This Glutathione is made by Kohjin for Talking Herbals They have been making Glutathione since 1968. One level teaspoon is 1500mg. There is approximately 33 servings per bottle. This is the purest Glutathione available today. Talking Herbals has been selling it since 1999.
Clinical Tests Demonstrate Long-Term Effectiveness of Oral Glutathione Supplements
Penn State College of Medicine researchers say supplementation can increase body’s glutathione stores.
We believe GSH supplementation may represent an effective intervention strategy for disease prevention and may enhance immune function -- Dr. John P. Richie
Hershey, PA (PRWEB) April 25, 2013
Glutathione deficiency has been found to be virtually universal in autoimmune diseases. This deficiency has two major implications: detox failure and viral/microbial activation. Glutathione plays a major role in detoxification. This deficiency impairs the body’s ability to get rid of toxins.
Consequently, people slowly become toxic, storing away poisons in fatty tissue, muscles, organs and the brain. This cellular detox failure can make people canaries to their environment.
To detoxify successfully, this glutathione deficiency must be addressed.
Because glutathione is a potent antiviral and anti-microbial weapon, glutathione deficiency compromises antiviral and anti-microbial defenses, and actually stimulates viral replication. Raising glutathione levels inside the cells can stop the replication of almost any pathogen.
A glutathione deficiency compromises our ability to keep old viruses dormant and fight off bacteria. This is why so many people test positive for EBV, CMV, HHV6, Mycoplasma, and Chlamydia Pneumoniae, etc.
Indications are that glutathione can stop the replication of any intracellular microbe, including HHV6, Chlamydia Pneumoniae, and mycoplasma. .
There has been a good deal of research that show how important glutathione is.
Immune depressed individuals have lower glutathione levels when fighting disease. Lymphocytes, cells vital for your immune response, depend on glutathione for their proper function and replication. Immunology 61: 503-508 1987 .
Cellular depletion of Glutathione has been implicated as a causative, or contributory factor in many pathologies including Parkinson\'s, Alzheimer\'s, cataracts, arteriosclerosis, cystic fibrosis, malnutrition, aging, AIDS and cancer (Bounous et al., 1991).
In addition, Glutathione is essential in supporting the immune system, including natural killer cells (Droege et al., 1997) and in the maintenance of T-lymphocytes (Gutman, 1998).
It is known that as we age, there is a precipitous drop in glutathione levels. Lower Glutathione levels are implicated in many diseases associated with aging, including Cataracts, Alzheimer\'s disease, Parkinson\'s, atherosclerosis and others. Journal of Clinical Epidemiology 47: 1021-28 1994
Antioxidants are well documented to play vital roles in health maintenance and disease prevention. Glutathione is our cell\'s own major antioxidant. Why not use what is natural? Biochemical Pharmacology 47:2113-2123 1994
Low glutathione has been demonstrated in neurodegenerative diseases such as MS (Multiple Sclerosis), ALS (Lou Gehrig\'s Disease), Alzheimer\'s, and Parkinson\'s, among others. The Lancet 344: 796-798 1994
Glutathione detoxifies many pollutants, carcinogens and poisons, including many in fuel exhaust and cigarette smoke. It retards damage from radiation such as seen with loss of the ozone. Annual Review of Biochemistry 52: 711-780 1983.
The liver is the main detoxification organ of the body. In the liver we find very high concentrations of glutathione, as it is a major factor in numerous biochemical detoxification pathways. Numerous studies have demonstrated that patients with compromised liver function due to alcohol abuse have significant reduction of glutathione in the liver. (Lamestro, 1995)
Glutathione is essential for the maintenance of Vitamin C and vitamin E levels according to Martensson. He found that as glutathione levels decreased, a corresponding decrease in ascorbic acid and vitamin E followed, which led to systematic mitochondrial death, which in turn leads to a cessation of cellular metabolism.
(It is this mitochondrial death, at first just a dysfunction, that may cause the fatigue found in autoimmune illnesses.)
The over-toxicity causes extensive free radical damage. Inhibits cellular function. Disrupts energy production by the mitochondria. Consequently the primary energy the cells produce is anaerobic which leads to extensive lactic acid buildup in the cells. And more toxicity.
Cheney explains that fatigue becomes worse. Pain increases. You feel sicker. Memory suffers as toxins and free radicals damage the brain, and not enough oxygen gets into the brain. Deep brain structures like the hypothalamus eventually are injured and cause problems with virtually every hormone in your body. They lose their ability to rise and fall according to signals or demands from the body making it harder to respond to changing situations. Actual damage to the DNA of the energy producing mitochondria can occur. Further limiting energy.
As toxins cause free radical damage, you end up with low levels of all the free radical scavengers. They get used up dealing with excessive free radicals produced by the excessive toxins.
Glutathione is the body’s master antioxidant involved in protecting cells and tissues from oxidants and a large variety of other toxins and insults. Debate over whether orally administered glutathione could be effective at enhancing glutathione levels in cells and tissues has simmered for years. Now, a Penn State College of Medicine study shows oral supplementation is effective in increasing the body’s stores of this vital nutrient.
The study of 54 healthy adults revealed that glutathione (GSH) levels of those taking 1000mg of Glutathione a day for six months increased 30%-35% in many compartments including red blood cells, lymphocytes and plasma., Glutathione increased in whole blood. And as glutathione stores increased so did the function of natural killer (NK) cells, a marker for increased immune defense, said John P. Richie, Jr., Ph.D., professor of Public Health Sciences and Pharmacology at Penn State College of Medicine.
“A battery of immune function markers was examined after three months of glutathione supplementation and NK cytotoxicity was enhanced more than two-fold for participants taking 1000mg daily doses,” Dr. Richie said. “We believe GSH supplementation may represent an effective intervention strategy for disease prevention and may enhance immune function.”
There is a school of thought that contends that glutathione is broken down in the stomach and intestine and effective increases of GSH must come via intravenous administration. However, previous animal studies showed that orally administered glutathione is bioavailable and will enhance tissue GSH levels, Dr. Richie said.
“Our research showed that in most cases increases were dose and time dependent, and levels returned to baseline after a one-month washout,” he said. “By taking daily GSH supplements, we believe efficacious levels will persist, and that oral intake is an effective means of chronically enhancing the body’s stores.”
Dr. Richie presented the study findings – “Enhanced Glutathione Levels in Blood and Buccal Cells by Oral Glutathione Supplementation” – at the Experimental Biology 2013 conference in Boston on April 22. The study was a joint effort of the Pennsylvania Department of Public Health Sciences, the Penn State Hershey Cancer Institute, and the Penn State College of Medicine.
About John P. Richie, Ph.D.
Dr. Richie is professor, Public Health Sciences and Pharmacology, at Penn State College of Medicine, State College, Penn. He has researched has researched glutathione for more than 30 years, including its role in protecting against oxidative damage during aging and the development of cancer at numerous sites in the body. Dr. Richie\'s research focuses on the factors that regulate glutathione, oxidative stress and cancer risk in individuals and in various populations
What is Glutathione (GSH)?
Reduced Glutathione (GSH) is a linear tripeptide of L-glutamine, L-cysteine, and glycine. Technically N-L-gamma-glutamyl-cysteinyl glycine or L-Glutathione, the molecule has a sulfhydryl (SH) group on the cysteinyl portion, which accounts for its strong electron-donating character.
As electrons are lost, the molecule becomes oxidized, and two such molecules become linked (dimerized) by a disulfide bridge to form Glutathione disulfide or oxidized Glutathione (GSSG). This linkage is reversible upon re-reduction.
Glutathione is under tight homeostatic control both intracellularly and extracellularly. A dynamic balance is maintained between GSH synthesis, it’s recycling from GSSG/oxidized Glutathione, and its utilization.
Glutathione synthesis involves two closely linked, enzymatically-controlled reactions that utilize ATP. First, cysteine and glutamate are combined by gamma-glutamyl cysteinyl synthetase. Second, GSH synthetase combines gamma-glutamylcysteine with glycine to generate Glutathione. As Glutathione levels rise, they self-limit further GSH synthesis; otherwise, cysteine availability is usually rate-limiting. Fasting, protein-energy malnutrition, or other dietary amino acid deficiencies limit Glutathione synthesis.
Glutathione recycling is catalyzed by Glutathione disulfide reductase, which uses reducing equivalents from NADPH to reconvert GSSG to 2GSH. The reducing power of ascorbate helps conserve systemic Glutathione.
Glutathione is used as a cofactor by (1) multiple peroxidase enzymes, to detoxify peroxides generated from oxygen radical attack on biological molecules; (2) transhydrogenases, to reduce oxidized centers on DNA, proteins, and other biomolecules; and (3) Glutathione S-transferases (GST) to conjugate Gluathione with endogenous substances (e.g., estrogens), exogenous electrophiles (e.g., arene oxides, unsaturated carbonyls, organic halides), and diverse xenobiotics. Low GST activity may increase risk for disease—but paradoxically, some Glutathione conjugates can also be toxic.
Direct attack by free radicals and other oxidative agents can also deplete Glutathione. The homeostatic Glutathione redox cycle attempts to keep Glutathione repleted as it is being consumed. Amounts available from foods are limited (less that 150 mg/day), and oxidative depletion can outpace synthesis.
The liver is the largest Glutathione reservoir. The parenchymal cells synthesize GSH for P450 conjugation and numerous other metabolic requirements—then export GSH as a systemic source of SH-reducing power. Glutathione is carried in the bile to the intestinal luminal compartment. Epithelial tissues of the kidney tubules, intestinal lining and lung have substantial P450 activity—and modest capacity to export Glutathione.
Glutathione equivalents circulate in the blood predominantly as cystine, the oxidized and more stable form of cysteine. Cells import cystine from the blood, reconvert it to cysteine (likely using ascorbate as cofactor), and from it synthesize GSH. Conversely, inside the cell, Glutathione helps re-reduce oxidized forms of other antioxidants—such as ascorbate and alpha-tocopherol.
Mechanism of Action:
Glutathione is an extremely important cell protectant. It directly quenches reactive hydroxyl free radicals, other oxygen-centered free radicals, and radical centers on DNA and other biomolecules. Glutathione is a primary protectant of skin, lens, cornea, and retina against radiation damage and other biochemical foundations of P450 detoxification in the liver, kidneys, lungs, intestinal, epithelia and other organs.
Glutathione is the essential cofactor for many enzymes that require thiol-reducing equivalents, and helps keep redox-sensitive active sites on enzyme in the necessary reduced state. Higher-order thiol cell systems, the metallothioneins, thioredoxins and other redox regulator proteins are ultimately regulated by Glutathione levels—and the GSH/GSSG redox ratio. GSH/GSSG balance is crucial to homeostasis—stabilizing the cellular biomolecular spectrum, and facilitating cellular performance and survival.
Glutathione and its metabolites also interface with energetics and neurotransmitter syntheses through several prominent metabolic pathways. Glutathione availability down-regulates the pro-inflammatory potential of leukotrienes and other eicosanoids. Recently discovered S-nitroso metabolites, generated in vivo from Glutathione and NO (nitric oxide), further diversify Glutathione's impact on metabolism
Glutathione Used in Various Disease States:
Acetaminophen Toxicity, ALS Alzheimer's, ASD (Autism Spectrum Disorder), Cancer, Chronic Fatigue, Cardiovascular Disease, COPD, Lung Disorders, Cystic Fibrosis, Diabetes, Gum Disease, Heavy Metal Toxicity, HIV, Huntington’s Disease, Liver Disease, Lyme Disease, Macular Degeneration, Multiple Sclerosis, Other Neurodegenerative Disease States, Parkinsons Disease, Stroke