319 lines
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319 lines
34 KiB
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<strong>MULTIPLE SCLEROSIS AND OTHER HORMONE-RELATED BRAIN SYNDROMES (1993)</strong>
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Since I am trying to discuss a complex matter in a single article, I have separately outlined the essential
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technical points of the argument in a section at the beginning, then I explain how my ideas on the subject
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developed, and finally there is a glossary. If you start with "Short-day brain stress," "Estrogen's
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effects," and "Symptoms and therapies," you will have the general picture, and can use the other sections to
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fill in the technical details.
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<strong> </strong>
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<strong>THE ARGUMENT: </strong> 1) The hormones pregnenolone, thyroid, and estrogen are
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involved in several ways with the changes that occur in multiple sclerosis, but no one talks about them. 2)
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The process of myelination is known to depend on the thyroid hormone. The myelinating cells are the
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oligodendroglia (oligodendrocytes) which appear to stop functioning in MS (and sometimes to a milder
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degree in Alzheimer's disease, and other conditions). The cells' absorption of thyroid hormone
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is influenced by dietary factors. 3) The oligodendrocytes are steroid-producing cells (1), and
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steroidogenesis is dependent on thyroid hormone, and on thyroid-dependent respiratory enzymes and on
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the heme-enzyme P-450scc, which are all sensitive (2) to poisoning by carbon monoxide and cyanide. The
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steroid produced by the oligodendrocytes is pregnenolone, which is known to have a profound
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anti-stress action (3), and which appears to be the main brain-protective steroid. 4) Lesions
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resembling those of MS can be produced experimentally by carbon monoxide or cyanide poisoning.(4) The
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lesions tend to be associated with individual small blood vessels, which are likely to contain
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clots. (Since all animals have enzymes to detoxify cyanide, this poison is apparently a
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universal problem, and can originate in the bowel. "Detoxified" cyanide is still toxic to the
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thyroid.) 5) Pregnenolone and progesterone protect against nerve damage (5) by the excitotoxic amino
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acids (glutamic acid, aspartic acid, monosodium glutamate, aspartame, etc.), while estrogen (6) and cortisol
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(7) are nerve-destroying, acting through the excitotoxic amino acids. Excitotoxins destroy certain
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types of nerve, especially the dopaminergic and cholinergic types, leaving the noradrenergic types (8),
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paralleling the changes that occur in aging. The clustering of oligodendrocytes around deteriorating
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nerve cells could represent an adaptive attempt to provide pregnenolone to injured nerve cells. 6) The
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involvement of hormones and environmental factors probably accounts for the intermittent progress of
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multiple sclerosis. To the extent that the environmental factors can be corrected, the disease can
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probably be controlled.
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<strong> SHORT-DAY BRAIN STRESS</strong>
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Shortly after I moved from Mexico to Montana, one of my students, a 32 year old woman, began having the same
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sensory symptoms her older sister had experienced at the same age, at the onset of multiple sclerosis.
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Vertigo and visual distortions of some sort made her consider withdrawing from the university. I'm not sure
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why she tried eating a whole can of tuna for lunch a couple of days after the onset of symptoms, but it
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seemed to alleviate the symptoms, and she stayed on a high protein diet and never had a recurrence.
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She told me some of the lore of MS: That it mostly affects young adults between the ages of 20 and 40, that
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it is common in high latitudes and essentially unknown in the tropics, and that it is sometimes exacerbated
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by pregnancy and stress. (Later, I learned that systemic lupus erythematosis and other "auto-immune"
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diseases also tend to occur mainly during the reproductive years. I discussed some of the implications
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of this in "Bean Syndrome.") Having enjoyed the mild climate of Mexico, I became very conscious of the harm
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done to us by northern winters, and began developing the idea of "winter sickness." In 1966-67,
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allergies, PMS, weight gain, colitis, and arthritis came to my attention as winter-related problems, and I
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assumed that the high-latitude incidence of MS related to what I was seeing and experiencing. Studies
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in Leningrad began revealing that mitochondria are injured during darkness, and repaired during
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daylight. I observed that hamsters' thymus glands shrank in the winter and regenerated in the summer;
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shrinkage of the thymus gland is a classical feature of stress, and usually reflects the dominance of
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cortisone, though estrogen and testosterone also cause it to shrink. Winter's darkness is stressful in
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a very fundamental way, and like any stress it tends to suppress thyroid function. In the hypothyroid
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state, any estrogen which is produced tends to accumulate in the body, because of liver sluggishness. I
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began to see that PMS could be controlled by certain things--extra light, supplements of sodium and
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magnesium, high quality protein, and correction of deficiencies of thyroid and progesterone. In
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working on my dissertation, I saw that tissue hypoxia (lower than optimal concentrations of oxygen in the
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blood) may result from estrogen excess, vitamin E deficiency, or aging. There is a close biological
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parallel between estrogen-dominance and the other hypoxic states, such as stress/shock, and aging.
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<strong>ESTROGEN'S EFFECTS</strong>
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As a portrait painter, I had been very conscious of the blue aspect that can often be seen in the skin of
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young women. In pale areas, the color may actually be blue, and in areas with a rich supply of blood, such
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as the lips, the color is lavender during times of high estrogen influence--around ovulation and puberty,
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for example. During these times of estrogen dominance, the blood is not only poorly oxygenated, but it
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has other special properties, such as an increased tendency to clot. The Shutes' work in the 1930s
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began with the use of vitamin E to antagonize estrogen's clot-promoting tendency, and led them to the
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discovery that vitamin E can be very therapeutic in heart disease. More recently, it has been found
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that men with heart disease have abnormally high estrogen (9), that women using oral contraceptives have
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higher mortality from heart attacks (10), and that estrogen tends to promote spasm of blood vessels
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(11). (These reactions are probably related to the physiology of menstruation, in which
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progesterone withdrawal causes spasms in the spiral arteries of the uterus, producing endometrial
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anoxia and cell death.) In toxemia of late pregnancy, or eclampsia, the exaggerated clotting tendency caused
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by excess estrogen (or by inadequately opposed estrogen, i.e., progesterone deficiency), can cause
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convulsions and strokes. Vascular spasms could be involved here, too. The stasis caused by the
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vasospasm would facilitate clotting. (Vascular spasm has been observed in epilepsy, too. Epilepsy can
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be brought on by the premenstrual excess of estrogen, and in that situation there is no evidence that
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clotting is involved. Leakage of hemoglobin out of red cells can cause vasospasm, so bleeding,
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clotting, strokes, and seizures can interact complexly.) The brains of women who have
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died following eclampsia show massive clotting in the blood vessels, and their livers are
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characteristically injured, with clots (12). Tom Brewer and others have shown very clearly that
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malnutrition, especially protein deficiency, is the cause of toxemia of late pregnancy. (In Nutrition
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for Women, I discussed the importance of protein in allowing the liver to eliminate estrogen.) Various
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researchers have demonstrated that the plaques of MS usually occur in the area served by a single blood
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vessel (13, 14), and some have suggested that clotting is the cause. MS patients have been found to
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have an abnormal clotting time, and it has been suggested that an altered diet might be able to correct the
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clotting tendency. Studies in animals have shown clearly that a protein deficiency increases the fibrinogen
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content of blood. (Field and Dam, 1946.) Other factors that increase blood clotting are elevated
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adrenalin and cortisone. Protein deficiency causes an adaptive decrease in thyroid function, which
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leads to a compensatory increase in adrenaline and cortisone. The combination of high estrogen with
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high adrenaline increases the tendency for both clots and spasms of the blood vessels (11). In experimental
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poisoning of animals with carbon monoxide or cyanide, the brain lesions resembling MS include blood
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clots. The patchy distribution of these spots in the brain suggests that the clotting is secondary to
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metabolic damage in the brain. Presumably, the same would be true in ordinary MS, with clots and
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spasms being induced in certain areas by metabolic abnormalities in brain cells. The injured cells
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that are responsible for myelination of nerve fibers are steroid-forming cells. A failure to secrete
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their protective pregnenolone could cause a local spasm of a blood vessel. The circulatory problem
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would exacerbate the respiratory problem. Steroid production is dependent on NADH and NADPH, and so requires
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adequate energy supplies and energy metabolism. The phenomenon of blood-sludging, studied by M.
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Knisely at the University of Chicago in the l930s and l940s, is apparently a general result of decreased
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energy metabolism, and is likely to be a factor in energy-and-circulatory vicious circles.
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<strong> </strong>
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<strong>SYMPTOMS AND THERAPIES </strong>
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Around 1976 I met a woman in her mid-thirties who heard about my work with progesterone in animals.
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She had been disabled by a brain disease that resembled MS or Devic's disease, inflammation of the optic
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nerves. It would sometimes cause blindness and paralysis that persisted for weeks at a time.
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During remissions, sometimes using a wheelchair, she would go to the medical school library to try to
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understand her condition. She came across Katherina Dalton's work with progesterone, and convinced a
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physician to give her a trial injection. Although she had trouble finding people who were willing to
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give her progesterone, her recovery was so complete that she was able to climb stairs and drive her car, and
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she came to my endocrinology class and gave a very good (and long) lecture on progesterone
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therapy. Although her sensory and motor functions became normal, she remained very fat, and
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chronically suffered from sore areas on her arms and legs that seemed to be abnormal blood vessels, possibly
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with phlebitis. She appeared to need thyroid hormone as well as larger amounts of progesterone, but
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never found a physician who would cooperate, as far as I know. In the late 1970s I was seeing a lot of
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people who had puzzling health problems. In a period of two or three years, there were five people who
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had been diagnosed by neurologists as having multiple sclerosis. In talking to them, it seemed clear
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that they had multiple symptoms of hypothyroidism. They weren't severely disabled. Since they
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weren't fat or lethargic, their physicians hadn't thought they could be hypothyroid. When they tried
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taking a thyroid supplement, all of their symptoms disappeared, including those that had led to their MS
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diagnosis. One of the women went to her doctor to tell him that she felt perfectly healthy since
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taking thyroid, and he told her to stop taking it, because people who have MS need a lot of rest, and she
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wouldn't get enough rest if she was living in a normally active way. The assumption seemed to be that the
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diagnosis was more important than the person. (When I refer to a "thyroid supplement" I mean one that
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contains some T3. Many people experience "neurological symptoms" when they take thyroxine by
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itself. Experimentally, it has been found to suppress brain respiration, probably by diluting the T3
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that was already present in the brain tissue.)
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<strong> </strong>
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<strong>METABOLISM OF THE OLIGODENDROCYTES</strong>
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The rate-regulating step in steroid synthesis involves the entry of cholesterol into the mitochondria, where
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the heme-enzyme P-450scc then removes the side-chain of cholesterol (by introducing oxygen atoms), to
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produce pregnenolone. This enzyme can be poisoned by carbon monoxide or cyanide, and light can
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eliminate the poison (15); this could be one aspect of the winter-sickness problem. Peripheral nerves
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are myelinated by essentially the same sort of cell that is called an oligodendrocyte in the brain, but
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outside the brain it is called a Schwann cell. It is easier to study the myelin sheath in peripheral
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nerves, and the electrical activity of a nerve is the most easily studied aspect of its physiology.
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Certain experiments seemed to indicate a "jumping" (saltatory) kind of conduction along the nerve between
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Schwann cells, and it was argued that the insulating function of the myelin sheath made this kind of
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conduction possible. This idea has become a standard item in physiology textbooks, and its familiarity
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leads many people to assume that the presence of myelin sheaths in the brain serves the same "insulating"
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function. For a long time it has been known that heat production during nerve conduction reveals a more
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continuous mode of conduction, that doesn't conform to the idea of an electrical current jumping
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around an insulator. Even if the myelin functioned primarily to produce "saltatory conduction" in
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peripheral nerves, it isn't clear how this process could function in the brain. I think of the issue
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of "saltatory conduction at the nodes of Ranvier" as another of the fetish ideas that have served to
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obstruct progress in biology in the United States. A more realistic approach to nerve function can be
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found in Gilbert Ling's work. Ling has demonstrated in many ways that the ruling dogma of "cell
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membrane" function isn't coherently based on fact. He found that hormones such as progesterone
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regulate the energetic and structural stability of cells. Many people, unaware of his work, have felt
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that it was necessary to argue against the idea that there are anesthetic steroids with generalized
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protective functions, because of their commitment to a textbook dogma of "cell membrane" physiology. I think
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the myelinating cells do have relevance to nerve conduction, but I don't think they serve primarily as
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electrical insulators. If the adrenal cortex were inside the heart, it would be obvious to ask whether
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its hormones aren't important for the heart's function. Since the oligodendrocytes are
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steroid-synthesizers, it seems obvious to ask whether their production of pregnenolone in response to stress
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or fatigue isn't relevant to the conduction processes of the nerves they surround.
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<strong> </strong>
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<strong>OLD AGE</strong>
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A biologist friend of mine who was about 85 became very senile. His wife started giving him thyroid,
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progesterone, DHEA and pregnenolone, and within a few days his mental clarity had returned. He
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continued to be mentally active until he was 89, when his wife interfered with his access to the hormones.
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In old age the brain steroids fall to about 5% of their level in youth. Pregnenolone and DHEA improve
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memory in old rats, and improve mood stability and mental clarity of old people. Pregnenolone's action
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in improving the sense of being able to cope with challenges probably reflects a quieting and coordinating
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of the "sequencing" apparatus of the forebrain, which is the area most sensitive to energy
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deprivation. This is the area that malfunctions in hyperactive and "dyslexic" children.
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Weakening of the sequencing and sorting processes probably explains the common old-age inability to extract
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important sounds from environmental noise, creating a kind of "confusion deafness." Insomnia, worry
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and "restless legs" at bedtime are problems for many old people, and I think they are variations of the
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basic energy-depletion problem. The oligodendrocytes were reported (Hiroisi and Lee, 1936) to be the source
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of the senile plaques or amyloid deposits of Alzheimer's disease.(16) Hiroisi and Lee showed the cells
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in different stages of degeneration, ending with translucent "mucoid" spots that stained the same as
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amyloid, the material in the senile plaques. This type of cell also appears to form a halo or crown
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around degenerating nerve cells--possibly in a protective reaction to provide the nerve cell with any
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pregnenolone the oligodendrocytes are able to make. The oligodendrocytes, the source of the
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brain steroids (that people previously believed came from the adrenals and gonads, and were just stored in
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the brain), myelinate nerve fibers under the influence of thyroid hormone (17). Thyroid is
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responsible for both myelination and hormone formation. In old age, glial cells become more numerous,
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and nerve cells become structurally and functionally abnormal, but usually there is no problem
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with the formation of myelin. In MS, the problem is just with myelination, and there are no
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senile plaques or defects in the nerve cells themselves. These differences
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suggest the possibility that Alzheimer's disease involves a specific premature loss of brain
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pregnen- olone production, but not of thyroid. Recent work suggests a central role for
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pregnenolone and progesterone in the regulation of consciousness (18), and possibly in the brain's
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detoxifying system. Elsewhere, I have suggested that vitamin A deficiency might cause the excessive
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production of the "amyloid" protein. A vitamin A deficiency severely inhibits steroid synthesis.
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(It is used so massively in steroid synthesis that a progesterone supplement can prevent the symptoms of
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vitamin A deficiency.) I suspect that vitamin A is necessary for the side-chain cleavage that converts
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cholesterol to pregnenolone. Iron-stimulated lipid peroxidation is known to block steroid formation,
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and vitamin A is very susceptible to destruction by iron and oxidation. Iron tends to
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accumulated in tissues with aging. Gajdusek has demonstrated that brain deterioration is
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associated with the retention of whatever metal happens to be abundant in the person's environment, not just
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with aluminum. (One type of glial cell is known for its metal-binding function, causing them to be
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called "metallophils."). According to Gajdusek, "calcium and other di- and trivalent elements" are
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"deposited as hydroxyapatites in brain cells" in brain degeneration of the Alzheimer's type.(19) Even early
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forms of Alzheimer's disease begin at an age when the youth-associated steroids have begun to decline.
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If MS involves a deficiency of thyroid (or of T3 within the oligodendrocytes, where T3 normally can be
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made from thyroxine; many things, including protein deficiency, can block the conversion of T4 to T3), those
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cells would necessarily be deficient in their ability to produce pregenolone, but in young people the
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brain would still be receiving a little pregnenolone, progesterone, and DHEA from the adrenals and
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gonads. This relatively abundant youthful supply of hormones would keep most of the body's organs in
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good condition, and could keep the bodies of the major brain cells from deteriorating. But if proper
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functioning of the nerve fibers requires that they be fed a relatively high concentration of pregnenolone
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from their immediately adjacent neighbors (with the amount increasing during stress and fatigue), then their
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function would be impaired when they had to depend on the hormones that arrived from the blood stream. For
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many years it has been recognized that the brain atrophy of "Alzheimer's disease" resembles the changes seen
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in the brain in many other situations: The traumatic dementia of boxers; toxic dementia; the
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slow-virus diseases; exposure of the brain to x-<span class="il">rays</span> (20); ordinary old age;
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and in people with Down's syndrome who die around the age of thirty.
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In menopause, certain nerve cells have lost their ability to regulate the ovaries, because of
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prolonged exposure to estrogen (6). The cells that fail as a result of prolonged estrogen exposure
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aren't the same cells that fail from prolonged exposure to the glucocorticoids (7), but they have in common
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the factor of excitatory injury. Since people who experience premature menopause are known to be more likely
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than average to die prematurely, it is reasonable to view menopause as a model of the aging process. It is
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now well established that progesterone fails to be produced at the onset of menopause (the first missed
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period, increased loss of calcium, symptoms such as hot flashes, etc.), and that estrogen continues to be
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produced at monthly intervals for about four years. The essential question for aging, in the present
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context, is why the anesthetic steroids are no longer produced at a rate that allows them to protect
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tissues, including brain cells, from the excitotoxins. Using menopause as a model for aging, we can
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make the question more answerable by asking why progesterone stops being produced. During stress, we are
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designed not to get pregnant, and the simplest aspect of this is that ACTH, besides stimulating the adrenals
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to produce stress-related hormones, inhibits the production of progesterone by the ovary. Other
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stress-induced factors, such as increased prolactin and decreased thyroid, also inhibit progesterone
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production. Stress eventually makes us more susceptible to stress. Menopause and other landmarks
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of aging simply represent upward inflections in the rate-of-aging curve. Individual variations in type
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of stress, hormonal response and diet, etc., probably govern the nature of the aging process in an
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individual. The amphetamine-like action of estrogen, which undoubtedly contributes to the general
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level of stress and excitotoxic abuse of nerve cells, is probably the only "useful" facet of
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estrogen treatment, but a little cocaine might achieve the same effect with no more harm, possibly
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less. The toxicity of catecholamines has been known for over thirty years, and estrogen's stimulating
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effects are partly the result of its conversion to catechol-estrogens which increase the activity of brain
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catecholamines. Estrogen's powerful ability to nullify learning seems never to be mentioned by the
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people who promote its use. The importance of a good balance of brain steroids for mood, attention,
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memory, and reasoning is starting to be recognized, but powerful economic forces militate against its
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general acceptance. Since the brain is the organ that can allow us to adapt without undergoing stress in the
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hormonal sense, it is very important to protect its flexibility and to keep its energy level high, so it can
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work in a relaxed way. It is the low energy cellular state that leads to the retention of calcium and
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iron, and to the production of age pigment, and other changes that constitute the vicious circle of
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aging. And mental activity that challenges obsession and rigidity might be the most important brain
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energizer. Pseudo-optimism, humor-as-therapy, has a certain value, but a deeper optimism involves a
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willingness to assimilate new information and to change plans accordingly.
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<strong> </strong>
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<strong>SUPPLEMENTS</strong>
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Nutritional supplements that might help to prevent or correct these brain syndromes include: Vitamin E
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and coconut oil; vitamin A; magnesium, sodium; thyroid which includes T3; large amounts of
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animal protein, especially eggs; sulfur, such as magnesium sulfate or flowers of sulfur, but not
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to take continuously, because of sulfur's interference with copper absorption; pregnenolone; progesterone if
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needed. Bright light, weak in the blue end of the spectrum and with protection against ultraviolet,
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activates respiratory metabolism and quenches free radicals. Raw carrot fiber and/or laxatives if
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needed; charcoal occasionally for gas or bowel irritation. Coconut oil serves several
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purposes. Its butyric acid is known to increase T3 uptake by glial cells. It has a general
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pro-thyroid action, for example by diluting and displacing antithyroid unsaturated oils, its short- and
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medium-chain fatty acids sustain blood sugar and have antiallergic actions, and it protects mitochondria
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against stressinjury. P.S.: In 1979, a woman whose husband was suffering from advanced
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Amyotrophic Lateral Sclerosis (ALS) asked me if I had any ideas for slowing his decline. I described
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my suspicion that ALS involved defective metabolism or regulation of testosterone. In some tissues,
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testosterone is selectively concentrated to prevent atrophy, and ALS is a disease of middle-age, when
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hormone regulation often becomes a special problem. In the late 1970s, there was discussion of a
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higher incidence of ALS in males, and especially in athletes. I told her about progesterone's general
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protective effects, its antagonism to testosterone, and its prevention of atrophy in various tissues.
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She decided to ask her doctor to try progesterone for her husband. Later, I learned that her husband
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had gone into a very rapid decline immediately after the injection, and died within a week; the physician
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had given him testosterone, since, he said, "testosterone and progesterone are both male hormones."
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Besides making me more aware of the problems patients have in communicating with physicians, this tended to
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reinforce my feeling that a hormone imbalance is involved in ALS. Although I haven't written much
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about testosterone's toxicity, Marian Diamond's work showed that prenatal testosterone is similar to
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prenatal estrogen, in causing decreased thickness of the cortex of the brain; both of those hormones oppose
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progesterone's brain-protecting and brain-promoting actions.
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<strong><h3>REFERENCES</h3></strong>
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1) Z. Y. Hu, et al., P.N.A.S. (USA) 84, 8215-9, 1987. 2) P. F. Hall, Vitamins and Hormones 42,
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315-370, 1985. 3) J. J. Lambert, et al., Trends in Pharmac. Sci. 8, 224-7, 1987. 4) W. A. D. A.
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Anderson, Pathology (second edition), C. V. Mosby, St. Louis, 1953. 5) S. S. Smith, et al., Brain Res.
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422, 52-62, 1987. 6) P. M. Wise, Menopause, 1984; S. S. Smith, et al., Brain Res. 422, 40-51, 1987.
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7) R. M. Sapolsky, et al., J. Neuroscience 5, 1222-1227, 1985; R. M. Sapolsky and W. Pulsinelli,
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Science 229, 1397-9, 1985. 8) C. B. Nemeroff, (Excitotoxins) 290-305, 1984. 9) G. B.
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Phillips, Lancet 2, 14-18, 1976; G. B. Phillips, et al., Am. J. Med. 74, 863-9, 1983; M. H. Luria, et al.,
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Arch Intern Med 142, 42-44, 1982; E. L. Klaiber, et al., Am J Med 73, 872-881, 1982. 10) J. I. Mann,
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et al., Br Med J 2, 241-5, 1975. 11) V. Gisclard and P. M. Vanhoutte, Physiologist 28, 324(48.1).
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12) W. A. D. A. Anderson, Pathology, 1953; H. H. Reese, et al., editors, 1936 Yearbook of
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Neurology, Psychiatry, and Endocrinology, Yearbook Publishers, Chicago, 1937. 13)
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T. J. Putnam, Ann Int Med 9, 854-63, 1936; JAMA 108, 1477, 1937. 14) R. S. Dow and G. Berglund, Arch
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Neurol and Psychiatry 47, 1, 1992. 15) R. W. Estabrook, et al., Biochem Z. 338, 741-55, 1963.
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16) S. Hiroisi and C. C. Lee, Arch Neurol and Psychiat 35, 827-38, 1936. 17) J. M. Matthieu, et
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al., Ann Endoc. 1974. 18) K. Iwaharhi, et al., J Ster Biochem and Mol Biol 44(2), 163-4, 1993.
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19) D. C. Gajdusek, Chapter 63, page 1519 in Virology (B. N. Fields, et al., editors), Raven Press,
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N.Y., 1985. 20) K. Lowenberg-Scharenberg and R. C. Bassett, J Neuropath and Exper Neurol 9, 93, 1950.
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GLOSSARY 1. Amyloid is the old term for the "starchy" appearing (including the way it
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stains) proteins seen in various diseases, and in the brain in Alzheimer's disease. 2. Cytochrome
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P450scc. The cytochromes are "pigments," in the same sense that they contain the colored "heme" group
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|
that gives hemoglobin its color. P450 means "protein that absorbs light at a wavelength of 450.
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|
The scc means "side-chain cleaving," which refers to the removal of the 6 carbon atoms that distinguish
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cholesterol from pregnenolone. Other Cyt P450 enzymes are important for their detoxifying oxidizing action,
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and some of these are involved in brain metabolism. 3. Glial means "glue-like," and glial cells are
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mostly spidery-shaped cells that used to be thought of as just connective, supportive cells in the brain.
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4. Mitochondria (the "thread-like bodies") are the structures in cells which produce most of our
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metabolic energy by respiration, in response to the thyroid hormones. 5. Mucoid--refers to a
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mucoprotein, a protein which contains some carbohydrate. A glycoprotein; usually not intended as a
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|
precise term. 6. Myelination. Myelin is a multilayered enclosure of the axons (the long
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|
processes) of nerve cells, composed of proteins and complex lipids, including cholesterol. The layered
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material is a flat, thin extension of the cytoplasm of the oligodendroglial cells. 7. Oligodendrocytes
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are one of the kinds of glial (or neuroglial) cells, and structurally they are unusual in having sheet-like,
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rather than just thread-like processes; they have a sensitivity ("receptors") to stress and valium, and
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|
produce pregnenolone when activated. Under the influence of thyroid hormone, they wrap themselves in
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thin layers around the conductive parts of nerve cells, leaving a multilayered "myelin" coating. Their
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absorption of thyroid hormone is promoted by butyrate, an anti-stress substance found in butter and coconut
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oil. 8. Steroidogenesis is the creation of steroids, usually referring to the conversion of
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cholesterol to hormones.
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© Ray Peat Ph.D. 2013. All Rights Reserved. www.RayPeat.com
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