Aging And Glutathione

Most Doctors agree that Aging and Disease are caused by Oxidative Stress and Free Radical damage. Oxidative Stress and Free Radical Damage occurs in our bodies as a normal course of daily living. It comes from exercise, pollutants in the air, even the food we eat and drink. If left unchecked our bodies would deteriorate from the inside out. The good news is that we were created with the ability to produce a molecule (found in every cell in our body) that is called GLUTATHIONE (GSH). Surprisingly, glutathione was discovered circa 1888 but not until the last 20 years have scientists really understood its importance. Scientists now refer to glutathione as The Master Antioxidant. Without GSH we literally cannot survive. The key to understanding the importance of GSH is that many of the diseases we know of are associated with low levels of glutathione. Therefore, elevated levels of Glutathione fight against MS, Alzheimer's, AIDS, Diabetes, Heart Disease, Cancer, Crohns Disease, Lung Disease, Parkinson's, Lupus and many more. The production is dependent upon the availability of the amino acid Cysteine. After 25 years of research Immunocal was the discovery of Gustavo Bounous, MD which is the Ideal Source of Cysteine. Immunocal is an Undenatured Whey Protein Isolate that has 10 Method of Use Patents in 80 countries worldwide. This is a critical distinction when compared to any product that only have a composition patent. Unfortunately, some misinformation also exists that can confuse the average person who is just trying to improve their health. Some companies try to sell glutathione pills that are just passed thruough your body as waste. They do nothing or at best, very little to increase glutathione serum levels. The only proven safe and natural whey to improve your health is by providing your body with the precursor or building block Cysteine found in Immunocal.

Glutathione metabolism during aging and in Alzheimer disease. Liu H, Wang H, Shenvi S, Hagen TM, Liu RM. Department of Immunology, School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama 35294-0022, USA. The concentration of glutathione (GSH), the most abundant intracellular nonprotein thiol and important antioxidant, declines with age and in some age-related diseases. The underlying mechanism, however, is not clear. The previous studies from our laboratory showed that the agedependent decline in GSH content in Fisher 344 rats was associated with a downregulation of glutamate cysteine ligase (GCL), the rate-limiting enzyme in de novo GSH synthesis. Our recent studies further indicated that the activity and mRNA content of glutathione synthase (GS), which catalyzes the second reaction in de novo GSH synthesis, were also decreased with age in some tissues. No age-associated change was observed in glutathione reductase or gamma-glutamyl transpeptidase activities. Also, although GSH content declined with age in both male and female mice, male mice experienced more dramatic age-associated decline in many tissues/organs than female mice. Furthermore, we found that GSH content was significantly decreased in the red blood cells from male Alzheimer disease patients, which was associated with decreases in GCL and GS activities. Finally, we showed that estrogen increased GSH content, GS and GR activities, and GCL gene expression in the liver of both male and female mice. Taken together, our results suggest that (1) GCL plays a critical role in maintaining GSH homeostasis under both physiological and pathological conditions; (2) decreased GSH content may be involved in AD pathology in humans; and (3) estrogen increases GSH content in mice by multiple mechanisms. PMID: 15247041 [PubMed - indexed for MEDLINE]

Aberrant Insulin Receptor Signaling and Amino Acid Homeostasis as a Major Cause of Oxidative Stress in Aging WULF DRÖGE and RALF KINSCHERF The mechanisms leading to the increase in free radical-derived oxidative stress in “normal aging” remains obscure. Here we present our perspective on studies from different fields that reveal a previously unnoticed vicious cycle of oxidative stress. The plasma cysteine concentrations during starvation in the night and early morning hours (the postabsorptive state) decreases with age. This decrease is associated with a decrease in tissue concentrations of the cysteine derivative and quantitatively important antioxidant glutathione. The decrease in cysteine reflects changes in the autophagic protein catabolism that normally ensures free amino acid homeostasis during starvation. Autophagy is negatively regulated by the insulin receptor signaling cascade that is enhanced by oxidative stress in the absence of insulin. This synopsis of seemingly unrelated processes reveals a novel mechanism of progressive oxidative stress in which decreasing antioxidant concentrations and increasing basal (postabsorptive) insulin receptor signaling activity compromise not only the autophagic protein catabolism but also the activity of FOXO transcription factors (i.e., two functions that were found to have an impact on lifespan in several animal models of aging). In addition, the aging-related decrease in glutathione levels is likely to facilitate certain “secondary” disease-related mechanisms of oxidative stress. Studies on cysteine supplementation show therapeutic promise. Antioxid. Redox Signal. 10, 661–678.

Erythrocytic Glutathione and Plasma Cysteine Status of Human Immunodeficient Patients Calvin A. Lang,1, Anna Huang, Julio A. Ramirez and Marcia C. Liu Departments of Biochemistry and Molecular Biology and Medicine, University of Louisville School of Medicine, Louisville, Kentucky 40292 http://www.ebmonline.org/cgi/content/full/226/9/866 In later studies, glutathione (GSH) concentrations in various tissues were determined during the life span. A noteworthy discovery was a sharp decline in tissue GSH levels in the senescent C57BL/6J mouse and the yellow fever mosquito, Aedes aegypti (2–4). Another key finding was that the blood GSH profile in the mature and aging mouse was paralleled in less accessible organs such as heart, liver, kidneys, lung, spleen, and brain (5, 6, 8, 9). Thus, blood GSH reflected the whole body status. A similar GSH and aging relationship occurs in humans. Healthy males and females from ages 20 to 94 years old were recruited from Louisville, Kentucky and their blood GSH status was determined. Normal GSH concentration was determined in the 20- to 40-year-old subjects. Reduced glutathione (GSSH) deficiency occurred in subjects older than 40 year and the number increased with age, reaching as high as 50% of the 60- to 79-year-old age group (10). GSH deficiency was also found in another group of elderly subjects in Michigan with an inverse relationship between age and GSH level. In that epidemeologic study, GSH together with age and measure of suppressed anger accounted for 39% of the variance of an index for morbidity (11). The findings in healthy persons suggested an investigation of GSH in unhealthy subjects (12). Newly admitted hospital patients who had a variety of major chronic diseases were consecutively recruited along with healthy controls. Blood GSH levels were determined and correlated with their diagnoses. Over 36% of the 74 patients were GSH deficient (P < 0.001).

At this time we became aware of reports that GSH was deficient in plasma and its cellular components of HIV-seropositive subjects, regardless of CD4 lymphocyte level (13–17). Since Cys is the rate-limiting precursor of GSH, its decrease inferred that Cys deficiency was the cause of low GSH levels and implicated low levels of both GSH and Cys in the pathogenesis of HIV infection. The importance of GSH and Cys to HIV infection has been well documented in these articles. ***** Drs. Richie and Lang, of the Department of Biochemistry, University of Louisville, were the first to propose that a glutathione deficiency might be a biochemical cause of the aging process. They demonstrated that glutathione levels decline with age in a number of organisms, including mosquitoes, mice, and man. They proposed that restoring glutathione tissue concentrations to those of younger organisms might result in an extension of the lifespan.

A decrease in cysteine levels causes the glutathione deficiency of aging in the mosquito. Richie JP Jr, Lang CA. Department of Biochemistry, University of Louisville School of Medicine, Kentucky 40292.

Our previous results indicated that a glutathione (GSH) deficiency is a determinant of the aging process in many tissues and organisms. Correction of this deficiency in the aging mosquito by feeding the cysteine (Cys) precursor magnesium thiazolidine carboxylic acid (MgTc) suggested that the cause could be a lack of Cys. ***** Contact: Randy Grover Immunotec Consultant

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