Glutathione plays an important role in our ear nose throat eyes (ENT) health.
The primary way everything enters our body both good and bad is through the ear nose throat eyes. Actually our eyes are a secondary portal of entry.
The things entering can be good such as breathing, sound and food. It can also be potentially damaging to the body. These include toxins, bacteria's, viruses, and carcinogens. It would only seem natural that the human body would have a defense systems to protect the points of entry.
The good news...it does. It is called the immune system. It is a formidable military force. The strongest front line defense is the marine like tripeptide glutathione. It is not only in each cell, it is in the respiratory tract lining fluid (RTLF). Glutathione is the main antioxidant in this fluid.
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The Upper Respiratory Tract
It depletes with age
The weakest point of the human body would be the place of greatest risk of attack by infection and toxins. Glutathione is the primary defense for the nose and throat.
General Otolaryngology
LaryngitisParotitis (inflammation of the parotid gland)
Pharyngitis (inflammation of the pharynx producing symptoms similar to tonsillitis)
Sleep apneaSnoringTonsillitis (inflammation of tonsils producing pain)
odynophagia (painful swallowing fever etc)
HyperthyroidismThyroid cancer
Sore throat
Strep throat
Esophageal cancer
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Showing posts with label cancer. Show all posts
Showing posts with label cancer. Show all posts
Tuesday, February 12, 2008
Monday, February 11, 2008
Dietary antioxidants
The effect of dietary intake of the antioxidants ascorbate, tocopherol, and carotenoids is difficult to disentangle by epidemiological studies from other important vitamins and ingredients in fruits and vegetables.
Nevertheless, several arguments suggest that the antioxidants content of fruits and vegetables is a major contributor to their protective effect.
1) Biochemical data, discussed above shows that oxidative damage is massive and is likely to be the major endogenous damage to DNA, proteins, and lipids.
2) Studies showing that oxidative damage to sperm DNA is increased when dietary ascorbate is insufficient
3) Epidemiological studies and intervention trials on prevention of cancer and heart disease in people taking antioxidants supplements are suggestive, though larger studies need to be done. Clinical trials using antioxidants will be the critical test for many of the ideas.
4) Studies on oxidative mechanisms and epidemiology on antioxidants protection for individual degenerative diseases.
Small molecule dietary antioxidants such as Vitamin C (ascorbate), Vitamin E (tocopherol), and carotenoids have generated particular interest as anticarcinogens and as defenses against degenerative diseases. Most carotenoids have antioxidants activity, particularly against singlet oxygen and many, including ß-carotene, can be metabolized to Vitamin A (retinal)
We have called attention to a number of previously neglected physiological antioxidants including urate, bilirubin, carnosine, and ubiquinol. Ubiquinone (CoQ10), for example, is the critical small molecule for transporting electrons in mitochondria for the generation of energy. Its reduced form, ubiquinol, is an effective antioxidants in membranes.
Optimal levels of dietary ubiquinone/ubiquinol could be of importance in many of the
degenerative diseases.
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Nevertheless, several arguments suggest that the antioxidants content of fruits and vegetables is a major contributor to their protective effect.
1) Biochemical data, discussed above shows that oxidative damage is massive and is likely to be the major endogenous damage to DNA, proteins, and lipids.
2) Studies showing that oxidative damage to sperm DNA is increased when dietary ascorbate is insufficient
3) Epidemiological studies and intervention trials on prevention of cancer and heart disease in people taking antioxidants supplements are suggestive, though larger studies need to be done. Clinical trials using antioxidants will be the critical test for many of the ideas.
4) Studies on oxidative mechanisms and epidemiology on antioxidants protection for individual degenerative diseases.
Small molecule dietary antioxidants such as Vitamin C (ascorbate), Vitamin E (tocopherol), and carotenoids have generated particular interest as anticarcinogens and as defenses against degenerative diseases. Most carotenoids have antioxidants activity, particularly against singlet oxygen and many, including ß-carotene, can be metabolized to Vitamin A (retinal)
We have called attention to a number of previously neglected physiological antioxidants including urate, bilirubin, carnosine, and ubiquinol. Ubiquinone (CoQ10), for example, is the critical small molecule for transporting electrons in mitochondria for the generation of energy. Its reduced form, ubiquinol, is an effective antioxidants in membranes.
Optimal levels of dietary ubiquinone/ubiquinol could be of importance in many of the
degenerative diseases.
Click here for more about Glutathione and its benefits to our body.
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Antioxidants Protect Against Disease
Many defense mechanisms within the organism have evolved to limit the levels of reactive oxidants and the damage they inflict. Among the defenses are enzymes such as superoxide dismutase, catalase, and glutathione peroxidase. The glutathione S-transferases inactivate reactive electrophilic mutagens, including the aldehyde products of lipid peroxidation.
There are also many structural defenses such as sequestering H202 generating enzymes in peroxisomes and chelating any free iron or copper salts in transferrin and ferritin or ceruloplasmin to avoid Fenton chemistry. Superoxide, however, can release iron from ferritin.
Oxidized DNA is repaired by a series of glycosylases that are specific for particular oxidized bases and possibly by non-specific excision repair enzymes. In the absence of cell division these oxidative lesions are removed from DNA quite effectively and the mutation rate is kept to a minimum. Oxidized proteins are degraded by proteases. Lipid hydroperoxides are destroyed by glutathione peroxidase.
Almost all of these defenses appear to be inducible, as are most other types of defenses, i.e., the amounts increase in response to damage. There is a large literature showing that cells respond to low levels of radiation, an oxidative mutagen, by inducing antioxidant defenses that help to protect them against mutation by high levels of radiation.
There is a tradeoff however, since the induction of these defenses makes the cell more sensitive to alkylating mutagens.
In addition to the protective effects of endogenous enzymatic antioxidant defenses, consumption of dietary antioxidants appears to be of great importance. Fruits and vegetables, the main source of antioxidants in the diet, are associated with a lowered risk of degenerative diseases. Block and her colleagues have recently reviewed 172 studies in the epidemiological literature that relate, with great consistency, the lack of adequate consumption of fruits and vegetables to cancer incidence.
The quarter of the population with low dietary intake of fruits and vegetables compared to the quarter with high intake has double the cancer rate for most types of cancer (lung, larynx, oral cavity, esophagus, stomach, colon and rectum, bladder, pancreas, cervix, and ovary). Data on the types of cancer known to be associated with hormone levels are not as consistent and show less protection by fruits and vegetables: for breast cancer the protective effect was about 30%. There is also literature on the protective effect of fruit and vegetable consumption on heart disease and stroke. Only 9% of Americans eat five servings of fruits and vegetables per day, the intake recommended by the National Cancer Insitute and the National Research Council. European countries with low fruit and vegetable intake (e.g., Scotland) are generally in poorer health and have higher rates of heart disease and cancer than countries with high intake (e.g., Greece).
The cost of fruits and vegetables is an important factor in discouraging consumption. Poorer people spend a higher percentage of their income on food, eat less fruits and vegetables, and have shorter life expectancy than wealthier people. A major contributor to health in this century was synthetic pesticides which markedly decreased the cost of food production and ensured that most of the crops planted would be eaten by humans rather than insects. Synthetic pesticide residues do not appear to be a significant cause of cancer.
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There are also many structural defenses such as sequestering H202 generating enzymes in peroxisomes and chelating any free iron or copper salts in transferrin and ferritin or ceruloplasmin to avoid Fenton chemistry. Superoxide, however, can release iron from ferritin.
Oxidized DNA is repaired by a series of glycosylases that are specific for particular oxidized bases and possibly by non-specific excision repair enzymes. In the absence of cell division these oxidative lesions are removed from DNA quite effectively and the mutation rate is kept to a minimum. Oxidized proteins are degraded by proteases. Lipid hydroperoxides are destroyed by glutathione peroxidase.
Almost all of these defenses appear to be inducible, as are most other types of defenses, i.e., the amounts increase in response to damage. There is a large literature showing that cells respond to low levels of radiation, an oxidative mutagen, by inducing antioxidant defenses that help to protect them against mutation by high levels of radiation.
There is a tradeoff however, since the induction of these defenses makes the cell more sensitive to alkylating mutagens.
In addition to the protective effects of endogenous enzymatic antioxidant defenses, consumption of dietary antioxidants appears to be of great importance. Fruits and vegetables, the main source of antioxidants in the diet, are associated with a lowered risk of degenerative diseases. Block and her colleagues have recently reviewed 172 studies in the epidemiological literature that relate, with great consistency, the lack of adequate consumption of fruits and vegetables to cancer incidence.
The quarter of the population with low dietary intake of fruits and vegetables compared to the quarter with high intake has double the cancer rate for most types of cancer (lung, larynx, oral cavity, esophagus, stomach, colon and rectum, bladder, pancreas, cervix, and ovary). Data on the types of cancer known to be associated with hormone levels are not as consistent and show less protection by fruits and vegetables: for breast cancer the protective effect was about 30%. There is also literature on the protective effect of fruit and vegetable consumption on heart disease and stroke. Only 9% of Americans eat five servings of fruits and vegetables per day, the intake recommended by the National Cancer Insitute and the National Research Council. European countries with low fruit and vegetable intake (e.g., Scotland) are generally in poorer health and have higher rates of heart disease and cancer than countries with high intake (e.g., Greece).
The cost of fruits and vegetables is an important factor in discouraging consumption. Poorer people spend a higher percentage of their income on food, eat less fruits and vegetables, and have shorter life expectancy than wealthier people. A major contributor to health in this century was synthetic pesticides which markedly decreased the cost of food production and ensured that most of the crops planted would be eaten by humans rather than insects. Synthetic pesticide residues do not appear to be a significant cause of cancer.
Click here for more about Glutathione and its benefits to our body.
Aging is slowed by calorie or protein restriction
In rodents a calorie restricted diet, significantly increases lifespan, decreases reproduction, and markedly decreases cancer rates.
It has been suggested that Darwinian fitness in animals is increased by the delay of reproductive function during periods of low food availability and that the saved resources are invested in maintenance of the body until food resources are available for successful reproduction.
Protein restriction appears to have the same effects on rodents as calorie restriction, though it is less well-studied. An understanding of mechanisms for this marked effect on aging and cancer is becoming clearer and may in good part be due to reduced oxidative damage.
The suggestion that maintenance functions are enhanced in calorie-restricted rats thus resulting in less oxidative damage is supported by the findings of more efficient DNA repair, better coupled mitochondrial respiration and a delay in the age-dependent decline of antioxidant defenses.
The higher level of antioxidant defenses could also account for the enhanced immune response in restricted animals. We have recently shown that either calorie or protein restriction decreases the rate of accumulation of oxidized protein that accompanies aging in rats and preliminary results suggest a decrease in preneoplastic foci and oxidative lesions in DNA as well.
Thus, the overall effect of these enhanced maintenance activities appears to be a reduction in oxidative damage to DNA and protein, a decrease in DNA and protein lesions, and a decrease in somatic mutations. Markedly lower mitotic rates are observed in a variety of tissues in calorie restricted compared to ad libitum fed rodent, which may also contribute to the decrease in tumor incidence.
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*Dietary restriction activates the pituitary adrenocorticotropic axis resulting in a decrease in the release of reproductive and mitogenic hormones. Decreases in mitogenic hormones such as insulin, TSH, growth hormone, estrogen, and prolactin decrease the likelihood of hormone-induced cancers, as has been shown in various animal studies. This is consistent with suppression of mitogenic hormones and decreased proto-oncogene expression. The lowered incidence of mammary tumors observed in calorie-restricted rats has been attributed to reduced circulating levels of the mammotropic hormones estrogen and prolactin.
Click here for more about Glutathione and its benefits to our body.
It has been suggested that Darwinian fitness in animals is increased by the delay of reproductive function during periods of low food availability and that the saved resources are invested in maintenance of the body until food resources are available for successful reproduction.
Protein restriction appears to have the same effects on rodents as calorie restriction, though it is less well-studied. An understanding of mechanisms for this marked effect on aging and cancer is becoming clearer and may in good part be due to reduced oxidative damage.
The suggestion that maintenance functions are enhanced in calorie-restricted rats thus resulting in less oxidative damage is supported by the findings of more efficient DNA repair, better coupled mitochondrial respiration and a delay in the age-dependent decline of antioxidant defenses.
The higher level of antioxidant defenses could also account for the enhanced immune response in restricted animals. We have recently shown that either calorie or protein restriction decreases the rate of accumulation of oxidized protein that accompanies aging in rats and preliminary results suggest a decrease in preneoplastic foci and oxidative lesions in DNA as well.
Thus, the overall effect of these enhanced maintenance activities appears to be a reduction in oxidative damage to DNA and protein, a decrease in DNA and protein lesions, and a decrease in somatic mutations. Markedly lower mitotic rates are observed in a variety of tissues in calorie restricted compared to ad libitum fed rodent, which may also contribute to the decrease in tumor incidence.
Click here for more about Glutathione and its benefits to our body.
*Dietary restriction activates the pituitary adrenocorticotropic axis resulting in a decrease in the release of reproductive and mitogenic hormones. Decreases in mitogenic hormones such as insulin, TSH, growth hormone, estrogen, and prolactin decrease the likelihood of hormone-induced cancers, as has been shown in various animal studies. This is consistent with suppression of mitogenic hormones and decreased proto-oncogene expression. The lowered incidence of mammary tumors observed in calorie-restricted rats has been attributed to reduced circulating levels of the mammotropic hormones estrogen and prolactin.
Click here for more about Glutathione and its benefits to our body.
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Aging and Dietary Restriction
Evolutionary biologists have argued that aging is inevitable because of several tradeoffs. One tradeoff is that a considerable proportion of an animal's resources is devoted to reproduction at a cost to maintenance, which means that the maintenance of somatic tissues is less than that required for indefinite survival. Of the vast array of maintenance processes that are necessary to sustain normal function in somatic cells, those that defend the cell against metabolism derived oxidants are likely to play an important role.
Metabolism has costs: oxidants by-products of normal energy metabolism extensively damage DNA, proteins, and other molecules in the cell, and this damage accumulates with age.
Another tradeoff is that nature selects for many genes that have immediate survival value, but that may have long term deleterious consequences. The oxidative burst from phagocytic cells, for example, protects against death from bacterial and viral infections, but contributes to DNA damage, mutation, and cancer.
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Metabolism has costs: oxidants by-products of normal energy metabolism extensively damage DNA, proteins, and other molecules in the cell, and this damage accumulates with age.
Another tradeoff is that nature selects for many genes that have immediate survival value, but that may have long term deleterious consequences. The oxidative burst from phagocytic cells, for example, protects against death from bacterial and viral infections, but contributes to DNA damage, mutation, and cancer.
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Tobacco, cancer, and heart disease
Smoking, which we and others argue is a major oxidative stress in addition to a source of mutagens, contributes to about one-third of U.S. cancer, about one-quarter of U.S. heart disease and, about 400,000 premature deaths per year in the U.S..
Tobacco is a major global cause of cancer, but it causes even more deaths by other diseases. Tobacco will cause about 3 million deaths per year worldwide in the l990s and will, at present rates of smoking, cause about l0 million deaths per year a few decades from now.
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Tobacco is a major global cause of cancer, but it causes even more deaths by other diseases. Tobacco will cause about 3 million deaths per year worldwide in the l990s and will, at present rates of smoking, cause about l0 million deaths per year a few decades from now.
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Monday, January 21, 2008
Glutathione Fact 2 - slow down the aging process
Glutathione has been shown to slow down the aging process, detoxify and improve liver function, strengthen the immune system, and reduce the chances of developing cancer.
Glutathione also works to help improve mental functions, increase energy, improve concentration, permit increased exercise, and improve heart and lung function - just to name a few.
Among the uses that have been reported for glutathione are:
treatment of poisoning, particularly heavy metal poisons
treatment of idiopathic pulmonary firbosis
increasing the effectiveness and reducing the toxicity of cis-platinum, a chemo drug used to treat breast cancer
treating Parkinson's disease
lowering blood pressure in patients with diabetes
increasing male sperm counts in humans and animals
treatment of liver cancer
treatment of sickle cell anemia
Glutathione also works to help improve mental functions, increase energy, improve concentration, permit increased exercise, and improve heart and lung function - just to name a few.
Among the uses that have been reported for glutathione are:
treatment of poisoning, particularly heavy metal poisons
treatment of idiopathic pulmonary firbosis
increasing the effectiveness and reducing the toxicity of cis-platinum, a chemo drug used to treat breast cancer
treating Parkinson's disease
lowering blood pressure in patients with diabetes
increasing male sperm counts in humans and animals
treatment of liver cancer
treatment of sickle cell anemia
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Friday, January 18, 2008
GSH has five major functions
Antioxidant:
Antioxidant is a substance that neutralizes destructive free radicals; some are manufactured by the metabolic processes of the body, others are derived from foods, the air we breath, exercise, stress and disease.GSH is the most powerful Antioxidant occurring naturally in the cells of the body. Through its significant reducing power, GSH also makes major contributions to the recycling of other Antioxidant that have become oxidized. Healthy cells homeostatically oppose free radicals through the use of Antioxidant, of which GSH plays a significant role. The effectiveness of other Antioxidant like vitamins C and E depends on the availability of GSH.
Help Prevent Disease:
Oxidative related diseases: accelerated aging, cell destruction, causes damage to DNA cellular patterns which leads to cancer, arteriosclerosis, coronary artery disease, Parkinson’s disease, diseases of the immune system, diabetes, cataract formation, Alzheimer’s, macular degeneration, COPD, allergy/asthma, stroke.
Detoxification:
GSH also plays a main role in detoxification..primarily in Phase II Liver detox. It "binds" to many toxins by its sulfur molecules and aids in forming a complex which the body then rids itself of.
Immune System Support:
When the immune system responds to an invader, it releases a blitz of free radicals to aid in the offensive agent's demise. This could create damage to local tissue and your body, but GSH rallies around the area to quench the free radicals that are produced in excess.
Protection from Radiation:
A recent research article published in the journal Radiology states that “radiation from a single whole-body scan is equal to that from 100 mammograms and is similar to that received by survivors of the atomic bombings of Hiroshima and Nagasaki, Japan – about 1 mile from the explosions – according to radiation biologist, David J. Brenner of Columbia University. The radiation from one scan is enough to produce a tumor in one out of 1200 people, and for those who have annual scans the risk increases to one tumor in every 50 people. With inadequate intracellular GSH the risk is greatly increased.
Antioxidant is a substance that neutralizes destructive free radicals; some are manufactured by the metabolic processes of the body, others are derived from foods, the air we breath, exercise, stress and disease.GSH is the most powerful Antioxidant occurring naturally in the cells of the body. Through its significant reducing power, GSH also makes major contributions to the recycling of other Antioxidant that have become oxidized. Healthy cells homeostatically oppose free radicals through the use of Antioxidant, of which GSH plays a significant role. The effectiveness of other Antioxidant like vitamins C and E depends on the availability of GSH.
Help Prevent Disease:
Oxidative related diseases: accelerated aging, cell destruction, causes damage to DNA cellular patterns which leads to cancer, arteriosclerosis, coronary artery disease, Parkinson’s disease, diseases of the immune system, diabetes, cataract formation, Alzheimer’s, macular degeneration, COPD, allergy/asthma, stroke.
Detoxification:
GSH also plays a main role in detoxification..primarily in Phase II Liver detox. It "binds" to many toxins by its sulfur molecules and aids in forming a complex which the body then rids itself of.
Immune System Support:
When the immune system responds to an invader, it releases a blitz of free radicals to aid in the offensive agent's demise. This could create damage to local tissue and your body, but GSH rallies around the area to quench the free radicals that are produced in excess.
Protection from Radiation:
A recent research article published in the journal Radiology states that “radiation from a single whole-body scan is equal to that from 100 mammograms and is similar to that received by survivors of the atomic bombings of Hiroshima and Nagasaki, Japan – about 1 mile from the explosions – according to radiation biologist, David J. Brenner of Columbia University. The radiation from one scan is enough to produce a tumor in one out of 1200 people, and for those who have annual scans the risk increases to one tumor in every 50 people. With inadequate intracellular GSH the risk is greatly increased.
Tuesday, January 15, 2008
Genetic determinants of lung cancer short-term survival: the role of glutathione-related genes
Survival of lung cancer patients has been dismal. Glutathione enzymes are directly involved in the metabolism of platinum compounds, a group of important chemotherapeutic drugs in cancer treatment. We tested the hypothesis that genes encoding Glutathione enzymes may predict lung cancer short-term survival. Methods: We studied DNA polymorphisms of 250 primary lung cancer patients at four Glutathione-related loci: GSTP1, GSTM1, GSTT1 and γ-GCS that encode Glutathione-S-transferase-π,Glutathione-S-transferase-μ, Glutathione-S-transferase-θ, and γ-glutamylcysteine synthetase, respectively. Pearson's χ2-square tests, Kaplan–Meier survival curves, log rank tests, and Cox regression models were applied in the analysis.
Results: There were 150 (60%) men and 100 (40%) women in this study. Seventeen percent of the patients had never smoked cigarettes, and 61% had stopped smoking at least 6 months prior to their lung cancer diagnosis. Among never smokers, those with null (N) or low (L) genotype experienced a better 1-year-survival rate than those with a positive (P) or high (H) genotype. Patients with P or H at two loci (PP or PH) were compared with patients with N or L at one or both loci (other). Among never smokers, 1-year-survival rates were 60–78% for patients with PP or PH genotypes compared with 89–100% for other types. The survival advantage was greater among advanced-stage patients who were NL or NN than low-stage patients. Similar results were not observed among smokers.
Conclusions: Glutathione-related genes may determine lung cancer survival. Our results, if confirmed, would suggest new directions to enhance cancer treatment, and provide easily measurable markers for clinicians to plan patient-specific therapy.
Ping Yangab, Akira Yokomizoc, Henry D Tazelaarc, Randolph S Markse, Timothy G Lesnicka, Daniel L Millerd, Jeff A Sloana, Eric S Edellf, Rebecca L Meyera, James Jettef, Wanguo Liuc
Results: There were 150 (60%) men and 100 (40%) women in this study. Seventeen percent of the patients had never smoked cigarettes, and 61% had stopped smoking at least 6 months prior to their lung cancer diagnosis. Among never smokers, those with null (N) or low (L) genotype experienced a better 1-year-survival rate than those with a positive (P) or high (H) genotype. Patients with P or H at two loci (PP or PH) were compared with patients with N or L at one or both loci (other). Among never smokers, 1-year-survival rates were 60–78% for patients with PP or PH genotypes compared with 89–100% for other types. The survival advantage was greater among advanced-stage patients who were NL or NN than low-stage patients. Similar results were not observed among smokers.
Conclusions: Glutathione-related genes may determine lung cancer survival. Our results, if confirmed, would suggest new directions to enhance cancer treatment, and provide easily measurable markers for clinicians to plan patient-specific therapy.
Ping Yangab, Akira Yokomizoc, Henry D Tazelaarc, Randolph S Markse, Timothy G Lesnicka, Daniel L Millerd, Jeff A Sloana, Eric S Edellf, Rebecca L Meyera, James Jettef, Wanguo Liuc
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Glutathione could well be involved in protecting against cancer
The best known functions of selenium at nutritionally adequate, but not at excessive, levels are its role as a part of the enzyme Glutathione peroxidase and its interaction with heavy metals. Glutathione peroxidase destroys hydroperoxides and lipoperoxides, thereby protecting the constituents of the cells against free radical damage. Ip and Sinha (1981) have shown that selenium, through its function in Glutathione peroxidase, could well be involved in protecting against cancer induced by high intakes of fat, especially polyunsaturated fatty acids. Glutathione peroxidase activity in human blood increases with increasing selenium intakes, but reaches a plateau at intakes well below those customary in the United States (Thomson and Robinson, 1980). Thus, if the antitumorigenic effect of selenium is mediated through its function in Glutathione peroxidase, attempts to increase the enzyme activity by selenium supplementation, superimposed on an adequate diet in the United States, would not be successful. The second function of selenium is to protect against acute and chronic toxicity of certain heavy metals. Although selenium is known to interact with cadmium and mercury, the mechanism of action is not known. Selenium does not cause an increased elimination of the toxic elements, but, rather, an increased accumulation in some nontoxic form (National Academy of Sciences, 1971). It is conceivable that carcinogenic effects of these, and perhaps other heavy metals, could be counteracted by selenium, in a manner similar to its protection against their general toxicity. Diet Nutrition Cancer by National Research Council, page 168
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Cancer
Numerous studies suggest that an inverse association exists between selenium levels and cancer incidence (Hocman, 1988; Willett and Stampfer, 1986; Milner, 1985). Associations appear to be particularly strong with cancers that are also associated with high-fat, low-fiber diets (i.e., breast, colon, prostrate, etc.). The mechanism for selenium's reported protective effects is likely due to its function in antioxidant synthesis. Glutathione peroxidase, the primary enzyme that converts hydrogen peroxide to water (and thus prevents lipid peroxidation) is selenium-dependent. Inhibition of lipid or bile acid oxidation may account for its protective role (reviewed by Linder 1991:496-7). Selenium may also act as an immune stimulant. Selenium deficiency inhibits macrophage-mediated tumor destruction, and inhibits tumor necrosis factor-alpha production in animals (Kiremidjian-Schumacher et al., 1992). Dietary supplementation with selenium produced the opposite effects. Cancer And Natural Medicine by John Boik, page 146
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Glutathione, oxidative stress and aging
The theory of aging proposes that the impairment in physiological performance associated with aging is caused by the detrimental effects of oxygen free radicals. This is interesting because it provides us with a theoretical framework to understand aging and because it suggests a rationale for intervention, i.e., antioxidant administration. Thus, the study of antioxidant systems of the cell may be very important in gerontological studies. Glutathione is one of the main nonprotein antioxidant in the cell which, together with its related enzymes, constitute the “Glutathione system.” The involvement of Glutathione in aging has been known since the early seventies. Several studies have reported that reduced Glutathione is decreased in cells from old animals, whereas oxidized Glutathione tends to be increased. Recent experiments from our laboratory have underscored the importance of cellular compartmentation of Glutathione. MitochondrialGlutathione plays a key role in the protection against free radical damage associated with aging. Oxidative damage to mitochondrial DNA is directly related to an oxidation of mitochondrialGlutathione. In fact, aging is associated with oxidative damage to proteins, nucleic acids, and lipids. These molecular lesions may be responsible for the low physiological performance of aged cells. Thus, antioxidant supplementation may be a rational way to partially protect against age-associated impairment in performance. Apoptosis, a programmed cell death, is an area of research which has seen an explosive growth. Glutathione is involved in apoptosis: apoptotic cells have lower levels of reduced Glutathione, and administration of Glutathione precursors prevent, or at least delay, apoptosis. Age-associated diseases constitute a major concern for researchers involved in aging. Free radicals are involved in many such diseases; for instance, cancer, diabetes or atherosclerosis. The key role of Glutathione and other antioxidant in the pathophysiology of aging and age-associated diseases is discussed in this review.
Juan Sastre1, Federico V. Pallardó1 and Jose Viña Department of Physiology, Faculty of Medicine, University of Valencia, Spain Dept. Fisiologia, Facultad de Medicina, Avenida Blasco Ibanez 17, 46010 Valencia, Spain
Juan Sastre1, Federico V. Pallardó1 and Jose Viña Department of Physiology, Faculty of Medicine, University of Valencia, Spain Dept. Fisiologia, Facultad de Medicina, Avenida Blasco Ibanez 17, 46010 Valencia, Spain
The role of glutathione in aging and cancer.
The incidence and mortality rates from most cancers increase exponentially with age. It is likely that this aging phenomenon is partially due to specific changes that occur in the host resulting in an increased susceptibility to neoplasia. Our hypothesis is that one such host factor is a deficiency in GSH, based on the importance of this compound in the detoxification of a wide variety of exogenous and endogenous carcinogens and free radicals, as well as in the maintenance of immune function. American Health Foundation, Valhalla, New York 10595.
PMID: 1426093 [PubMed - indexed for MEDLINE]
Antioxidants are well documented and known to possess vital roles in health maintenance and disease prevention. Glutathione is your cell's own major antioxidant. Maintaining elevated glutathione levels aids the body's natural antioxidant function.
Click here for more about Glutathione and its benefits to our body.
PMID: 1426093 [PubMed - indexed for MEDLINE]
Antioxidants are well documented and known to possess vital roles in health maintenance and disease prevention. Glutathione is your cell's own major antioxidant. Maintaining elevated glutathione levels aids the body's natural antioxidant function.
Click here for more about Glutathione and its benefits to our body.
Thursday, January 10, 2008
Glutathione and Cancer
Free radicals are involved in the processes leading to cancer.
Unfortunately, Glutathione, which could normally help mount a defense against the free radicals, is often depleted in patients with cancer.
In one study of 52 bladder cancer patients and 24 healthy adult controls, levels of malondialdehyde, a free-radical promoting substance, were significantly higher and Glutathione levels significantly lower in cancer patients compared to controls.
In other studies of lung6 and breast cancer levels of glutathione-dependent enzymes were markedly altered, depending on the disease stage.
Animal studies also have indicated that Glutathione deficiency is linked to DNA damage.By Kimberly Pryor
Click here for more about Glutathione and its benefits to our body.
Unfortunately, Glutathione, which could normally help mount a defense against the free radicals, is often depleted in patients with cancer.
In one study of 52 bladder cancer patients and 24 healthy adult controls, levels of malondialdehyde, a free-radical promoting substance, were significantly higher and Glutathione levels significantly lower in cancer patients compared to controls.
In other studies of lung6 and breast cancer levels of glutathione-dependent enzymes were markedly altered, depending on the disease stage.
Animal studies also have indicated that Glutathione deficiency is linked to DNA damage.By Kimberly Pryor
Click here for more about Glutathione and its benefits to our body.
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Antioxidant Supports Lung, Liver, Gastric and Cerebral Health while Guarding Against DNA Damage
Glutathione is the king of all antioxidants.
It rules our body’s cells, for without it, they would be helpless during the fatal onslaught of free radicals.
Glutathione plays a prominent role in regulation of cellular events including gene expression, DNA and protein synthesis, cell proliferation and apoptosis (programmed cell death), and immune response.
Glutathione deficiency contributes to oxidative stress, which is involved in aging and the development of such diseases as Alzheimer’s, Parkinson's, liver disease, cystic fibrosis, sickle cell anemia, HIV and AIDS, cancer, strokes—even H. pylori infections.1-2 Recently, an abundance of research has emerged on Glutathione’s role in health. By Kimberly Pryor
It rules our body’s cells, for without it, they would be helpless during the fatal onslaught of free radicals.
Glutathione plays a prominent role in regulation of cellular events including gene expression, DNA and protein synthesis, cell proliferation and apoptosis (programmed cell death), and immune response.
Glutathione deficiency contributes to oxidative stress, which is involved in aging and the development of such diseases as Alzheimer’s, Parkinson's, liver disease, cystic fibrosis, sickle cell anemia, HIV and AIDS, cancer, strokes—even H. pylori infections.1-2 Recently, an abundance of research has emerged on Glutathione’s role in health. By Kimberly Pryor
Wednesday, January 9, 2008
Supplementation may help and prevent the following conditions
Supplementation may prevent, or be helpful with, the following conditions:
Aging
Alcoholism
Asthma
Atherosclerosis (heart disease)
Cancer
Cataracts
Dizziness
Hepatitis
Immunodepression (immune function)
Infertility (male)
Memory Loss (Alzheimer's disease, dementia)
Osteoarthritis
Parkinson's Disease
Peptic Ulcers
Why is Glutathione Essential to Health?
Glutathione's three major roles in the body are summarized by the letters A-B-C.
- Anti-oxidant
- Blood Booster
- Cell Detoxifier
Click here to buy Glutathione
Aging
Alcoholism
Asthma
Atherosclerosis (heart disease)
Cancer
Cataracts
Dizziness
Hepatitis
Immunodepression (immune function)
Infertility (male)
Memory Loss (Alzheimer's disease, dementia)
Osteoarthritis
Parkinson's Disease
Peptic Ulcers
Why is Glutathione Essential to Health?
Glutathione's three major roles in the body are summarized by the letters A-B-C.
- Anti-oxidant
- Blood Booster
- Cell Detoxifier
Click here to buy Glutathione
Labels:
Aging,
Alcoholism,
Asthma,
Atherosclerosis,
cancer,
glutathione
Friday, January 4, 2008
Possible Related Side Effects of Chronic Fatigue Syndrome
Orthostatic HypotensionOrthostatic hypotension is defined as an excessive fall in blood pressure on standing, usually greater than 20/10 mmHg. It is considered to be a manifestation of abnormal blood pressure regulation due to a variety of causes.
Hypotension, particularly orthostatic hypotension, is a common symptom in chronic fatigue patients. Many people with Chronic Fatigue Syndrome have chronic low blood pressure (the normal is 120/80 mmHg), which is made even worse on standing. This may be a particular problem in the morning, when standing can cause dizziness. Exercise or a heavy meal may exacerbate the symptoms. Syncope is a loss of consciousness and postural tone caused by diminished cerebral blood flow. Syncope often occurs during the morning shower, perhaps due to the vasodilating effect of hot water.
There are several mechanisms that govern blood pressure. Upon standing, a large amount of blood pools in the veins of the legs and trunk. The transient decrease in venous return to the heart results in a low blood pressure. The body responds with a sympathetic-mediated release of catacholamines that increase heart rate contraction and vasoconstrict the arteries. With continued standing, antidiuretic hormone (ADH) is secreted which activates the renin-angiotensin-aldosterone system, subsequently causing sodium and water retention and an expansion of the circulating blood volume.
There are many causes of orthostatic hypotension, including:
Hypovolemia (low blood volume) induced by excessive use of diuretic agents (e.g., loop diuretics, such as furosemide, bumetanide, and ethacrynic acid) and relative hypovolemia due to vasodilator therapy with nitrate preparations and calcium antagonists (verapamil, nifedipine, or diltiazem) or with angiotensin converting enzyme (ACE) inhibitors.
Histamine, a key player in allergic reactions, induces vasodilation and hypotension.
Potassium deficiency (hypokalemia) impairs the reactivity of vascular smooth muscle and may limit the increase in peripheral vascular resistance on standing
The adrenocortical hypofunction of Addison's disease may lead to orthostatic hypotension in the absence of adequate salt intake.
Several classes of drugs reversibly impair autonomic reflexes and reduce blood pressure on standing as an important adverse effect. These include many drugs used to treat psychiatric disorders such as the monoamine oxidase inhibitors (MAOIs) (isocarboxazid, phenelzine, and tranylcypromine) used to treat depression; the tricyclic antidepressants (nortriptyline, amitriptyline, desipramine, imipramine, and protriptyline) or tetracyclic antidepressants; and the phenothiazine antipsychotic drugs (chlorpromazine, promazine, and thioridazine). Other drugs that may produce orthostatic hypotension are quinidine, L-dopa, barbiturates, and alcohol.
Elevated Homocysteine LevelsHomocysteine is a sulfur-containing amino acid that is produced as a byproduct of methionine metabolism. When the body has an adequate supply of cofactors, such as vitamins B6, B12, and folic acid, homocysteine is detoxified, rendering compounds useful for other functions. Currently, homocysteine levels are in the forefront as a cardiovascular risk because of the damage that can occur to blood vessels and arteries when homocysteine levels are high.
A study of 12 women who fulfilled the criteria for both fibromyalgia and Chronic Fatigue Syndrome found that, in all the patients, the homocysteine levels were increased in the cerebrospinal fluid (CSF). There was a significant positive correlation between CSF homocysteine and B12 levels and fatigue-ability, as rated on the Comprehensive Psychopathological Rating Scale. The authors concluded that "increased homocysteine levels in the central nervous system characterize patients fulfilling the criteria for both fibromyalgia and Chronic Fatigue Syndrome ." They also noted that B12 deficiency caused a deficient remethylation of homocysteine. Therefore, a vitamin B12 deficiency can be considered a contributing factor to the higher homocysteine elevations found in these patient groups (Regland et al. 1997).
Glutathione Deficiency
Glutathione is a tripeptide made up of three amino acids: glycine, cysteine, and gamma-glutamic acid. Glutathionee functions as a modulator of cellular homeostasis, including detoxification of oxyradicals and metals. It also acts as a potent free radical scavenger that can help prevent damage to DNA and RNA, detoxify heavy metals, boost immune function, and assist the liver in detoxification through its various enzymes. Levels of intracellular Glutathione decrease with age, lowering the body's ability to detoxify free radicals and the many important enzymes Glutathione makes.
An article in the journal Medical Hypothesis proposed that Glutathione, an antioxidant essential for lymphocyte function, may be depleted in Chronic Fatigue Syndrome patients. Glutathione is needed for both the immune system and for aerobic muscular contraction. The authors proposed that Glutathione depletion by an activated immune systemalso causes the muscular fatigue and myalgia associated with Chronic Fatigue Syndrome (Bounous et al. 1999).'
Cysteine is a precursor to Glutathione. It has been hypothesized that Glutathione and cysteine metabolism may play a role in skeletal muscle wasting and muscle fatigue. The combination of abnormally low plasma cysteine and Glutathione levels, low natural killer (NK) cell activity (with a resulting susceptibility to viral infection), skeletal muscle wasting or muscle fatigue, and increased rates of urea production define a complex of abnormalities that is tentatively called "low CG syndrome." These symptoms are found in patients with HIV infection, cancer, major injuries, sepsis, Crohn's disease, ulcerative colitis, Chronic Fatigue Syndrome , and to some extent in overtrained athletes (Droge et al. 1997).
Click here to demonstrate to you why Glutathione is so important to your health and well-being
Hypotension, particularly orthostatic hypotension, is a common symptom in chronic fatigue patients. Many people with Chronic Fatigue Syndrome have chronic low blood pressure (the normal is 120/80 mmHg), which is made even worse on standing. This may be a particular problem in the morning, when standing can cause dizziness. Exercise or a heavy meal may exacerbate the symptoms. Syncope is a loss of consciousness and postural tone caused by diminished cerebral blood flow. Syncope often occurs during the morning shower, perhaps due to the vasodilating effect of hot water.
There are several mechanisms that govern blood pressure. Upon standing, a large amount of blood pools in the veins of the legs and trunk. The transient decrease in venous return to the heart results in a low blood pressure. The body responds with a sympathetic-mediated release of catacholamines that increase heart rate contraction and vasoconstrict the arteries. With continued standing, antidiuretic hormone (ADH) is secreted which activates the renin-angiotensin-aldosterone system, subsequently causing sodium and water retention and an expansion of the circulating blood volume.
There are many causes of orthostatic hypotension, including:
Hypovolemia (low blood volume) induced by excessive use of diuretic agents (e.g., loop diuretics, such as furosemide, bumetanide, and ethacrynic acid) and relative hypovolemia due to vasodilator therapy with nitrate preparations and calcium antagonists (verapamil, nifedipine, or diltiazem) or with angiotensin converting enzyme (ACE) inhibitors.
Histamine, a key player in allergic reactions, induces vasodilation and hypotension.
Potassium deficiency (hypokalemia) impairs the reactivity of vascular smooth muscle and may limit the increase in peripheral vascular resistance on standing
The adrenocortical hypofunction of Addison's disease may lead to orthostatic hypotension in the absence of adequate salt intake.
Several classes of drugs reversibly impair autonomic reflexes and reduce blood pressure on standing as an important adverse effect. These include many drugs used to treat psychiatric disorders such as the monoamine oxidase inhibitors (MAOIs) (isocarboxazid, phenelzine, and tranylcypromine) used to treat depression; the tricyclic antidepressants (nortriptyline, amitriptyline, desipramine, imipramine, and protriptyline) or tetracyclic antidepressants; and the phenothiazine antipsychotic drugs (chlorpromazine, promazine, and thioridazine). Other drugs that may produce orthostatic hypotension are quinidine, L-dopa, barbiturates, and alcohol.
Elevated Homocysteine LevelsHomocysteine is a sulfur-containing amino acid that is produced as a byproduct of methionine metabolism. When the body has an adequate supply of cofactors, such as vitamins B6, B12, and folic acid, homocysteine is detoxified, rendering compounds useful for other functions. Currently, homocysteine levels are in the forefront as a cardiovascular risk because of the damage that can occur to blood vessels and arteries when homocysteine levels are high.
A study of 12 women who fulfilled the criteria for both fibromyalgia and Chronic Fatigue Syndrome found that, in all the patients, the homocysteine levels were increased in the cerebrospinal fluid (CSF). There was a significant positive correlation between CSF homocysteine and B12 levels and fatigue-ability, as rated on the Comprehensive Psychopathological Rating Scale. The authors concluded that "increased homocysteine levels in the central nervous system characterize patients fulfilling the criteria for both fibromyalgia and Chronic Fatigue Syndrome ." They also noted that B12 deficiency caused a deficient remethylation of homocysteine. Therefore, a vitamin B12 deficiency can be considered a contributing factor to the higher homocysteine elevations found in these patient groups (Regland et al. 1997).
Glutathione Deficiency
Glutathione is a tripeptide made up of three amino acids: glycine, cysteine, and gamma-glutamic acid. Glutathionee functions as a modulator of cellular homeostasis, including detoxification of oxyradicals and metals. It also acts as a potent free radical scavenger that can help prevent damage to DNA and RNA, detoxify heavy metals, boost immune function, and assist the liver in detoxification through its various enzymes. Levels of intracellular Glutathione decrease with age, lowering the body's ability to detoxify free radicals and the many important enzymes Glutathione makes.
An article in the journal Medical Hypothesis proposed that Glutathione, an antioxidant essential for lymphocyte function, may be depleted in Chronic Fatigue Syndrome patients. Glutathione is needed for both the immune system and for aerobic muscular contraction. The authors proposed that Glutathione depletion by an activated immune systemalso causes the muscular fatigue and myalgia associated with Chronic Fatigue Syndrome (Bounous et al. 1999).'
Cysteine is a precursor to Glutathione. It has been hypothesized that Glutathione and cysteine metabolism may play a role in skeletal muscle wasting and muscle fatigue. The combination of abnormally low plasma cysteine and Glutathione levels, low natural killer (NK) cell activity (with a resulting susceptibility to viral infection), skeletal muscle wasting or muscle fatigue, and increased rates of urea production define a complex of abnormalities that is tentatively called "low CG syndrome." These symptoms are found in patients with HIV infection, cancer, major injuries, sepsis, Crohn's disease, ulcerative colitis, Chronic Fatigue Syndrome , and to some extent in overtrained athletes (Droge et al. 1997).
Click here to demonstrate to you why Glutathione is so important to your health and well-being
Oxidative Stress and Chronic Fatigue Syndrome
Studies have shown that oxidative stress plays a role in the development of Chronic Fatigue Syndrome (Fulle et al. 2000; Richards et al. 2000; Logan et al. 2001). Oxidative stress is a term used to describe the body's prolonged exposure to oxidative factors that cause more free radicals than the body can neutralize. Free radicals are produced as a byproduct of normal metabolic functions. When there are enough free radical scavengers present, such as glutathione and vitamins C, E, and A, along with zinc and other nutrients, through normal metabolic functioning, the body will "mop up" or neutralize the free radicals. When free radicals are not neutralized, the body can become vulnerable to cellular destruction.
A relationship between abnormal oxidative stress and Chronic Fatigue Syndrome can be found in the literature. An article in the journal Life Science described a study that showed that patients with Chronic Fatigue Syndrome had lower serum transferrin levels and higher lipoprotein peroxidation. These results indicate that patients with Chronic Fatigue Syndrome have increased susceptibility of LDL and VLDL to copper-induced peroxidation and that this is related both to their lower levels of serum transferrin and to other unidentified pro-oxidizing effects of Chronic Fatigue Syndrome (Manuel y Keenoy et al. 2001).
Exercise has been shown to increase the production of oxidants. Fortunately, regular endurance exercise results in adaptations in the skeletal muscle antioxidant capacity, which protects myocytes (muscle cells) against the deleterious effects of oxidants and prevents extensive cellular damage (McCully et al. 1996; Powers et al. 1999).
A study of the oxygen delivery to muscles in patients with Chronic Fatigue Syndrome found that oxygen delivery and oxidative metabolism was significantly reduced in Chronic Fatigue Syndrome patients after exercise (compared with sedentary controls) (McCully et al. 1999).
Click here to demonstrate to you why Glutathione is so important to your health and well-being
A relationship between abnormal oxidative stress and Chronic Fatigue Syndrome can be found in the literature. An article in the journal Life Science described a study that showed that patients with Chronic Fatigue Syndrome had lower serum transferrin levels and higher lipoprotein peroxidation. These results indicate that patients with Chronic Fatigue Syndrome have increased susceptibility of LDL and VLDL to copper-induced peroxidation and that this is related both to their lower levels of serum transferrin and to other unidentified pro-oxidizing effects of Chronic Fatigue Syndrome (Manuel y Keenoy et al. 2001).
Exercise has been shown to increase the production of oxidants. Fortunately, regular endurance exercise results in adaptations in the skeletal muscle antioxidant capacity, which protects myocytes (muscle cells) against the deleterious effects of oxidants and prevents extensive cellular damage (McCully et al. 1996; Powers et al. 1999).
A study of the oxygen delivery to muscles in patients with Chronic Fatigue Syndrome found that oxygen delivery and oxidative metabolism was significantly reduced in Chronic Fatigue Syndrome patients after exercise (compared with sedentary controls) (McCully et al. 1999).
Click here to demonstrate to you why Glutathione is so important to your health and well-being
Metal Sensitivity and Chronic Fatigue Syndrome
The effect of dental metal (amalgam) removal was studied in 111 patients with metal hypersensitivity and symptoms resembling Chronic Fatigue Syndrome. After consultation with a dentist, the patients decided to replace their metal restorations with nonmetallic materials. A significant number of patients had metal-specific lymphocytes in the blood. Nickel was the most common, followed by inorganic mercury, gold, phenyl-mercury, cadmium, and palladium. As compared to lymphocyte responses in healthy subjects, the Chronic Fatigue Syndrome group had significantly increased responses to several metals, especially to inorganic mercury, phenyl-mercury, and gold. Following dental metal removal, 83 patients (76%) reported long-term health improvement; 24 patients (22%) reported unchanged health; and two patients (2%) reported worsening of symptoms. Following dental metal replacement, the lymphocyte reactivity to metals decreased as well (Stejskal et al. 1999) (see "Mercury Amalgam Toxicity" in the May 2001 issue of Life Extension Magazine).
Click here to demonstrate to you why Glutathione is so important to your health and well-being
Click here to demonstrate to you why Glutathione is so important to your health and well-being
Multiple Chemical Sensitivity and Chronic Fatigue Syndrome
Multiple chemical sensitivity (MCS) is a controversial term. Synonyms for MCS are twentieth century disease, Environmental Illness, Total Allergy syndrome, Chemical AIDS, and Idiopathic Environmental Illness. It is believed by some that exposure to a chemical (or many chemicals) can trigger a complex of symptoms called MCS. It appears to affect young women at a higher rate than men. There has not been a consensus on the specific definition for MCS. The disorder is characterized by recurring symptoms affecting multiple organ systems. The individual demonstrates symptoms of MCS when exposed to many unrelated chemicals, in doses that are far below those recognized to cause harm in the general population. No single, widely accepted test of physiologic function can be correlated with the symptoms (Cullen 1987a; 1987b).
The theories for MCS include, but are not limited to, dysfunction of the immune system and neurological abnormalities--specifically, chemical sensitization of the limbic system--and various psychological theories. To date, no studies have validated any theory. One study points out that MCS, fibromyalgia, Chronic Fatigue Syndrome, and post-traumatic stress disorder are overlapping diseases, sharing common symptoms. Very often, each disorder seems to be induced by a relatively short-term stress, which is followed by a chronic pathology, suggesting that the stress may act by inducing a self-perpetuating vicious cycle.
Pall et al. (2001b) believe that the vicious cycle mechanism is the explanation for the etiology of Chronic Fatigue Syndrome and MCS, based on the elevated levels of nitric oxide and its potent oxidant product, peroxynitrite, found in both conditions.
Beckman et al. reported that peroxynitrite reacts with and inactivates several important mitochondrial enzymes leading to metabolic energy dysfunction (Beckman et al. 1993; Radi et al. 1994), characteristics of both Chronic Fatigue Syndrome and MCS.
Click here to demonstrate to you why Glutathione is so important to your health and well-being
The theories for MCS include, but are not limited to, dysfunction of the immune system and neurological abnormalities--specifically, chemical sensitization of the limbic system--and various psychological theories. To date, no studies have validated any theory. One study points out that MCS, fibromyalgia, Chronic Fatigue Syndrome, and post-traumatic stress disorder are overlapping diseases, sharing common symptoms. Very often, each disorder seems to be induced by a relatively short-term stress, which is followed by a chronic pathology, suggesting that the stress may act by inducing a self-perpetuating vicious cycle.
Pall et al. (2001b) believe that the vicious cycle mechanism is the explanation for the etiology of Chronic Fatigue Syndrome and MCS, based on the elevated levels of nitric oxide and its potent oxidant product, peroxynitrite, found in both conditions.
Beckman et al. reported that peroxynitrite reacts with and inactivates several important mitochondrial enzymes leading to metabolic energy dysfunction (Beckman et al. 1993; Radi et al. 1994), characteristics of both Chronic Fatigue Syndrome and MCS.
Click here to demonstrate to you why Glutathione is so important to your health and well-being
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