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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
style="font-size: medium"
><strong>MULTIPLE SCLEROSIS AND OTHER HORMONE-RELATED BRAIN SYNDROMES (1993)</strong></span></span
></span>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>Since I am trying to discuss a complex matter in a single article, I have separately outlined the
essential technical points of the argument in a section at the beginning, then I explain how my
ideas on the subject developed, and finally there is a glossary. If you start with
"Short-day brain stress," "Estrogen's effects," and "Symptoms and therapies," you will have the
general picture, and can use the other sections to fill in the technical details.</span></span
></span>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
style="font-size: small"
><strong>THE ARGUMENT:</strong></span></span></span>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>1) The hormones pregnenolone, thyroid, and estrogen are involved in several ways with the changes
that occur in multiple sclerosis, but no one talks about them.</span></span></span>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>2) The process of myelination is known to depend on the thyroid hormone. The myelinating
cells are the oligodendroglia (oligodendrocytes) which appear to stop functioning in MS
(and sometimes to a milder degree in Alzheimer's disease, and other
conditions). The cells' absorption of thyroid hormone is influenced by dietary
factors.</span></span></span>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>3) The oligodendrocytes are steroid-producing cells (1), and steroidogenesis is dependent on
thyroid hormone, and on thyroid-dependent respiratory enzymes and on the heme-enzyme
P-450scc, which are all sensitive (2) to poisoning by carbon monoxide and cyanide. The
steroid produced by the oligodendrocytes is pregnenolone, which is known to have a
profound anti-stress action (3), and which appears to be the main brain-protective
steroid.</span></span></span>
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<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>4) Lesions resembling those of MS can be produced experimentally by carbon monoxide or cyanide
poisoning.(4) The lesions tend to be associated with individual small blood vessels,
which are likely to contain clots. (Since all animals have enzymes to
detoxify cyanide, this poison is apparently a universal problem, and can originate in the
bowel. "Detoxified" cyanide is still toxic to the thyroid.) </span></span></span>
</blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>5) Pregnenolone and progesterone protect against nerve damage (5) by the excitotoxic amino acids
(glutamic acid, aspartic acid, monosodium glutamate, aspartame, etc.), while estrogen (6) and
cortisol (7) are nerve-destroying, acting through the excitotoxic amino acids.
Excitotoxins destroy certain types of nerve, especially the dopaminergic and cholinergic types,
leaving the noradrenergic types (8), paralleling the changes that occur in aging. The
clustering of oligodendrocytes around deteriorating nerve cells could represent an adaptive
attempt to provide pregnenolone to injured nerve cells.</span></span></span>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>6) The involvement of hormones and environmental factors probably accounts for the intermittent
progress of multiple sclerosis. To the extent that the environmental factors can be
corrected, the disease can probably be controlled.</span></span></span>
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<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
style="font-size: small"
><span style="font-style: normal"><strong>SHORT-DAY BRAIN STRESS</strong></span></span></span></span
>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>Shortly after I moved from Mexico to Montana, one of my students, a 32 year old woman, began having
the same sensory symptoms her older sister had experienced at the same age, at the onset of
multiple sclerosis. Vertigo and visual distortions of some sort made her consider
withdrawing from the university. I'm not sure why she tried eating a whole can of tuna for lunch
a couple of days after the onset of symptoms, but it seemed to alleviate the symptoms, and she
stayed on a high protein diet and never had a recurrence. She told me some of the lore of
MS: That it mostly affects young adults between the ages of 20 and 40, that it is common in high
latitudes and essentially unknown in the tropics, and that it is sometimes exacerbated by
pregnancy and stress. (Later, I learned that systemic lupus erythematosis and other
"auto-immune" diseases also tend to occur mainly during the reproductive years. I
discussed some of the implications of this in "Bean Syndrome.")</span></span></span>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>Having enjoyed the mild climate of Mexico, I became very conscious of the harm done to us by
northern winters, and began developing the idea of "winter sickness." In 1966-67,
allergies, PMS, weight gain, colitis, and arthritis came to my attention as winter-related
problems, and I assumed that the high-latitude incidence of MS related to what I was seeing and
experiencing. Studies in Leningrad began revealing that mitochondria are injured during
darkness, and repaired during daylight. I observed that hamsters' thymus glands shrank in
the winter and regenerated in the summer; shrinkage of the thymus gland is a classical feature
of stress, and usually reflects the dominance of cortisone, though estrogen and testosterone
also cause it to shrink. Winter's darkness is stressful in a very fundamental way, and
like any stress it tends to suppress thyroid function. In the hypothyroid state, any
estrogen which is produced tends to accumulate in the body, because of liver sluggishness.</span
></span></span>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>I began to see that PMS could be controlled by certain things--extra light, supplements of sodium
and magnesium, high quality protein, and correction of deficiencies of thyroid and
progesterone. In working on my dissertation, I saw that tissue hypoxia (lower than optimal
concentrations of oxygen in the blood) may result from estrogen excess, vitamin E deficiency, or
aging. There is a close biological parallel between estrogen-dominance and the other
hypoxic states, such as stress/shock, and aging.</span></span></span>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
style="font-size: small"
><span style="font-style: normal"><strong>ESTROGEN'S EFFECTS</strong></span></span></span></span>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>As a portrait painter, I had been very conscious of the blue aspect that can often be seen in the
skin of young women. In pale areas, the color may actually be blue, and in areas with a rich
supply of blood, such as the lips, the color is lavender during times of high estrogen
influence--around ovulation and puberty, for example. During these times of estrogen
dominance, the blood is not only poorly oxygenated, but it has other special properties, such as
an increased tendency to clot. The Shutes' work in the 1930s began with the use of vitamin
E to antagonize estrogen's clot-promoting tendency, and led them to the discovery that vitamin E
can be very therapeutic in heart disease. More recently, it has been found that men with
heart disease have abnormally high estrogen (9), that women using oral contraceptives have
higher mortality from heart attacks (10), and that estrogen tends to promote spasm of
blood vessels (11). (These reactions are probably related to the physiology of
menstruation, in which progesterone withdrawal causes spasms in the spiral arteries of the
uterus, producing endometrial anoxia and cell death.)</span></span></span>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>In toxemia of late pregnancy, or eclampsia, the exaggerated clotting tendency caused by excess
estrogen (or by inadequately opposed estrogen, i.e., progesterone deficiency), can cause
convulsions and strokes. Vascular spasms could be involved here, too. The stasis
caused by the vasospasm would facilitate clotting. (Vascular spasm has been observed in
epilepsy, too. Epilepsy can be brought on by the premenstrual excess of estrogen, and in
that situation there is no evidence that clotting is involved. Leakage of hemoglobin out
of red cells can cause vasospasm, so bleeding, clotting, strokes, and seizures can interact
complexly.) The brains of women who have died following eclampsia show massive
clotting in the blood vessels, and their livers are characteristically injured, with clots
(12).</span></span></span>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>Tom Brewer and others have shown very clearly that malnutrition, especially protein deficiency, is
the cause of toxemia of late pregnancy. (In Nutrition for Women, I discussed the
importance of protein in allowing the liver to eliminate estrogen.)</span></span></span>
</blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>Various researchers have demonstrated that the plaques of MS usually occur in the area served by a
single blood vessel (13, 14), and some have suggested that clotting is the cause. MS
patients have been found to have an abnormal clotting time, and it has been suggested that an
altered diet might be able to correct the clotting tendency.</span></span></span>
</blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>Studies in animals have shown clearly that a protein deficiency increases the fibrinogen content of
blood. (Field and Dam, 1946.) Other factors that increase blood clotting are elevated
adrenalin and cortisone. Protein deficiency causes an adaptive decrease in thyroid
function, which leads to a compensatory increase in adrenaline and cortisone. The
combination of high estrogen with high adrenaline increases the tendency for both clots and
spasms of the blood vessels (11).</span></span></span>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>In experimental poisoning of animals with carbon monoxide or cyanide, the brain lesions resembling
MS include blood clots. The patchy distribution of these spots in the brain suggests that
the clotting is secondary to metabolic damage in the brain. Presumably, the same would be
true in ordinary MS, with clots and spasms being induced in certain areas by metabolic
abnormalities in brain cells. The injured cells that are responsible for myelination of
nerve fibers are steroid-forming cells. A failure to secrete their protective pregnenolone
could cause a local spasm of a blood vessel. The circulatory problem would exacerbate the
respiratory problem. Steroid production is dependent on NADH and NADPH, and so requires adequate
energy supplies and energy metabolism. The phenomenon of blood-sludging, studied by M.
Knisely at the University of Chicago in the l930s and l940s, is apparently a general result of
decreased energy metabolism, and is likely to be a factor in energy-and-circulatory vicious
circles.</span></span></span>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
style="font-size: small"
><span style="font-style: normal"><strong>SYMPTOMS AND THERAPIES</strong></span></span></span></span
>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>Around 1976 I met a woman in her mid-thirties who heard about my work with progesterone in
animals. She had been disabled by a brain disease that resembled MS or Devic's disease,
inflammation of the optic nerves. It would sometimes cause blindness and paralysis that
persisted for weeks at a time. During remissions, sometimes using a wheelchair, she would
go to the medical school library to try to understand her condition. She came across
Katherina Dalton's work with progesterone, and convinced a physician to give her a trial
injection. Although she had trouble finding people who were willing to give her
progesterone, her recovery was so complete that she was able to climb stairs and drive her car,
and she came to my endocrinology class and gave a very good (and long) lecture on
progesterone therapy. Although her sensory and motor functions became normal, she remained
very fat, and chronically suffered from sore areas on her arms and legs that seemed to be
abnormal blood vessels, possibly with phlebitis. She appeared to need thyroid hormone as
well as larger amounts of progesterone, but never found a physician who would cooperate, as far
as I know.</span></span></span>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>In the late 1970s I was seeing a lot of people who had puzzling health problems. In a period
of two or three years, there were five people who had been diagnosed by neurologists as having
multiple sclerosis. In talking to them, it seemed clear that they had multiple symptoms of
hypothyroidism. They weren't severely disabled. Since they weren't fat or
lethargic, their physicians hadn't thought they could be hypothyroid. When they tried
taking a thyroid supplement, all of their symptoms disappeared, including those that had led to
their MS diagnosis. One of the women went to her doctor to tell him that she felt
perfectly healthy since taking thyroid, and he told her to stop taking it, because people who
have MS need a lot of rest, and she wouldn't get enough rest if she was living in a normally
active way. The assumption seemed to be that the diagnosis was more important than the person.
(When I refer to a "thyroid supplement" I mean one that contains some T3. Many people
experience "neurological symptoms" when they take thyroxine by itself. Experimentally, it
has been found to suppress brain respiration, probably by diluting the T3 that was already
present in the brain tissue.) </span></span></span>
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<span style="color: #222222"><span style="font-size: small"><span
style="font-family: georgia, times, serif"
><span style="font-style: normal"><strong>METABOLISM OF THE OLIGODENDROCYTES</strong></span></span
></span></span>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>The rate-regulating step in steroid synthesis involves the entry of cholesterol into the
mitochondria, where the heme-enzyme P-450scc then removes the side-chain of cholesterol
(by introducing oxygen atoms), to produce pregnenolone. This enzyme can be poisoned by
carbon monoxide or cyanide, and light can eliminate the poison (15); this could be one aspect of
the winter-sickness problem. </span></span></span>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>Peripheral nerves are myelinated by essentially the same sort of cell that is called an
oligodendrocyte in the brain, but outside the brain it is called a Schwann cell. It is
easier to study the myelin sheath in peripheral nerves, and the electrical activity of a nerve
is the most easily studied aspect of its physiology. Certain experiments seemed to
indicate a "jumping" (saltatory) kind of conduction along the nerve between Schwann cells, and
it was argued that the insulating function of the myelin sheath made this kind of conduction
possible. This idea has become a standard item in physiology textbooks, and its
familiarity leads many people to assume that the presence of myelin sheaths in the brain serves
the same "insulating" function.</span></span></span>
</blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>For a long time it has been known that heat production during nerve conduction reveals a more
continuous mode of conduction, that doesn't conform to the idea of an electrical
current jumping around an insulator. Even if the myelin functioned primarily to produce
"saltatory conduction" in peripheral nerves, it isn't clear how this process could function in
the brain. I think of the issue of "saltatory conduction at the nodes of Ranvier" as
another of the fetish ideas that have served to obstruct progress in biology in the United
States. A more realistic approach to nerve function can be found in Gilbert Ling's
work. Ling has demonstrated in many ways that the ruling dogma of "cell membrane" function
isn't coherently based on fact. He found that hormones such as progesterone regulate the
energetic and structural stability of cells. Many people, unaware of his work, have felt
that it was necessary to argue against the idea that there are anesthetic steroids with
generalized protective functions, because of their commitment to a textbook dogma of "cell
membrane" physiology.</span></span></span>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>I think the myelinating cells do have relevance to nerve conduction, but I don't think they serve
primarily as electrical insulators. If the adrenal cortex were inside the heart, it would
be obvious to ask whether its hormones aren't important for the heart's function. Since
the oligodendrocytes are steroid-synthesizers, it seems obvious to ask whether their production
of pregnenolone in response to stress or fatigue isn't relevant to the conduction processes of
the nerves they surround.</span></span></span>
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<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
style="font-size: small"
><span style="font-size: small"><strong>OLD AGE</strong></span></span></span></span>
</blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>A biologist friend of mine who was about 85 became very senile. His wife started giving him
thyroid, progesterone, DHEA and pregnenolone, and within a few days his mental clarity had
returned. He continued to be mentally active until he was 89, when his wife interfered
with his access to the hormones.</span></span></span>
</blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>In old age the brain steroids fall to about 5% of their level in youth. Pregnenolone and DHEA
improve memory in old rats, and improve mood stability and mental clarity of old people.
Pregnenolone's action in improving the sense of being able to cope with challenges probably
reflects a quieting and coordinating of the "sequencing" apparatus of the forebrain, which is
the area most sensitive to energy deprivation. This is the area that malfunctions in
hyperactive and "dyslexic" children. Weakening of the sequencing and sorting processes
probably explains the common old-age inability to extract important sounds from environmental
noise, creating a kind of "confusion deafness." Insomnia, worry and "restless legs" at
bedtime are problems for many old people, and I think they are variations of the basic
energy-depletion problem.</span></span></span>
</blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>The oligodendrocytes were reported (Hiroisi and Lee, 1936) to be the source of the senile plaques
or amyloid deposits of Alzheimer's disease.(16) Hiroisi and Lee showed the cells in
different stages of degeneration, ending with translucent "mucoid" spots that stained the same
as amyloid, the material in the senile plaques. This type of cell also appears to form a
halo or crown around degenerating nerve cells--possibly in a protective reaction to provide the
nerve cell with any pregnenolone the oligodendrocytes are able to make. The
oligodendrocytes, the source of the brain steroids (that people previously believed came from
the adrenals and gonads, and were just stored in the brain), myelinate nerve fibers under
the influence of thyroid hormone (17). Thyroid is responsible for both myelination
and hormone formation. In old age, glial cells become more numerous, and nerve cells
become structurally and functionally abnormal, but usually there is no problem with
the formation of myelin. In MS, the problem is just with myelination, and there are
no senile plaques or defects in the nerve cells themselves. </span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"> <span style="font-family: georgia, times, serif"><span
style="font-size: small"
><span style="font-style: normal"><span style="font-weight: normal"
>These differences suggest the possibility that Alzheimer's disease involves a
specific premature loss of brain pregnen- olone production, but not of
thyroid. Recent work suggests a central role for pregnenolone and progesterone in
the regulation of consciousness (18), and possibly in the brain's detoxifying
system. Elsewhere, I have suggested that vitamin A deficiency might cause the
excessive production of the "amyloid" protein. A vitamin A deficiency severely
inhibits steroid synthesis. (It is used so massively in steroid synthesis that a
progesterone supplement can prevent the symptoms of vitamin A deficiency.) I
suspect that vitamin A is necessary for the side-chain cleavage that converts
cholesterol to pregnenolone. Iron-stimulated lipid peroxidation is known to block
steroid formation, and vitamin A is very susceptible to destruction by iron and
oxidation. Iron tends to accumulated in tissues with aging. Gajdusek
has demonstrated that brain deterioration is associated with the retention of
whatever metal happens to be abundant in the person's environment, not just with
aluminum. (One type of glial cell is known for its metal-binding function, causing
them to be called "metallophils."). According to Gajdusek, "calcium and other di-
and trivalent elements" are "deposited as hydroxyapatites in brain cells" in brain
degeneration of the Alzheimer's type.(19)</span></span></span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>Even early forms of Alzheimer's disease begin at an age when the youth-associated steroids
have begun to decline. If MS involves a deficiency of thyroid (or of T3 within the
oligodendrocytes, where T3 normally can be made from thyroxine; many things, including protein
deficiency, can block the conversion of T4 to T3), those cells would necessarily be deficient in
their ability to produce pregenolone, but in young people the brain would still be
receiving a little pregnenolone, progesterone, and DHEA from the adrenals and gonads. This
relatively abundant youthful supply of hormones would keep most of the body's organs in good
condition, and could keep the bodies of the major brain cells from deteriorating. But if
proper functioning of the nerve fibers requires that they be fed a relatively high concentration
of pregnenolone from their immediately adjacent neighbors (with the amount increasing during
stress and fatigue), then their function would be impaired when they had to depend on the
hormones that arrived from the blood stream.</span></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>For many years it has been recognized that the brain atrophy of "Alzheimer's disease" resembles the
changes seen in the brain in many other situations: The traumatic dementia of boxers;
toxic dementia; the slow-virus diseases; exposure of the brain to x-rays (20); ordinary old age;
and in people with Down's syndrome who die around the age of thirty.
</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>In menopause, certain nerve cells have lost their ability to regulate the ovaries, because of
prolonged exposure to estrogen (6). The cells that fail as a result of prolonged estrogen
exposure aren't the same cells that fail from prolonged exposure to the glucocorticoids (7), but
they have in common the factor of excitatory injury.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>Since people who experience premature menopause are known to be more likely than average to die
prematurely, it is reasonable to view menopause as a model of the aging process. It is now well
established that progesterone fails to be produced at the onset of menopause (the first missed
period, increased loss of calcium, symptoms such as hot flashes, etc.), and that estrogen
continues to be produced at monthly intervals for about four years. The essential question
for aging, in the present context, is why the anesthetic steroids are no longer produced at a
rate that allows them to protect tissues, including brain cells, from the excitotoxins.
Using menopause as a model for aging, we can make the question more answerable by asking why
progesterone stops being produced.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>During stress, we are designed not to get pregnant, and the simplest aspect of this is that ACTH,
besides stimulating the adrenals to produce stress-related hormones, inhibits the production of
progesterone by the ovary. Other stress-induced factors, such as increased prolactin and
decreased thyroid, also inhibit progesterone production. Stress eventually makes us more
susceptible to stress. Menopause and other landmarks of aging simply represent upward
inflections in the rate-of-aging curve. Individual variations in type of stress, hormonal
response and diet, etc., probably govern the nature of the aging process in an individual.</span
></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>The amphetamine-like action of estrogen, which undoubtedly contributes to the general level
of stress and excitotoxic abuse of nerve cells, is probably the only "useful" facet
of estrogen treatment, but a little cocaine might achieve the same effect with no
more harm, possibly less. The toxicity of catecholamines has been known for over thirty
years, and estrogen's stimulating effects are partly the result of its conversion to
catechol-estrogens which increase the activity of brain catecholamines. Estrogen's
powerful ability to nullify learning seems never to be mentioned by the people who promote its
use. The importance of a good balance of brain steroids for mood, attention, memory, and
reasoning is starting to be recognized, but powerful economic forces militate against its
general acceptance.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>Since the brain is the organ that can allow us to adapt without undergoing stress in the hormonal
sense, it is very important to protect its flexibility and to keep its energy level high, so it
can work in a relaxed way. It is the low energy cellular state that leads to the retention
of calcium and iron, and to the production of age pigment, and other changes that constitute the
vicious circle of aging. And mental activity that challenges obsession and rigidity might
be the most important brain energizer. Pseudo-optimism, humor-as-therapy, has a certain
value, but a deeper optimism involves a willingness to assimilate new information and to change
plans accordingly.</span></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
style="font-size: small"
><span style="font-size: small"><strong>SUPPLEMENTS</strong></span></span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>Nutritional supplements that might help to prevent or correct these brain syndromes include:
Vitamin E and coconut oil; vitamin A; magnesium, sodium; thyroid which includes T3;
large amounts of animal protein, especially eggs; sulfur, such as magnesium sulfate or
flowers of sulfur, but not to take continuously, because of sulfur's interference with
copper absorption; pregnenolone; progesterone if needed. Bright light, weak in the blue
end of the spectrum and with protection against ultraviolet, activates respiratory metabolism
and quenches free radicals. Raw carrot fiber and/or laxatives if needed; charcoal
occasionally for gas or bowel irritation. Coconut oil serves several purposes.
Its butyric acid is known to increase T3 uptake by glial cells. It has a general
pro-thyroid action, for example by diluting and displacing antithyroid unsaturated oils, its
short- and medium-chain fatty acids sustain blood sugar and have antiallergic actions, and it
protects mitochondria against stressinjury. </span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>P.S.: In 1979, a woman whose husband was suffering from advanced Amyotrophic Lateral
Sclerosis (ALS) asked me if I had any ideas for slowing his decline. I described my
suspicion that ALS involved defective metabolism or regulation of testosterone. In some
tissues, testosterone is selectively concentrated to prevent atrophy, and ALS is a disease of
middle-age, when hormone regulation often becomes a special problem. In the late 1970s,
there was discussion of a higher incidence of ALS in males, and especially in athletes. I
told her about progesterone's general protective effects, its antagonism to testosterone, and
its prevention of atrophy in various tissues. She decided to ask her doctor to try
progesterone for her husband. Later, I learned that her husband had gone into a very rapid
decline immediately after the injection, and died within a week; the physician had given him
testosterone, since, he said, "testosterone and progesterone are both male hormones."
Besides making me more aware of the problems patients have in communicating with physicians,
this tended to reinforce my feeling that a hormone imbalance is involved in ALS. Although
I haven't written much about testosterone's toxicity, Marian Diamond's work showed that prenatal
testosterone is similar to prenatal estrogen, in causing decreased thickness of the cortex of
the brain; both of those hormones oppose progesterone's brain-protecting and brain-promoting
actions.</span></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
style="font-size: small"
><strong><h3>REFERENCES</h3></strong></span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>1) Z. Y. Hu, et al., P.N.A.S. (USA) 84, 8215-9, 1987.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>2) P. F. Hall, Vitamins and Hormones 42, 315-370, 1985.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>3) J. J. Lambert, et al., Trends in Pharmac. Sci. 8, 224-7, 1987.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>4) W. A. D. A. Anderson, Pathology (second edition), C. V. Mosby, St. Louis, 1953.</span
></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>5) S. S. Smith, et al., Brain Res. 422, 52-62, 1987.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>6) P. M. Wise, Menopause, 1984; S. S. Smith, et al., Brain Res. 422, 40-51, 1987.</span
></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>7) R. M. Sapolsky, et al., J. Neuroscience 5, 1222-1227, 1985; R. M. Sapolsky and W.
Pulsinelli, Science 229, 1397-9, 1985.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>8) C. B. Nemeroff, (Excitotoxins) 290-305, 1984.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>9) G. B. Phillips, Lancet 2, 14-18, 1976; G. B. Phillips, et al., Am. J. Med. 74, 863-9,
1983; M. H. Luria, et al., Arch Intern Med 142, 42-44, 1982; E. L. Klaiber, et al., Am J Med 73,
872-881, 1982.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>10) J. I. Mann, et al., Br Med J 2, 241-5, 1975.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>11) V. Gisclard and P. M. Vanhoutte, Physiologist 28, 324(48.1).</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>12) W. A. D. A. Anderson, Pathology, 1953; H. H. Reese, et al., editors, 1936 Yearbook
of Neurology, Psychiatry, and Endocrinology, Yearbook Publishers, Chicago, 1937.
</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>13) T. J. Putnam, Ann Int Med 9, 854-63, 1936; JAMA 108, 1477, 1937.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>14) R. S. Dow and G. Berglund, Arch Neurol and Psychiatry 47, 1, 1992.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>15) R. W. Estabrook, et al., Biochem Z. 338, 741-55, 1963.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>16) S. Hiroisi and C. C. Lee, Arch Neurol and Psychiat 35, 827-38, 1936.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>17) J. M. Matthieu, et al., Ann Endoc. 1974.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>18) K. Iwaharhi, et al., J Ster Biochem and Mol Biol 44(2), 163-4, 1993.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>19) D. C. Gajdusek, Chapter 63, page 1519 in Virology (B. N. Fields, et al., editors), Raven
Press, N.Y., 1985.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>20) K. Lowenberg-Scharenberg and R. C. Bassett, J Neuropath and Exper Neurol 9, 93,
1950.</span></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>GLOSSARY </span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>1. Amyloid is the old term for the "starchy" appearing (including the way it stains) proteins
seen in various diseases, and in the brain in Alzheimer's disease.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>2. Cytochrome P450scc. The cytochromes are "pigments," in the same sense that they
contain the colored "heme" group that gives hemoglobin its color. P450 means "protein that
absorbs light at a wavelength of 450. The scc means "side-chain cleaving," which refers to
the removal of the 6 carbon atoms that distinguish cholesterol from pregnenolone. Other Cyt P450
enzymes are important for their detoxifying oxidizing action, and some of these are involved in
brain metabolism.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>3. Glial means "glue-like," and glial cells are mostly spidery-shaped cells that used to be
thought of as just connective, supportive cells in the brain.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>4. Mitochondria (the "thread-like bodies") are the structures in cells which produce most of
our metabolic energy by respiration, in response to the thyroid hormones.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>5. Mucoid--refers to a mucoprotein, a protein which contains some carbohydrate. A
glycoprotein; usually not intended as a precise term.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>6. Myelination. Myelin is a multilayered enclosure of the axons (the long processes) of
nerve cells, composed of proteins and complex lipids, including cholesterol. The layered
material is a flat, thin extension of the cytoplasm of the oligodendroglial cells.</span></span
></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>7. Oligodendrocytes are one of the kinds of glial (or neuroglial) cells, and structurally
they are unusual in having sheet-like, rather than just thread-like processes; they have a
sensitivity ("receptors") to stress and valium, and produce pregnenolone when activated.
Under the influence of thyroid hormone, they wrap themselves in thin layers around the
conductive parts of nerve cells, leaving a multilayered "myelin" coating. Their absorption
of thyroid hormone is promoted by butyrate, an anti-stress substance found in butter and coconut
oil.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"
>8. Steroidogenesis is the creation of steroids, usually referring to the conversion of
cholesterol to hormones.</span></span></span>
</blockquote>
<p> </p>
© Ray Peat Ph.D. 2013. All Rights Reserved. www.RayPeat.com
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