much more active than a-tocopherol. On day 6 the extracts of the olives and the oil continued to be more effective than a-tocopherol (Keceli & Gordon, 2001).

The biological activity of phenolic compounds of olive oil is not limited to their antioxidant ability but extends to their interaction with important enzymic systems. In particular, it has been found out that olive oil phenols: inhibit platelet aggregation; reduce pro-inflammatory molecule formation such as thromboxane B2 and leucotriene B4; inhibit the use of oxygen in human neutrophils; increase NO production by the macrophages of rats exposed to endotoxin – they therefore act by up regulating the immune system.

Other biological actions of phenolic compounds have been discovered that can be important for their effects on human health. For example, caffeic acid could have cytoprotective effects on endothelial cells, correlated not only with its action as an antioxidant agent but also with its ability to block the increase of the concentration of intracellular Ca2þ in response to lipoprotein oxidation (Vieira et al. 1998). The ability of polyphenolic compounds to react with metal ions could make them pro-oxidant. It has in fact been widely observed that caffeic acid, a simple polyphenol with an ortho-diphenolic structure, can have pro-oxidant activity on LDL oxidation induced by Cu2þ (Yamanaka et al. 1997). However, this pro-oxidant activity has been found only in the propagation phase of oxidation, and not in the initiation phase, in which caffeic acid inhibits lipoprotein oxidation, as has been found in previous studies (Laranjinha et al. 1994; Nardini et al. 1995).

The effects of the antioxidant activity of olive oil polyphenols on the integrity and function of the cells have been studied in erythrocytes and intestinal cells (Caco-2). The capacity of polyphenols to prevent damage in these cells was verified when they were exposed to oxidative stress, as in treatment with H2O2. Human erythrocytes were chosen because they are the cells most exposed to oxidative risk, since their specific role is to carry oxygen.

The main target of H2O2 is Hb, which is oxidised to methaemoglobin. Exposure of erythrocytes to H2O2 also causes lipid peroxidation, and alterations in proteins, for example the formation of carbonyl dimers. As a consequence of this oxidative damage, the shape of the erythrocytes changes, causing haemolysis. The spontaneous oxidation of Hb produces superoxide anion radicals that cause the dismutation of H2O2. In the presence of reduced metal ions, especially Fe, these compounds form the highly reactive hydroxyl radical that can damage the cellular membrane, with consequent haemolysis (Sadrzadeh et al. 1984; van Dyke & Saltman, 1996).

Some studies on isolated erythrocyte membranes have demonstrated that the ATP dependent ion transport (such as amino acid transport) is considerably compromised by oxidative damage (Rohn et al. 1993). Under physiological conditions, ROS are quickly removed by both enzymic and non-enzymic systems; however, if ROS production is excessive, or if antioxidant defence is impaired, serious oxidative damage can occur, to both the plasma membrane and the cytosol, which finally leads to haemolysis. Erythrocytes pre-treated with phenols extracted from extra-virgin olive oil show significantly less lipid oxidation and haemolysis after treatment with H2O2.

In erythrocytes pre-treated with H2O2 and incubated in the presence of [3H]methionine or [3H]leucine, there is a marked reduction in the absorption of both the amino acids compared with control erythrocytes. 3,4-Dihydroxyphenyl-ethanol, or hydroxytyrosol, prevents the alteration of amino acid transport by H2O2 in intact erythrocytes (Manna et al. 1999). Similarly in intestinal tumour cells (Caco-2) treated with H2O2, pre-treatment with olive oil polyphenols exerts a strong antioxidant effect.

H2O2 induces a clear increase in the intracellular concentration of malonyldialdehyde and the paracellular transport of inulin, respectively indicating the occurrence of lipid peroxidation and changes in cellular permeability. Preincubation of the Caco-2 cells with hydroxytyrosol totally prevents the alterations induced by H2O2 (Manna et al. 1999).

    Now, Get This Folks!
Phenolic Components As Compounds With Anti–inflammatory Activity

Lipid radicals are also produced during reactions involved in the metabolism of arachidonic acid, during the sysnthesis of the eicosanoids by the action of the lipo–oxygenase and cyclo–oxygenase...[These latter two are inflammatory Substances!]

During these reactions, the radicals that are generated are partially inactivated by glutathione peroxidase (Eling et al. 1986; Mirochnitchenko et al. 2000). Some studies hypothesizse an inhibitory activity on cyclo–oxygenase (Petroni et al. 1995; de La Pueta et al. 2000 and lipo–oxygenase by olive oil phenolic compounds (Kohyama et al. 1997; DeLa Puerta et al. 1999; Martinez–Dominguez et al. 2001).

Considering the functions of the prostaglandins and leucotrienes, the results of these studies have important implication for the genesis of the inflammatory response and for atherosclerosis. In one these studies, the effects of hydroxytyrosol and of the polyphenols extracted from waste waters inhibited in vitro platelet aggregation induced by collagen and thromboxane B2 production.

The effectiveness of hydroxytyrosol (One of the Main Ingredients in the 'Real Stuff; the other is Oleuropein. These two give real extra–virgin olive oil its bitter, pungent taste) in inhibition of the aggregation induced by collagen is similar to that of aspirin, a drug that is well known for its powerful activity in platelet anti–aggregation and cyclo–oxygenase inhibition (Petroni et al. 1995)

    What Is It The Researchers Discovered About Olive Oil In Its Relation To Radiation? Olive Oil, the kind we're talking about, Inhibits; or, blocks Radiation Damage! It does this by blocking the damage to the cells' free fatty acids that are polyunsaturated! How Is This? Because Olive Oil, the 'Right Stuff' is a powerful antioxidant, like Aspirin!

Enter Saturated Fat!

    It would be best to start immediately on eating the foods that contain real saturated fat, such as Tropical oils (Unrefined Coconut Oil, Palm Kernel Oil, and real Butter). Using aspirin as a prevention, as well as for purposes of healing, will be advantageous when the total Chaos, spoken of above, arrives in its various forms. Aspirin will prevent heart disease, including lung disease too! It can inhibit brain dysfunction, such as degeneration, and cancer.

    Aspirin not only facilitates in cancer protection, but many of its sequelae; such as, cachexia—wasting of tissue, strokes and immunosuppression.

    Many take Opiates; but they increase histamine and this works with substances from a tumor to inhibit the body's own immune system protection and enhances the growth of tumors! This is a Catch–22 Situation: Giving Opiates minimally to control cancer pain; yet, it does those other things negatively to the cancerous body!

    Niacinamide, T3, Magnesium are substances that are protective, in addition to aspirin for degenerative diseases of nerve tissue, such as Alzheimer's disease, and Parkinson's disease. Glutamate induced excitotoxicity, rancidity, and ande dopamine toxicity, is inhibited or protected by Aspirin. And, as given earlier, facilitates mitochondria respiration as does the chemicals just mention.

    When caught without hospitals, tent hospitals with this coming Chastisement, carbon dioxide, as generated from 1 teaspoon of sodium bicarbonate in 16 ounces of pure water, with 1 teaspoon of cain sugar added, ingesting about a tablespoon several times daily, are very important in multiple organ failure, which will be caused by the Chaos coming, that generates through profound shock (low–blood pressure), infections, hard or blunt trauma, and Severe Stress, as the kind that most have never seen, finds that aspirin is an excellent modality. However, for helping in multiple organ failure, glucose hypertonicity, sodium and carbon dioxide will be more suitable.

    Many reading this have been caught up in the dogma espoused by pharmaceutical companies, that aspirin make you Bleed! It order to see other of their latest produces, they performed experments designed to demonize aspirin by shown a number of negative things it did, one just stated.

    Reading this, you're going to find, 'Hell Ain't Half Full!' Dr. Ray Peat in his newsletter of 2006 writes:
Although the animals studies that showed stomach damage from aspirin often used single doses equivalent to 10 or 100 aspirin tablets, the slight irritation produced by a normal dose of aspirin can be minimized by dissolving the aspirin in water. The stomach develops a tolerance for aspirin over a period of a few days, allowing the dose to be increase if necessary. And both aspirin and salicylic acid can be absorbed through the skin, so rheu\matic problems have been treated by add the drugh to bath water.

The unsaturated (n–6 and n–3) fats that accumulate in our tissues, instead of being part of the system for reestablishing order and stability, tend to amplify the instability that is triggered by excitation, by estrogen, or by external stresses.

I think it's important that we don't allow the drug publicists to obscure the broad importance of substances such as aspirin, vitamin E, progesterone, and thyroid. For 60 years, a myth that was created to sell estrogen has harmed both science ande the health of many people.


    Many women learned, who had bought into the myth about aspirin, discovered It reduced excessive menstrual monthly discharge (bleeding).


As Given By Dr. Ray Peat, Endocrine Physiologist

Free Radic Biol Med 2000 Dec 1;29(11):1135-42. Synergistic inhibition of cyclooxygenase-2 expression by vitamin E and aspirin. Abate A, Yang G, Dennery PA, Oberle S, Schroder H.

Proc Natl Acad Sci U S A 1995 Aug 15;92(17):7926-30. The mode of action of aspirin-like drugs: effect on inducible nitric oxide synthase. Amin AR, Vyas P, Attur M, Leszczynska-Piziak J, Patel IR, Weissmann G, Abramson SB. "These studies indicate that the inhibition of iNOS expression and function represents another mechanism of action for aspirin, if not for all aspirin-like drugs."

Obstet Gynecol 2001 Mar;97(3):423-7. Aspirin effects on endometrial cancer cell growth. Arango HA, Icely S, Roberts WS, Cavanagh D, Becker JL.

J Neurochem 2001 Mar;76(6):1895-904. Neuroprotective effects of non-steroidal anti-inflammatory drugs by direct scavenging of nitric oxide radicals. Asanuma M, Nishibayashi-Asanuma S, Miyazaki I, Kohno M, Ogawa N.

J Neurochem 1998 Oct;71(4):1635-42. Aspirin and salicylate protect against MPTP-induced dopamine depletion in mice. Aubin N, Curet O, Deffois A, Carter C.

Psychopharmacology (Berl) 1998 Aug;138(3-4):369-74. The influence of acetylsalicylic acid on cognitive processing: an event-related potentials study. Austermann M, Grotemeyer KH, Evers S, Rodding D, Husstedt IW.

Brain Res 1999 Oct 2; 843(1-2): 118-29. Cyclooxygenase-2 selective inhibitors aggravate kainic acid induced seizure and neuronal cell death in the hippocampus. Baik EJ, Kim EJ, Lee SH, Moon C.

Cancer Lett 1978 Jun;4(6):333-42. Inflammatory, tumor initiating and promoting activities of polycyclic aromatic hydrocarbons and diterpene esters in mouse skin as compared with their prostaglandin releasing potency in vitro. Brune K, Kalin H, Schmidt R, Hecker E.

J Neurooncol 2000;46(3):215-29. Acetaminophen selectively reduces glioma cell growth and increases radiosensitivity in culture. Casper D, Lekhraj R, Yaparpalvi US, Pidel A, Jaggernauth WA, Werner P, Tribius S, Rowe JD, LaSala PA "Glioblastoma multiforme (GBM) is a highly lethal brain cancer. Using cultures of rodent and human malignant glioma cell lines, we demonstrated that millimolar concentrations of acetylsalicylate, acetaminophen, and ibuprofen all significantly reduce cell numbers after several days of culture."

Neurosci Lett 2000 Aug 11;289(3):201-4. Ibuprofen protects dopaminergic neurons against glutamate toxicity in vitro. Casper D, Yaparpalvi U, Rempel N, Werner P. "We examined the effects of aspirin, acetaminophen, and ibuprofen on cultured primary rat embryonic neurons from mesencephalon, the area primarily affected in Parkinson's disease. We evaluated whether these drugs protect dopaminergic neurons against excitotoxicity. All three NSAIDs significantly attenuated the decrease in dopamine uptake caused by glutamate, indicating preservation of neuronal integrity."

Lipids 1996 Aug;31(8):829-37. Effect of dietary n-9 eicosatrienoic acid on the fatty acid composition of plasma lipid fractions and tissue phospholipids. Cleland LG, Neumann MA, Gibson RA, Hamazaki T, Akimoto K, James MJ "Dietary enrichment with ETrA warrants further investigation for possible beneficial effects in models of inflammation and autoimmunity, as well as in other conditions in which mediators derived from n-6 fatty acids can affect homeostasis adversely."

Can J Ophthalmol 1981 Jul;16(3):113-8. Senile cataracts: evidence for acceleration by diabetes and deceleration by salicylate. Cotlier E.

Int Ophthalmol 1981 May;3(3):173-7. Aspirin effect on cataract formation in patients with rheumatoid arthritis alone or combined with diabetes. Cotlier E. "The effects of aspirin on cataract formation may result from 1) lowering of plasma tryptophan levels and increased excretion of tryptophan metabolites, 2) inhibition of aldose reductase and sorbitol formation in the diabetic lens, 3) inhibition of tryptophan or kynurenine binding to lens protein."

Arterioscler Thromb Vasc Biol 2001 Feb;21(2):255-61. Tamoxifen and cardiac risk factors in healthy women: Suggestion of an anti-inflammatory effect. Cushman M, Costantino JP, Tracy RP, Song K, Buckley L, Roberts JD, Krag DN.

Med Sci Sports Exerc 2001 Dec;33(12):2029-35. Acetylsalicylic acid inhibits the pituitary response to exercise-related stress in humans. Di Luigi L, Guidetti L, Romanelli F, Baldari C, Conte D.

Ann Med 2000 Dec;32 Suppl 1:21-6. Cyclo-oxygenase products and atherothrombosis. FitzGerald GA, Austin S, Egan K, Cheng Y, Pratico D.

Acta Diabetol Lat 1981;18(1):27-36. Effects of acetylsalicylic acid on plasma glucose, free fatty acid, betahydroxybutyrate, glucagon and C-peptide responses to salbutamol in insulin-dependent diabetic subjects. Giugliano D, Passariello N, Torella R, Cerciello T, Varricchio M, Sgambato S.

J Reprod Fertil 1994 Aug;101(3):523-9. Relationships among GnRH, substance P, prostaglandins, sex steroids and aromatase activity in the brain of the male lizard Podarcis sicula sicula during reproduction. Gobbetti A, Zerani M, Di Fiore MM, Botte V "Acetylsalicylic acid decreased PGF2 alpha, oestradiol and aromatase activity, but increased the amount of androgens released."

Natl Med J India 1998 Jan-Feb;11(1):14-7. Aspirin: a neuroprotective agent at high doses? Gomes I.

Radiat Res 1991 Sep;127(3):317-24. Effects of some nonsteroidal anti-inflammatory agents on experimental radiation pneumonitis. Gross NJ, Holloway NO, Narine KR.

Micron 2001 Apr;32(3):307-15. Collagen as a model system to investigate the use of aspirin as an inhibitor of protein glycation and crosslinking. Hadley J, Malik N, Meek K.

J Pharmacol Exp Ther 1981 Aug;218(2):464-9. Protective effects of aspirin in endotoxic shock. Halushka PV, Wise WC, Cook JA.

J Pharmacol Exp Ther 2000 May; 293(2):417-25. Cyclooxygenase-2 contributes to N-methyl-D-aspartate-mediated neuronal cell death in primary cortical cell culture. Hewett SJ, Uliasz TF, Vidwans AS, Hewett JA.

Med Hypotheses 1999 Apr;52(4):291-2. Genetic induction and upregulation of cyclooxygenase (COX) and aromatase (CYP19): an extension of the dietary fat hypothesis of breast cancer. Harris RE, Robertson FM, Abou-Issa HM, Farrar WB, Brueggemeier R A novel model of mammary carcinogenesis is proposed involving sequential induction and upregulation of cyclooxygenase and aromatase genes by essential fatty acids prominent in the US diet.

J Clin Endocrinol Metab 2001 Sep; 86(9):4216-22. Differential effects of E and droloxifene on C-reactive protein and other markers of inflammation in healthy postmenopausal women. Herrington DM, Brosnihan KB, Pusser BE, Seely EW, Ridker PM, Rifai N, MacLean DB. "E treatment resulted in 65.8% higher levels of C-reactive protein (P = 0.0002) and 48.1% higher levels of IL-6...." "These data provide additional evidence of a proinflammatory effect of E that may have adverse cardiovascular consequences."

J Natl Cancer Inst 1998 Mar 18;90(6):455-60. Expression of cyclooxygenase-1 and cyclooxygenase-2 in human breast cancer. Hwang D, Scollard D, Byrne J, Levine E "Our results suggest that overexpression of COX may not be unique to colon cancer and may be a feature common to other epithelial tumors."

Ginekol Pol 1999 Mar;70(3):126-34. [Evaluation of the effectiveness of a low-dose aspirin in the treatment of intrauterine growth retardation (IUGR)]. Kalinka J, Sieroszewski P, Hanke W, Laudanski T, Suzin J.

J Cardiovasc Pharmacol 1995 Feb;25(2):273-81. Inhibitory effects of aspirin on coronary hyperreactivity to autacoids after arterial balloon injury in miniature pigs. Kuga T, Ohara Y, Shimokawa H, Ibayashi S, Tomoike H, Takeshita A. "Coronary vasoconstriction induced by histamine and serotonin were examined angiographically before, 1 h, 1 week, and 1 month after balloon injury in 29 hypercholesterolemic miniature pigs." "Hyperconstriction induced by the autacoids 1 h after injury were significantly less in groups B and C than in group A (p < 0.01). hyperconstriction induced by autacoids 1 week after injury were significantly less in group b than in group a (p < 0.01) and were significantly less in group c than in group a (p < 0.01) or group b (p < 0.05)."

Proc Soc Exp Biol Med 1975 Feb;148(2):329-32. Correlation of anti-inflammatory activity with inhibition of prostaglandin synthesis activity of nonsteroidal anti-estrogens and estrogens (38532). Lerner EJ, Carminati P, Schiatti P.

Proc Soc Exp Biol Med 1985 Feb;178(2):250-3. Salicylic acid blocks indomethacin-induced cyclooxygenase inhibition and lesion formation in rat gastric mucosa. Ligumsky M, Guth PH, Elashoff J, Kauffman GL Jr, Hansen D, Paulsen G. "Salicylic acid has been shown to decrease gastric mucosal lesions induced by indomethacin in the rat."

Z Naturforsch [C] 2001 May-Jun; 56(5-6):455-63. Constant expression of cyclooxygenase-2 gene in prostate and the lower urinary tract of estrogen-treated male rats. Luo C, Strauss L, Ristimaki A, Streng T, Santti R.

Neuropharmacology 2000 Apr 27;39(7):1309-18. Mechanisms of the neuroprotective effect of aspirin after oxygen and glucose deprivation in rat forebrain slices. Moro MA, De Alba J, Cardenas A, De Cristobal J, Leza JC, Lizasoain I, Diaz-Guerra MJ, Bosca L, Lorenzo P "Apart from its preventive actions against stroke due to its antithrombotic properties, recent data in the literature suggest that high concentrations of ASA also exert direct neuroprotective effects." "We have found that ASA inhibits neuronal damage at concentrations lower than those previously reported (0.1-0.5 mM), and that these effects correlate with the inhibition of excitatory amino acid release, of NF-kappaB translocation to the nucleus and iNOS expression caused by ASA." "Our results also show that the effects of ASA are independent of COX inhibition. Taken together, our present findings show that ASA is neuroprotective in an in vitro model of brain ischaemia at doses close to those recommended for its antithrombotic effects."

Pediatrics 1987 Nov;80(5):638-42. A catch in the Reye. Orlowski JP, Gillis J, Kilham HA.

Prostaglandins Leukot Med 1982 Jul;9(1):109-15. Effect of acetaminophen and salicylate on aspirin-induced inhibition of human platelet cyclo-oxygenase. Rao GH, Reddy KR, White JG. "Recent studies have shown that salicylic acid, a metabolite of aspirin, effectively competes for the same site on the platelet cyclo-oxygenase enzyme."

Stroke 1997 Oct;28(10):2006-11. Acetylsalicylic acid increases tolerance against hypoxic and chemical hypoxia. Riepe MW, Kasischke K, Raupach A.

Cancer Res 1998 Dec 1;58(23):5354-60. Prevention of NNK-induced lung tumorigenesis in A/J mice by acetylsalicylic acid and NS-398. Rioux N, Castonguay A.

J Endocrinol 1989 Jun;121(3):513-9. Indomethacin inhibits the effects of oestrogen in the anterior pituitary gland of the rat. Rosental DG, Machiavelli GA, Chernavsky AC, Speziale NS, Burdman JA.

Int J Cancer 2001 Aug 15;93(4):497-506. Cyclooxygenase inhibitors retard murine mammary tumor progression by reducing tumor cell migration, invasiveness and angiogenesis. Rozic JG, Chakraborty C, Lala PK.

Res Commun Mol Pathol Pharmacol 1998 Sep;101(3):259-68. Protective ability of acetylsalicylic acid (aspirin) to scavenge radiation induced free radicals in J774A.1 macrophage cells. Saini T, Bagchi M, Bagchi D, Jaeger S, Hosoyama S, Stohs SJ.

Mol Cell Biochem 1999 Sep;199(1-2):93-102. Antioxidant properties of aspirin: characterization of the ability of aspirin to inhibit silica-induced lipid peroxidation, DNA damage, NF-kappaB activation, and TNF-alpha production. Shi X, Ding M, Dong Z, Chen F, Ye J, Wang S, Leonard SS, Castranova V, Vallyathan V.

J Physiol Paris 2001 Jan-Dec;95(1-6):51-7. Protection by aspirin of indomethacin-induced small intestinal damage in rats: mediation by salicylic acid. Takeuchi K, Hase S, Mizoguchi H, Komoike Y, Tanaka A. "Most of non-steroidal anti-inflammatory drugs (NSAIDs) except aspirin (ASA) produce intestinal damage in rats." "ASA did not provoke any damage, despite inhibiting (prostaglandin) PG production, and prevented the occurrence of intestinal lesions induced by indomethacin, in a dose-related manner."

FASEB J 2001 Oct;15(12):2057-72. Cyclooxygenase-independent actions of cyclooxygenase inhibitors. Tegeder I, Pfeilschifter J, Geisslinger G.

J Indian Med Assoc 1997 Feb;95(2):43-4, 47. Role of low dose aspirin in prevention of pregnancy induced hypertension. Tewari S, Kaushish R, Sharma S, Gulati N.

J Chromatogr B Biomed Appl 1995 Jul 21;669(2):404-7. Aspirin inhibits collagen-induced platelet serotonin release, as measured by microbore high-performance liquid chromatography with electrochemical detection. Tsai TH, Tsai WJ, Chen CF.

Clin Exp Immunol 1991 Nov;86(2):315-21. Piroxicam, indomethacin and aspirin action on a murine fibrosarcoma. Effects on tumour-associated and peritoneal macrophages. Valdez JC, Perdigon G. "We also studied the effect on tumour development of three inhibitors of prostaglandin synthesis: indomethacin, piroxicam and aspirin. Intraperitoneal administration of these drugs during 8 d was followed by the regression of palpable tumours. Indomethacin (90 mg/d) induced 45% regression, while with piroxicam (two 400 mg/d doses and six 200 mg/d doses) and aspirin (1 mg/d) 32% and 30% regressions, respectively, were observed. The growth rate of nonregressing tumours, which had reached different volumes by the end of the treatment, was delayed to a similar extent by the three anti-inflammatory non-steroidal drugs (NSAID)."

Int J Radiat Biol 1995 May;67(5):587-96. Amelioration of radiation nephropathy by acetylsalicylic acid. Verheij M, Stewart FA, Oussoren Y, Weening JJ, Dewit L.

Semin Perinatol 1986 Oct;10(4):334-55. The role of arachidonic acid metabolites in preeclampsia. Walsh SW, Parisi VM.

Proc Natl Acad Sci U S A 1999 Apr 27;96(9):5292-7. Suppression of inducible cyclooxygenase 2 gene transcription by aspirin and sodium salicylate. Xu XM, Sansores-Garcia L, Chen XM, Matijevic-Aleksic N, Du M, Wu KK. "Aspirin and sodium salicylate at therapeutic concentrations equipotently blocked COX-2 mRNA and protein levels induced by interleukin-1beta and phorbol 12-myristate 13-acetate."

Hum Reprod 1994 Oct;9(10):1954-7. The benefits of low-dose aspirin therapy in women with impaired uterine perfusion during assisted conception. Wada I, Hsu CC, Williams G, Macnamee MC, Brinsden PR. "Higher pregnancy rates (47 versus 17%) were achieved in those taking aspirin from day 1 of HRT." "The addition of low-dose aspirin to a standard HRT protocol in women with impaired uterine perfusion is associated with improved blood flow and satisfactory pregnancy rates."

J Ethnopharmacol 1991 Sep;34(2-3):215-9. Radiation-protective and platelet aggregation inhibitory effects of five traditional Chinese drugs and acetylsalicylic acid following high-dose gamma-irradiation. Wang HF, Li XD, Chen YM, Yuan LB, Foye WO.

Fertil Steril 1997 Nov;68(5):927-30. Low-dose aspirin for oocyte donation recipients with a thin endometrium: prospective, randomized study. Weckstein LN, Jacobson A, Galen D, Hampton K, Hammel J. "Low-dose aspirin therapy improves implantation rates in oocyte donation recipients with a thin endometrium."

Dermatologica 1978;156(2):89-96. Effect of topical salicylic acid on animal epidermopoiesis. Weirich EG, Longauer JK, Kirkwood AH. In contrast to its antihyperplastic effect on pathological proliferation of the epidermis, salicylic acid promotes epidermopoiesis in the normal guinea pig skin. After the application of 1% w/w salicylic acid in acetone-ethanol for 4 weeks, the thickness of the surface epithelium was increased by 40% and that of the deep epithelium by 19%. The mitotic index rose by 17%.

Arch Exp Veterinarmed 1981;35(3):465-70. [Control of implantation in rats and sows by peroral administration of prostaglandin synthetase inhibitors. 2. Effects of prostaglandin F2 alpha, progesterone/estrone, and acetylsalicylic acid on implantation and various biochemical parameters of amniotic fluid in the rat] Wollenhaupt K, Steger H. "The highest number of normally developed (97 per cent) and the lowest number of degenerated foetuses (three per cent) were recorded following acetylsalicylic acid treatment, as compared to the control group (91 and nine per cent)."

Biomed Pharmacother 1999 Aug;53(7):315-8. Aspirin induced apoptosis in gastric cancer cells. Wong BC, Zhu GH, Lam SK.

Scand J Immunol 2000 Oct;52(4):393-400. Tamoxifen decreases renal inflammation and alleviates disease severity in autoimmune NZB/W F1 mice. Wu WM, Lin BF, Su YC, Suen JL, Chiang BL. "It has been documented that sex hormone may play a role in the pathogenesis of murine lupus."

Science 2001 Aug 31;293(5535):1673-7. Reversal of obesity- and diet-induced insulin resistance with salicylates or targeted disruption of Ikkbeta. Yuan M, Konstantopoulos N, Lee J, Hansen L, Li ZW, Karin M, Shoelson SE.

Comet Hitting Rotating Earth!

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