642 lines
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642 lines
48 KiB
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<head><title>Diabetes, scleroderma, oils and hormones</title></head>
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<body>
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<h1>
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Diabetes, scleroderma, oils and hormones
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</h1>
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<p>
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The basic argument: Stress and aging make cells less responsive in many ways by damaging their ability to
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produce energy and to adapt. The polyunsaturated fats are universally toxic to the energy producing system,
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and act as a "misleading signal" channeling cellular adaptation down certain self-defeating pathways.
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Diabetes is just one of the "terminal" diseases that can be caused by the polyunsaturated vegetable oils.
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Coconut oil, in diabetes as in other degenerative diseases, is highly protective.
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</p>
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<p>
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When the oral contraceptive pill was new (Enovid), it was found to produce signs of diabetes, including
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decreased glucose tolerance. Spellacy and Carlson (1966) suggested that an elevation of circulating free
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fatty acids might be responsible, and remarked that "Free fatty acids can block the Krebs cycle, with
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relative insulin action resistance resulting." "The potential danger of the oral contraceptives is one of
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prolonged pancreatic stimulation." Recent papers are reporting that the estrogen used to "treat menopause"
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causes an increase in free fatty acids. Spellacy and Carlson suggested that estrogen's effect was mediated
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by growth hormone, and that is now the consensus. Women are much more likely than men to develop diabetes.
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</p>
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<p>
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Ephraim Racker observed that free unsaturated fatty acids inhibit mitochondrial respiration, and recent
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studies are finding that free linoleic and linolenic acids act as intracellular regulators, stimulating the
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protein kinase C (PKC) system, which is also stimulated by estrogen and the (cancer promoting) phorbol
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esters. They stimulate the cell while blocking the energy it needs to respond.
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</p>
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<p>
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Scleroderma, or systemic sclerosis, is a supposedly mysterious condition in which tissues harden, with an
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excessive deposition of fibrous material. Besides hardening the skin, it can involve fibrosis of the heart
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and other organs, and can cause changes in blood vessels of the kidneys like those seen in some types of
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hypertension, and often involves Raynaud's phenomenon and osteoporosis of the fingers. (Silicone functions
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as an adjuvant, making exposure to irritants, solvents or infections more harmful. This seems to be the
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reason for the association between breast implants and scleroderma.) Another type of disease that involves
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hardening of the skin is scleredema, in which the skin thickens with an accumulation of "mucin" between
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collagen bundles, and in which fibroblasts are overactive in producing collagen. (Varga, et al.) This
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condition is believed to often follow a "febrile illness" and is associated with diabetes. My interest in
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these conditions comes from my awareness that estrogen promotes collagen formation, and that changes in the
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connective tissue are deeply associated with the processes of stress and aging, following the ideas of
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Metchnikov and Selye.
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</p>
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<p>
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Many people are still committed to the various old theories of diabetes, though a few are showing ways in
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which multiple causes can lead to diabetes. Increasingly, old age itself is seen to be "like diabetes
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(Meneilly, et al.; Smith, et al.), and the situation is ripe for a recentering of our understanding of
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diabetes around some of the general facts about aging and stress.
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</p>
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<p>
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Diabetes mellitus, as named, refers to excessive urination and sugary urine, but it is now often diagnosed
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in people who neither urinate excessively nor pass glucose in the urine, on the basis of a high level of
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glucose in the blood. Many other signs (abnormal mucopolysaccharide metabolism with thickening of basement
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membranes, leakage of albumin through capillary walls and into the urine, a high level of free fatty acids
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in the blood, insensitivity of tissues to insulin, or reduced sensitivity of the beta cells to glucose) are
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considered diagnostic by some people, who believe that the worst aspects of the disease can be prevented if
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they can diagnose early and take preventive measures. This attitude derives largely from the genetic theory
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of causation, though it incorporates a belief that (environmental) intervention can ameliorate the course of
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the disease. When I wrote Nutrition for Women, I mentioned that the sudden appearance of diabetes in
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non-European Jews when they moved to Isreal made the genetic theory of diabetes untenable, and since then
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other studies have made the similar point that environmental factors seem crucial. (Shaltout, et al.) Many
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people are arguing for the racial/genetic theory of diabetes, but they are failing to consider some simple
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dietary factors, especially the high consumption of unsaturated seed oils and the combination of nutritional
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deficiencies and environmental stress.
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</p>
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<p>
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I have known adults and children who were diagnosed as diabetic, and given insulin (and indoctrinated with
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the idea that they had a terminal degenerative disease) on the strength of a single test showing excessive
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glucose. When I taught at the naturopathic medical school in Portland, I tried to make it clear that
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"diabetes" (a term referring to excessive urination) is a function, and that a high level of glucose in the
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blood or urine is also a function, and that the use of insulin should require a greater diagnostic
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justification than the use of aspirin for a headache does, because insulin use itself constitutes a serious
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health problem. (And we seldom hear the idea that "diabetes" might have a positive side [Robinson and
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Johnston], for example that it reduces the symptoms of asthma [Vianna and Garcialeme], which get worse when
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insulin is given. Normal pregnancy can be considered "diabetic" by some definitions based on blood sugar. I
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got interested in this when I talked to a healthy "diabetic" woman who had a two year old child whose IQ
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must have been over 200, judging by his spontaneous precocious hobbies. Old gynecologists told me that it
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was common knowledge that "diabetic" women had intellectually precocious children.)
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</p>
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<p>
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When non-diabetic apes were given insulin treatments, they developed some of the same "complications of
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diabetes" that are seen in humans, and antibodies to insulin were found in their retinas, suggesting that
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some "complications of diabetes" were complications of insulin treatment. Patients were seldom well informed
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of the arguments against the use of insulin, but the justification for the new genetically engineered human
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insulin is precisely that it avoids immunological damage.
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</p>
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<p>
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Insulin was introduced into medicine in the 1920s. According to the Britannica Book of the Year for 1947,
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page 265, "Mortality from diabetes in 1920 in the United States was 16.0 per 100,000, 14,062 deaths, but in
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1944, it was 26.4 per 100,000, 34,948 deaths."
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</p>
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<p>
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One of the theories of the cause of diabetes is that a virus damages the beta cells in the pancreas, and the
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main argument for that in the 1970s was that the onset of diabetes in children can often be dated to a time
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shortly after a severe viral infection. It is true that intense sickness and a high fever (and high doses of
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drugs given to treat the sickness) can cause very high levels of glucose in the blood, and even glucose in
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the urine, but this is a fairly well recognized consequence of stress. High doses of cortisone (prednisone,
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etc.) typically cause elevated glucose levels. Cushing's syndrome usually involves hyperglycemia. Normally,
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this is just a functional response to an excess of glucocorticoids, but studies in dogs suggested that
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intense and/or prolonged stress can damage the insulin-secreting cells in the pancreas. Dogs had half of
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their pancreas removed, to increase the burden put on the remaining tissue, and after a large dose of
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cortisone the dogs became (and remained) diabetic.
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</p>
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<p>
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One of the problems associated with diabetes is the calcification of blood vessels, though now there is more
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emphasis on fatty degeneration. Other blood vessel problems include hypertension, and poor circulation in
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general, leading to gangrene of the feet, impotence, and degeneration of the retina. In muscles, and
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probably in other tissues of diabetics, capillaries are more widely spaced, as if the basal oxidative
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requirement were lower than normal. However, mitochondria contain more respiratory enzymes, as if to partly
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compensate for the poor delivery of oxygen to the cells. Osteoporosis or osteopenia is a common complication
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of diabetes, and seems to be associated with the calcification of soft tissues.
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</p>
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<p>
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F. Z. Meerson's description of the stress-injured heart is very similar to the general changes that occur in
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chronic diabetes. He found that the stressed heart becomes rigid and unable to contract completely, or to
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relax completely. Excess calcium enters cells, and fatty acids are mobilized both locally and systemically,
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and both of these tend to damage the mitochondria. In diabetes, fatty acids are mobilized and oxidized
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instead of glucose, and calcium enters cells, increasing their rigidity and preventing relaxation of muscles
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in blood vessels. (I'm not sure whether it is relevant to cell physiology, but the presence of an excess of
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free unsaturated fatty acids, and of calcium, in cells makes me think of the insoluble soap that these
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substances form in other situations, including the intestine. It seems that this could form a harmful
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deposit in cells, blocking many metabolic processes.)
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</p>
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<p></p>
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<p>
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For many years, histologists have observed that calcium and iron tend to be deposited together in
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"devitalized" tissues. Now we know that cell death from a great variety of causes involves the cell's
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absorption of increased amounts of calcium. Simply the lack of energy increases the amount of calcium in a
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cell, and stimulation or excitation does the same, creating or exaggerating a deficiency of energy. In low
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thyroid people, many (if not all) tissues are very easily damaged. Since glucose is needed by liver cells to
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produce the active (T3) form of thyroid, diabetes almost by definition will produce hypothyroidism, since in
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diabetes glucose can't be absorbed efficiently by cells.
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</p>
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<p>
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In the form of cell damage caused by the "excitotoxins," glutamic and aspartic acids, the damage seems to
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require both stimulation, and difficulty in maintaining adequate energy production. This combination leads
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to both calcium uptake and lipid peroxidation. When cells are de-energized, they tend to activate iron by
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chemical reduction, producing lipid peroxidation. This could explain the presence of chemically active iron,
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but an actual increase in the iron concentration suggests that there has been prolonged injury (oxidative
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stress) to the cell, with increased production of the heme group, which binds iron.
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</p>
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<p>
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Hans Selye found that he could produce scleroderma (hardening and calcification of the skin) in rats by
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giving them a toxic dose of a heavy metal, and then irritating the skin a little by plucking hair. Iron is
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now tending to be recognized as a factor in inflammation. Vitamin E was able to prevent the development of
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scleroderma under Selye's experimental conditions, suggesting that the irritation allowed the heavy metal to
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cause oxidative damage to the skin. Selye found other ways to cause calcification of tissues, including the
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walls of arteries, but he directed most of his attention to the role of "pro-inflammatory" hormones. A
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decreased blood supply was often used to predispose an organ to calcification. In diabetes, a characteristic
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feature is that the blood supply is relatively remote from cells in muscle and skin, so the oxygen and
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nutrients have to diffuse farther than in normal individuals, and the ATP level of cells is
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characteristically lower than normal. In blood cells, both red (Garnier, et al.) and white cells are
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probably more rigid in diabetes, because of lower ATP production, and higher intracellular calcium and
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sodium.
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</p>
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<p>
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Magnesium in the cell is largely associated with ATP, as the complex Mg-ATP. When ATP is "used" or converted
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to ADP, this lower-energy substance associates with calcium, as Ca-ADP. In a hypothyroid state, the energy
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charge can be depleted by stress, causing cells to lose magnesium. ATP is less stable when it isn't
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complexed with magnesium, so the stress-induced loss of magnesium makes the cell more susceptible to stress,
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by acting as a chronic background stimulation, forcing the cell to replace the ATP which is lost because of
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its instability. In this state, the cell takes up an excess of calcium.
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</p>
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<p>
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The picture that I think explains many of the features of diabetes is that an energy deficit produces an
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alarm state, causing increased production of adrenalin and cortisol. Adrenalin mobilizes fat from storage,
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and the free fatty acids create a chronic problem involving 1) blocked ATP production, 2) activation of the
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protein kinase C system (increasing tension in blood vessels), 3) inhibition of thyroid function with its
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energetic, hormonal, and tissue-structure consequences, 4) availability of fats for prostaglandin synthesis,
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and 5) possibly a direct effect on clot dissolving, besides the PAI-1 (plasminogen activator inhibitor)
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effect seen in diabetes (Ceriello, et al., Udvardy, et al., Vague, et al.). (Estrogen has many pro-clotting
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effects, and one of them is a decreased activity of vascular plasminogen activator. K. E. Miller and S. V.
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Pizzo, "Venous and arterial thromboembolic disease in women using oral contraceptives," Am. J. Obst. Gyn.
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144, 824, 1982. In 1968, D. G. Daniel et al., reported that estrogen promotes thromboembolism by increasing
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clotting factor IX in the blood.)
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</p>
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<p>
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Increased entry of calcium into cells is complexly related to increased exposure to unsaturated fatty acids,
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decreased energy, and lipid peroxidation. Osteoporosis, calcification of soft tissues and high blood
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pressure are promoted by multiple stresses, hypothyroidism, and magnesium deficiency. The particular
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direction a disease takes--diabetes, scleroderma, lupus, Alzheimer's, stroke, etc.--probably results from
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the balance between resources and demands within a particular organ or system. Calcium overload of cells
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can't be avoided by avoiding dietary calcium, because the bones provide a reservoir from which calcium is
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easily drawn during stress. (In fact, the reason calcium can temporarily help prevent muscle cramps seems to
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be that it makes magnesium more available to the muscles.)
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</p>
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<p>
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If we want to stop a disease that involves abnormal calcification or contraction of muscle (see Zenere, et
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al.), we can increase our consumption of magnesium, and to cause cells to absorb and retain the magnesium,
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we can increase our thyroid function. The use of coconut oil provides energy to stabilize blood sugar while
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protecting mitochondria and the thyroid system from the harmful effects of unsaturated fats.
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</p>
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<p>
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In 1947, B. A. Houssay found that a diet based on sugar as a source of energy was more protective against
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diabetes than a diet based on lard, while the most protective diet was based on coconut oil. Lard reflects
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the pigs' diet, and is usually extremely unsaturated, especially since it became standard to fatten them on
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soybeans and corn. Essentially, his study seems to show that unsaturated (pork) fat permits diabetes to
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develop, sugar is slightly protective, and coconut oil is very protective against the form of diabetes
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caused by a poison.
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</p>
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<p>
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At the same time, A. Lazarow was demonstrating that a low protein diet made animals more sensitive to
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diabetes, and that cysteine, glutathione, and thioglycolic acid (antioxidants) are protective against
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diabetes. The chelator of metals, BAL (British anti-lewisite), was also found to protect against diabetes.
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</p>
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<p>
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Taken together, those studies suggest that the oxidizable unsaturated fats are involved in the process of
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producing diabetes. At the same time, other studies were showing that the unsaturated oils suppress the
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thyroid, and that coconut oil increases the metabolic rate, apparently by normalizing thyroid function.
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Hypothyroidism is known to include deposition of mucopolysaccharides in tissues, increased permeability of
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capillaries with leakage of albumin out of the blood, elevated adrenalin which can lead to increased
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production of cortisol, decreased testosterone production, high risk of heart and circulatory disease,
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including a tendency to ulceration of the extremities, and osteoporosis, all of which are recognized
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"complications of diabetes." Broda Barnes gave all of his diabetic patients a thyroid supplement, and found
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that none of them developed the expected complications of diabetes.
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</p>
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<p>
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Recently, a high safflower oil diet was found to cause diabetes (Ikemoto, et al.), and obesity itself is
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thought to be a factor in developing diabetes. The hormone patterns associated with obesity can be seen as
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either cause or effect of the obesity (or both cause and effect), since, for example, low thyroid can
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increase both estrogen and cortisol, which support the formation of fat, and the fat cells can become a
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chronic source of estrogen synthesis.
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</p>
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<p>
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On a diet lacking the "essential" unsaturated fatty acids, Benhamou (1995) found that nonobese diabetic mice
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didn't develop diabetes, that is, the unsaturated fats themselves, without obesity, are sufficient to cause
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diabetes. (Also see Girard; Golay, et al., and Kusunoki, et al.)
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</p>
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<p>
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Estrogen and the polyunsaturated fatty acids (PUFA), linoleic and linolenic acid, alike activate the protein
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kinase C (PKC) system of cellular activation. Many of the functions of PUFA are similar to the functions of
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estrogen (e.g., antagonism to thyroid function, promotion of age pigment/lipofuscin), so this information
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showing that they both act similarly on the same basic regulatory pathway is important. Estrogen increases
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secretion of growth hormone (GH; it's closely associated with prolactin, also increased by estrogen), and GH
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causes an increase in free fatty acids in the blood. Estrogen promotes iron retention, so it sets the stage
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for oxidative stress. At least in some systems, both estrogen and PUFA promote the entry of calcium into the
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cell.
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</p>
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<p>
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In diabetes, there is a generalized excess activation of the PKC system. The starch-based diet, emphasizing
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grains, beans, nuts, and vegetables, has been promoted with a variety of justifications. When people are
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urged to reduce their fat and sugar consumption, they are told to eat more starch. Starch stimulates the
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appetite, promotes fat synthesis by stimulating insulin secretion, and sometimes increases the growth of
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bacteria that produce toxins. It is often associated with allergens, and according to Gerhard Volkheimer,
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whole starch grains can be "persorbed" from the intestine directly into the blood stream where they may
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block arterioles, causing widely distributed nests of cell-death. I have heard dietitians urge the use of
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"complex carbohydrates" (starch) instead of sugar. In the first physiology lab I took, we fed rats a large
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blob of moist cornstarch with a stomach tube, and then after waiting a few minutes, were told to dissect the
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rat to find out "how far the starch had gone." In such a short time, we were surprised to find that not a
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trace of the starch could be found. The professor's purpose was to impress us with the rapidity with which
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starch is digested and absorbed. Various studies have demonstrated that starch (composed of pure glucose)
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raises blood glucose more quickly than sucrose (half fructose, half glucose) does. The sudden increase of
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blood glucose is sometimes thought to contribute to the development of diabetes, but if it does, it is
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probably mediated by fat metabolism and the hormones other than just insulin.
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</p>
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<p>
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Brewer's yeast has been used successfully to treat diabetes. In the l930s, my father had severe diabetes,
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but after a few weeks of living on brewer's yeast, he recovered and never had any further evidence of
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diabetes. Besides its high B-vitamin and protein content, yeast is an unusual food that should be sparingly
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used, because of its high phosphorous/calcium ratio, high potassium to sodium ratio, and high estrogen
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content. The insulin-producing beta cells of the pancreas have estrogen receptors, but I don't know of any
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new research investigating this aspect of yeast therapy. In rabbit studies, diabetes produced by alloxan
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poisoning, which kills the beta cells, was cured by DHEA treatment, and beta cells were found to have
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regenerated in the pancreatic islets.
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</p>
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<p>
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I think the basic anti-aging diet is also the best diet for prevention and treatment of diabetes,
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scleroderma, and the various "connective tissue diseases." This would emphasize high protein, low
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unsaturated fats, low iron, and high antioxidant consumption, with a moderate or low starch consumption. In
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practice, this means that a major part of the diet should be milk, cheese, eggs, shellfish, fruits and
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coconut oil, with vitamin E and salt as the safest supplements. It should be remembered that amino acids,
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especially in eggs, stimulate insulin secretion, and that this can cause hypoglycemia, which in turn causes
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cortisol secretion. Eating fruit (or other carbohydrate), coconut oil, and salt at the same meal will
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decrease this effect of the protein. Magnesium carbonate and epsom salts can also be useful and safe
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supplements, except when the synthetic material causes an allergic bowel reaction..
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</p>
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<p>
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Although I started this newsletter with the thought of discussing the Mead acids--the unsaturated (n-9) fats
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that are formed under certain conditions, especially when the dietary polyunsaturated fatty acids are
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"deficient"--and their prostaglandin derivatives as a distinct anti-stress, anti-aging system, the loss of
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which makes us highly susceptible to injury, I will save that argument for a future time, leaving this
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newsletter as an addition to the view that an excess of the polyunsaturated fats is central to the
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development of degenerative diseases: Cancer, heart disease, arthritis, immunodeficiency, diabetes,
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hypertension, osteoporosis, connective tissue disease, and calcification.
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</p>
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<p>
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<strong><h3>
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REFERENCES WITH EXCERPTS AND COMMENTS
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</h3></strong>
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</p>
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<p>
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A. A. Alzaid, et al., "Effects of insulin on plasma magnesium in noninsulin-dependent diabetes mellitus:
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Evidence for insulin resistance," J. of Clin. Endocr. and Metab. 80(4), 1376-1381, 1995. "...insulin
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resistance in subjects with NIDDM impairs the ability of insulin to stimulate magnesium as well as glucose
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uptake."
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</p>
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<p>
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A. B. Akella, et al., "Diminished Ca++ sensitivity of skinned cardiac muscle contractility coincident with
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troponin T-band shifts in the diabetic rat," Circulation Research 76(4), 600-606, 1995.D. A. Antonetti, et
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al., "Increased expression of mitochondrial-encoded genes in skeletal muscle of humans with diabetes
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mellitus--Rapid publication," J. of Clinical Investigation 95(3), 1383-1388, 1995. "The increased
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mitochondrial gene expression may contribute to the increase in mitochondrial respiration observed in
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uncontrolled diabetes." (Low ATP with high respiration would suggest uncoupling; unsaturated fatty acids are
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known uncouplers of respiration from energy production.)
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</p>
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<p>
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S. Asakuma, et al., "The effects of antianginal drugs on energy expernditure during exercise in normal
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subjects," Japanese Circulation Journal--English Edition 59(3), 137-145, 1995. "RQ (carbohydrate consumption
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relative to fat consumption) during exercise was significantly increased and VO2 was decreased after
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propranolol, metoprolol and amosulalol." "These data suggest that propranolol, metoprolol and amosulalol
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[beta-blockers] increase the efficiency of energy expenditure during ordinary physical activity by
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increasing the utilization of carbohydrate and by decreasing the utilization of fat."
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</p>
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<p>
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M. Bardicef, et al., "Extracellular and intracellular magnesium depletion in pregnancy and gestational
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diabetes," Amer. J. of Obst. and Gyn. 172(3), 1009-1013, 1995.
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</p>
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<p>
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P. E. Beales, et al., "Baclofen, a gamma-aminobutyric acid-b receptor agonist, delays diabetes onset in the
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non-obese diabetic mouse," Acta Diabetologica 32(1), 53-56, 1995.
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</p>
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<p>
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P. Y. Benhamou, et al., :"Essential fatty acid deficiency prevents autoimmune diabetes in nonobese diabetic
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mice through a positive impact on antigen-presenting cells and Th2 lymphocytes," Pancreas 11(1), 26-37,
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1995.
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</p>
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<p>
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C. D. Berdanier, "Diet, autoimmunity, and insulin-dependent diabetes mellitus: A controversy," Proc. Soc.
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Exp. Biol. Med. 209(3), 223-230, 1995. "The majority of the genetic mutations that result in the phenotypic
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expression of the insulin-dependent diabetes mellitus genotype are in the immune system." Antibodies to milk
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protein can be found in the patient, but these probably represent antigen mimicry, resulting from the loss
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of antibody specificity which is a feature of autoimmune disease.
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</p>
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<p>
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G. Bianchi, et al., "Thyroid volume in type 1 diabetes patients without overt thyroid disease," Acta
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Diabetologica 32(1), 49-52, 1995. "An association between insulin-dependent diabetes mellitus (type 1) and
|
|
thyroid diseases has long been reported...."
|
|
</p>
|
|
<p>
|
|
P. Bjorntorp, "Insulin resistance: The consequence of a neuroendocrine disturbance?" Int. J. Obes. 19(Suppl.
|
|
1), S6-S10, 1995. "The decreased capillary density may...be of importance for the apparent insulin
|
|
resistance."
|
|
</p>
|
|
<p>
|
|
R. Bouillon, et al., "Influence of age, sex, and insulin on osteoblast function: Osteoblast dysfunction in
|
|
diabetes mellitus," J. of Clin. Endocr. and Metab. 80(4), 1194-1202, 1995. "...the osteoblast function is
|
|
significantly decreased in diabetic patients...."
|
|
</p>
|
|
|
|
<p>
|
|
A. Ceriello, et al., "The defence against free radicals protects endothelial cells from
|
|
hyperglycaemia-induced plasminogen activator inhibitor 1 over-production," Blood Coagulation &
|
|
Fibrinolysis 6(2), 133-137, 1995. "The hypothesis that oxidative stress may play an important role in the
|
|
pathogenesis of diabetic complications is ... supported by this study." [GSH reduced PAI-1.]
|
|
</p>
|
|
<p>
|
|
V. Coiro, et al., "Low-dose ovine corticotropin-releasing hormone stimulation test in diabetes mellitus with
|
|
or without neuropathy," Metabolism--Clinical and Experimental 44(4), 538-542, 1995. "...basal and
|
|
CRH-induced cortisol levels were significantly higher in diabetics than in normal controls." "...even
|
|
uncomplicated diabetes mellitus is associated with adrenal hyperfunction."
|
|
</p>
|
|
|
|
<p>
|
|
S. R. Colberg, et al., "Skeletal muscle utilization of free fatty acids in women with visceral obesity," J.
|
|
Clin. Invest. 95(4), 1846-1853, 1995. "Visceral obesity is strongly associated with insulin resistance."
|
|
"...visceral adiposity is clearly associated with skeletal muscle insulin resistance but this is not due to
|
|
glucose-FFA [free fatty acid] substrate competition. Instead, women with visceral obesity have reduced
|
|
postabsorptive FFA utilization by muscle."
|
|
</p>
|
|
<p>
|
|
G. A. Colditz, et al., "Weight gain as a risk factor for clinical diabetes mellitus in women," Annals of
|
|
Internal Medicine 122(7), 481-486, 1995.
|
|
</p>
|
|
<p>
|
|
C. Douillet and M. Ciavatti, "Effect of vitamin E treatment on tissue fatty acids and cholesterol content in
|
|
experimental diabetes," J. Nutr. Biochem. 6(6), 319-326, 1995. "Diabetes induced a decrease of
|
|
monounsaturated fatty acids and particularly palmitoleic acid in all studied tissues: liver, aorta, plasma."
|
|
C18:3 n-6 and C20:4 n-6 were increased by diabetes.
|
|
</p>
|
|
<p>
|
|
M. Garnier, et al., "Red blood cell sodium conent in NID diabetic patients with hemorheological
|
|
abnormalities," Clinical Hemorheology 15(3), 325-333, 1995.
|
|
</p>
|
|
<p>
|
|
K. D. Gerbitz, et al., "Mitochondrial diabetes mellitus: A review," BBA--Mol. Basis Dis. 1271(1), 253-260,
|
|
1995. This particular kind of diabetes, which is combined with deafness in 60% of the patients, involves a
|
|
variant mitochondrial gene and occurs in about 1.5% of diabetics. "The underlying pathomechanism is probably
|
|
a delayed insulin secretion due to an impaired mitochondrial ATP production in consequence of the mtDNA
|
|
defect." To know the "causal" value of this gene we have to know how often it occurs in people who never
|
|
develop diabetes. It is interesting that it is suggested to operate by way of impaired ATP production, which
|
|
can be the result of so many factors, such as excess unsaturated fats, low thyroid, low magnesium, low
|
|
copper, etc. Pages 141-151 of the same journal as an article by D. C. Wallace, et al., "Mitochondrial DNA
|
|
mutations in human degenerative diseases and aging," which makes the point that "Generally, individuals
|
|
inheriting these mitochondrial diseases are relatively normal in early life, develop symptoms during
|
|
childhood, mid-life, or old age depending on the severity of the ... mutation; and then undergo a
|
|
progressive decline." Their energy-producing systems are supposedly more susceptible to the effects of
|
|
aging.
|
|
</p>
|
|
|
|
<p>
|
|
J. Girard, "Role of free fatty acids in insulin resistance of subjects with non-insulin-dependent diabetes,"
|
|
Diabetes Metab. 21(2), 79-88, 1995. "Studies performed in the rat suggest that impaired glucose-induced
|
|
insulin secretion could also be related to chronic exposure of pancreatic beta cells to elevated plasma free
|
|
fatty acid levels." [This direct effect of free fatty acids on the beta cells is extremely important.
|
|
Estrogen--probably via GH--increases free fatty acids, and adrenalin--which is elevated in
|
|
hypothyroidism--increases the release of free fatty acids from storage. Free fatty acids impair
|
|
mitochondrail energy production.]
|
|
</p>
|
|
<p>
|
|
A. Golay, et al., "Effect of lipid oxidation on the regulation of glucose utilization in obese patients,"
|
|
Acta Diabetologica 32(1), 44-48, 1995. [Free fatty acids strongly and quickly depress the ability to oxidize
|
|
or store glucose.]
|
|
</p>
|
|
<p>
|
|
A. Gomes, et al., "Anti-hyperglycemic effect of black tea (Camellia sinensis) in rat," J. of
|
|
Ethnopharmacology 45(3), 223-226, 1995. It "was found to possess both preventive and curative effects on
|
|
experimentally produced diabetes in rats."
|
|
</p>
|
|
<p>
|
|
Y. Hattori, et al., "Phorbol esters elicit Ca++-dependent delayed contractions in diabetic rat aorta," Eur.
|
|
J. Pharmacol. 279(1), 51-58, 1995. [Diabetic tissue is more responsive to activation of protein kinase C by
|
|
phorbol esters.]
|
|
</p>
|
|
<p>
|
|
B. A. Houssay and C. Martinez, "Experimental diabetes and diet," Science 105, 548-549, 1947. [Mortality was
|
|
zero on the high coconut oil diet, 100% on the high lard diet. It was 90% on the low protein diet, and 33%
|
|
on the high protein diet. With a combination of coconut oil and lard, 20%.]
|
|
</p>
|
|
<p>
|
|
B. A. Houssay, et al., "Accion de la administracion prolongada de glucosa sobre la diabetes de la rata,"
|
|
Rev. Soc. argent. de biol. 23, 288-293, 1947.
|
|
</p>
|
|
<p>
|
|
S. Ikemoto, et al., "High fat diet-induced hyperglycemia: Prevention by low level expression of a glucose
|
|
transporter (GLUT4) minigene in transgenic mice," Proc. Nat. Acad. Sci. USA 92(8), 3096-3099, 1995. "...mice
|
|
fed a high-fat (safflower oil) diet develop defective glycemic control, hyperglycemia, and obesity."
|
|
</p>
|
|
<p>
|
|
M. Inaba, et al., "Influence of high glucose on 1,25-dihydroxyvitamin D-3-induced effect on human
|
|
osteoblast-like MG-63 cells," J. Bone Miner. Res. 10(7), 1050-1056, 1995.
|
|
</p>
|
|
<p>
|
|
J. S. Jensen, et al., "Microalbuminuria reflects a generalized transvascular albumin leakiness in clinically
|
|
healthy subjects," Clin. Sci. 88(6), 629-633, 1995.
|
|
</p>
|
|
<p>
|
|
G. Jorneskog, et al., "Skin capillary circulation severely impaired in toes of patients with IDDM, with and
|
|
without late diabetic complications," Diabetologia 38(4), 474-480, 1995.
|
|
</p>
|
|
<p>
|
|
A. M. Kahn and T. Song, "Insulin inhibits dog vascular smooth muscle contraction and lowers Ca++[i] by
|
|
inhibiting Ca++ influx," J. of Nutrition 125(6 Suppl.), S1732-S1737, 1995.
|
|
</p>
|
|
<p>
|
|
F. Kuhlencordt, et al., "Examination of the skeleton in diabetic patients up to age 45," Deutsche med.
|
|
Wchnschr. 91, 1913-1917, 1966. "Some patients have a generalized osteoporosis-like process, and some have
|
|
localized bone lesions...."
|
|
</p>
|
|
<p>
|
|
M. Kusunoki, et al., "Amelioration of high fat feeding-induced insulin resistance in skeletal muscle with
|
|
the antiglucocorticoid RU486," Diabetes 44(6), 718-720, 1995. "These results suggest that glucocorticoids
|
|
play, in a tissue-specific manner, a role in the maintenance and/or production of insulin resistance
|
|
produced by high-fat feeding."
|
|
</p>
|
|
<p>
|
|
A. Lazarow, "Protection against alloxan diabetes," Anat. Rec. 97, 353, 1947.
|
|
</p>
|
|
<p>
|
|
A. Lazarow, "Protective effect of glutathione and cysteine against alloxan diabetes in the rat," Proc. Soc.
|
|
Exp. Biol. & Med. 61, 441-447, 1946. [While certain doses of cysteine, glutathione, and thioglycolic
|
|
acid completely prevented alloxan diabetes, it was interesting that all of the rats receiving ascorbic acid
|
|
became diabetic. To me, this argues for the free radical cause of diabetes, rather than just the sulfhydryl
|
|
oxidation. Lazarow suggested that succinic dehydrogenase, and various other sulfhydryl enzymes, including
|
|
those involved in fatty acid oxidation, might be involved.]
|
|
</p>
|
|
<p>
|
|
R. B. Lipton and J. A. Fivecoate, "High risk of IDDM in African-American and Hispanic children in Chicago,
|
|
1985-1990," Diabetes Care 18(4), 476-482, 1995. "The relatively early age at onset may point to an
|
|
environmental factor associated with this high incidence of the disease."
|
|
</p>
|
|
<p>
|
|
G. S. Meneilly, et al., "Insulin-mediated increase in blood flow is impaired in the elderly," J. Clin.
|
|
Endocrinol. Metab. 80(6), 1899-1903, 1995. "Normal aging is characterized by resistance to insulin-mediated
|
|
glucose uptake."
|
|
</p>
|
|
<p>
|
|
J. Ma, et al., "Associations of serum and dietary magnesium with cardiovascular disease, hypertension,
|
|
diabetes, insulin, and carotid arterial wall thickness: The ARIC study," J. Clin. Epidemiol. 48(7), 927-940,
|
|
1995. [Carotid wall thickness increased in women as serum Mg level decreased.]
|
|
</p>
|
|
<p>
|
|
Y. Matsumoto, et al., "Creatine kinase kinetics in diabetic cardiomyopathy," Amer. J. Physiol.-Endocrinol.
|
|
Met. 31(5), E1070-E1076, 1995.
|
|
</p>
|
|
<p>
|
|
F. Mercure and G. Vanderkraak, "Inhibition of gonadotropin-stimulated ovarian steroid production by
|
|
polyunsaturated fatty acids in teleost fish," Lipids 30(6), 547-554, 1995. "The inhibitory actions by PUFAs
|
|
were not restricted to long-chain PUFAs, as linoleic and linolenic acids had similar actions in the
|
|
goldfish. The inhibitory action of EPA on testosterone production was reversible upon removal of the PUFA
|
|
from medium." "[Stimulated] ...testosterone production ... was attenuated by PUFAs...."
|
|
</p>
|
|
|
|
<p>
|
|
H. Mulder, et al., "Non-parallelism of islet amyloid polypeptide (amylin) and insulin gene expression in rat
|
|
islets following dexamethasone treatment," Diabetologia 38(4), 395-402, 1995.
|
|
</p>
|
|
<p>
|
|
S. Nagasaka, et al., "Effect of glycemic control on calcium and phosphorus handling and parathyroid hormone
|
|
level in patients with non-insulin-dependent diabetes mellitus," Endocr. J. 42(3), 377-383, 1995.
|
|
"...hyperglycemia causes excess urinary calcium and phosphorus excretion in patients with NIDDM. In response
|
|
to urinary calcium loss, PTH secretion is mildly stimulated. Bone formation seems to be suppressed in the
|
|
hyperglycemic state in spite of increased PTH secretion." [These are the changes I would expect to see in
|
|
hypothyroid people with high cortisol.]
|
|
</p>
|
|
<p>
|
|
B. Oztas and M. Kucuk, "Influence of acute arterial hypertension on blood-brain barrier permeability in
|
|
streptozocin-induced diabetic rats," Neuroscience Letters 188(1), 53-56, 1995.
|
|
</p>
|
|
|
|
<p>
|
|
S. Phillips, et al., "Neuropathic arthropathy of the spine in diabetes," Diabetes Care 18(6), 876-869, 1995.
|
|
</p>
|
|
<p>
|
|
J. F. Pouliot and R. Beliveau, "Palmitoylation of the glucose transporter in blood-brain barrier
|
|
capillaries," Bioch. et Bioph. Acta--Biomembranes 1234(2), 191-196, 1995. "Palmitoylation may be involved in
|
|
the regulation of glucose transport activity in hyperglycemia."
|
|
</p>
|
|
<p>
|
|
R. Ramakrishnan and A. Namasivayam, "Norepinephrine and epinephrine levels in the brain of alloxan diabetic
|
|
rats," Neuroscience Letters 186(2-3), 200-202, 1995. [Epinephrine increased in striatum, hippocampus and
|
|
hypothalamus, Norepinephrine increased in hypothalamus and decreased in pons and medulla.]
|
|
</p>
|
|
<p>
|
|
J. G. Regensteiner, et al., "Effects of non-insulin-dependent diabetes on oxygen consumption during
|
|
treadmill exercise," Med. Sci. Sports Exerc. 27(6), 874-881, 1995. "The reduced rate of increase in oxygen
|
|
consumption during increasing submaximal work loads in NIDDM suggests that limitations in oxygen delivery
|
|
may impair exercise performance in otherwise healthy persons with diabetes."
|
|
</p>
|
|
<p>
|
|
A. A. Shaltout, et al., "High incidence of childhood-onset IDDM in Kuwait," Diabetes Care 18(7), 923-927,
|
|
1995. The incidence of IDDM in children is high in the region and has apparently increased nearly fourfold
|
|
in the last decade. This is especially significant, since diabetes that appears in childhood is especially
|
|
important for the theory of genetic causation. This study should give the gene people real trouble. They
|
|
might have to call in the "gene for bed-wetting" people to help with their case.
|
|
</p>
|
|
|
|
<p>
|
|
M. A. Smith, et al., "Radical AGEing in Alzheimer's disease," Trends in Neurosciences 18(4), 172-176, 1995.
|
|
</p>
|
|
<p>
|
|
A. Tchernof, et al., "Relation of steroid hormones to glucose tolerance and plasma insulin levels in men:
|
|
Importance of visceral adipose tissue," Diabetes Care 28(3), 292-299, 1995.
|
|
</p>
|
|
<p>
|
|
A. Tchernof, et al., "Reduced testosterone and adrenal C-19 steroid levels in obese men," Metabolism--Clin.
|
|
and Exp. 44(4), 513-519, 1995. "...reduced concentrations of testosterone and adrenal C-19 steroid
|
|
precursors are associated with increased body fatness rather than with excess visceral fat accumulation."
|
|
[These results] "...emphasize the importance of adrenal steroids as correlates of body composition in men."
|
|
</p>
|
|
|
|
<p>
|
|
B. G. Trumper, et al., "Circadian variation of insulin requirement in insulin dependent diabetes
|
|
mellitus--The relationship between circadian change in insulin demand and diurnal patterns of growth
|
|
hormone, cortisol and glucagon during euglycemia," Hormone and Metabolic Research 27(3), 141-147, 1995. "The
|
|
results of the study showed that the early morning rise in the insulin demand is related to the increased
|
|
early morning cortisol secretion and to the nocturnal peaks of growth hormone concentration."
|
|
</p>
|
|
<p>
|
|
M. Udvardy, et al., "Altered lysis resistance of platelet-rich clots in patients with insulin-dependent
|
|
diabetes mellitus," Thromb. Res. 79(1), 57-63, 1995. Suppression of clot-dissolving "...was remarkably
|
|
stronger in IDDM, along with the highest PAI-1 activity concentration ratio of the platelet lysates,
|
|
compared to plasmatic levels."
|
|
</p>
|
|
<p>
|
|
P. Vague, et al., "Hypofibrinolysis and the insulin resistance syndrome," Int. J. Obes. 19(Suppl. 1),
|
|
S11-S15, 1995. Hypofibrinolysis is observed among obese subjects and it has been shown that an excess of
|
|
plasminogen activator inhibitor 1 (PAI 1) the main regulator of the fibrinolytic system, is closely
|
|
associated to other components of the insulin resistance syndrome, namely, excessive body weight, high waist
|
|
to hip ratio, elevated blood pressure, hyperinsulinemia and hypertriglyceridemia."
|
|
</p>
|
|
|
|
<p>
|
|
E. O. Vianna and J. Garcialeme, "Allergen-induced airway inflammation in rats: Role of insulin," American J.
|
|
of Respiratory and Critical Care Med. 151(3), 809-814, 1995. "Clinical asthma appears to be less severe when
|
|
diabetes mellitus is superimposed."
|
|
</p>
|
|
<p>
|
|
A. Warley, et al., "Capillary surface area is reduced and tissue thickness from capillaries to myocytes is
|
|
increased in the left ventricle of streptozotocin-diabetic rats," Diabetologia 38(4), 413-421, 1995.
|
|
</p>
|
|
<p>
|
|
G. C. Weir, "Which comes first in non-insulin-dependent diabetes mellitus: Insulin resistance or beta-cell
|
|
failure? Both come first," JAMA 273(23), 1878-1879, 1995.
|
|
</p>
|
|
|
|
<p>
|
|
N. R. Williams, et al., "Plasma, granulocyte and mononuclear cell copper and zinc in patients with diabetes
|
|
mellitus," Analyst 120(3), 887-890, 1995. "...the copper and zinc status of these diabetic patients was
|
|
reduced, providing further evidence of a role for these antioxidant" trace elements in this disease.
|
|
</p>
|
|
<p>
|
|
T. Yamakawa, et al., "Augmented production of tumor necrosis factor-alpha in obese mice," Clinical
|
|
Immunology and Immunopathology 75(1), 51-56, 1995. "...the TNF-alpha derived from adipose tissues might be
|
|
involved in the induction of peripheral insulin resistance..."
|
|
</p>
|
|
<p>
|
|
T. Yamashita, et al., "Increased transendothelial permeation of albumin by high glucose concentration,"
|
|
Metabolism 44(6), 739-744, 1995.
|
|
</p>
|
|
<p>
|
|
M. B. Zemel, "Insulin resistance vs. hyperinsulinemia in hypertension: Insulin regulation of Ca++ transport
|
|
and Ca++-regulation of insulin sensitivity," Journal of Nutrition 125(6 Suppl.), S1738-S1743, 1995.
|
|
</p>
|
|
<p>
|
|
B. M. Zenere, et al., "Noninvasive detection of functional alterations of the arterial wall in IDDM patients
|
|
with and without microalbuminuria," Diabetes Care 18(7), 975-982, 1995. [There is a reduced vasodilatory
|
|
capacity in diabetes, and especially in patients who are leaking albumin.]
|
|
</p>
|
|
<p>
|
|
D. B. Zilvermit, et al., "Oxidation of glucose labelled with radioactive carbon by normal and
|
|
alloxandiabetic rats," J. Biol. Chem. 176, 389-400, 1948. [Diabetic rats had the same rate of glucose
|
|
oxidation as normal rats, in this experiment. This is an artificial form of diabetes that doesn't
|
|
immediately involve an excess of unsaturated fatty acids, as occurs during stress, estrogen excess,
|
|
hypothyroidism, or diets high in polyunsaturated fats which can cause a more "natural" kind of diabetes. The
|
|
artificial alloxandiabetes forces the animal to oxidize an excess of fatty acids, and eventually should lead
|
|
to the same kind of mitochondrial damage seen in natural diabetes.]
|
|
</p>
|
|
|
|
<p>
|
|
© Ray Peat 2006. All Rights Reserved. www.RayPeat.com
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|
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