Controlling Symptoms In Multiple Sclerosis And Stress-.

charlie

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Controlling symptoms in multiple sclerosis and stress-related diseases.

My previous articles suggested that conventional doctrines about MS were mistaken, and showed reasons for trying other therapies. Emerging information suggests that the orthodox treatments based on misunderstanding the nature of the problem are harming patients. I think the basic problem is that physicians think in terms of attacking "the disease," instead of supporting the patient.

Physicians commonly say that the cause of MS isn't known, but they are confident of the involvement of "genes" and the "immune system," with "autoimmunity" possibly triggered by a previous viral infection, such as measles. Glucocorticoids and other "more sophisticated" immunosuppressants have been the standard treatments.

Because the incidence of MS is greater at high latitudes, with less ultraviolet exposure, a vitamin D deficiency is now often suspected to be involved. But the hypothetical "triggering factors" of an autoimmune reaction don't guide the conventional approaches to treatment, which focus on the immune system and the cells that are supposedly attacking the myelin sheaths of nerves. Identifying "autoimmunity" as the essence of the disease has the advantage that it can be treated with the same immunosuppressant drugs used for treating psoriasis, cancer, arthritis, lupus, etc., such as azathioprine, cyclophosphamide, cyclosporin A, methotrexate, mitoxantrone, and glucocorticoids. Since its approval for use in multiple sclerosis in 1993, the immune system "modulator" beta-interferon has been widely used, and its sales are now worth about $500 million per year.

These chemicals do kill some of the cells that are involved in the elimination of the myelin sheaths. Their disadvantage is that they are extremely toxic, and can cause diseases such as leukemia, and they can damage systems that are essential for recovery of functions (e.g., Smith and Franklin, 2001). Their long-range effects are still unknown. We normally begin learning about the adverse effects of a drug around the time that its patent is expiring.

Interferon-beta has recently been identified as a link between two important mediators of inflammation that can cause brain damage or death (Caso, et al., 2007; Cartwright, et al., 2007; Kim, et al., 2007; Thomas, et al., 2006). It increases cortisol and prolactin (Then Bergh, 2007).

The drug-centered medical culture guides research relating to multiple sclerosis. A university group (Gregg, et al., 2007) has proposed that prolactin might be used to treat MS patients. Knowing that patients often have a remission during pregnancy, they studied the myelin-forming cells in pregnant mice, and found that they regenerate quickly in the presence of increased prolactin. Their reasoning was able to convince the people who funded them, and the editors who published their paper.

Drug companies are eagerly waiting for new drugs to sell for MS. Genzyme General, which is involved in marketing beta-interferon for treating multiple sclerosis, has patents on recombinant transgenic prolactin, and the company is planning to promote its use in medicine.

But prolactin has an important role in producing inflammation in humans and other species. It induces at least two of the most important factors that specifically contribute to the brain damage in MS.

The antiinflammatory pregnancy hormone that is associated with MS remission is progesterone, and it is well known as one of the hormones--along with thyroid and pregnenolone--required for synthesizing myelin. In rodents prolactin is well known as a stimulus for the production of progesterone, but in humans increased prolactin suppresses progesterone synthesis, which accounts for infertility during lactation (Konner and Worthman, 1980). During the first three months postpartum there is a higher risk of new attacks than before the pregnancy.

Researchers working with rodents are assumed to understand the important physiological differences between rodents and humans, but the present culture encourages experiments to be designed to justify potential new billion dollar drugs, rather than to advance general physiological knowledge.

If the principle, "First do no harm," were applied, the pharmaceutical industry would be in trouble.

When people who are diagnosed with diabetes, or cancer, or Alzheimer's disease refuse treatment and go home and get well after doing something nonmedical, the official medical conclusion is that the diagnosis must have been incorrect, because those conditions have highly predictable courses.

But with multiple sclerosis, the situation is different. Those people who get well are said to still have multiple sclerosis, because both temporary and permanent remissions are considered to be compatible with "having" multiple sclerosis. Some physicians encourage them to continue treatments even when they have no symptoms.

Even if many people seem to recover from MS while doing something inexpensive, that won't necessarily seriously impact the treatment industry, or the national economy.

Medical spending in the US is now more than 4 times greater than military spending. Medical research and publication are oriented toward increased profits. Information which threatens those profits is easily ignored.

The incidence and prevalence of multiple sclerosis have been increasing very rapidly in most places in the world. In some places incidence increased fourfold in 30 years. (Grimaldi, et al., 2007) During this time, the cost of drugs used to treat it has increased from a few dollars to more than $1000 per month, and the annual cost of drugs to treat it in the US is expected to rise quickly from $4 billion to $6 billion.

There is general agreement that inflammation is involved, and that stress aggravates the problem. If the meaning of stress could be clarified in relation to MS, a systematic approach to minimize it would seem desirable. Little attention has been given to that approach, because of the powerful fetishes of "genes" and "autoimmunity."

Stress and inflammation, especially in the case of MS, are very closely related. An imbalance between increased excitation and decreased ability to efficiently produce energy leads to cellular fatigue and maladaptive changes.

Everything is influenced by changing conditions. When their internal coherence and energy reserves are adequate, organisms adapt to stress in constructive ways, for example by increasing the synthesis of some substances or by increasing cell division. When that isn't possible, the organism may resort to defensive processes, in which metabolic requirements are decreased, as in hibernation. These defensive reactions are commonly involved in degenerative diseases.

The defensive reactions that reduce the metabolic rate typically act on the respiratory enzyme, cytochrome oxidase. This is the most important enzyme activated by the thyroid hormone, and the thyroid activity itself is quickly depressed by a stress as mild as a decrease in blood sugar. In multiple sclerosis, the brain's metabolic rate is slowed.

Cortisol, which is increased by stress, lowers the activity of cytochrome oxidase (Simon, et al., 1998).

With decreased activity of the respiratory enzyme, the brain will be in a relatively reduced state, with a higher ratio of NADH to NAD (Pasichna, et al., 2004; Steen, et al., 1987). Cells are more susceptible to free radical damage in the reduced state, and this contributes to lipid peroxidation. In MS, lipid peroxidation, indicating oxidative stress, is increased (Toshniwal and Zarling, 1992). Increased nitric oxide synthesis occurs in the MS brain (Calabrese, et al., 2002), some of it originating in the endothelial cells of blood vessels. Isoprostanes, produced by polyunsaturated fats during oxidative stress, are increased in the cerebrospinal fluid in MS. Oxidatively damaged myelin is recognized as foreign, and stimulates cells to remove it.

One of the molecules produced by many kinds of stress, nitric oxide, at first counters the stress, by opening blood vessels to deliver more blood, and by inhibiting the respiratory enzyme, to reduce the need for oxygen. This shifts metabolism to the glycolytic production of energy, forming lactic acid instead of carbon dioxide when oxygen is scarce. This tends to raise the cell's pH, and to increase the ratio of NADH/NAD. The temporary inhibition of the respiratory enzyme can easily become permanent, and the dilated vessels become more permeable, allowing molecules to leak from the plasma into the tissues. Lactate itself contributes to vascular permeability, as well as interfering with respiratory energy production.

Many stress-induced factors besides NO contribute to vascular leakiness, including cortisol, estrogen, prolactin, histamine, serotonin, carbon monoxide, polyunsaturated fatty acids, prostaglandins, and probably endogenous opiates, such as beta-endorphin. During hypoxia, beta-endorphin also suppresses respiration (Xu, et al., 1999), and lowers the metabolic rate (Lin and Su, 1979).

Stress can cause vascular leakiness in any organ, and can disrupt the blood brain barrier, causing leakiness into the brain. Fibrin and fibrinogen, the blood clotting proteins, and their breakdown products, and other proteins, fats, and even red blood cells, can pass from the blood into the brain (Esposito, et al., 2001, 2002; Theoharides, et al., 2007). The entry of fibrin and related proteins into the brain precedes the entry of cells (Floris, et al., 2003).

In multiple sclerosis, there is an increased viscosity of the blood (Brunetti, et al., 1981), causing it to clot too quickly, and a decreased ability to remove clots.

The energy failure that leads to vascular leakage is preceded by oxidative stress and nitric oxide formation (Jacobson, et al., 2005). Histamine's promotion of vascular permeability is mediated by nitric oxide (Mayhan, 1994). Many things contribute to the release of histamine from mast cells, but endotoxin and estrogen are among the most important mast cell activators.

These events all tend to contradict the standard doctrine that cells from the immune system start the problem by attacking myelin. It appears that the actual causes of the problem precede the invasion of inflammatory thymus cells and the removal of the myelin by phagocytic cells.

In the intestine, emotional or physical stress reduces blood circulation, and the resulting hypoxia makes the blood vessels more permeable, allowing bacterial endotoxin to enter the blood stream in larger amounts. Endotoxin is a powerful stimulus to the enzyme nitric oxide synthase, increasing the amount of nitric oxide in the blood systemically. It also increases the production of cortisol, fibrinogen, and inflammatory cytokines, increases the tendency of the blood to coagulate spontaneously, and makes blood vessels more permeable. The loss of blood volume is a factor in the shock produced by a large amount of endotoxin. Endotoxin also increases estrogen, prolactin, endorphins, leptin, prostaglandins, free fatty acids, TNF, histamine, serotonin, and other proinflammatory substances. Some of these activate the formation of nitric oxide. Luteinizing hormone, progesterone, T3, TSH, and testosterone are usually decreased by endotoxin.

The endorphins and nitric oxide and estrogen that are produced by stress can contribute to increased prolactin secretion. Prolactin is increased in association with MS.

The effect of chronic mild exposure to endotoxin can be seen by the effect of an antibiotic, or by eating raw carrots---in women with low progesterone and high estrogen and cortisol, those antibacterial substances can increase progesterone, and lower estrogen and cortisol. (Carrots suppress bacteria by both chemical and physical means.) The effect of antibiotics on the steroid hormones had been seen in animals, but it was discovered in women by accident when infertile women were given antibiotics experimentally, and noticed that they stopped having the premenstrual syndrome. There have been reports of improvement in MS patients treated with antibiotics, but the assumption has commonly been that they are treating a bacterial infection in the brain, rather than reducing inflammation caused by endotoxin from the bowel (Mikhailoff, 1953).

Autoimmune diseases, including neurological diseases, have frequently been associated with increased permeability of the bowel (e.g., Hadjivassiliou, et al., 1996; Roth, et al., 2006). People with MS have increased antibodies to gluten and gliadin (Reichelt and Jensen, 2004), supporting the idea of an association between celiac disease and MS. Gerhard Volkheimer's comments on the immunological implications of persorbed starch particles are clearly relevant, though generally ignored.

The tetracylines and erythromycin inhibit the synthesis of nitric oxide (Kohri, et al., 2000; Milano, et al., 1997) and protect the brain against endotoxin (Fan, et al., 2005) and against microglial activation and oxidative damage (Choi, et al, 2005).
Studies in animals have shown clearly that a protein deficiency increases the fibrinogen content of blood (Field and Dam, 1946). The stressful effects of a protein deficiency are very similar to those of endotoxin poisoning. Protein deficiency can cause increased tryptophan in the brain (Miller, et al., 1977), and excess tryptophan contributes to oxidative stress (Feksa, et al., 2006). A daily intake of at least 80 grams of protein is probably protective against MS. Gelatin, because of the brain-protective effects of its high glycine content, and its lack of tryptophan, is probably one of the most protective proteins.

Histamine, serotonin, endorphins and other brain peptides, nitric oxide, estrogen, and cortisol are some of the factors in the stress response that can be modified therapeutically.

The classical "stress response" involves the production of cortisol, which increases blood sugar and suppresses inflammation (but also suppresses respiration). Falling blood sugar is sufficient to trigger the reactive secretion of cortisol. An injury (or stressor) that impairs tissue energy production causes the rapid conversion of glucose to lactic acid. Lactic acid, as well as falling glucose, will trigger cortisol release. Simply eating sucrose inhibits cortisol production. The minerals in fruits help to metabolize the sugars. Good thyroid function is essential for keeping the blood sugar steady, and helps to minimize fluctuations in cortisol and other stress hormones.

Orange juice contains the antiinflammatory chemicals naringin and naringenin, which protect against endotoxin by suppressing the formation of nitric oxide and prostaglandins (Shiratori, et al., 2005).

Women normally have higher cortisol levels than men do, because of estrogen's effects, and women are much more susceptible to MS than men are--four times as likely, according to a recent study (Cutter, 2007). Cortisol, like prolactin, shifts the blood's equilibrium toward clotting, though it does provide some protection against endotoxin and other inflammatory agents. Although too much protein in the diet can activate the stress hormones, a deficiency makes it impossible for the thyroid to function fully, and leads to a chronic excess of estrogen, and often prolactin.

Adequate diet and good thyroid function will correct over-production of prolactin, but the drug bromocriptine is commonly used to lower it, and it has been reported to have beneficial effects in MS (Azar and Yamout, 1999; Bissay, et al., 1994). Excess prolactin is involved in several other "autoimmune" conditions (Compan Gonzalez, 1996). Bromocriptine treatment often corrects a progesterone deficiency, because of prolactin's suppressive effect on the ovary (del Pozo, et al., 1979; Seppala, et al., 1976).

The use of antihistamines (histamine-1 blockers) such as Benadryl has been associated with a greatly reduced risk (0.2) of developing MS (Alonso, et al., 2006). Benadryl blocks histamine's stimulating effect on prolactin secretion (Rivier and Vale, 1977).

The mast cells, which release histamine and other inflammation-provoking materials in the brain, are an important link between stress and the inflammation that produces demyelination in MS. The histamine they release activates nitric oxide formation, and damages the blood-brain barrier. The number of mast cells in the brain is variable, and can be significantly altered within a few days simply by changed living arrangements (Asarian, et al., 2002).

Estrogen is an activator of mast cells, and it appears to be involved in their myelin-damaging effects (Theoharides, et al., 1993). Progesterone inhibits mast cell activation (Vasiadi, et al., 2006), and acts like an antihistamine in blocking its effects in the brain (Uchida, et al., 2003).

Reports of MS symptoms worsening in association with menstruation (Zorgdrager and De Keyser, 1997) and the association between the number of brain lesions and high estrogen, low progesterone (Bansil, et al., 1999), suggests that treatment with progesterone would be reasonable. It inhibits the synthesis of nitric oxide and many other mediators of inflammation. Progesterone synthesis is blocked by endotoxin and nitric oxide (Mishra and Dhali, 2007).

Because of the importance of myelin, thyroid treatment would seem to be one of the first things that neurologists would think of for treating MS patients, since thyroid hormone accelerates the synthesis of myelin, and hypothyroidism is often associated with demyelinating nerve symptoms (Shirabe, et al., 1975; Zampollo, et al., 1983; Jagannathan, et al., 1998). Thyroid has many antiinflammatory effects, besides inhibiting prolactin secretion.

Vitamin D and vitamin K both inhibit nitric oxide synthesis, and have some antiestrogenic properties (e.g., Otsuka, et al., 2005), and they both help to prevent abnormal spontaneous clotting (Koyama and Hirosawa, 1999), and they regulate calcium. Supplemental calcium itself inhibits prolactin secretion.

Medical people have focused on ultraviolet light as the protective factor in sunlight. One of the important effects of ordinary visible light is the restoration of the respiratory enzyme. More than 80 years ago Otto Warburg demonstrated this effect, and since then others have demonstrated a variety of mechanisms through which light restores activity to inhibited cytochrome oxidase. For example, it frees the enzyme from inhibition by nitric oxide (Borutaite, et al., 2000).

When the respiratory pigment functions properly, cells produce carbon dioxide rather than lactic acid, and carbon dioxide is an important compound in preserving cellular integrity and preventing inflammation. For example, a decrease in carbon dioxide in the blood causes serotonin to be released, increasing vascular permeability and the tendency of the blood to clot.

Carbon dioxide concentrations can be increased by the drug acetazolamide (Diamox), and this drug has been used to treat some of the symptoms of MS (Hamasaki, et al., 1998; Voiculescu, et al., 1975). There is some evidence that acetazolamide decreases nitric oxide (Taki, et al., 1999).

Aspirin has several antiinflammatory nerve-protecting actions, including the inhibition of nitric oxide synthase and nitrite production (Amin, et al., 1995) and the scavenging of nitric oxide radicals (Asanuma, et al., 2001). Another inhibitor of nitric oxide synthesis, aminoguanidine, protects against experimental autoimmune encaphalomyelitis in mice (Cross, et al., 1994).

Niacinamide inhibits nitric oxide synthesis (Fukuzawa, et al., 1997; Fujimura, et al., 1997) and protects against some of its toxic effects (Narang and Krishna, 2005). Women are more likely than men to be deficient in niacin, and are twice as likely to develop pellagra from a niacin deficiency. This is because estrogen shifts tryptophan metabolism toward the formation of serotonin, and away from synthesizing niacin. Niacin has many other effects that would be beneficial in multiple sclerosis, for example inhibiting the release of free fatty acids from tissues.

The effects of estrogen, stress, and polyunsaturated fats on tryptophan metabolism suggest that a diet with minimal tryptophan could be helpful in the stress related diseases. Choosing foods such as gelatin, lacking tryptophan, and supplying an abundance of glycine, would tend to reduce nitric oxide formation (e.g., Fang, et al., 2003).

Eliminating polyunsaturated fats from the diet reduces the formation of prostaglandins, isoprostanes, and neuroprostanes, increases respiratory metabolism, and reduces vascular leakiness. The polyunsaturated fatty acids can increase nitric oxide (Chaet, et al., 1994), and many other factors that promote inflammation (Jia and Turek, 2005).

Caffeine and other methylxanthines alleviate symptoms in EAE, the animal model of MS (Tsutsui, et al., 2004). Caffeine and theophylline reduce the formation of nitric oxide (Bereta, et al., 1994).

Among the stress-related factors involved in inflammation that I have mentioned, there are several---tryptophan, serotonin, estrogen, endorphins, polyunsaturated fats, and even nitric oxide---that have had cultural niches as "good things." Viagra/sildenafil made nitric oxide famous as the erection chemical, and the drug has even been used to treat women with sexual problems related to MS.

The industry connections to most of them are obvious, except in the case of the endorphins. (Although beta-endorphin hasn't been approved as a drug for human use, it has been patented, and the industry occasionally produces hopeful press releases about it.) Athletes and the media created a cultural mystique about the endorphins that makes it confusing to physicians when a patient expresses an interest in lowering it.

Although one of the antiendorphin drugs, naloxone, is usually sold in 0.4 mg ampules for injection, a nearly identical drug, naltrexone, has been sold in 50 mg tablets for oral use. Naloxone has been used to treat opiate overdoses, but naltrexone is now being used to treat immunodeficiency, cancer, and MS, but some of its proponents call their method "low dose naltrexone" therapy, because they use doses ranging from 3 mg to 10 mg per day, and argue that it is effective because it is increasing, rather than lowering, the endorphins. The evidence is pretty clear that it produces its antistress, antiinflammatory effects by lowering, as well as antagonizing, the endorphins. This results in lowering the formation of nitric oxide, and probably reducing excitotoxic cell damage (Agrawal, 2006).

It happens that these same antiinflammatory factors are helpful for many diseases, and none is as harmful as even the safest of the drugs commonly used to treat MS. Some people are allergic to acetazolamide, a few people have allergy-like reactions to aspirin and bromocriptine, and very prolonged use of naloxone or naltrexone hasn't been studied, so those should be used cautiously.

Both patients and physicians are influenced by a culture in which a "serious disease" diagnosis calls for an "aggressive medical attack" on the disease, even when those attacks on "the disease" cause undeniable damage to the patient. But the fact that remissions are common in multiple sclerosis might give patients a sense that they have time to try some procedures that are based on well understood mechanisms that reduce stress and inflammation.
 

Kray

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Re: Controlling Symptoms in Multiple Sclerosis and Stress-..

Charlie, I found this article fascinating. Are you the author? I have a friend who has MS (63yo female) who I love to share things with about MS as I find them. I don't know if she is in active treatment anymore, but might I be bold enough to share this with her? Maybe one of the alternative docs she has seen in the past would help her to implement some of the more nutritional, and less invasive/expensive approaches covered in this article. Ironically, a neighbor is one of the top dogs in MS research. What would be your take on sharing this with him? (operative word "research" = institutionalized approach?) :)

Thank you for sharing!
 

charlie

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Re: Controlling Symptoms in Multiple Sclerosis and Stress-..

Ray Peat wrote all the articles in this section. :)
 

Kray

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Re: Controlling Symptoms in Multiple Sclerosis and Stress-..

Charlie said:
Ray Peat wrote all the articles in this section. :)

:oops: I didn't see that. Thanks anyway for sharing the link. I've probably read that article before, but because I'm not a science person, it was like reading it the first time :) But little by little, as I read his material, I am beginning to appreciate and better understand the amazing physiology of the human body. He is able to make things clear enough for people like myself, giving us not only the knowledge, but the potential power to good health!
 
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