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360 lines
39 KiB
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<strong>
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Glucose and sucrose for diabetes</strong>
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</p>Diabetes has been known since ancient times as a wasting disease in which sugar was lost in the urine, but
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more recently the name has been used to describe the presence of more than the normal amount of glucose in the
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blood, even in the absence of glucose in the urine. Some of the medical ideas regarding the original form of the
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condition have been applied to the newer form. Cultural "paradigms" or ideologies are so convenient that people
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often don't bother to doubt them, and they are sometimes so rigorously enforced that people learn to keep their
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doubts to themselves. Public concern about diabetes has been growing for decades, but despite the introduction
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of insulin and other drugs to treat it, and massive campaigns to "improve" eating habits, mortality from
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diabetes has been increasing during the last 100 years. Diabetes ("type 1") has been increasing even among
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children (Barat, et al., 2008).A basic meaning of homeopathic medicine is the support of the organism's ability
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to heal itself; the essence of allopathy is that the physician fights "a disease" to cure the patient, e.g., by
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cutting out tumors or killing germs. Confidence in the organism's essential rationality led the doctors with a
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homeopathic orientation to see a fever as part of a recuperative process, while their allopathic opponents
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sometimes saw fever as the essence of the sickness to be cured. Homeopaths concentrated on the nature of the
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patient; allopaths concentrated on a disease entity in itself, and were likely to ignore the patient's
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idiosyncrasies and preferences.Diabetes was named for the excessive urination it causes, and for the sugar in
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the urine. It was called the sugar disease, and physicians were taught that sugar was the problem. Patients were
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ordered to avoid sweet foods, and in hospitals they were sometimes locked up to keep them from finding sweets.
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The practice was derived from ideology, not from any evidence that the treatment helped.In 1857, M. Piorry in
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Paris and William Budd in Bristol, England, reasoned that if a patient was losing a pound of sugar every day in
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10 liters of urine, and was losing weight very rapidly, and had an intense craving for sugar, it would be
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reasonable to replace some of the lost sugar, simply because the quick weight loss of diabetes invariably led to
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death. Keeping patients from eating what they craved seemed both cruel and futile. After Budd's detailed reports
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of a woman's progressive recovery over a period of several weeks when he prescribed 8 ounces of sugar every day,
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along with a normal diet including beef and beef broth, a London physician, Thomas Williams, wrote sarcastically
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about Budd's metaphysical ideas, and reported his own trial of a diet that he described as similar to Budd's.
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But after two or three days he decided his patients were getting worse, and stopped the experiment. Williams'
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publication was presented as a scientific refutation of Budd's deluded homeopathic ideas, but Budd hadn't
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explained his experiment as anything more than an attempt to slow the patient's death from wasting which was
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sure to be the result of losing so much sugar in the urine. The following year Budd described another patient, a
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young man who had become too weak to work and who was losing weight at an extreme rate. Budd's prescription
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included 8 ounces of white sugar and 4 ounces of honey every day, and again, instead of increasing the amount of
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glucose in the urine, the amount decreased quickly as the patient began eating almost as much sugar as was being
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lost initially, and then as the loss of sugar in the urine decreased, the patient gained weight and recovered
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his strength. Drs. Budd and Piorry described patients recovering from an incurable disease, and that has usually
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been enough to make the medical profession antagonistic. Even when a physician has himself diagnosed diabetes
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and told a patient that it would be necessary to inject insulin for the rest of his life, if that patient
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recovers by changing his diet, the physician will typically say that the diagnosis was wrong, because diabetes
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is incurable.Twenty-five years ago, some rabbits were made diabetic with a poison that killed their
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insulin-secreting pancreatic beta-cells, and when some of them recovered from the diabetes after being given
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supplemental DHEA, it was found that their beta-cells had regenerated. The more recent interest in stem cells
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has led several research groups to acknowledge that in animals the insulin-producing cells are able to
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regenerate. It is now conceivable that there will be an effort to understand the factors that damage the
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beta-cells, and the factors that allow them to regenerate. The observations of Budd and Piorry would be a good
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place to start such a reconsideration. For many years, physicians have been taught that diabetes is either
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"genetic" or possibly caused by a viral infection, that might trigger an "autoimmune reaction," but the study of
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cellular respiration and energy metabolism and endocrinology has provided more convincing explanations. The
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antibodies that are found in the "autoimmune" conditions are evidence of tissue damage, but the damage may have
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been done by metabolic toxins, with the immune system's involvement being primarily the removal of defective
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cells. In the 1940s, Bernardo Houssay found that coconut oil protected animals from poison-induced diabetes,
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while a lard-based diet failed to protect them. Later, glucose itself was found to protect the pancreatic
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beta-cells from poisons.In 1963, P.J. Randle clearly described the inhibition of glucose oxidation by free fatty
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acids. Later, when lipid emulsions came into use for intravenous feeding in hospitals, it was found that they
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blocked glucose oxidation, lowered the metabolic rate, suppressed immunity, and increased lipid peroxidation and
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oxidative stress.Estrogen and stress are both known to create some of the conditions of diabetes, while
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increasing fat oxidation and inhibiting glucose oxidation. Emotional stress, overwork, trauma, and infections
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have been known to initiate diabetes. Estrogen increases free fatty acids and decreases glycogen storage, and
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when birth control pills were becoming popular, some researchers warned that they might cause diabetes. But the
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food oil industry and the estrogen industry were satisfied with the medical doctrine that diabetes was caused by
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eating too much sugar.If the essence of diabetes is the presence of too much sugar, then it seems reasonable to
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argue that it is the excess sugar that's responsible for the suffering and death associated with the disease,
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otherwise, how would the prohibition of sugar in the diet be justified? In fact, the argument is made (e.g.,
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Muggeo, 1998) that it is the hyperglycemia that causes problems such as hypertension, kidney failure, heart
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failure, neuropathy, blindness, dementia, and gangrene.As information about the many physiological and
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biochemical events associated with diabetes has accumulated, the basic doctrine that "sugar causes diabetes" has
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extended itself to whatever the topic of discussion is<strong>: </strong>"Glucose causes" the death of
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beta-cells, glucose causes blood vessels to become leaky, glucose causes cells to be unable to absorb glucose,
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glucose causes the formation of free radicals, glucose impairs immunity and wound healing, but causes
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inflammation while preventing the "respiratory burst" in which free radicals are produced by cells that cause
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inflammation, it disturbs enzyme functions, impairs nerve conduction and muscle strength, etc., and it is also
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addictive, causing people to irrationally seek the very material that is poisoning them. Tens of thousands of
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publications describe the pathogenic effects of sugar. To prove their point, they grow cells in a culture dish,
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and find that when they are exposed to excess glucose, often 5 times the normal amount, they deteriorate. In the
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artificial conditions of cell culture, the oversupply of glucose causes lactic acid to accumulate, leading to
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toxic effects. But in the organism, the hyperglycemia is compensating for a sensed deficiency of glucose, a need
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for more energy. If diabetes means that cells can't absorb or metabolize glucose, then any cellular function
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that requires glucose will be impaired, despite the presence of glucose in the blood. It is the intracellular
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absence of glucose which is problematic, rather than its extracellular excess. Neuroglycopenia (or
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neuroglucopenia) or intracellular glycopenia refers to the deficit of glucose in cells. When the brain senses a
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lack of glucose, nerves are activated to increase the amount of glucose in the blood, to correct the problem. As
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long as the brain senses the need for more glucose, the regulatory systems will make the adjustments to the
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blood glucose level. The antagonism between fat and sugar that Randle described can involve the suppression of
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sugar oxidation when the concentration of fats in the bloodstream is increased by eating fatty food, or by
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releasing fats from the tissues by lipolysis, but it can also involve the suppression of fat oxidation by
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inhibiting the release of fatty acids from the tissues, when a sufficient amount of sugar is eaten. When a
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normal person, or even a "type 2 diabetic," is given a large dose of sugar, there is a suppression of lipolysis,
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and the concentration of free fatty acids in the bloodstream decreases, though the suppression is weaker in the
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diabetic (Soriguer, et al., 2008). Insulin, released by the sugar, inhibits lipolysis, reducing the supply of
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fats to the respiring cells.Free fatty acids suppress mitochondrial respiration (Kamikawa and Yamazaki, 1981),
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leading to increased glycolysis (producing lactic acid) to maintain cellular energy. The suppression of
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mitochondrial respiration increases the production of toxic free radicals, and the decreased carbon dioxide
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makes the proteins more susceptible to attack by free radicals. The lactate produced under the influence of
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excessive fat metabolism stimulates the release of endorphins, which are lipolytic, releasing more free fatty
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acids from the tissues. Acting through cytokines such as interleukin-6, lactate shifts the balance toward the
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catabolic hormones, leading to tissue wasting.Lactic acid itself, and the longer chain fatty acids, inhibit the
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regulatory enzyme pyruvate dehydrogenase (which is activated by insulin), reducing the oxidative production of
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energy. Drugs to activate this enzyme are being studied by the pharmaceutical industry as treatments for
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diabetes and cancer (for example, DCA, dichloroacetate).Oxidative damage of proteins is often described as
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glycation or glycosylation, but it really consists of many addition and crosslinking reactions, most often onto,
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or between, lysine groups. Carbon dioxide normally associates with lysine groups, so the destructive reactions
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are favored when carbon dioxide is displaced by lactic acid. The reactive fragments of polyunsaturated fatty
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acids are much more often the source of the protein-damaging radicals than the carbohydrates are. The importance
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of the fats in causing type-2 diabetes is coming to be accepted, for example Li, et al., recently (2008) said
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"The cellular link between fatty acids and ROS (reactive oxygen species) is essentially the mitochondrion, a key
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organelle for the control of insulin secretion. Mitochondria are the main source of ROS and are also the primary
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target of oxidative attacks."But much earlier (Wright, et al., 1988) it had been demonstrated that a deficiency
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of the "essential fatty acids" prevents toxin-induced diabetes and greatly increases resistance to inflammation
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(Lefkowith, et al., 1990). The lack of those so-called "essential fatty acids" also prevents autoimmune diabetes
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in a strain of diabetic mice (Benhamou, et al., 1995),Suppressing fatty acid oxidation improves the contraction
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of the heart muscle and increases the efficiency of oxygen use (Chandler, et al., 2003). Various drugs are being
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considered for that purpose, but niacinamide is already being used to improve heart function, since it lowers
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the concentration of free fatty acids.The antimetabolic and toxic effects of the polyunsaturated fatty acids can
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account for the "insulin resistance" that characterizes type-2 diabetes, but similar actions in the pancreatic
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beta-cells can impair or kill those cells, creating a deficiency of insulin, resembling type-1 diabetes.The
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suppression of mitochondrial respiration causes increased free radical damage, and the presence of
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polyunsaturated fatty acids in the suppressed cell increases the rate of fat decomposition and production of
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toxins.Increasing the rate of respiration by replacing the fats with glucose reduces the availability of
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electrons that can trigger lipid peroxidation and produce toxic free radicals, and the shift of fuel also
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increases the amount of carbon dioxide produced, which can protect the protein amino groups such as lysine from
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glycation and lipoxidation.While it's clear that it is the excessive oxidation of fat that damages cells in the
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"diabetic" state in which cells aren't able to use glucose, it's important to look at some of the situations in
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which so many researchers are blaming problems on hyperglycemia.Important problems in diabetes are slow wound
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healing, excessive permeability or leakiness of blood vessels which allows molecules such as albumin to be
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extravasated, and the impaired function and survival of pancreatic beta-cells.During the healing of a wound in a
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diabetic individual, the local concentration of glucose decreases and then entirely disappears, as healing
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stops. Applying glucose and insulin topically to the wound, it heals quickly. The very old practice of treating
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deep wounds with honey or granulated sugar has been studied in controlled situations, including the treatment of
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diabetic ulcers, infected deep wounds following heart surgery, and wounds of lepers. The treatment eradicates
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bacterial infections better than some antiseptics, and accelerates healing without scarring, or with minimal
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scarring. The sugar regulates the communication between cells, and optimizes the synthesis of collagen and
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extracellular matrix. An excess of insulin, causing hypoglycemia, can cause blood vessels, for example in the
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brain and kidneys, to become leaky, and this has been claimed to be an effect of insulin itself. However, the
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same leakiness can be produced by an analog of glucose that can't be metabolized, so that intracellular
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glycopenia is produced. The harmful effect that has been ascribed to excessive insulin can be prevented by
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maintaining an adequate supply of glucose (Uezu and Murakami, 1993), showing that it is the lack of glucose,
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rather than the excess insulin, that causes the vascular malfunction. Fructose also reduces the leakiness of
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blood vessels (Plante, et al., 2003). Many of the complications of diabetes are caused by increased vascular
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leakiness (Simard, et al., 2002).Sugar can protect the beta-cells from the free fatty acids, apparently in the
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same ways that it protects the cells of blood vessels, restoring metabolic energy and preventing damage to the
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mitochondria. Glucose suppresses superoxide formation in beta-cells (Martens, et al., 2005) and apparently in
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other cells including brain cells.<u> </u>(Isaev, et al., 2008).The beta-cell protecting effect of glucose is
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supported by bicarbonate and sodium. Sodium activates cells to produce carbon dioxide, allowing them to regulate
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calcium, preventing overstimulation and death. For a given amount of energy released, the oxidation of glucose
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produces more carbon dioxide and uses less oxygen than the oxidation of fatty acids. The toxic excess of
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intracellular calcium that damages the insulin-secreting cells in the relative absence of carbon dioxide is
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analogous to the increased excitation of nerves and muscles that can be produced by hyperventilation.In every
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type of tissue, it is the failure to oxidize glucose that produces oxidative stress and cellular damage. Even
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feeding enough sucrose to cause fat deposition in the liver can protect the liver from oxidative stress
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(Spolarics and Meyenhofer, 2000), possibly by mechanisms such as those involved in the treatment of alcoholic
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liver disease with saturated fats.The active thyroid hormone, T3, protects the heart by supporting the oxidation
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of glucose (Liu, et al., 1998). The amount of T3 produced by the liver depends mainly on the amount of glucose
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available.Animals that have been made diabetic with relatively low doses of the poison streptozotocin can
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recover functional beta-cells spontaneously, and the rate of recovery is higher in pregnant animals (Hartman, et
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al., 1989). Pregnancy stabilizes blood sugar at a higher level, and progesterone favors the oxidation of glucose
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rather than fats.A recent study suggests that recovery of the pancreas can be very fast. A little glucose was
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infused for 4 days into rats, keeping the blood glucose level normal, and the mass of beta-cells was found to
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have increased 2.5 times. Cell division wasn't increased, so apparently the additional glucose was preventing
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the death of beta-cells, or stimulating the conversion of another type of cell to become insulin-secreting
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beta-cells (Jetton, et al., 2008).That study is very important in relation to stem cells in general, because it
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either means that glandular cells are turning over ("streaming") at a much higher rate than currently recognized
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in biology and medicine, or it means that (when blood sugar is adequate) stimulated cells are able to recruit
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neighboring cells to participate in their specialized function. Either way, it shows the great importance of
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environmental factors in regulating our anatomy and physiology."Diabetologists" don't regularly measure their
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patients' insulin, but they usually make the assumption that insulin is the main factor regulating blood sugar.
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In one study, it was found that the insulin molecule itself, immunoreactive insulin, accounted for only about 8%
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of the serum's insulin-like action. The authors of that study believed that potassium was the main other factor
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in the serum that promoted the disposition of glucose. Since potassium and glucose are both always present in
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the blood, their effects on each other have usually been ignored. Cellular activation (by electrical, nervous,
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chemical, or mechanical stimulation) causes glucose to be absorbed and oxidized, even in the absence of insulin
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and in otherwise insulin-resistant individuals. I think this local interaction between the need for energy and
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the production of energy predominates in good health, with insulin and other hormones facilitating the process
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in times of stress. A variety of local tissue regulators, including GABA and glutamate, probably participate in
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these interactions, in the brain, endocrine glands, muscles, and other tissues, and are probably involved in the
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relaxing and analgesic actions of the sugars. The GABA system (GABA is highly concentrated in the beta-cells) is
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involved in regulating blood sugar, inhibiting the release of glucagon when glucose isn't needed, and apparently
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allowing the beta cells to discriminate between amino acids and glucose (Gu, et al., 1993) and acting as a
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survival and growth factor for neighboring cells (Ligon, et al., 2007). The damaged beta-cells lose the enzyme
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(glutamate dehydrogenase) that makes GABA, and their ratio of linoleic acid to saturated and monounsaturated fat
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increases, a change that corresponds to a decreased metabolism of glucose.The free intracellular calcium that
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can become toxic is normally bound safely by well-energized mitochondria, and in the bloodstream it is kept
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safely complexed with carbon dioxide. The thyroid hormone, producing carbon dioxide, helps to sustain the level
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of ionized calcium (Lindblom, et al., 2001). In a vitamin D deficiency, or a calcium deficiency, the parathyroid
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hormone increases, and this hormone can contribute to many inflammatory and degenerative processes, including
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diabetes. Consuming enough calcium and vitamin D to keep the parathyroid hormone suppressed is important to
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protect against the degenerative conditions.When animals were fed an otherwise balanced diet lacking vitamin D,
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with the addition of either 68% sucrose or 68% starch, the bones of those on the starch diet failed to develop
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normally, as would be expected with a vitamin D deficiency, and their serum calcium was low. However, the bones
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of those on the diet with sucrose developed properly, and didn't show evidence of being calcium deficient,
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though they weren't quite as heavy as those that also received an adequate amount of vitamin D (Artus, 1975).
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This study suggests that the famous dietetic emphasis on the "complex carbohydrates," i.e., starches, has made
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an important contribution to the prevalence of osteoporosis, as well as obesity and other degeneration
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conditions.Both vitamin D and vitamin K, another important calcium-regulating nutrient, are now known to prevent
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diabetes. Both of these vitamins require carbon dioxide for disposing of calcium properly, preventing its
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toxicity. When carbon dioxide is inadequate, for example from simple hyperventilation or from hypothyroidism,
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calcium is allowed to enter cells, causing inappropriate excitation, sometimes followed by calcification.Keeping
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an optimal level of carbon dioxide (for example, when adapted to high altitude) causes calcium to be controlled,
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resulting in lowered parathyroid hormone, an effect similar to supplementing with calcium, vitamin D, and
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vitamin K. (E.g., Nicolaidou, et al, 2006.) Glycine, like carbon dioxide, protects proteins against oxidative
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damage (Lezcano, et al., 2006), so including gelatin (very rich in glycine) in the diet is probably protective.
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The contribution of PTH to inflammation and degeneration is just being acknowledged (e.g., Kuwabara, 2008), but
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the mechanism undoubtedly involves the fact that it is lipolytic, increasing the concentration of free fatty
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acids that suppress metabolism and interfere with the use of glucose.When we talk about increasing the metabolic
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rate, and the benefits it produces, we are comparing the rate of metabolism in the presence of thyroid, sugar,
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salt, and adequate protein to the "normal" diet, containing smaller amounts of those "stimulating" substances.
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It would be more accurate if we would speak of the suppressive nature of the habitual diet, in relation to the
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more optimal diet, which provides more energy for work and adaptation, while minimizing the toxic effects of
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free radicals.Feeding animals a normal diet with the addition of Coca-Cola, or with a similar amount of sucrose,
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has been found to let them increase their calorie intake by 50% without increasing their weight gain
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(Bukowiecki, et al., 1983). Although plain sucrose can alleviate the metabolic suppression of an average diet,
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the effect of sugars in the diet is much more likely to be healthful in the long run when they are associated
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with an abundance of minerals, as in milk and fruit, which provide potassium and calcium and other protective
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nutrients. Avoiding the starches such as cereals and beans, and using fruits as a major part of the diet helps
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to minimize the effects of the polyunsaturated fats. Celiac disease or gluten sensitivity is associated with
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diabetes and hypothyroidism. There is a cross reaction between the gluten protein molecule and an enzyme which
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is expressed under the influence of estrogen. This is another reason for simply avoiding cereal
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products.Brewers' yeast has been used traditionally to correct diabetes, and its high content of niacin and
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other B vitamins and potassium might account for its beneficial effects. However, eating a large quantity of it
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is likely to cause gas, so some people prefer to extract the soluble nutrients with hot water. Yeast contains a
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considerable amount of estrogen, and the water extract probably leaves much of that in the insoluble starchy
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residue. Liver is another rich source of the B vitamins as well as the oily vitamins, but it can suppress
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thyroid function, so usually one meal a week is enough.The supplements that most often help to correct
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diabetes-like conditions are niacinamide, thiamine, thyroid, and progesterone or pregnenolone. Vitamins D and K
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are clearly protective against developing diabetes, and their effects on many regulatory processes suggest that
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they would also help to correct existing hyperglycemia.Drinking coffee seems to be very protective against
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developing diabetes. Its niacin and magnesium are clearly important, but it is also a rich source of
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antioxidants, and it helps to maintain normal thyroid and progesterone production. Chocolate is probably
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protective too, and it is a good source of magnesium and antioxidants.A recent study (Xia, et al., 2008) showed
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that inhibition of cholesterol synthesis by beta-cells impairs insulin synthesis, and that replenishing
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cholesterol restores the insulin secretion. Green tea contains this type of inhibitor, but its use has
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nevertheless been associated with a reduced risk of diabetes. Caffeine is likely to be the main protective
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substance in these foods. Although antioxidants can be protective against diabetes, not all things sold as
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"antioxidants" are safe; many botannical "antioxidants" are estrogenic. Hundreds of herbal products can lower
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blood sugar, but many of them are simply toxic, and the reduction of blood glucose can make some problems
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worse.The supplements I mention above--including caffeine--have antiinflammatory, antioxidative and
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energy-promoting effects. Inflammation, interfering with cellular energy production, is probably the essential
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feature of the things called diabetes.Aspirin has a very broad spectrum of antiinflammatory actions, and is
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increasingly being recommended for preventing complications of diabetes. One of the consequences of inflammation
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is hyperglycemia, and aspirin helps to correct that (Yuan, et al., 2001), while protecting proteins against
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oxidative damage (Jafarnejad, et al, 2001).If Dr. Budd's thinking (and results) had been more widely accepted
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when his publications appeared, thinking about "diabetes" might have led to earlier investigation of the
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syndromes of stress and tissue wasting, with insulin being identified as just one of many regulatory substances,
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and a large amount of useless and harmful activity treating hyperglycemia as the enemy, rather than part of an
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adaptive reaction, might have been avoided. <span style="white-space: pre-wrap"> </span>
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<h3>REFERENCES</h3>Ann Nutr Aliment. 1975;29(4):305-12. <strong>[Effects of administering diets with starch or
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sucrose basis on certain parameters of calcium metabolism in the young, growing rat]</strong> Artus
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M.Diabetes Metab. 2008 Oct 24. <strong>The growing incidence of type 1 diabetes in children: The 17-year French
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experience in Aquitaine.</strong> Barat P, Valade A, Brosselin P, Alberti C, Maurice-Tison S, L"vy-Marchal
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C.Pancreas. 1995 Jul;11(1):26-37. <strong>Essential fatty acid deficiency prevents autoimmune diabetes in
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nonobese diabetic mice through a positive impact on antigen-presenting cells and Th2 lymphocytes.</strong>
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Benhamou PY, Mullen Y, Clare-Salzler M, Sangkharat A, Benhamou C, Shevlin L, Go VL.The Retrospect of Medicine,
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XXXVII January-June, 1858 Edited by W. Braithwaite, p. 122: SUGAR AND DIABETES: A CASE. By Dr. William Budd,
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Senior Physician to the Bristol Royal Infirmary.Am J Physiol. 1983 Apr;244(4):R500-7. <strong>Effects of
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sucrose, caffeine, and cola beverages on obesity, cold resistance, and adipose tissue cellularity.</strong>
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Bukowiecki LJ, Lupien J, Foll"a N, Jahjah L.Cardiovasc Res. 2003 Jul 1;59(1):143-51. <strong>Partial inhibition
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of fatty acid oxidation increases regional contractile power and efficiency during demand-induced ischemia.
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</strong>Chandler MP, Chavez PN, McElfresh TA, Huang H, Harmon CS, Stanley WC.Med Sci (Paris). 2003
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Aug-Sep;19(8-9):827-33.<strong>
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[Contribution of free fatty acids to impairment of insulin secretion and action: mechanism of beta-cell
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lipotoxicity]</strong> [Article in French] Girard J.Diabetes Metab. 21(2), 79-88, 1995. <strong>Role of free
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fatty acids in insulin resistance of subjects with non-insulin-dependent diabetes,</strong> Girard J.
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"Studies performed in the rat suggest that impaired glucose-induced insulin secretion could also be related to
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chronic exposure of pancreatic beta cells to elevated plasma free fatty acid levels." [This direct effect of
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free fatty acids on the beta cells is extremely important. Estrogen--probably via GH--increases free fatty
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acids, and adrenalin--which is elevated in hypothyroidism--increases the release of free fatty acids from
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storage. Free fatty acids impair mitochondrail energy production.]Med Sci (Paris). 2005 Dec;21 Spec No:19-25.
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<strong>[Contribution of free fatty acids to impairment of insulin secretion and action. mechanism of beta-cell
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