SULFUR AMINO ACIDS: Cysteine & Glutathione; Taurine; Methionine; Homocysteine

Cysteine and Glutathione – The Detoxifiers

Cysteine is important in energy metabolism. As cystine, it is a structural component of many tissues and hormones.

But what makes L-cysteine and all the chemical variants of it that are used in modern medicine-N-acetylcysteine, D-penicillamine (di-methylcysteine), gamma glutamyl cystine, and cysteamine-so active pharmacologically is that cysteine is a precursor of the ubiquitous tripeptide glutathione.

Glutathione is a compound synthesized from cysteine, perhaps the most important member of the body’s toxic waste disposal team.

Like cysteine, glutathione contains the crucial thiol (-SH) group that makes it an effective antioxidant. There are virtually no living organisms on this planet-animal or plant whose cells don’t contain some glutathione. Scientists have speculated that glutathione was essential to the very development of life on earth.

Glutathione has many roles; in none does it act alone. It is a coenzyme in various enzymatic reactions. The most important of these are redox reactions, in which the thiol grouping on the cysteine portion of cell membranes protects against peroxidation; and conjugation reactions, in which glutathione (especially in the liver) binds with toxic chemicals in order to detoxify them. Glutathione is also important in red and white blood cell formation and throughout the immune system. (See Selenium also)

Through these basic functions, glutathione is important Everyone is likely to be exposed to many of the pollutants GSH detoxifies, including lead, mercury, radiation, pesticides herbicides, fungicides, plastics, nitrates, cigarette smoke, birth control pills and other drugs. At the same time, cysteine, by its rapid conversion to GSH, protects against these toxins.

Glutathione’s clinical uses include the prevention of oxygen toxicity in hyperbaric oxygen therapy, treatment of lead and other heavy metal poisoning, lowering of the toxicity of chemotherapy and radiation in cancer treatments, and reversal of cataracts. In one study, oral glutathione was able to reverse advanced liver cancer in rats (Novi, 1981). Other potential uses may be in increasing the recovery chances of stroke victims, preventing or even reversing liver cirrhosis, and alleviating arthritis, psychosis and allergy.

Cysteine itself, in addition to the detoxifying function that results from its ability to increase glutathione levels, has clinical uses ranging from baldness to psoriasis to preventing smoker’s hack. N-acetylcysteine is available in liquid or aerosol and is great for mucus-burdened bronchial passages. In some cases, oral cysteine therapy has proved excellent for treatment of asthmatics, enabling them to stop theophylline and other medications.

Cysteine also enhances the effect of topically applied silver, tin and zinc salts in preventing dental cavities. In the future, cysteine may play a role in the treatment of cobalt toxicity, diabetes, psychosis, cancer and seizures.

At the Brain Bio Center, our standard dose of L-cysteine is 500 mg two times per day, often given with selenium. Measurement of plasma sulfur amino acids provides a guide to therapy and is essential for scientific treatment.

Taurine – Fights Seizures

Taurine is a sulfur amino acid like methionine, cystine, cysteine and homocysteine. It is a lesser-known amino acid because it is not incorporated into the structural building blocks of protein. Yet taurine is an essential amino acid in pre-term and newborn infants of humans and many other species. Adults can synthesize their own taurine, yet are probably dependent in part on dietary taurine. Taurine is abundant in the brain, heart, breast, gallbladder and kidney and has important roles in health and disease in these organs.

Taurine has many diverse biological functions serving as a neurotransmitter in the brain, a stabilizer of cell membranes and a facilitator in the transport of ions such as sodium, potassium, calcium and magnesium. Taurine is highly concentrated in animal and fish protein, which are good sources of dietary taurine. It can be synthesized by the body from cysteine when vitamin B6 is present. Deficiency of taurine occurs in premature infants and neonates fed formula milk, and in various disease states.

Inborn errors of taurine metabolism have been described, With, low blood taurine resulting in early signs of depression, lethargy, fatigability, sleep disturbances, progressive weight loss and depth perception impairment. Later, a Parkinson’s syndrome developed and progressed to coma and then death.

Another inborn error of taurine metabolism has been described, with mitral valve prolapse associated with a rapidly progressive form of congestive cardiomyopathy. These patents have elevated urinary taurine levels and depressed levels of myocardial (heart muscle) taurine. There may be a subcategory of taurine-responsive mitral valve prolapse patients.

Taurine, after GABA, is the second most important inhibitory neurotransmitter in the brain. Its inhibitory effect is one source of taurine’s anticonvulsant and antianxiety properties. It also lowers glutamic acid in the brain, and preliminary clinical trials suggest taurine may be useful in some forms of epilepsy. Taurine in the brain is usually associated with zinc or manganese. The amino acids alanine and glutamic acid, as well as pantothenic acid, inhibit taurine metabolism while vitamins A and B6, zinc and manganese help build taurine. Cysteine and B6 are the nutrients most directly involved in taurine synthesis. Taurine levels have been found to decrease significantly in many depressed patients.

One reason that the findings are not entirely clear is because taurine is often elevated in the blood of epileptics who need it. It is often difficult to distinguish compensatory changes in human biochemistry from true metabolic or deficiency disease.

Low levels of taurine are found in retinitis pigmentosa. Taurine deficiency in experimental animals produces degeneration of light-sensitive cells. Therapeutic applications of taurine to eye disease are likely to be forthcoming.

Taurine has many important metabolic roles. Supplements can stimulate prolactin and insulin release. The parathyroid gland makes a peptide hormone called glutataurine (glutamic acid-taurine), which further demonstrates taurine’s role in endocrinology. Taurine increases bilirubin and cholesterol excretion in bile, critical to normal gallbladder function. It seems to inhibit the effect of morphine and potentiate the effects of opiate antagonists.

Low plasma taurine levels have been found in a variety of conditions, i.e., depression, hypertension, hypothyroidism, gout, institutionalized patients, infertility, obesity, kidney failure and others.

Megataurine therapy has been proven to be useful in many patient groups, i.e., those with post myocardial infarction, congestive heart failure, elevated cholesterol or preventricular arrhythmias. Dying heart muscle quickly becomes depleted of taurine. Taurine may prove to be useful in patients with epilepsy, gallstones, mitral valve prolapse, hypertension, hyperbilirubinemia, retinitis pigmentosa, photosensitivity and diabetes. Effective supplements range from 500 mg to 5 g orally. Therapy can be guided by plasma amino acid determination. Taurine is usually well absorbed, and taurine levels can increase to five times normal during therapy without ill effects.

Methionine – Allergy Fighter

Claims for methionine in medicine were initiated by Adelle Davis (1970), who suggested that methionine was deficient in toxemia of pregnancy, childhood rheumatic fever and hair loss. Today, we see a more defined role for methionine as a treatment for some forms of depression, schizophrenia and Parkinson’s disease.

Methionine is one of the essential amino acids needed by humans and higher animals; bacteria can make it from aspartic acid. Some methionine may be absorbed from the bacteria of the gut flora under starvation conditions. The average human needs about 10 mg/kg of methionine and cysteine or as much as 700 mg a day of methionine. This minimal daily requirement is significantly less than the optimal need for methionine.

Methionine-deficient diets in experimental animals result in impaired growth and elevated blood spermidine. Normal methionine metabolism depends on the utilization of folic acid which can be elevated in the serum of methionine deficient patients. Some foods are rich in methionine. A cup of low-fat cottage cheese can contain up to a gram of methionine. Most cheeses contain 100 to 200 mg per ounce.

Methionine supplements lower blood histamine by increasing the breakdown of histamine. It is also a useful treatment for copper poisoning and for lowering serum copper. Methionine’s three major metabolic roles are as methyl and sulfur donor and a precursor to other sulfur amino acids such as cysteine and taurine.

Methionine supplementation is unusual because the D, L form is probably more effective than just the L form. This is probably due to D-L salt formation. Methionine is well absorbed in the brain where it is converted into SAM, which can increase adrenalin-like neurotransmitters in the brain. Methionine, the methyl donor, may produce active brain stimulants and degrade blood histamine. Methionine supplementation has been particularly useful in depressing the high histamine type (histadelia). It has been found to be more effective than MAO inhibitors in depression.

Methionine is a useful adjunct therapy in some cases of Parkinson’s disease, because it can stimulate the production of dopa. Methionine may be of value in acrodermatitis enteropathica, a rare disease of zinc deficiency. Methionine, like other sulfur amino acids, protects against the effects of radiation.

Methionine supplementation may help patients with heroin addiction, who often are unusually high in histamine and have a low pain threshold. Detoxification and withdrawal from barbiturates or amphetamines may also be assisted by methionine. Methionine may be useful for patients with chronic pain and is thought to lower blood cholesterol.

At present, we use methionine for patients with high blood histamine, depression, high copper, high cholesterol and chronic pain, allergies and asthma. Measurement of plasma levels is useful for guiding therapy. Doses of 1 to 2 g of methionine can raise plasma methionine levels 2 to 4 times above normal.

There are usually small elevations in other amino acids. We have had one case where taurine levels were raised as high as the methionine levels and other cases where taurine was not significantly elevated. Elevated levels of taurine, a methionine metabolite, are a hidden benefit of methionine therapy. These elevations may be the basis of methionine’s therapeutic effects.

Homocystine – Worse Than Cholesterol

Homocystine is a natural amino acid metabolite of the essential amino acid methionine, but it occurs only transiently before being converted to the harmless cystathionine via a vitamin B6-dependent enzyme. Homocystine is the double-bonded form of homocysteine. Homocysteine metabolism is related to sulfur amino acid metabolism (methionine, taurine and cysteine) and is dependent on vitamin B12, folic acid, vitamin B6 and betaine as primary cofactors. Homocysteine metabolism is relevant to the understanding of psychosis, arteriosclerosis and the biochemical basis of all nutrient therapies.

Homocysteine excess is still another metabolic cause of psychosis and mental retardation. Nutrients-vitamin B6, folic acid, betaine, cysteine and vitamin B12 can help various inborn errors of homocysteine metabolism. We’ve identified a similar form of psychosis, called pyroluria, which accounts for about 30 percent of psychotic patients (Pfeiffer, 1975). These patients are vitamin B6 and zinc dependent.

Furthermore, S-adenosyl homocysteine can be a useful therapy in certain forms of psychosis. Homocysteine, which presumably accumulates as a result of insufficient vitamin B6, is identified as a chief culprit in initiating the vascular lesions leading to arteriolosclerosis. Zinc deficiency also may have a role in this process. With this knowledge, the nutrient basis of heart disease prevention is expanded beyond the simplistic theory related to cholesterol and the restricted consumption of eggs. Beyond the treatment of arteriosclerosis by reduction of cholesterol is treatment by reduction of homocystine. Homocystine excess is related to vitamin B6 deficiency and probably a zinc deficiency, which has a role in the body’s ability to repair cells. Marginal deficiency of vitamin B6 and zinc is widespread in this country (Pfeiffer, 1975).