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782 lines
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<html>
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<head><title>Food-junk and some mystery ailments: Fatigue, Alzheimer's, Colitis, Immunodeficiency.</title></head>
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<body>
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<h1>
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Food-junk and some mystery ailments: Fatigue, Alzheimer's, Colitis, Immunodeficiency.
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</h1>
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<article class="posted">
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Years ago, I noticed that Oregon was one of the few states that still had real whipping cream and cottage
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cheese without additives, so I have been trustingly using cream in my coffee every day. Last week, I noticed
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that my cream listed carrageenan in its ingredients. Over the years, I have avoided carrageenan-containing
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foods such as apple cider, hot dogs, most ice creams and prepared sauces and jellies, because they caused me
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to have serious allergic symptoms. Carrageenan has been found to cause colitis and anaphylaxis in humans,
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but it is often present in baby “formulas” and a wide range of milk products, with the result that many
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people have come to believe that it was the milk-product that was responsible for their allergic symptoms.
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Because the regulators claim that it is a safe natural substance, it is very likely that it sometimes
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appears in foods that don’t list it on the label, for example when it is part of another ingredient.<p>
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In the 1940s, carrageenan, a polysaccharide made from a type of seaweed, was recognized as a dangerous
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allergen. Since then it has become a standard laboratory material to use to produce in-flammatory tumors
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(granulomas), immunodeficiency, arthritis, and other in-flammations. It has also become an increasingly
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common material in the food industry. Articles are often written to praise its usefulness and to claim
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that it doesn't produce cancer in healthy animals. Its presence in food, like that of the polyester
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imitation fat, microcrystalline cellulose, and many other polymers used to stabilize emulsions or to
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increase smoothness, is often justified by the doctrine that these molecules are too large to be
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absorbed. There are two points that are deliberately ignored by the food-safety regulators, 1) these
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materials can interact dangerously with intestinal bacteria, and 2) they can be absorbed, in the process
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called "persorption."
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</p>
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<p>
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The sulfites (sodium bisulfite, potassium metabisulfite, etc.) have been used as preservatives in foods
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and drugs for a long time, even though they were known to cause intense allergic reactions in some
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people. Fresh vegetables and fish, dried fruits, ham and other preserved meats, hominy, pickles, canned
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vegetables and juices, and wines were commonly treated with large amounts of the sulfites to prevent
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darkening and the development of unpleasant odors. People with asthma were known to be more sensitive
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than other people, but the sulfites could cause a fatal asthma-like attack even in someone who had never
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had asthma. Even when this was known, drugs used to treat asthma were preserved with sulfites. Was the
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information just slow to reach the people who made the products? No, the manufacturers knew about the
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deadly nature of their products, but they kept on selling them. The FDA didn't answer letters on the
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subject, and medical magazines such as J.A.M.A. declined to publish even brief letters seriously
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discussing the issue. Obviously, since many people died from what the drug companies called "paradoxical
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bronchoconstriction" when they used the products, the drug companies had to be protected from lawsuits,
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and the medical magazines and the government regulators did that through the control of information.
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</p>
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<p>
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I think a similar situation exists now in relation to the effects of carrageenan.
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</p>
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<p>
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Stress and anxiety sharply reduce the circulation of blood to the intestine and liver. Prolonged stress
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damages the ability of the in-testinal cells to exclude large molecules. Local irritation and
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inflammation of the intestine also increase its permeability and decrease its ability to exclude harmful
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materials. But even the normal intestine is able to permit the passage of large molecules and particles,
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in many cases particles larger than the cells that line the intestine; this persorption of particles has
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been demonstrated using particles of plastic, starch grains which are sometimes several times larger
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than blood cells, and many other materials, including carrageenan. One of the reasons it has been easy
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to convince the public that persorption doesn't happen is that there is a powerful myth in our culture
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about the existence of a "semipermeable" "plasma membrane" on cells through which only certain specific
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substances may pass.
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</p>
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<p>
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About 30 years ago some biologists made a movie of living cells under the microscope, showing an ameboid
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cell entering another cell, swimming around, and leaving, without encountering any perceptible
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resistance; persorption of food particles, moving in one side of a cell and out the other, wouldn't seem
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so mysterious if more people had seen films of that sort.
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</p>
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<p>
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Also in the 1960s, Gerhard Volkheimer rediscovered the phenomenon of persorption, which had been
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demonstrated a century earlier. Starch grains, or other hard particles, can be found in the blood,
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urine, and other fluids after they have been ingested. The iodine stain for starch, and the
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characteristic shape of the granules, makes their observation very easy. The absorption of
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immunologically intact proteins and other particles has been demonstrated many times, but myth is more
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important than fact; all of my biol-ogy professors, for example, denied that proteins could be absorbed
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by any part of the digestive system.
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</p>
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<p>
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The accepted description of the absorption of chylomicrons, tiny particles of fat, helps to understand
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the way medical professors think about the intestine. These particles, they say, are disassembled by the
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intestine cells on one side, their molecular parts are taken up by the cells, and similar particles are
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excreted out the other side of the cells, into the lymphatic vessels. As they visualize one of these
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cells, it consists of at least four barriers, with each theoretical cell surface membrane consisting of
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an outer water-compatible phase, in intramembranal lipid region, and an inner water-compatible phase
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where the membrane rests on the “cell contents.” Endocytosis, for example the ingestion of a bacterial
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particle by a phagocyte, is described in a similar way, to avoid any breach in the “lipid bilayer
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membrane.”
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</p>
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<p>
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This mental armature has made it essentially impossible for the biomedical culture to assimilate the
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facts of persorption, which would have led 150 years ago to the scientific study of allergy and
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immunology in relation to the digestive system.
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</p>
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<p>
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Volkheimer found that mice fed raw starch aged at an abnormally fast rate, and when he dissected the
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starch-fed mice, he found a multitude of starch-grain-blocked arterioles in every organ, each of which
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caused the death of the cells that depended on the blood supplied by that arteriole. It isn’t hard to
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see how this would affect the functions of organs such as the brain and heart, even without considering
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the immunological and other implications of the presence of foreign particles randomly distributed
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through the tissue.
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</p>
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<p>
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In 1979 some of my students in Mexico wanted a project to do in the lab. Since several traditional foods
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are made with corn that has been boiled in alkali, I thought it would be valuable to see whether this
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treatment reduced the ability of the starch grains to be persorbed. For breakfast one day, they ate only
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atole, tamales, and tortillas, all made from the alkali treated corn. None of the students could find
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any starch grains after centrifuging their blood and urine. That led me to substitute those foods
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whenever possible for other starches.
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</p>
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<p></p>
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<p>
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I have written previously about some of the environmental factors, including radiation, estrogens, and
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unsaturated fats, that are known to damage the immune system and the brain, and that we have been
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increasingly exposed to since 1940.
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</p>
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<p>
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To better understand the nature of the diseases that are now becoming so common, we can look at them in
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a series, from the bowel, to the liver, to the immune system, and to the brain and hormones.
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</p>
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<p>
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The incidence of several inflammatory diseases, for example Crohn's disease, a chronic inflammation of
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the intestine, has been increasing during the last 50 years in the industrialized countries, and at the
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same time, the incidence of several liver diseases has also been increasing.
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</p>
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<p>
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The entry of bacteria into the blood stream, which can lead to septicemia, is ordinarily considered to
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be of importance only in extreme immunodeficiency states, such as old age or in premature infants, but
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the death rate of young adults from septicemia has been increasing rapidly since the 1940s.
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</p>
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<p>
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The permeability of the intestine that allows bacteria to enter the blood stream is very serious if the
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phagocytic cells are weakened. Carrageenan poisoning is one known cause of the disappearance of
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macrophages. Its powerful immunosuppression would tend to be superimposed onto the immunological damage
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that has been produced by radiation, unsaturated fats, and estrogens.
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</p>
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<p>
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The liver tumor that is characteristic of young women using the oral contraceptive pill is a
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hepatocellular adenoma, which is considered to be a premalignant tumor. In Japan, Mexico, and several
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European countries, the incidence of hepatocellular tu-mors has increased steadily and tremendously in
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recent decades, and it has increased in men as well as in women. This is the sort of tumor that very
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likely represents an increased burden of toxins absorbed from the bowel. Carrageenan contributes to the
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disappearance of the liver enzymes (the cytochrome P-450 system) that detoxify drugs, hormones, and a
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variety of other chemicals.
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</p>
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<p>
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Carrageenan enters even the intact, uninflamed gut, and damages both chemical defenses and immunological
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defenses. When it has produced inflammatory bowel damage, the amount absorbed will be greater, as will
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the absorption of bacterial endotoxin. Carra-geenan and endotoxin synergize in many ways, including
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their effects on nitric oxide, prostaglandins, toxic free radicals, and the defensive enzyme systems.
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</p>
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<p>
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The continuing efficient production of energy is a basic aspect of metabolic defense, and this is
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interrupted by carrageenan and endotoxin. The energy failure becomes part of a vicious circle, in which
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permeability of the intestine is increased by the very factors that it should exclude.
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</p>
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<p>
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Once the protective barrier-functions of the intestine and liver have been damaged, allergens and many
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materials with specific biological effects can enter the tissues. The polysaccharide components of
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connective tissue constitute a major part of our regulatory system for maintaining differentiated cell
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functioning, and absorbed starches act as “false signals,” with a great capacity for deranging cellular
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functioning. Several types of research indicate that carrageenan changes cellular function in complex
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ways, imitating changes seen in cancer, for example.
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</p>
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<p>
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R.J.V. Pulvertaft found "a close similarity between Burkitt cells and human lymphocytes stimulated by
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bean extract." He concluded that "…the possibility of a relation between Burkitt's lymphoma and a diet
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of beans should not be neglected," though he emphasized that other factors must be considered, since
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most people who eat beans don't develop the disease. The intestinal parasites which are common in
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tropical Africa can cause inflammation of the bowel, leading to the absorption of large amounts of
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antigens.
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</p>
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<p>
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Since the bowel becomes inflamed in influenze, it is reasonable to think that some of the symptoms of
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"the flu" are produced by absorbed bowel toxins.
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</p>
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<p>
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The variations in the post-influenza syndromes are very likely influenced by the nature of the bacteria
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or foods which are present, chronically or at the time of an uncompensated stress or inflammatory
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disease. K.M. Stevens has argued that while rheumatic fever and glomerulonephritis are caused by the
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antigens of streptococci, systemic lupus erythematosis (SLE) is probably caused by the antigens of
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gram-positive lactobacilli found in the normal flora.
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</p>
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<p>
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Migraine, SLE, chronic fatigue syndrome, thyroid problems, and some kinds of porphyria seem to be more
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common in women of re-productive age, and are often exacerbated by premenstrual hormone changes.
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According to Stevens, "SLE is almost entirely a disease of women of child-bearing age. One possibility
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for this selection could be that women during this period harbour a peculiar flora. This is indeed the
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case; large numbers of gram-positive lactobacilli are present in the vagina only during the thirty-odd
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years when regular menstrual activity is present."
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</p>
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<p>
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In 1974, I noticed that I consistently got a migraine headache after drinking a lactobacillus milk
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product, and stopped using (and recommending) yogurt and other lactobacillus foods, though I suspected
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it was the lactic acid which caused the immediate symptoms. Lactic acid is a metabolic burden,
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especially when combined with an estrogen excess, but Stevens' main point, about the significance of our
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immunological response to systemic bacterial antigens, deserves more attention.
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</p>
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<p>
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On a typical diet, tissues progressively accumulate linoleic acid, and this alters the structure of
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mitochondrial cardiolipin, which governs the response of the mitochondrial enzymes to the thyroid
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hormone. This process is especially evident in the female liver. In the “autoimmune” diseases, such as
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lupus, there are typically antibodies to cardiolipin, as if the body were trying to reject its own
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tissues, which have been altered by the storage of linoleic acid. The altered mitochondrial function,
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which is involved in so many symptoms, can become part of a vicious circle, with endotoxin and estrogen
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having central roles, once the stage has been set by the combination of diet, stress, and toxins.
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</p>
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<p>
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A few months ago I had a questionnaire circulated in a “fibromyositis” discussion group on the internet,
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and the consistency of responses was interesting.
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</p>
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<p>
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The questions were: 1) Have you noticed that any of your symptoms are worse premenstrually?
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</p>
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<p>
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2) Have you noticed that any symptom is less severe premenstrually?
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</p>
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<p>
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3) Do any symptoms seem to be worse periodically, but without being associated with the premenstrual
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time?
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</p>
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<p>
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4) Did your symptoms appear after use of oral contraceptives or IUD?
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</p>
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<p>
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Except for one woman who was taking oral contraceptives at the time she became sick, and kept taking
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them, and who didn’t notice any cycle, all of the answers to the first three questions (15 of the 16 who
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responded) were identical: 1) yes, 2) no, 3) no.
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</p>
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<p>
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The premenstrual estrogen-dominance usually leads progressively to higher prolactin and lower thyroid
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function. Estrogen is closely associated with endotoxinemia, and with histamine and nitric oxide
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formation, and with the whole range of inflammatory and “autoimmune” diseases. Anything that irritates
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the bowel, leading to increased endotoxin absorption, contributes to the same cluster of metabolic
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consequences.
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</p>
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<p>
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I have previously discussed the use of antibiotics (and/or carrot fiber and/or charcoal) to relieve the
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premenstrual syndrome, and have mentioned the study in which the lifespan was extended by occasionally
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adding charcoal to the diet. A few years ago, I heard about a Mexican farmer who collected his
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neighbors' runt pigs, and got them to grow normally by adding charcoal to their diet. This probably
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achieves the same thing as adding antibiotics to their food, which is practiced by pig farmers in the US
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to promote growth and efficient use of food. Charcoal, besides binding and removing toxins, is also a
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powerful catalyst for the oxidative destruction of many toxic chemicals. In a sense, it anticipates the
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action of the protective enzymes of the intestinal wall and the liver.
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</p>
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<p>
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Some women with premenstrual fatigue have found that the “premenstrual” phase tends to get longer and
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longer, until they have chronic fatigue. I found that to be one of the easiest "PMS" problems to
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correct. When people are older, and have been sick longer, the fatigue problem is likely to involve more
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systems of the body. The larger the quantity of "toxic fat" stored in the body, the more careful the
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person must be about increasing metabolic and physical activity. Using more vitamin E, short-chain
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saturated fats, and other anti-lipid-peroxidation agents is important.
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</p>
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<p>
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The inflammatory diseases that develop after prolonged stress are sometimes hard to correct. But
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avoiding exposure to the major toxic allergens--such as carrageenan--is an essential consideration, just
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as important as correcting the thyroid function and avoiding the antithyroid substances.
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</p>
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<p>
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Low cholesterol is very commonly involved in the diseases of stress, and--like inadequate dietary
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protein--will make the system less responsive to supplementary thryoid hormone.
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</p>
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<p>
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The proliferative aspects of the inflammatory diseases represent, I think, a primitive form of
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regeneration. Arthritis, atherosclerosis, various granulomatous processes, breast diseases, liver
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adenomas, etc., provide an opportunity for investigating the various systems and substances that guide
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cell proliferation toward reconstruction, rather than obstructive and deformative, degenerative,
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processes. Degenerative diseases probably all contain clues for understanding regeneration, as I have
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suggested in relation to Alzheimer’s disease and inflammation. I will be talking about these in other
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newsletters, but the first step will always be to minimize exposure to the disruptive substances.
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</p>
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<p></p>
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<hr />
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<p><h3>REFERENCES</h3></p>
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<p>
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Pathol Biol (Paris) 1979 Dec;27(10):615-626 [Biological and pharmacological effects of
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carrageenan].[Article in French] Roch-Arveiller M, Giroud JP “Carrageenan is sulfated polysaccharide
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which has been extensively used as emulsifier and thickening agent in the food industry, for its ability
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to induce acute inflammation in pharmacology and for its selectively toxic effect for macrophages in
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immunology. Carrageenan is a complex substance which displays various biological properties. The authors
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have shown the extent of these actions and reviewed the latest investigations on this subject.”
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</p>
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<p>
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Kirchheiner B J Allergy Clin Immunol 1995 May;95(5 Pt 1):933-936 Anaphylaxis to carrageenan: a
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pseudo-latex allergy. Tarlo SM, Dolovich J, Listgarten C “Anaphylactic reactions during a barium enema
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have been attributed to allergy to latex on the barium enema device. The observation of anaphylaxis
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during barium enema without latex exposure or latex allergy led to the performance of an allergy skin
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test to the barium enema solution.” “Individual components of the barium enema solution were obtained
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for double-blind skin testing. A RAST to identify specific IgE antibodies to the skin test active agent
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was established.” “Carrageenan, a component of the barium enema solution, produced positive reactions to
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allergy skin test and RAST. Gastrointestinal symptoms for which the patient was being investigated by
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the barium enema subsequently disappeared with a diet free of carrageenan. CONCLUSIONS: Carrageenan is a
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previously unreported cause of anaphylaxis during barium enema. It is an allergen widely distributed in
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common foods and potentially could account for some symptoms related to milk products or baby formula.”
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</p>
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<p>
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Cancer Detect Prev 1981;4(1-4):129-134 Harmful effects of carrageenan fed to animals. Watt J, Marcus R
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“An increased number of reports have appeared in the literature describing the harmful effects of
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degraded and undegraded carrageenan supplied to several animal species in their diet or drinking fluid.
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The harmful effects include foetal toxicity, teratogenicity, birth defects, pulmonary lesions,
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hepatomegaly, prolonged storage in Kupffer cells, ulcerative disease of the large bowel with
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hyperplastic, metaplastic, and polypoidal mucosal changes, enhancement of neoplasia by carcinogens, and,
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more ominously, colorectal carcinoma. Degraded carrageenan as a drug or food additive has been
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restricted in the United States by the FDA, but undegraded carrageenan is still widely used throughout
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the world as a food additive. Its harmful effects in animals are almost certainly associated with its
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degradation during passage through the gastrointestinal tract. There is a need for extreme caution in
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the use of carrageenan or carrageenan-like products as food additives in our diet, and particularly in
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slimming recipes.”
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</p>
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<p>
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Acta Pathol Microbiol Scand [A] 1980 May;88(3):135-141 Stereomicroscopic and histologic changes in the
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colon of guinea pigs fed degraded carrageenan. Olsen PS, Poulsen SS “A colitis-like state induced in
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Guinea Pigs fed degraded carrageenan orally. By means of a combined semimacroscopic and histologic
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technique the course of the disease was followed during 28 days. The changes were primarily seen and
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became most prominent in the caecum. The first lesions were observed following 24 hours of treatment as
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small rounded foci initially with degenerative changes and inflammation in the surface epithelium, later
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forming superficial focal ulcerations. Ulcerative changes gradually progressed during the experiment,
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forming linear and later large, geographical ulcerations. Topographically the ulcerative process was
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strongly related to the larger submucosal vessels. Nonulcerated parts of the mucosa were not changed
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until following 7-14 days of treatment. The mucosa became bulging, granulated and finally villus-like.
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Accumulation of macrophages was found under the surface epithelium after 7-17 days. Possible
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pathogenetic mechanisms are discussed, especially the development of the early lesions and the
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significance of the macrophages.
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</p>
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<p>
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Cancer Res 1997 Jul 15;57(14):2823-2826 Filament disassembly and loss of mammary myoepithelial cells
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after exposure to lambda-carrageenan. Tobacman JK “Carrageenans are naturally occurring sulfated
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polysaccharides, widely used in commercial food preparation to improve the texture of processed foods.
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Because of their ubiquity in the diet and their observed preneoplastic effects in intestinal cells,
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their impact on human mammary myoepithelial cells in tissue culture was studied. At concentrations as
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low as 0.00014%, lambda-carrageenan was associated with disassembly of filaments with reduced
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immunostaining for vimentin, alpha-smooth muscle-specific actin, and gelsolin; increased staining for
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cytokeratin 14; and cell death. The absence of mammary myoepithelial cells is associated with invasive
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mammary malignancy; hence, the destruction of these cells in tissue culture by a low concentration of a
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widely used food additive suggests a dietary mechanism for mammary carcinogenesis not considered
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previously.”
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</p>
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<p>
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Agents Actions 1981 May;11(3):265-273 Carrageenan: a review of its effects on the immune system. Thomson
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AW, Fowler EF “Carrageenans (kappa, lambda and iota) are sulphated polysaccharides isolated from marine
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algae that can markedly suppress immune responses both in vivo and in vitro. Impairment of complement
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activity and humoral responses to T-dependent antigens, depression of cell-mediated immunity,
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prolongation of graft survival and potentiation of tumour growth by carrageenans have been reported. The
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mechanism responsible for carrageenan-induced immune suppression is believed to be its selective
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cytopathic effect on macrophages. This property of carrageenan has led to its adoption as a tool for
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analysing the role of these cells in the induction and expression of immune reactivity. Systemic
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administration of carrageenan may, however, induce disseminated intravascular coagulation and inflict
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damage on both the liver and kidney. This is an important consideration in the interpretation of the
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effects of carrageenan in vivo and precludes its use as a clinical immune suppressant.”
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</p>
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<p>
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Biomedicine 1978 May;28(3):148-152 Carrageenan and the immune response. Thomson AW “Since the biological
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effects of carrageenan were reviewed in 1972 by Di Rosa it has become clear from a large number of
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reports that this algal polysaccharide markedly influences immune responses. Profound suppression of
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immunity evidenced by impaired antibody production, graft rejection, delayed hypersensitivity and
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anti-tumour immunity, has been observed in carrageenan-treated animals and the immunodepressive ability
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of carrageenan confirmed by in vitro studies. Efforts at analysis of carrageenan-induced immune
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suppression have focussed on the selective cy-totoxic effect of this agent onmononuclear phagocytes.
|
||
Faith in the ability of carrageenan to eliminate those cells has led to its use in examination of the
|
||
role played by mononuclear phagocytes in various aspects of immune reactivity. This review documents and
|
||
discusses the effects of carrageenan on immune responses and assesses the value of carrageenan as a
|
||
useful tool in both current and future work aimed at broadening our knowledge of mechanisms underlying
|
||
immune reactions.”
|
||
</p>
|
||
<p>
|
||
Teratology 1981 Apr;23(2):273-278 Teratogenic effect of lambda-carrageenan on the chick embryo. Monis B,
|
||
Rovasio RA “Carrageenans are widely used as food additives. Thus, it seemed of interest to test their
|
||
possible teratogenic action. For this purpose, 530 chick eggs were injected in the yolk sac with 0.1 ml
|
||
of a solution of 0.1% lambda-carrageenan in 0.9% sodium chloride. As controls, 286 eggs were injected
|
||
with 0.1 ml of 9.0% sodium chloride. In addition, 284 eggs received no treatment. After incubation for
|
||
48--50 hours at 39 degrees C, embryos were fixed, cleared, and observed with a stereoscopic microscope.
|
||
The frequency of abnormal embryos in the group receiving lambda-carrageenan was higher than in the
|
||
controls (p less than 0.04). Partial duplication of the body, abnormal flexures of the trunk,
|
||
anencephaly, a severely malformed brain, thickening of the neural tube wall, an irregular neural tube
|
||
lumen with segmentary occlusion and a reduction in crown-rump length and number of somites were
|
||
distinctly seen in thelambda-carrageenan-injected group. Moreover, the average number of anomalies per
|
||
embryo in the lambda-carrageenan-injected group was nearly twice that in the controls. Present data
|
||
indicate that lambda-carrageenan has teratogenic effects on early stages of the development of the chick
|
||
embryo.”
|
||
</p>
|
||
<p>
|
||
Food Addit Contam 1989 Oct;6(4):425-436 Intestinal uptake and immunological effects of
|
||
carrageenan--current concepts. Nicklin S, Miller K “Carrageenans are a group of high molecular weight
|
||
sulphated polygalactans which find extensive use inthe food industry as thickening, gelling and
|
||
protein-suspending agents. Although there is no evidence to suggest that the persorption of small
|
||
amounts of carrageenans across the intestinal barrier poses an acute toxic hazard, they are known to be
|
||
biologically active in a number of physiological systems and extended oral administration in laboratory
|
||
animals has been shown to modify both in vivo and in vitro immune competence. Whereas this effect could
|
||
be attributed to carrageenan having a selective toxic effect on antigen-processing macrophages,
|
||
additional studies suggest that macrophages can also influence immune responses by the timed release of
|
||
immunoregulatory mediators. Evidence in support of this comes from in vitro studies which demonstrate
|
||
that carrageenan-treated macrophages can, depending on conditions and time of administration, release
|
||
either stimulatory or inhibitory factors. The former is known to be the immunostimulatory agent
|
||
interleukin 1 (IL-1). The inhibitory factor, which is produced at an early stage following exposure to
|
||
non-toxic doses of carrageenans, has yet to be formally identified but it is believed to be a
|
||
prostaglandin because of its specific mode of action and short biological half-life. At present it is
|
||
impossible to relate these studies to the human situation. Although it is established that carrageenans
|
||
can cross the intestinal barrier of experimental animals, there is no evidence to suggest that the
|
||
limited uptake that may occur in man in any way interferes with normal immune competence. Nevertheless,
|
||
increased exposure may occur in the neonate during weaning, and adults and children following allergic
|
||
reactions and episodes of gastrointestinal disease. Further studies under such conditions now seem
|
||
warranted in order to elucidate the possible immunological consequences which may be associated with
|
||
enhanced uptake of carrageenans in vulnerable groups.”
|
||
</p>
|
||
<p>
|
||
Health Rep 1990;2(4):343-359 “Crohn's disease and ulcerative colitis: morbidity and mortality,” Rod
|
||
Riley. “This study analyzes hospital discharges and deaths from 1971 to 1986 for patients with
|
||
inflammatory bowel disease (IBD), which includes Crohn's disease and ulcerative colitis. The data are
|
||
based on hospital morbidity and mortality statistics provided to Statistics Canada by the provinces. For
|
||
Crohn's disease, age-standardized rates per 100,000 population for hospital discharges increased by 148%
|
||
for males and by 192% for females over the study period. In 1986, the rate for females was 48% higher
|
||
than the rate for males. For both males and females, age-specific discharge rates were highest in the
|
||
20-24 age group. For ulcerative colitis, male age-standardized discharge rates decreased by 17% from
|
||
1971 to 1977, and then increased by 41% from 1977 to 1986. For females, the rates decreased by 18% from
|
||
1971 to 1976, then remained fairly stable from 1976 to 1986. Male and female discharge rates were
|
||
similar over the study period. For females, rates were highest in the 20-34 age groups; for males, they
|
||
were highest in the 65 and older age groups. In 1971, rates for both types of IBD were almost the same,
|
||
but by the end of the study period the rate per 100,000 population for Crohn's disease was 34 for
|
||
females and 23 for males, while for ulcerative colitis the rates were 13 for females and 14 for males.
|
||
During the 16-year study period, cause of death data showed 556 deaths directly attributed to Crohn's
|
||
disease and 761 deaths at-tributed to ulcerative colitis. The under 45 age group accounted for 25% of
|
||
deaths due to Crohn's disease and for 17% of deaths due to ulcerative colitis. The time trends for IBD
|
||
hospital discharge rates in Canada closely parallel the findings of hospital discharge rates in the
|
||
United States and England-Wales. A comparison with epidemiological population surveys strongly suggests
|
||
that increased discharge rates are due mostly to increases in incidence and prevalence of IBD in the
|
||
general population.”
|
||
</p>
|
||
<p><hr /></p>
|
||
<p><hr /></p>
|
||
<p>
|
||
Gut 1988 Mar;29(3):346-351, Cardiff Crohn's disease jubilee: the incidence over 50 years. Rose JD,
|
||
Roberts GM, Williams G, Mayberry JF, Rhodes J “The incidence of Crohn's disease in Cardiff between 1931
|
||
and 1985 has been examined using hospital diagnostic indices supplemented in recent years by records
|
||
from clinicians, and the departments of pathology and radiology. Four hundred and seven new patients
|
||
were confirmed after all notes had been reviewed. There has been a large increase from 0.18 cases/10(5)
|
||
of the population per year in the 1930s to current values of 8.3/10(5)/year. The incidence continues to
|
||
rise and shows an increasing proportion of patients with colorectal disease. Peak age specific
|
||
incidences occur in the third and eighth decades of life.”
|
||
</p>
|
||
<p>
|
||
Am J Hematol 1992 Mar;39(3):176-182 Polysaccharide encapsulated bacterial infection in sickle cell
|
||
anemia: a thirty year epidemiologic experience. Wong WY, Powars DR, Chan L, Hiti A, Johnson C, Overturf
|
||
G “Annual age-specific incidence rates of Streptococcus pneumoniae or Haemophilus influenzae bacterial
|
||
septicemia in sickle cell anemia (SS) were determined for the years of 1957 through 1989. Forty-nine
|
||
patients had 64 episodes of septicemia among a population of 786 SS patients observed for 8,138
|
||
person-years. Peak frequency of infection occurred between 1968-1971 and 1975-1981 with a conspicuous
|
||
absence of episodes in 1972, 1973, 1982-1984, and 1986-1987, thus demonstrating cycles of high and low
|
||
attack rates. The annual age-specific incidence rate of septicemia varied from 64.5 (1965) to 421.1
|
||
(1980) per 1,000 person-years for those under 2 years of age and never exceeded 10.2 per 1,000 in those
|
||
over 4 years of age. Following the introduction of pneumococcal polyvalent vaccine in 1978, incidence of
|
||
infection decreased in SS children greater than 2 years of age. No modification of the risk of infection
|
||
was observed in immunized children less than 2 years of age. During these three decades, there has been
|
||
a ten-fold increase in the number of SS adults over 20 years of age. The relative risk of chronic sickle
|
||
complications comparing the survivors of septicemia to the non-infected patients was: subsequent death
|
||
1.76, retinopathy 4.06, avascular necrosis 1.95, symptomatic cholelithiasis 1.33, stroke 1.30, and
|
||
priapism 1.26. These data suggest that prognosis for lifetime severe SS is initially manifested as an
|
||
increased risk of septicemia during childhood.”
|
||
</p>
|
||
<p>
|
||
Gastroenterol Clin Biol 1986 Jun;10(6-7):468-474 [Trends of mortality from cirrhosis in France between
|
||
1925 and 1982 Coppere H, Audigier JC “In 1982, 13,866 deaths secondary to cirrhosis were reported.
|
||
Between 1925 and 1982, the number of deaths increased by 163 p. 100. This overall change was observed
|
||
gradually: profound drop in the cirrhosis mortality rate during the Second World War, increase between
|
||
1945 and 1967, stabilization between 1967 and 1975 and more pronounced decline from then on. Cirrhosis
|
||
mortality rate per 100,000 increased from 9.17 to 28.21 (+208 p. 100) in males and from 3.63 to 10.38
|
||
(+186 p. 100) in females from 1945 to 1982. The increase was approximately the same whatever the age. A
|
||
cohort effect was observed in both sexes. There were two successive waves of increased mortality
|
||
separated by an interval of non augmentation for the cohorts born between 1906 and 1915 and between 1931
|
||
and 1940. Since 1967, mortality due to cirrhosis has stopped increasing in both sexes. These changes may
|
||
be related to decreasing alcohol consumption in France, certainly one of the major objectives in present
|
||
day health programs. Abrupt reduction of alcohol consumption should be followed by a dramatic fall in
|
||
the number of deaths from cirrhosis. Progressive decline of consumption is possibly associated with a
|
||
decrease in the incidence of the disease. In 2,000, the rate for cirrhosis mortality is expected to be
|
||
the same as that observed in the middle of the 20th century.”
|
||
</p>
|
||
<p>
|
||
Cancer Res 1987 Sep 15;47(18):4967-4972 Changing incidence of hepatocellular carcinoma in Japan. Okuda
|
||
K, Fujimoto I, Hanai A, Urano Y “A trend in the incidence of hepatocellular carcinoma (HCC) in Japan was
|
||
studied from the data of the Osaka Cancer Registry (population, 8,512,351 in 1981) for the period of
|
||
1963-1983, the Vital Statistics of Japan, Ministry of Health and Welfare, and the Japan Autopsy Registry
|
||
which contained 594,132 individually filed cases in the 26-year period from 1958 to 1983. Both cancer
|
||
registry data and autopsy records showed a more than 2-fold increase in HCC incidence, particularly in
|
||
the last 10 years or so, among males and a less pronounced increase in females. The same trend was borne
|
||
out by the cancer registries of Nagasaki City and Miyagi Prefecture and the Vital Statistics. When
|
||
studied with the autopsy data, it was found that the numbers of autopsies for cirrhosis without HCC and
|
||
autopsies for HCC (with and without cirrhosis) were about the same in 1958-1961 and that currently
|
||
(1980-1983) the latter is about 2 times the former. As one of the possible causes of increase in HCC
|
||
incidence other than prolonged survival of patients with cirrhosis, chronic non-A, non-B hepatitis is
|
||
discussed. “
|
||
</p>
|
||
<p>
|
||
Hepatogastroenterology 1997 Sep;44(17):1401-1403 Hepatocellular carcinoma and hepatic cirrhosis in
|
||
Mexico: a 25 year necroscopy review. Cortes-Espinosa T, Mondragon-Sanchez R, Hurtado-Andrade H,
|
||
Sanchez-Cisneros R “BACKGROUND/AIMS: Hepatocellular carcinoma (HCC) is a common form of cancer which is
|
||
found throughout the world. In recent years, the rates of HCC seem to have increased in European and
|
||
North American countries.” “RESULTS: Of 12556 autopsies studied, 73 cases of histologically proven HCC
|
||
were reported, representing a total necropsy carcinoma incidence of 0.59%. Fifty-five cases were
|
||
associated with cirrhosis (0.43%), and 18 were not (0.14%). HCC was two times more common in males (67%)
|
||
than in females (33%), with a ratio of 2:1. During this period, the necropsy incidence of HCC rose
|
||
steadily to twice its original level (1965-69 incidence 0.35%; 1985-89 incidence 0.69%). The necropsy
|
||
incidence of cirrhosis was 4% (329 males, 185 females). The overall TC/T index was 75% (87% for males
|
||
and 50% for females). The overall TC/C index was 10.7% (13% for males and 6.4% for females).
|
||
CONCLUSIONS: There was a two-fold increase in the incidence of HCC in the Mexican population studied
|
||
over a 25-year period. HCC was associated with cirrhosis in the majority of cases. HCC was two times
|
||
more common in males than in females in patients with cirrhosis; in patients without cirrhosis, the
|
||
ratio was 1:1. The incidence of cirrhosis was 4%, which remained unchanged with the passage of time.”
|
||
</p>
|
||
<p>
|
||
Hepatogastroenterology 1984 Oct;31(5):215-217 Hepatocellular carcinoma and cirrhosis: a review of their
|
||
relative incidence in a 25-year period in the Florence area. Bartoloni St Omer F, Giannini A, Napoli P
|
||
“An eight-fold increase in the incidence of hepatocellular carcinoma in the Florence area was detected
|
||
in a 25-year retrospective review of adult autopsy records in the Institute of Pathology of the
|
||
University of Florence. During the same period, the incidence of cirrhosis did not show a parallel
|
||
increase. The relationship between hepatocellular carcinoma, cirrhosis and HB virus is briefly discussed
|
||
in the light of these findings.”
|
||
</p>
|
||
<p>
|
||
J Clin Pathol 1978 Feb;31(2):108-110 Hepatocellular carcinoma and hepatic cirrhosis in the west of
|
||
Scotland: a 25-year necropsy review. Burnett RA, Patrick RS, Spilg WG, Buchanan WM, Macsween RN “A
|
||
two-fold increase in the incidence of hepatocellular carcinoma in the west of Scotland is reported on
|
||
the basis of a 25-year retrospective necropsy review (313 cases). This increase is not accompanied by a
|
||
corresponding increase in the incidence of hepatic cirrhosis. The relationship between hepatocellular
|
||
carcinoma and hepatic cirrhosis is discussed in the light of these findings.”
|
||
</p>
|
||
<p>
|
||
J Hyg Epidemiol Microbiol Immunol 1990;34(4):343-348 “Increasing trend of hyperbilirubinemia incidence
|
||
in the blood donors population,” Pintera J.
|
||
</p>
|
||
<p>
|
||
Hepatogastroenterology 1984 Oct;31(5):211-214 Primary hepatic cancer and liver cirrhosis. Autopsy study
|
||
covering fifty years. Bethke BA, Schubert GE “Autopsy reports from 1931 to 1980 were used to study the
|
||
incidence of liver cirrhosis (LC) and the association between LC and hepatocellular carcinoma (HCC) in
|
||
our area (Wuppertal, Germany). An increase in LC and in LC with HCC has occurred since World War II,
|
||
with HCC being most frequently associated with postnecrotic cirrhosis. The prevalence of HCC in men with
|
||
LC was highest (13.5%) in 1966-1970, whereas the prevalence of HCC with LC in women rose abruptly to a
|
||
peak (11.8%) during the last 5 years of the study. Possible etiological factors for the association
|
||
between LC and HCC are discussed.”
|
||
</p>
|
||
<p>
|
||
Riv Eur Sci Med Farmacol 1990 Jun;12(3):165-168 [Oral contraceptive and hepatic effects].[Article in
|
||
Italian] Tarantino G, Morelli L, Califano C “The general use of synthetic estrogens like DC pointed out
|
||
that near many skilled collateral effects, some others that are showing with a decrease of bile
|
||
excretion (cholestasis), reversible with their administration interruption; with hepatic cells adenoma
|
||
that are potentially premalignant and can transform into hepatocellular carcinoma; with vascular
|
||
complications such as (most frequently in carcinomatousis) "hepatic peliosis" and "thrombosis" of
|
||
suprahepatic veins (Budd-Chiari's syndrome). There is no overall increase in the incidence of
|
||
gallbladder disease (cholelithiasis and cholecystitis).”
|
||
</p>
|
||
<p>
|
||
Hepatology 1990 Nov;12(5):1106-1110 Fatty liver hepatitis (steatohepatitis) and obesity: an autopsy
|
||
study with analysis of risk factors. Wanless IR, Lentz JS “Steatohepatitis (fatty liver hepatitis),
|
||
histologically identical to alcoholic disease, occurs in some obese patients after jejunoileal bypass. A
|
||
similar lesion occurs rarely in obese patients without bypass surgery, but the risk factors are poorly
|
||
understood. Hepatic steatosis, steatohepatitis and fibrosis were sought in 351 apparently nonalcoholic
|
||
patients at autopsy and various risk factors were evaluated.” “Thus this study supports the hypothesis
|
||
that fatty acids have a role in the hepatocellular necrosis found in some obese individuals.”
|
||
</p>
|
||
<p>
|
||
Prostaglandins 1977 Aug;14(2):295-307 Reduced exudation and increased tissue proliferation during
|
||
chronic inflammation in rats deprived of endogenous prostaglandin precursors. Bonta IL, Parnham MJ,
|
||
Adolfs MJ “Two models of chronic inflammation were studied in rats deprived of endogenous precursors of
|
||
prostaglandins by feeding the animals on essential fatty acid deficient (EFAD) food. During
|
||
kaolin-induced pouch-granuloma, exudate production was markedly reduced in EFAD rats, when compared with
|
||
normal animals. The exudates from normal rats contained large amounts of PGE, but in the exudates from
|
||
EFAD rats the amount of PGE was very markedly reduced. Similarly, with carrageenan-impregnated polyether
|
||
sponges, the exudative component of inflammation was reduced in EFAD rats. However, the proliferative
|
||
component was significantly increased, particularly in relation to the stunted growth of EFAD rats.
|
||
Sponge exudates from EFAD rats contained fewer leucocytes than those from normal animals but the fall in
|
||
leucocyte count was much smaller than the very marked reduction in PGE activity. EFAD rats also
|
||
exhibited a significant increase in adrenal weights. The results are discussed in the light of the
|
||
ambivalent (pro- or anti-inflammatory) role of endogenous PGS. It appears that, in the proliferative
|
||
phase of inflammation, the anti-inflammatory role of PGs is more dominant.”
|
||
</p>
|
||
<p>
|
||
J Hepatol 1997 Sep;27(3):578-582 Subfulminant hepatic failure in autoimmune hepatitis type 1: an unusual
|
||
form of presentation. Herzog D, Rasquin-Weber AM, Debray D, Alvarez F “Autoimmune hepatitis type 1 is
|
||
known to progress insidiously and in many cases cirrhosis is already established at the first
|
||
presentation of symptoms. It affects mostly females, with peaks of incidence around 10 and 50 years of
|
||
age. Subfulminant hepatic failure is an unusual initial form of presentation of AIH type 1 and it was
|
||
observed in three post-pubertal female patients. Rapid disease evolution or no response to
|
||
immunosuppressive therapy led to liver transplantation in all patients. Two did not have cirrhosis, and
|
||
the third had focal cirrhosis. The occurrence of the unusual subfulminant form of autoimmune hepatitis
|
||
in three latepubertal girls (Tanner V) suggests that estrogen may play a role in the severity of the
|
||
disease.”
|
||
</p>
|
||
<p>
|
||
Acta Hepatogastroenterol (Stuttg) 1977 Apr;24(2):97-101 Plasma prolactin and prolactin release in liver
|
||
cirrhosis. Wernze H, Schmitz E “A significant increase of basal plasma prolactin levels
|
||
(radioimmunoassayed) in 75 patients with liver cirrhosis was found in comparison to 50 male controls
|
||
(8.5+/-4.5 (SD) vs. 5.5+/-1.7 ng/ml p less than 0.001). The extent and incidence of hyperprolactinaemia
|
||
in 48 patients with alcoholic cirrhosis was more pronounced than in 27 cases of cirrhosis of
|
||
non-alcoholic aetiologies (mean 9.7+/-4.8 vs. 5.7+/-2.1 ng/ml). No relation to ascites formation as well
|
||
as to the development of gynaecomastia was apparent. Prolactin release following thyrotropin-releasing
|
||
hormone was markedly enhanced in alcoholic as compared to non-alcoholic cirrhosis. Possibly
|
||
hyperprolactinaemia and increased pituitary hormone reserve reflects hyperoestrogenism but changes of
|
||
the hypothalamic regulation cannot be excluded as yet.”
|
||
</p>
|
||
<p>
|
||
Jpn J Pharmacol 1991 Apr;55(4):551-554 Endotoxin- and inflammation-induced depression of the hepatic
|
||
drug metabolism in rats. Ishikawa M, Sasaki K, Nishimura K, Takayanagi Y, Sasaki K “Carrageenan-induced
|
||
inflammation and exposure to endotoxin considerably decreased the content of cytochrome P-450 and
|
||
activities of ethylmorphine N-demethylase and meperidine N-demethylase, but did not decrease the
|
||
activities of aniline hydroxylase or NADPH-cytochrome c reductase, compared with the respective
|
||
activities in rats treated with carrageenan alone. These results suggest that under these experimental
|
||
conditions, the two host-related environmental factors interact and enhance a decrease in rat hepatic
|
||
microsomal drug metabolizing enzymes depending on the substrate used.”
|
||
</p>
|
||
<p>
|
||
Infect Immun 1991 Feb;59(2):679-683 Enhancement of lipopolysaccharide-induced tumor necrosis factor
|
||
production in mice by carrageenan pretreatment. Ogata M, Yoshida S, Kamochi M, Shigematsu A, Mizuguchi Y
|
||
“Tumor necrosis factor (TNF) is a cytokine which mediates endotoxin shock and causes multiple organ
|
||
damage. It is thought that macrophage (MP) activation is necessary to increase lipopolysaccharide
|
||
(LPS)-induced TNF production and lethality. Carrageenan (CAR) is sulfated polygalactose which destroys
|
||
MP; it is used as a MP blocker. We found that CAR pretreatment can increase both endotoxin-induced TNF
|
||
production and the mortality rate in mice. The ddY mice (7 to 8 weeks old) were injected
|
||
intraperitoneally with CAR (5-mg dose) and challenged intravenously with LPS 24 h later. Without CAR
|
||
pretreatment, LPS doses of less than 10 micrograms did not induce TNF in sera. After pretreatment,
|
||
however, about 3 x 10(3) to 4 x 10(4) U of TNF per ml was produced after LPS injection at doses of 0.1
|
||
to 10 micrograms, respectively. TNF production was significantly increased by CAR pretreatment at LPS
|
||
doses of more than 10 micrograms. CAR pretreatment rendered the mice more sensitive to the lethal effect
|
||
of LPS; 50% lethal doses of LPS in CAR-pretreated mice and nonpretreated mice were 26.9 and 227
|
||
micrograms, respectively. The mortality of the two groups was significantly different at doses of 50,
|
||
100, and 200 mi-crograms of LPS. CAR increased LPS-induced TNF production and mortality within 2 h, much
|
||
earlier than MP activators, which needed at least 4 days. Our results made clear that TNF production is
|
||
enhanced not only by a MP activator but also by a MP blocker.”
|
||
</p>
|
||
<p>
|
||
Prog Clin Biol Res 1989;286:237-242 Effect of macrophage inhibition in carrageenan- and
|
||
D-galactosamine-induced sensitivity to low-dose endotoxin. Kujawa KI, Berning A, Odeyale C, Yaffe LJ.
|
||
</p>
|
||
<p>
|
||
J Surg Res 1984 Jul;37(1):63-68 Evidence for aerobic glycolysis in lambda-carrageenan-wounded skeletal
|
||
muscle. Caldwell MD, Shearer J, Morris A, Mastrofrancesco B, Henry W, Albina JE “Classically, increased
|
||
lactate production in wounded tissue is ascribed to anaerobic glycolysis although its oxygen consumption
|
||
has been found to be similar to normal tissue. This apparent inconsistency was studied in a standardized
|
||
isolated perfused wound model. Male Sprague-Dawley rats were wounded (group W) with intramuscular
|
||
injections of lambda-carrageenan and fed ad lib.; not wounded and pair fed to the decreased food intake
|
||
of the wounded animals (group PFC); or not wounded and fed ad lib. (group ALC). After 5 days, the
|
||
hindlimbs of animals from each group were either perfused using a standard perfusate with added
|
||
[U-14C]glucose or [1-14C]pyruvate or assayed for the tissue content of lactate and pyruvate. In
|
||
addition, the effect of a 30% hemorrhage on the tissue lactate and pyruvate concentration was examined.
|
||
Wounding increased glucose uptake and lactate production by 100 and 96%, respectively, above that seen
|
||
in ALC animals. Oxygen consumption was unchanged by wounding (5.74, 5.14, and 5.83 mumole/min/100 g in
|
||
W, PFC, and ALC, respectively). Glucose and pyruvate oxidation were also unaltered among the groups.
|
||
Hemorrhage resulted in a comparable increase in lactate and pyruvate in tissue from wounded and pair-fed
|
||
control animals (above those concentrations found in tissue harvested without preexisting hemorrhage).
|
||
As a consequence, the same relationship in L/P ratio was maintained after hemorrhage. Taken together,
|
||
these results confirm the presence of aerobic glycolysis in wounded tissue (unchanged oxygen
|
||
consumption, glucose, and pyruvate oxidation). In addition, pyruvate dehydrogenase activity in the wound
|
||
was apparently the same as that found in muscle from pair-fed control animals.”
|
||
</p>
|
||
<p>
|
||
Food Chem Toxicol 1984 Aug;22(8):615-621 Effect of orally administered food-grade carrageenans on
|
||
antibody-mediated and cell-mediated immunity in the inbred rat. Nicklin S, Miller K “Experiments were
|
||
performed to investigate the immunological consequences associated with the persorption of poorly
|
||
degradable carregeenans from the diet. Using an inbred strain of rat it was demonstrated
|
||
histochemically, by the carrageenan-specific Alcian blue staining technique, that small quantities of
|
||
food-grade carrageenans given at 0.5% in drinking-water for 90 days could penetrate the intestinal
|
||
barrier of adult animals. This apparently occurred via an intact mucosa in the absence of inflammatory
|
||
or pathological lesions. The carrageenan was demonstrated in macrophage-like cells present within the
|
||
villi and lamina propria of the small intestine. The oral administration of kappa, lambda or iota
|
||
food-grade carrageenans did not affect local (biliary) or systemic antibody responses to gut commensal
|
||
microorganisms, or to orally-administered sheep erythrocytes. However, when sheep red blood cells were
|
||
administered parenterally the ensuing anti-sheep red blood cell haemagglutinating antibody response was
|
||
temporarily suppressed in carrageenan-fed rats. lambda-Carrageenan and iota-carrageenan both
|
||
significantly (P less than or equal to 0.01 and P less than or equal to 0.05, respectively) reduced the
|
||
mid-phase (14-28 days) haemagglutinin response; kappa-carrageenan (L100) was less effective but caused
|
||
significant depression at day 21 (P less than or equal to 0.01). Individual responses were, however,
|
||
within the control range 35 days after sheep erythrocyte administration, thus indicating the temporary
|
||
nature of this effect. Although carrageenan administration depressed the anti-sheep erythrocyte antibody
|
||
response, it did not affect T-cell immune competence as measured by the popliteal lymph node assay for
|
||
graft-versus-host reactivity.”
|
||
</p>
|
||
<p>
|
||
J Nutr 1986 Feb;116(2):223-232 Effects of certain dietary fibers on apparent permeability of the rat
|
||
intestine. Shiau SY, Chang GW “Apparent intestinal permeability was determined indirectly by orally
|
||
administering a poorly absorbed dye, phenol red, to rats and measuring its recovery in feces and in
|
||
urine. Increased apparent permeability was recognized by increased dye recovery in urine and by an
|
||
increased ratio of urinary to fecal dye recovery. Guar gum, pectin, carrageenan type I (80% kappa, 20%
|
||
lambda), carra-geenan type II (iota) and cellulose were each fed at levels of 5 and 15% (wt/wt) of the
|
||
diet for 31 d to male Fischer 344 rats. The average initial weight of rats was 230 g. Rats fed 15% guar
|
||
gum gained significantly less weight than most of the other rats (P less than 0.05). Phenol red recovery
|
||
was measured at 2 and 4 wk after the beginning of the experiment. At 2 wk urinary recoveries of phenol
|
||
red were high in rats fed fiber-free and carrageenan type II diets, indicating increased apparent
|
||
permeability. By 4 wk, adaptation had apparently taken place.” “These data are consistent with the
|
||
hypothesis that intestinal permeability to foreign substances may be altered considerably by diet.”
|
||
</p>
|
||
<p>
|
||
Pathologe 1993 Sep;14(5):247-252 [Persorption of microparticles].[Article in German] Volkheimer G
|
||
“Solid, hard microparticles, such as starch granules, pollen, cellulose particles, fibres and crystals,
|
||
whose diameters are well into the micrometre range, are incorporated regularly and in considerable
|
||
numbers from the digestive tract. Motor factors play an important part in the paracellular penetration
|
||
of the epithelial cell layer. From the subepithelial region the microparticles are transported away via
|
||
lymph and blood vessels. They can be detected in body fluids using simple methods: only a few minutes
|
||
after oral administration they can be found in the peripheral blood-stream. We observed their passage
|
||
into urine, bile, cerebrospinal fluid, the alveolar lumen, the peritoneal cavity, breast milk, and
|
||
transplacentally into the fetal blood-stream. Since persorbed microparticles can embolise small vessels,
|
||
this touches on microangiological problems, especially in the region of the CNS. The long-term deposit
|
||
of embolising microparticles which consist of potential allergens or contaminants, or which are carriers
|
||
of contaminants, is of immunological and environmental-technical importance. Numerous ready-made
|
||
foodstuffs contain large quantities of microparticles capable of persorption.”
|
||
</p>
|
||
<p>
|
||
Eur J Pediatr 1993 Jul;152(7):592-594 Oral cornstarch therapy: is persorption harmless? Gitzelmann R,
|
||
Spycher MA ”Sediments prepared from freshly voided urine of four patients with glycogenosis Ia, or
|
||
leucine-sensitive hypoglycaemia, on oral cornstarch therapy contained starch granules, evidence for
|
||
persorption i.e. the incorporation of undissolved starch particles. In these patients, amyluria was more
|
||
marked than in untreated controls. While cornstarch therapy is successful and causes few side-effects,
|
||
the possibility of late adverse reactions to persorbed starch should not be disregarded.”
|
||
</p>
|
||
<p>
|
||
Med Hypotheses 1991 Jun;35(2):85-87 “Persorption of raw starch: a cause of senile dementia? Freedman BJ
|
||
“Intact starch granules in food can pass through the intestinal wall and enter the circulation. They
|
||
remain intact if they have not been cooked for long enough in the presence of water. Some of these
|
||
granules embolise arterioles and capillaries. In most organs the collateral circulation suffices for
|
||
continued function.In the brain, however, neurones may be lost. Over many decades the neuronal loss
|
||
could be of clinical importance. To test this hypothesis, there is a need to examine brains for the
|
||
presence of embolised starch granules. Examining tissues polariscopically clearly distinguishes starch
|
||
granules from other objects of similar appearance.”
|
||
</p>
|
||
<p>
|
||
Kitasato Arch Exp Med 1990 Apr;63(1):1-6 [The Herbst-Volkheimer effect]” [Article in German], Prokop, O.
|
||
“More than 150 years ago the foundations were laid for the so-called HERBST effect which was
|
||
subsequently forgotten. In the sixties the phenomenon was rediscovered by VOLKHEIMER at the Charite
|
||
Hospital in Berlin and then reviewed through many experiments and publications. What is meant by the
|
||
HERBST effect? If an experimental animal or even human being is given a larger amount of maize starch or
|
||
also biscuits or some other products containing starch, starch bodies can be detected rapidly in venous
|
||
blood already after minutes or half an hour later and in the urine after one hour and later. The term
|
||
"persorption" has been coined for this interesting phenomenon. It is indeed surprising that it has met
|
||
with so little attention. As a matter of fact, it constitutes the basis for our understanding of peroral
|
||
immunization and of allergies. In the same way, feeding of carbon particles results in their appearance
|
||
and detection in blood, kidney and urine. The same result is obtained by the intake of diatoms and what
|
||
is even more important with meat fibres. I hope you are aware of the implications. When Professor NAGAI
|
||
stayed in Berlin, we tried to receive the phenomenon. Since only a few cell nuclei are necessary for
|
||
"genetic fingerprinting" we thought that after intake of 200 or 400 g of raw meat the type of food eaten
|
||
could be determined from the urinary sediment by means of the fingerprint method which would be of
|
||
forensic significance. Therefore, we eat meat and raw liver and examined the urinary sediment.”
|
||
</p>
|
||
<p>
|
||
Z Arztl Fortbild (Jena) 1993 Mar 12;87(3):217-221 [The phenomenon of persorption--history and
|
||
facts].[Article in German] Volkheimer G.
|
||
</p>
|
||
<p>
|
||
J Pediatr 1994 Sep;125(3):392-399 Clinical and molecular epidemiology of enterococcal bacteremia in a
|
||
pediatric teaching hospital. Christie C, Hammond J, Reising S, Evans-Patterson J “An apparent increase
|
||
in the in-cidence of enterococcal bacteremias from 7 to 48/1000 bacteremias during 1986 to 1991 (p <
|
||
0.01) prompted this descriptive clinical and molecular epidemiologic study of 83 episodes occurring in
|
||
80 children between 1986 and 1992.” “The increase in enterococcal bacteremias was not due to a clonal
|
||
strain dissemination but to an increase in cases of heterogeneous enterococcal strains. We conclude that
|
||
enterococcal septicemia is now an important cause of serious morbidity and death in critically ill
|
||
children.”
|
||
</p>
|
||
<p>R.F.V. Pulvertaft, PHA in relation to Burkitt's tumour, Lancet sept 12, pp 552-554, 1964.</p>
|
||
<p>K.M. Stevens, The aetiology of SLE, Lancet, Sept. 5, 506-508, 1964.</p>
|
||
<p><hr /></p>
|
||
|
||
<p>Ray Peat's Newsletter</p>
|
||
<p>
|
||
Not for republication without written permission PO Box 5764, Eugene, OR 97405 Raymond PeatJuly, 1995
|
||
</p>
|
||
<p>
|
||
Persorption refers to a process in which relatively large particles pass through the intact wall of the
|
||
intestine and enter the blood or lymphatic vessels. It can be demonstrated easily, but food regulators
|
||
prefer to act as though it didn't exist. The doctrine that polymers--gums, starches, peptides, polyester
|
||
fat substitutes--and other particulate substances can be safely added to food because they are "too
|
||
large to be absorbed" is very important to the food in-dustry and its shills.
|
||
</p>
|
||
<p>
|
||
When the bowel is inflamed, toxins are absorbed. The natural bacterial endotoxin produces many of the
|
||
same inflammatory effects as the food additive, carrageenan. Like inflammatory bowel disease, the
|
||
incidence of liver tumors and cirrhosis has increased rapidly. Liver damage leads to hormonal imbalance.
|
||
Carrageenan produces inflammation and immunodeficiency, synergizing with estrogen, endotoxin and
|
||
unsaturated fatty acids.
|
||
</p>
|
||
<p>
|
||
“Volkheimer found that mice fed raw starch aged at an abnormally fast rate, and when he dissected the
|
||
starch-fed mice, he found a multitude of blocked arterioles in every organ, each of which caused the
|
||
death of the cells that depended on the blood supplied by that arteriole. It isn’t hard to see how this
|
||
would affect the functions of organs such as the brain and heart, even without considering the
|
||
immunological and other implications....”
|
||
</p>
|
||
<p></p>
|
||
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|
||
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