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djledda-web/raypeat-articles/processed/multiple-sclerosis.html

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  1. <html>

  2.     <head><title></title></head>

  3.     <body>

  4.         <h1></h1>

  5. 

  6.         <p></p>

  7.         <blockquote>

  8.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span

  9.                         style="font-size: medium"

  10.                     ><strong>MULTIPLE SCLEROSIS AND OTHER HORMONE-RELATED BRAIN SYNDROMES (1993)</strong></span></span

  11.                 ></span>

  12.         </blockquote>

  13.         <blockquote></blockquote>

  14.         <blockquote>

  15.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  16.                     >Since I am trying to discuss a complex matter in a single article, I have separately outlined the

  17.                         essential technical points of the argument in a section at the beginning, then I explain how my

  18.                         ideas on the subject developed, and finally there is a glossary.&nbsp; If you start with

  19.                         "Short-day brain stress," "Estrogen's effects," and "Symptoms and therapies," you will have the

  20.                         general picture, and can use the other sections to fill in the technical details.</span></span

  21.                 ></span>

  22.         </blockquote>

  23.         <blockquote></blockquote>

  24.         <blockquote>

  25.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span

  26.                         style="font-size: small"

  27.                     ><strong>THE ARGUMENT:</strong></span></span></span>

  28.         </blockquote>

  29.         <blockquote>

  30.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  31.                     >1) The hormones pregnenolone, thyroid, and estrogen are involved in several ways with the changes

  32.                         that occur in multiple sclerosis, but no one talks about them.</span></span></span>

  33.         </blockquote>

  34.         <blockquote>

  35.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  36.                     >2) The process of myelination is known to depend on the thyroid hormone.&nbsp; The myelinating

  37.                         cells are the oligodendroglia (oligodendrocytes) which appear to stop functioning in MS

  38.                         (and&nbsp; sometimes to a milder degree in Alzheimer's disease, and other&nbsp;

  39.                         conditions).&nbsp; The cells' absorption of thyroid hormone is influenced by dietary

  40.                         factors.</span></span></span>

  41.         </blockquote>

  42.         <blockquote>

  43.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  44.                     >3) The oligodendrocytes are steroid-producing cells (1),&nbsp; and steroidogenesis is dependent on

  45.                         thyroid hormone, and on&nbsp; thyroid-dependent respiratory enzymes and on the heme-enzyme

  46.                         P-450scc, which are all sensitive (2) to poisoning by carbon monoxide and cyanide.&nbsp; The

  47.                         steroid produced by the oligodendrocytes is pregnenolone, which is known to have a

  48.                         profound&nbsp; anti-stress action (3), and which appears to be the main&nbsp; brain-protective

  49.                         steroid.</span></span></span>

  50.         </blockquote>

  51.         <blockquote>

  52.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  53.                     >4) Lesions resembling those of MS can be produced experimentally by carbon monoxide or cyanide

  54.                         poisoning.(4)&nbsp; The lesions&nbsp; tend to be associated with individual small blood vessels,

  55.                         which &nbsp; are likely to contain clots.&nbsp; (Since all animals have enzymes to&nbsp;

  56.                         detoxify cyanide, this poison is apparently a universal problem,&nbsp; and can originate in the

  57.                         bowel. "Detoxified" cyanide is still toxic to the thyroid.)&nbsp;</span></span></span>

  58.         </blockquote>

  59.         <blockquote>

  60.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  61.                     >5) Pregnenolone and progesterone protect against nerve damage (5) by the excitotoxic amino acids

  62.                         (glutamic acid, aspartic acid, monosodium glutamate, aspartame, etc.), while estrogen (6) and

  63.                         cortisol (7) are nerve-destroying, acting through the excitotoxic amino acids.&nbsp;

  64.                         Excitotoxins destroy certain types of nerve, especially the dopaminergic and cholinergic types,

  65.                         leaving the noradrenergic types (8), paralleling the changes that occur in aging.&nbsp; The

  66.                         clustering of oligodendrocytes around deteriorating nerve cells could represent an adaptive

  67.                         attempt to provide pregnenolone to injured nerve cells.</span></span></span>

  68.         </blockquote>

  69.         <blockquote>

  70.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  71.                     >6) The involvement of hormones and environmental factors probably accounts for the intermittent

  72.                         progress of multiple sclerosis. To the extent that the environmental factors can be&nbsp;

  73.                         corrected, the disease can probably be controlled.</span></span></span>

  74.         </blockquote>

  75.         <blockquote></blockquote>

  76.         <blockquote>

  77.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span

  78.                         style="font-size: small"

  79.                     ><span style="font-style: normal"><strong>SHORT-DAY BRAIN STRESS</strong></span></span></span></span

  80.             >

  81.         </blockquote>

  82.         <blockquote>

  83.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  84.                     >Shortly after I moved from Mexico to Montana, one of my students, a 32 year old woman, began having

  85.                         the same sensory symptoms her older sister had experienced at the same age, at the onset of

  86.                         multiple sclerosis.&nbsp; Vertigo and visual distortions of some sort made her consider

  87.                         withdrawing from the university. I'm not sure why she tried eating a whole can of tuna for lunch

  88.                         a couple of days after the onset of symptoms, but it seemed to alleviate the symptoms, and she

  89.                         stayed on a high protein diet and never had a recurrence.&nbsp; She told me some of the lore of

  90.                         MS: That it mostly affects young adults between the ages of 20 and 40, that it is common in high

  91.                         latitudes and essentially unknown in the tropics, and that it is sometimes exacerbated by

  92.                         pregnancy and stress.&nbsp; (Later, I learned that systemic lupus erythematosis and other

  93.                         "auto-immune" diseases also tend to occur mainly during the reproductive years.&nbsp; I

  94.                         discussed some of the implications of this in "Bean Syndrome.")</span></span></span>

  95.         </blockquote>

  96.         <blockquote>

  97.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  98.                     >Having enjoyed the mild climate of Mexico, I became very conscious of the harm done to us by

  99.                         northern winters, and began developing the idea of "winter sickness."&nbsp; In 1966-67,

  100.                         allergies, PMS, weight gain, colitis, and arthritis came to my attention as winter-related

  101.                         problems, and I assumed that the high-latitude incidence of MS related to what I was seeing and

  102.                         experiencing.&nbsp; Studies in Leningrad began revealing that mitochondria are injured during

  103.                         darkness, and repaired during daylight.&nbsp; I observed that hamsters' thymus glands shrank in

  104.                         the winter and regenerated in the summer; shrinkage of the thymus gland is a classical feature

  105.                         of stress, and usually reflects the dominance of cortisone, though estrogen and testosterone

  106.                         also cause it to shrink.&nbsp; Winter's darkness is stressful in a very fundamental way, and

  107.                         like any stress it tends to suppress thyroid function.&nbsp; In the hypothyroid state, any

  108.                         estrogen which is produced tends to accumulate in the body, because of liver sluggishness.</span

  109.                     ></span></span>

  110.         </blockquote>

  111.         <blockquote>

  112.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  113.                     >I began to see that PMS could be controlled by certain things--extra light, supplements of sodium

  114.                         and magnesium, high quality protein, and correction of deficiencies of thyroid and

  115.                         progesterone.&nbsp; In working on my dissertation, I saw that tissue hypoxia (lower than optimal

  116.                         concentrations of oxygen in the blood) may result from estrogen excess, vitamin E deficiency, or

  117.                         aging.&nbsp; There is a close biological parallel between estrogen-dominance and the other

  118.                         hypoxic states, such as stress/shock, and aging.</span></span></span>

  119.         </blockquote>

  120.         <blockquote></blockquote>

  121.         <blockquote>

  122.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span

  123.                         style="font-size: small"

  124.                     ><span style="font-style: normal"><strong>ESTROGEN'S EFFECTS</strong></span></span></span></span>

  125.         </blockquote>

  126.         <blockquote>

  127.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  128.                     >As a portrait painter, I had been very conscious of the blue aspect that can often be seen in the

  129.                         skin of young women. In pale areas, the color may actually be blue, and in areas with a rich

  130.                         supply of blood, such as the lips, the color is lavender during times of high estrogen

  131.                         influence--around ovulation and puberty, for example.&nbsp; During these times of estrogen

  132.                         dominance, the blood is not only poorly oxygenated, but it has other special properties, such as

  133.                         an increased tendency to clot.&nbsp; The Shutes' work in the 1930s began with the use of vitamin

  134.                         E to antagonize estrogen's clot-promoting tendency, and led them to the discovery that vitamin E

  135.                         can be very therapeutic in heart disease.&nbsp; More recently, it has been found that men with

  136.                         heart disease have abnormally high estrogen (9), that women using oral contraceptives have

  137.                         higher mortality from heart attacks (10), and that estrogen tends to&nbsp; promote spasm of

  138.                         blood vessels (11).&nbsp; (These reactions are probably&nbsp; related to the physiology of

  139.                         menstruation, in which progesterone&nbsp;withdrawal causes spasms in the spiral arteries of the

  140.                         uterus,&nbsp; producing endometrial anoxia and cell death.)</span></span></span>

  141.         </blockquote>

  142.         <blockquote>

  143.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  144.                     >In toxemia of late pregnancy, or eclampsia, the exaggerated clotting tendency caused by excess

  145.                         estrogen (or by inadequately opposed estrogen, i.e., progesterone deficiency), can cause

  146.                         convulsions and strokes.&nbsp; Vascular spasms could be involved here, too.&nbsp; The stasis

  147.                         caused by the vasospasm would facilitate clotting. (Vascular spasm has been observed in

  148.                         epilepsy, too.&nbsp; Epilepsy can be brought on by the premenstrual excess of estrogen, and in

  149.                         that situation there is no evidence that clotting is involved.&nbsp; Leakage of hemoglobin out

  150.                         of red cells can cause vasospasm, so bleeding, clotting, strokes, and seizures can interact

  151.                         complexly.)&nbsp; The brains of women who have died&nbsp;following eclampsia show massive

  152.                         clotting in the blood vessels, and their livers are characteristically injured, with clots

  153.                         (12).</span></span></span>

  154.         </blockquote>

  155.         <blockquote>

  156.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  157.                     >Tom Brewer and others have shown very clearly that malnutrition, especially protein deficiency, is

  158.                         the cause of toxemia of late pregnancy.&nbsp; (In Nutrition for Women, I discussed the

  159.                         importance of protein in allowing the liver to eliminate estrogen.)</span></span></span>

  160.         </blockquote>

  161.         <blockquote>

  162.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  163.                     >Various researchers have demonstrated that the plaques of MS usually occur in the area served by a

  164.                         single blood vessel (13, 14), and some have suggested that clotting is the cause.&nbsp; MS

  165.                         patients have been found to have an abnormal clotting time, and it has been suggested that an

  166.                         altered diet might be able to correct the clotting tendency.</span></span></span>

  167.         </blockquote>

  168.         <blockquote>

  169.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  170.                     >Studies in animals have shown clearly that a protein deficiency increases the fibrinogen content of

  171.                         blood. (Field and Dam, 1946.)&nbsp; Other factors that increase blood clotting are elevated

  172.                         adrenalin and cortisone.&nbsp; Protein deficiency causes an adaptive decrease in thyroid

  173.                         function, which leads to a compensatory increase in adrenaline and cortisone.&nbsp; The

  174.                         combination of high estrogen with high adrenaline increases the tendency for both clots and

  175.                         spasms of the blood vessels (11).</span></span></span>

  176.         </blockquote>

  177.         <blockquote>

  178.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  179.                     >In experimental poisoning of animals with carbon monoxide or cyanide, the brain lesions resembling

  180.                         MS include blood clots.&nbsp; The patchy distribution of these spots in the brain suggests that

  181.                         the clotting is secondary to metabolic damage in the brain.&nbsp; Presumably, the same would be

  182.                         true in ordinary MS, with clots and spasms being induced in certain areas by metabolic

  183.                         abnormalities in brain cells.&nbsp; The injured cells that are responsible for myelination of

  184.                         nerve fibers are steroid-forming cells.&nbsp; A failure to secrete their protective pregnenolone

  185.                         could cause a local spasm of a blood vessel.&nbsp; The circulatory problem would exacerbate the

  186.                         respiratory problem. Steroid production is dependent on NADH and NADPH, and so requires adequate

  187.                         energy supplies and energy metabolism.&nbsp; The phenomenon of blood-sludging, studied by M.

  188.                         Knisely at the University of Chicago in the l930s and l940s, is apparently a general result of

  189.                         decreased energy metabolism, and is likely to be a factor in energy-and-circulatory vicious

  190.                         circles.</span></span></span>

  191.         </blockquote>

  192.         <blockquote></blockquote>

  193.         <blockquote>

  194.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span

  195.                         style="font-size: small"

  196.                     ><span style="font-style: normal"><strong>SYMPTOMS AND THERAPIES</strong></span></span></span></span

  197.             >

  198.         </blockquote>

  199.         <blockquote>

  200.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  201.                     >Around 1976 I met a woman in her mid-thirties who heard about my work with progesterone in

  202.                         animals.&nbsp; She had been disabled by a brain disease that resembled MS or Devic's disease,

  203.                         inflammation of the optic nerves.&nbsp; It would sometimes cause blindness and paralysis that

  204.                         persisted for weeks at a time.&nbsp; During remissions, sometimes using a wheelchair, she would

  205.                         go to the medical school library to try to understand her condition.&nbsp; She came across

  206.                         Katherina Dalton's work with progesterone, and convinced a physician to give her a trial

  207.                         injection.&nbsp; Although she had trouble finding people who were willing to give her

  208.                         progesterone, her recovery was so complete that she was able to climb stairs and drive her car,

  209.                         and she came&nbsp; to my endocrinology class and gave a very good (and long) lecture on

  210.                         progesterone therapy.&nbsp; Although her sensory and motor functions became normal, she remained

  211.                         very fat, and chronically suffered from sore areas on her arms and legs that seemed to be

  212.                         abnormal blood vessels, possibly with phlebitis.&nbsp; She appeared to need thyroid hormone as

  213.                         well as larger amounts of progesterone, but never found a physician who would cooperate, as far

  214.                         as I know.</span></span></span>

  215.         </blockquote>

  216.         <blockquote>

  217.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  218.                     >In the late 1970s I was seeing a lot of people who had puzzling health problems.&nbsp; In a period

  219.                         of two or three years, there were five people who had been diagnosed by neurologists as having

  220.                         multiple sclerosis.&nbsp; In talking to them, it seemed clear that they had multiple symptoms of

  221.                         hypothyroidism. &nbsp; They weren't severely disabled.&nbsp; Since they weren't fat or

  222.                         lethargic, their physicians hadn't thought they could be hypothyroid.&nbsp; When they tried

  223.                         taking a thyroid supplement, all of their symptoms disappeared, including those that had led to

  224.                         their MS diagnosis.&nbsp; One of the women went to her doctor to tell him that she felt

  225.                         perfectly healthy since taking thyroid, and he told her to stop taking it, because people who

  226.                         have MS need a lot of rest, and she wouldn't get enough rest if she was living in a normally

  227.                         active way. The assumption seemed to be that the diagnosis was more important than the person.

  228.                         (When I refer to a "thyroid supplement" I mean one that contains some T3.&nbsp; Many people

  229.                         experience "neurological symptoms" when they take thyroxine by itself.&nbsp; Experimentally, it

  230.                         has been found to suppress brain respiration, probably by diluting the T3 that was already

  231.                         present in the brain tissue.) &nbsp;</span></span></span>

  232.         </blockquote>

  233.         <blockquote></blockquote>

  234.         <blockquote>

  235.             <span style="color: #222222"><span style="font-size: small"><span

  236.                         style="font-family: georgia, times, serif"

  237.                     ><span style="font-style: normal"><strong>METABOLISM OF THE OLIGODENDROCYTES</strong></span></span

  238.                     ></span></span>

  239.         </blockquote>

  240.         <blockquote>

  241.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  242.                     >The rate-regulating step in steroid synthesis involves the entry of cholesterol into the

  243.                         mitochondria, where the heme-enzyme P-450scc then removes the side-chain of cholesterol&nbsp;

  244.                         (by introducing oxygen atoms), to produce pregnenolone.&nbsp; This enzyme can be poisoned by

  245.                         carbon monoxide or cyanide, and light can eliminate the poison (15); this could be one aspect of

  246.                         the winter-sickness problem. &nbsp;</span></span></span>

  247.         </blockquote>

  248.         <blockquote></blockquote>

  249.         <blockquote>

  250.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  251.                     >Peripheral nerves are myelinated by essentially the same sort of cell that is called an

  252.                         oligodendrocyte in the brain, but outside the brain it is called a Schwann cell.&nbsp; It is

  253.                         easier to study the myelin sheath in peripheral nerves, and the electrical activity of a nerve

  254.                         is the most easily studied aspect of its physiology.&nbsp; Certain experiments seemed to

  255.                         indicate a "jumping" (saltatory) kind of conduction along the nerve between Schwann cells, and

  256.                         it was argued that the insulating function of the myelin sheath made this kind of conduction

  257.                         possible.&nbsp; This idea has become a standard item in physiology textbooks, and its

  258.                         familiarity leads many people to assume that the presence of myelin sheaths in the brain serves

  259.                         the same "insulating" function.</span></span></span>

  260.         </blockquote>

  261.         <blockquote>

  262.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  263.                     >For a long time it has been known that heat production during nerve conduction reveals a more

  264.                         continuous mode of&nbsp; conduction, that doesn't conform to the idea of an electrical&nbsp;

  265.                         current jumping around an insulator.&nbsp; Even if the myelin functioned primarily to produce

  266.                         "saltatory conduction" in peripheral nerves, it isn't clear how this process could function in

  267.                         the brain.&nbsp; I think of the issue of "saltatory conduction at the nodes of Ranvier" as

  268.                         another of the fetish ideas that have served to obstruct progress in biology in the United

  269.                         States.&nbsp; A more realistic approach to nerve function can be found in Gilbert Ling's

  270.                         work.&nbsp; Ling has demonstrated in many ways that the ruling dogma of "cell membrane" function

  271.                         isn't coherently based on fact.&nbsp; He found that hormones such as progesterone regulate the

  272.                         energetic and structural stability of cells.&nbsp; Many people, unaware of his work, have felt

  273.                         that it was necessary to argue against the idea that there are anesthetic steroids with

  274.                         generalized protective functions, because of their commitment to a textbook dogma of "cell

  275.                         membrane" physiology.</span></span></span>

  276.         </blockquote>

  277.         <blockquote>

  278.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  279.                     >I think the myelinating cells do have relevance to nerve conduction, but I don't think they serve

  280.                         primarily as electrical insulators.&nbsp; If the adrenal cortex were inside the heart, it would

  281.                         be obvious to ask whether its hormones aren't important for the heart's function.&nbsp; Since

  282.                         the oligodendrocytes are steroid-synthesizers, it seems obvious to ask whether their production

  283.                         of pregnenolone in response to stress or fatigue isn't relevant to the conduction processes of

  284.                         the nerves they surround.</span></span></span>

  285.         </blockquote>

  286.         <blockquote></blockquote>

  287.         <blockquote>

  288.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span

  289.                         style="font-size: small"

  290.                     ><span style="font-size: small"><strong>OLD AGE</strong></span></span></span></span>

  291.         </blockquote>

  292.         <blockquote>

  293.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  294.                     >A biologist friend of mine who was about 85 became very senile.&nbsp; His wife started giving him

  295.                         thyroid, progesterone, DHEA and pregnenolone, and within a few days his mental clarity had

  296.                         returned.&nbsp; He continued to be mentally active until he was 89, when his wife interfered

  297.                         with his access to the hormones.</span></span></span>

  298.         </blockquote>

  299.         <blockquote>

  300.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  301.                     >In old age the brain steroids fall to about 5% of their level in youth.&nbsp; Pregnenolone and DHEA

  302.                         improve memory in old rats, and improve mood stability and mental clarity of old people.&nbsp;

  303.                         Pregnenolone's action in improving the sense of being able to cope with challenges probably

  304.                         reflects a quieting and coordinating of the "sequencing" apparatus of the forebrain, which is

  305.                         the area most sensitive to energy deprivation.&nbsp; This is the area that malfunctions in

  306.                         hyperactive and "dyslexic" children.&nbsp; Weakening of the sequencing and sorting processes

  307.                         probably explains the common old-age inability to extract important sounds from environmental

  308.                         noise, creating a kind of "confusion deafness."&nbsp; Insomnia, worry and "restless legs" at

  309.                         bedtime are problems for many old people, and I think they are variations of the basic

  310.                         energy-depletion problem.</span></span></span>

  311.         </blockquote>

  312.         <blockquote>

  313.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  314.                     >The oligodendrocytes were reported (Hiroisi and Lee, 1936) to be the source of the senile plaques

  315.                         or amyloid deposits of Alzheimer's disease.(16)&nbsp; Hiroisi and Lee showed the cells in

  316.                         different stages of degeneration, ending with translucent "mucoid" spots that stained the same

  317.                         as amyloid, the material in the senile plaques.&nbsp; This type of cell also appears to form a

  318.                         halo or crown around degenerating nerve cells--possibly in a protective reaction to provide the

  319.                         nerve cell&nbsp; with any pregnenolone the oligodendrocytes are able to make.&nbsp; The&nbsp;

  320.                         oligodendrocytes, the source of the brain steroids (that people previously believed came from

  321.                         the adrenals and gonads, and were just stored in the brain), myelinate nerve fibers under

  322.                         the&nbsp; influence of thyroid hormone (17).&nbsp; Thyroid is responsible for both myelination

  323.                         and hormone formation.&nbsp; In old age, glial cells become more numerous, and nerve cells

  324.                         become structurally&nbsp; and functionally abnormal, but usually there is no problem&nbsp; with

  325.                         the formation of myelin.&nbsp; In MS, the problem is just with&nbsp; myelination, and there are

  326.                         no senile plaques or defects in the&nbsp; nerve cells themselves. &nbsp;</span></span></span>

  327.         </blockquote>

  328.         <blockquote>

  329.             <span style="color: #222222">&nbsp;&nbsp; &nbsp; <span style="font-family: georgia, times, serif"><span

  330.                         style="font-size: small"

  331.                     ><span style="font-style: normal"><span style="font-weight: normal"

  332.                             >These differences suggest the possibility that Alzheimer's&nbsp; disease involves a

  333.                                 specific premature loss of brain pregnen-&nbsp; olone production, but not of

  334.                                 thyroid.&nbsp; Recent work suggests a central role for pregnenolone and progesterone in

  335.                                 the regulation of consciousness (18), and possibly in the brain's detoxifying

  336.                                 system.&nbsp; Elsewhere, I have suggested that vitamin A deficiency might cause the

  337.                                 excessive production of the "amyloid" protein.&nbsp; A vitamin A deficiency severely

  338.                                 inhibits steroid synthesis.&nbsp; (It is used so massively in steroid synthesis that a

  339.                                 progesterone supplement can prevent the symptoms of vitamin A deficiency.)&nbsp; I

  340.                                 suspect that vitamin A is necessary for the side-chain cleavage that converts

  341.                                 cholesterol to pregnenolone.&nbsp; Iron-stimulated lipid peroxidation is known to block

  342.                                 steroid formation, and vitamin A is very susceptible to destruction&nbsp; by iron and

  343.                                 oxidation.&nbsp; Iron tends to accumulated in tissues&nbsp; with aging.&nbsp; Gajdusek

  344.                                 has demonstrated that brain deterioration&nbsp; is associated with the retention of

  345.                                 whatever metal happens to be abundant in the person's environment, not just with

  346.                                 aluminum.&nbsp; (One type of glial cell is known for its metal-binding function, causing

  347.                                 them to be called "metallophils.").&nbsp; According to Gajdusek, "calcium and other di-

  348.                                 and trivalent elements" are "deposited as hydroxyapatites in brain cells" in brain

  349.                                 degeneration of the Alzheimer's type.(19)</span></span></span></span></span>

  350.         </blockquote>

  351.         <blockquote>

  352.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  353.                     >Even early forms of Alzheimer's disease begin at an age&nbsp; when the youth-associated steroids

  354.                         have begun to decline. If&nbsp; MS involves a deficiency of thyroid (or of T3 within the

  355.                         oligodendrocytes, where T3 normally can be made from thyroxine; many things, including protein

  356.                         deficiency, can block the conversion of T4 to T3), those cells would necessarily be deficient in

  357.                         their ability to produce pregenolone, but in&nbsp; young people the brain would still be

  358.                         receiving a little pregnenolone, progesterone, and DHEA from the adrenals and gonads.&nbsp; This

  359.                         relatively abundant youthful supply of hormones would keep most of the body's organs in good

  360.                         condition,&nbsp; and could keep the bodies of the major brain cells from deteriorating. But if

  361.                         proper functioning of the nerve fibers requires that they be fed a relatively high concentration

  362.                         of pregnenolone from their immediately adjacent neighbors (with the amount increasing during

  363.                         stress and fatigue), then their function would be impaired when they had to depend on the

  364.                         hormones that arrived from the blood stream.</span></span></span>

  365.         </blockquote>

  366.         <blockquote></blockquote>

  367.         <blockquote>

  368.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  369.                     >For many years it has been recognized that the brain atrophy of "Alzheimer's disease" resembles the

  370.                         changes seen in the brain in many other situations:&nbsp; The traumatic dementia of boxers;

  371.                         toxic dementia; the slow-virus diseases; exposure of the brain to x-rays (20); ordinary old age;

  372.                         and in people with Down's syndrome who die around the age of thirty.&nbsp; &nbsp; &nbsp; &nbsp;

  373.                         &nbsp; &nbsp;</span></span></span>

  374.         </blockquote>

  375.         <blockquote>

  376.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  377.                     >In menopause, certain nerve cells have lost their ability to regulate the ovaries, because of

  378.                         prolonged exposure to estrogen (6).&nbsp; The cells that fail as a result of prolonged estrogen

  379.                         exposure aren't the same cells that fail from prolonged exposure to the glucocorticoids (7), but

  380.                         they have in common the factor of excitatory injury.</span></span></span>

  381.         </blockquote>

  382.         <blockquote>

  383.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  384.                     >Since people who experience premature menopause are known to be more likely than average to die

  385.                         prematurely, it is reasonable to view menopause as a model of the aging process. It is now well

  386.                         established that progesterone fails to be produced at the onset of menopause (the first missed

  387.                         period, increased loss of calcium, symptoms such as hot flashes, etc.), and that estrogen

  388.                         continues to be produced at monthly intervals for about four years.&nbsp; The essential question

  389.                         for aging, in the present context, is why the anesthetic steroids are no longer produced at a

  390.                         rate that allows them to protect tissues, including brain cells, from the excitotoxins.&nbsp;

  391.                         Using menopause as a model for aging, we can make the question more answerable by asking why

  392.                         progesterone stops being produced.</span></span></span>

  393.         </blockquote>

  394.         <blockquote>

  395.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  396.                     >During stress, we are designed not to get pregnant, and the simplest aspect of this is that ACTH,

  397.                         besides stimulating the adrenals to produce stress-related hormones, inhibits the production of

  398.                         progesterone by the ovary.&nbsp; Other stress-induced factors, such as increased prolactin and

  399.                         decreased thyroid, also inhibit progesterone production.&nbsp; Stress eventually makes us more

  400.                         susceptible to stress.&nbsp; Menopause and other landmarks of aging simply represent upward

  401.                         inflections in the rate-of-aging curve.&nbsp; Individual variations in type of stress, hormonal

  402.                         response and diet, etc., probably govern the nature of the aging process in an individual.</span

  403.                     ></span></span>

  404.         </blockquote>

  405.         <blockquote></blockquote>

  406.         <blockquote>

  407.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  408.                     >The amphetamine-like action of estrogen, which undoubtedly&nbsp; contributes to the general level

  409.                         of stress and excitotoxic&nbsp; abuse of nerve cells, is probably the only "useful" facet

  410.                         of&nbsp; estrogen treatment, but a little cocaine might achieve the&nbsp; same effect with no

  411.                         more harm, possibly less.&nbsp; The toxicity of catecholamines has been known for over thirty

  412.                         years, and estrogen's stimulating effects are partly the result of its conversion to

  413.                         catechol-estrogens which increase the activity of brain catecholamines.&nbsp; Estrogen's

  414.                         powerful ability to nullify learning seems never to be mentioned by the people who promote its

  415.                         use.&nbsp; The importance of a good balance of brain steroids for mood, attention, memory, and

  416.                         reasoning is starting to be recognized, but powerful economic forces militate against its

  417.                         general acceptance.</span></span></span>

  418.         </blockquote>

  419.         <blockquote>

  420.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  421.                     >Since the brain is the organ that can allow us to adapt without undergoing stress in the hormonal

  422.                         sense, it is very important to protect its flexibility and to keep its energy level high, so it

  423.                         can work in a relaxed way.&nbsp; It is the low energy cellular state that leads to the retention

  424.                         of calcium and iron, and to the production of age pigment, and other changes that constitute the

  425.                         vicious circle of aging.&nbsp; And mental activity that challenges obsession and rigidity might

  426.                         be the most important brain energizer.&nbsp; Pseudo-optimism, humor-as-therapy, has a certain

  427.                         value, but a deeper optimism involves a willingness to assimilate new information and to change

  428.                         plans accordingly.</span></span></span>

  429.         </blockquote>

  430.         <blockquote></blockquote>

  431.         <blockquote>

  432.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span

  433.                         style="font-size: small"

  434.                     ><span style="font-size: small"><strong>SUPPLEMENTS</strong></span></span></span></span>

  435.         </blockquote>

  436.         <blockquote>

  437.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  438.                     >Nutritional supplements that might help to prevent or correct these brain syndromes include:

  439.                         Vitamin E and&nbsp; coconut oil; vitamin A; magnesium, sodium; thyroid which&nbsp; includes T3;

  440.                         large amounts of animal protein, especially&nbsp; eggs; sulfur, such as magnesium sulfate or

  441.                         flowers of&nbsp; sulfur, but not to take continuously, because of sulfur's interference with

  442.                         copper absorption; pregnenolone; progesterone if needed.&nbsp; Bright light, weak in the blue

  443.                         end of the spectrum and with protection against ultraviolet, activates respiratory metabolism

  444.                         and quenches free radicals.&nbsp; Raw carrot fiber and/or laxatives if needed; charcoal

  445.                         occasionally for gas or bowel&nbsp; irritation.&nbsp; Coconut oil serves several purposes.&nbsp;

  446.                         Its butyric acid is known to increase T3 uptake by glial cells.&nbsp; It has a general

  447.                         pro-thyroid action, for example by diluting and displacing antithyroid unsaturated oils, its

  448.                         short- and medium-chain fatty acids sustain blood sugar and have antiallergic actions, and it

  449.                         protects mitochondria against stressinjury.&nbsp;</span></span></span>

  450.         </blockquote>

  451.         <blockquote>

  452.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  453.                     >P.S.:&nbsp; In 1979, a woman whose husband was suffering from advanced Amyotrophic Lateral

  454.                         Sclerosis (ALS) asked me if I had any ideas for slowing his decline.&nbsp; I described my

  455.                         suspicion that ALS involved defective metabolism or regulation of testosterone.&nbsp; In some

  456.                         tissues, testosterone is selectively concentrated to prevent atrophy, and ALS is a disease of

  457.                         middle-age, when hormone regulation often becomes a special problem.&nbsp; In the late 1970s,

  458.                         there was discussion of a higher incidence of ALS in males, and especially in athletes.&nbsp; I

  459.                         told her about progesterone's general protective effects, its antagonism to testosterone, and

  460.                         its prevention of atrophy in various tissues.&nbsp; She decided to ask her doctor to try

  461.                         progesterone for her husband.&nbsp; Later, I learned that her husband had gone into a very rapid

  462.                         decline immediately after the injection, and died within a week; the physician had given him

  463.                         testosterone, since, he said, "testosterone and progesterone are both male hormones."&nbsp;

  464.                         Besides making me more aware of the problems patients have in communicating with physicians,

  465.                         this tended to reinforce my feeling that a hormone imbalance is involved in ALS.&nbsp; Although

  466.                         I haven't written much about testosterone's toxicity, Marian Diamond's work showed that prenatal

  467.                         testosterone is similar to prenatal estrogen, in causing decreased thickness of the cortex of

  468.                         the brain; both of those hormones oppose progesterone's brain-protecting and brain-promoting

  469.                         actions.</span></span></span>

  470.         </blockquote>

  471.         <blockquote></blockquote>

  472.         <blockquote>

  473.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span

  474.                         style="font-size: small"

  475.                     ><strong><h3>REFERENCES</h3></strong></span></span></span>

  476.         </blockquote>

  477.         <blockquote>

  478.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  479.                     >1)&nbsp; Z. Y. Hu, et al., P.N.A.S. (USA) 84, 8215-9, 1987.</span></span></span>

  480.         </blockquote>

  481.         <blockquote>

  482.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  483.                     >2)&nbsp; P. F. Hall, Vitamins and Hormones 42, 315-370, 1985.</span></span></span>

  484.         </blockquote>

  485.         <blockquote>

  486.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  487.                     >3)&nbsp; J. J. Lambert, et al., Trends in Pharmac. Sci. 8, 224-7, 1987.</span></span></span>

  488.         </blockquote>

  489.         <blockquote>

  490.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  491.                     >4)&nbsp; W. A. D. A. Anderson, Pathology (second edition), C. V. Mosby, St. Louis, 1953.</span

  492.                     ></span></span>

  493.         </blockquote>

  494.         <blockquote>

  495.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  496.                     >5)&nbsp; S. S. Smith, et al., Brain Res. 422, 52-62, 1987.</span></span></span>

  497.         </blockquote>

  498.         <blockquote>

  499.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  500.                     >6)&nbsp; P. M. Wise, Menopause, 1984; S. S. Smith, et al., Brain Res. 422, 40-51, 1987.</span

  501.                     ></span></span>

  502.         </blockquote>

  503.         <blockquote>

  504.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  505.                     >7)&nbsp; R. M. Sapolsky, et al., J. Neuroscience 5, 1222-1227, 1985; R. M. Sapolsky and W.

  506.                         Pulsinelli, Science 229, 1397-9, 1985.</span></span></span>

  507.         </blockquote>

  508.         <blockquote>

  509.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  510.                     >8)&nbsp; C. B. Nemeroff, (Excitotoxins)&nbsp; 290-305, 1984.</span></span></span>

  511.         </blockquote>

  512.         <blockquote>

  513.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  514.                     >9)&nbsp; G. B. Phillips, Lancet 2, 14-18, 1976; G. B. Phillips, et al., Am. J. Med. 74, 863-9,

  515.                         1983; M. H. Luria, et al., Arch Intern Med 142, 42-44, 1982; E. L. Klaiber, et al., Am J Med 73,

  516.                         872-881, 1982.</span></span></span>

  517.         </blockquote>

  518.         <blockquote>

  519.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  520.                     >10)&nbsp; J. I. Mann, et al., Br Med J 2, 241-5, 1975.</span></span></span>

  521.         </blockquote>

  522.         <blockquote>

  523.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  524.                     >11)&nbsp; V. Gisclard and P. M. Vanhoutte, Physiologist 28, 324(48.1).</span></span></span>

  525.         </blockquote>

  526.         <blockquote>

  527.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  528.                     >12)&nbsp; W. A. D. A. Anderson, Pathology, 1953; H. H. Reese, et al.,&nbsp; editors, 1936 Yearbook

  529.                         of Neurology, Psychiatry, and Endocrinology,&nbsp; Yearbook Publishers, Chicago, 1937.&nbsp;

  530.                         &nbsp;</span></span></span>

  531.         </blockquote>

  532.         <blockquote>

  533.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  534.                     >13)&nbsp; T. J. Putnam, Ann Int Med 9, 854-63, 1936; JAMA 108, 1477, 1937.</span></span></span>

  535.         </blockquote>

  536.         <blockquote>

  537.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  538.                     >14)&nbsp; R. S. Dow and G. Berglund, Arch Neurol and Psychiatry 47, 1, 1992.</span></span></span>

  539.         </blockquote>

  540.         <blockquote>

  541.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  542.                     >15)&nbsp; R. W. Estabrook, et al., Biochem Z. 338, 741-55, 1963.</span></span></span>

  543.         </blockquote>

  544.         <blockquote>

  545.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  546.                     >16)&nbsp; S. Hiroisi and C. C. Lee, Arch Neurol and Psychiat 35, 827-38, 1936.</span></span></span>

  547.         </blockquote>

  548.         <blockquote>

  549.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  550.                     >17)&nbsp; J. M. Matthieu, et al., Ann Endoc. 1974.</span></span></span>

  551.         </blockquote>

  552.         <blockquote>

  553.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  554.                     >18)&nbsp; K. Iwaharhi, et al., J Ster Biochem and Mol Biol 44(2), 163-4, 1993.</span></span></span>

  555.         </blockquote>

  556.         <blockquote>

  557.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  558.                     >19)&nbsp; D. C. Gajdusek, Chapter 63, page 1519 in Virology (B. N. Fields, et al., editors), Raven

  559.                         Press, N.Y., 1985.</span></span></span>

  560.         </blockquote>

  561.         <blockquote>

  562.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  563.                     >20)&nbsp; K. Lowenberg-Scharenberg and R. C. Bassett, J Neuropath and Exper Neurol 9, 93,

  564.                         1950.</span></span></span>

  565.         </blockquote>

  566.         <blockquote></blockquote>

  567.         <blockquote>

  568.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  569.                     >GLOSSARY&nbsp;&nbsp;</span></span></span>

  570.         </blockquote>

  571.         <blockquote>

  572.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  573.                     >1.&nbsp; Amyloid is the old term for the "starchy" appearing (including the way it stains) proteins

  574.                         seen in various diseases, and in the brain in Alzheimer's disease.</span></span></span>

  575.         </blockquote>

  576.         <blockquote>

  577.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  578.                     >2.&nbsp; Cytochrome P450scc.&nbsp; The cytochromes are "pigments," in the same sense that they

  579.                         contain the colored "heme" group that gives hemoglobin its color.&nbsp; P450 means "protein that

  580.                         absorbs light at a wavelength of 450.&nbsp; The scc means "side-chain cleaving," which refers to

  581.                         the removal of the 6 carbon atoms that distinguish cholesterol from pregnenolone. Other Cyt P450

  582.                         enzymes are important for their detoxifying oxidizing action, and some of these are involved in

  583.                         brain metabolism.</span></span></span>

  584.         </blockquote>

  585.         <blockquote>

  586.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  587.                     >3.&nbsp; Glial means "glue-like," and glial cells are mostly spidery-shaped cells that used to be

  588.                         thought of as just connective, supportive cells in the brain.</span></span></span>

  589.         </blockquote>

  590.         <blockquote>

  591.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  592.                     >4.&nbsp; Mitochondria (the "thread-like bodies") are the structures in cells which produce most of

  593.                         our metabolic energy by respiration, in response to the thyroid hormones.</span></span></span>

  594.         </blockquote>

  595.         <blockquote>

  596.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  597.                     >5.&nbsp; Mucoid--refers to a mucoprotein, a protein which contains some carbohydrate.&nbsp; A

  598.                         glycoprotein; usually not intended as a precise term.</span></span></span>

  599.         </blockquote>

  600.         <blockquote>

  601.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  602.                     >6.&nbsp; Myelination.&nbsp; Myelin is a multilayered enclosure of the axons (the long processes) of

  603.                         nerve cells, composed of proteins and complex lipids, including cholesterol.&nbsp; The layered

  604.                         material is a flat, thin extension of the cytoplasm of the oligodendroglial cells.</span></span

  605.                 ></span>

  606.         </blockquote>

  607.         <blockquote>

  608.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  609.                     >7.&nbsp; Oligodendrocytes are one of the kinds of glial (or neuroglial) cells, and structurally

  610.                         they are unusual in having sheet-like, rather than just thread-like processes; they have a

  611.                         sensitivity ("receptors") to stress and valium, and produce pregnenolone when activated.&nbsp;

  612.                         Under the influence of thyroid hormone, they wrap themselves in thin layers around the

  613.                         conductive parts of nerve cells, leaving a multilayered "myelin" coating.&nbsp; Their absorption

  614.                         of thyroid hormone is promoted by butyrate, an anti-stress substance found in butter and coconut

  615.                         oil.</span></span></span>

  616.         </blockquote>

  617.         <blockquote>

  618.             <span style="color: #222222"><span style="font-family: georgia, times, serif"><span style="font-size: small"

  619.                     >8.&nbsp; Steroidogenesis is the creation of steroids, usually referring to the conversion of

  620.                         cholesterol to hormones.</span></span></span>

  621.         </blockquote>

  622.         <p>&nbsp;</p>

  623. 

  624.         © Ray Peat Ph.D. 2013. All Rights Reserved. www.RayPeat.com

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