Glutathione is a powerful antioxidant. It is water-soluble and is primarily synthesized in the liver and helpful in many conditions including for oxidative stress and more in heart disease (atherosclerosis and hypercholesterolemia).
Glutathione deficiency contributes to oxidative stress, which plays a key role in aging and the worsening of many diseases including heart attacks and anaemia. Age-related depletion of glutathione levels may be especially damaging to metabolically active tissues, such as the heart and brain. Studies show that Glutathione in the aging heart and brain are thought to decline by 58-66% relative to young controls.
Although Glutathione is present in fruits, vegetables and meats, the levels in the body do not seem to correlate to dietary intake. Your body synthesizes Glutathione primarily from L-Cysteine which acts as a precursor. However, L-Cysteine is quite unstable, which is why we have always used the more effective and expensive, but stable form of Acetyl-L-Cysteine to help the body produce L-Glutathione.
Some people still cannot effectively synthesize the precursors and end up with a shortage of L-Glutathione in their cells, which leads to all sorts of health complications and premature aging.
Because depletion of L-Glutathione has been noted in so many diseases many researchers throughout the world worked on ways of trying to figure out how to replenish L-Glutathione in the cells. This was a very difficult task as 'normal' L-Glutathione is ineffective when taken orally... for two reasons. One... the molecule is too large to pass through the cell membranes and two... it is useless if released into the stomach as per normal capsules and tablets!
Scientists ultimately figured out how to make the molecule smaller so it could pass through the cell membranes. Reduced Glutathione, such as we use in our Total Balance formula, is well absorbed by the body. It is able to benefit you in all the same ways as Glutathione, but is additionally important as it helps to increase and maintain the functions of other antioxidants. For example, as a ‘ground’ for antioxidant enzyme activity such as for Glutathione peroxidase (a powerful enzyme and scavenger of free radicals, which defuses damaging peroxides (formed by the oxidation of lipids and further causing rancidity).
So, this solved the first problem! This meant that there was only the one outstanding issue of how to get the Glutathione to the cells. It cannot be released in the stomach because the stomach acid would destroy it. It needs to be released in the upper intestine, where it can be safely and wholly absorbed.
Fortunately the technology to achieve this has been used in the pharmaceutical industry for some time. It is called enteric coating, and Xtend-Life has employed this technique in the manufacturing process, without having to increase costs onto the consumer.
Published Clinical Studies
L-Glutathione
Nutritional regulation of glutathione in stroke.3
College of Pharmacy and Nutrition, The Cameco MS Neuroscience Research Center, University of Saskatchewan, 110 Science Place, Saskatoon, SK S7N 5C9, Canada.
In contrast to cardiovascular disease, the impact of nutritional status on the prevention and outcome of stroke has received limited investigation. We present a mechanism based on animal studies, clinical data, and epidemiological data by which protein-energy status in the acute stroke and immediate postinjury periods may affect outcome by regulating reduced glutathione (GSH), a key component of antioxidant defense. As cysteine is the limiting amino acid for GSH synthesis, the GSH concentration of a number of nonneural tissues has been shown to be decreased by fasting, low-protein diets, or diets limiting in sulfur amino acids. The mechanism may also be relevant in brain since GSH in some brain regions is responsive to dietary sulfur amino acid supply and to the pro-cysteine drug, L-2-oxothiazolidine-4-carboxylate. The latter is an intracellular cysteine delivery system used to overcome the toxicity associated with cysteine supplementation. These findings may provide the mechanism to explain both the inverse correlation between dietary protein and stroke mortality and the documented association between suboptimal protein-energy status and diminished functional status following a stroke. Future investigations should examine the role of nutritional intervention in neuroprotective strategies aimed at improving stroke outcome. Pharmacological interventions such as L-2-oxothiazolidine-4-carboxylate should be investigated in animal models of stroke, as well as the impact of nutritional status on the response to these agents. Finally, micronutrient deficiencies that may accompany protein-energy malnutrition, such as selenium, should also be investigated for their role in antioxidant defense in cerebral ischemia.
Glutathione deficiency intensifies ischaemia-reperfusion induced cardiac dysfunction and oxidative stress
Department of Kinesiology and Nutritional Science, University of Wisconsin-Madison, WI, USA.
The efficacy of glutathione (GSH) in protecting ischaemia-reperfusion (I-R) induced cardiac dysfunction and myocardial oxidative stress was studied in open-chest, stunned rat heart model. Female Sprague-Dawley rats were randomly divided into three experimental groups: (1) GSH-depletion, by injection of buthionine sulphoxamine (BSO, 4 mmol kg(-1), i.p.) 24 h prior to I-R, (2) BSO injection (4 mmol kg(-1), i.p.) in conjunction with acivicin (AT125, 0.05 mmol kg(-1), i.v.) infusion 1 h prior to I-R, and (3) control (C), receiving saline treatment. Each group was further divided into I-R, with surgical occlusion of the main left coronary artery (LCA) for 30 min followed by 20 min reperfusion, and sham. Myocardial GSH content and GSH : glutathione disulphide (GSSG) ratio were decreased by approximately 50% (P < 0.01) in both BSO and BSO + AT125 vs. C. Ischaemia-reperfusion suppressed GSH in both left and right ventricles of C (P < 0.01) and left ventricles of BSO and BSO + AT125 (P < 0.05). Contractility (+dP/dt and -dP/dt) in C heart decreased 55% (P < 0.01) after I and recovered 90% after I-R, whereas +/-dP/dt in BSO decreased 57% (P < 0.01) with ischaemia and recovered 76 and 84% (P < 0.05), respectively, after I-R. For BSO + AT125, +/-dP/dt were 64 and 76% (P < 0.01) lower after ischaemia, and recovered only 67 and 61% (P < 0.01) after I-R. Left ventricular systolic pressure in C, BSO and BSO + AT125 reached 95 (P > 0.05) 87 and 82% (P < 0.05) of their respective sham values after I-R. Rate-pressure double product was 11% (P > 0.05) and 25% (P < 0.05) lower in BSO and BSO + AT125, compared with Saline, respectively. BSO and BSO + AT125 rats demonstrated significantly lower liver GSH and heart Mn superoxide dismutase activity than C rats after I-R. These data indicate that GSH depletion by inhibition of its synthesis and transport can exacerbate cardiac dysfunction inflicted by in vivo I-R. Part of the aetiology may involve impaired myocardial antioxidant defenses and whole-body GSH homeostasis.