Whey protein contains proteins like alpha-lactalbumin which is is rich in sulphur-containing amino acids.
Heating or pasteurization destroys the delicate disulphide bonds that give these proteins their bioactivity.
Undenatured whey protein is a non-heated product that preserves bioactive amino acids like cystine. It has been shown in numerous scientific studies and clinical trials to optimize glutathione levels.
Glutathione's three major roles in the body are summarized by the letters A-B-C.
- Anti-oxidant- Blood Booster- Cell Detoxifier
Click here for more about Glutathione and its benefits to our body.
Showing posts with label Blood Booster. Show all posts
Showing posts with label Blood Booster. Show all posts
Wednesday, January 23, 2008
Monday, January 21, 2008
Glutathione Fact 1 - produced naturally in our cells
Glutathione (GSH) is a small protein produced naturally in our cells when certain required elements are present
It functions both as an antioxidant and an antitoxin and is a major defense system against illness and aging.
Our glutathione level actually indicates our state of health and can predict longevity. Although there are more than 60,000 published papers on the beneficial effects of glutathione replacement, it is still largely ignored by mainstream medicine.
In the near future the importance of glutathione will be widely recognized because it has the ability to boost the immune system and fight off the damage of free radicals on the cells.
Glutathione's three major roles in the body are summarized by the letters A-B-C.
- Anti-oxidant- Blood Booster- Cell Detoxifier
It functions both as an antioxidant and an antitoxin and is a major defense system against illness and aging.
Our glutathione level actually indicates our state of health and can predict longevity. Although there are more than 60,000 published papers on the beneficial effects of glutathione replacement, it is still largely ignored by mainstream medicine.
In the near future the importance of glutathione will be widely recognized because it has the ability to boost the immune system and fight off the damage of free radicals on the cells.
Glutathione's three major roles in the body are summarized by the letters A-B-C.
- Anti-oxidant- Blood Booster- Cell Detoxifier
Friday, January 18, 2008
HOW TO GET GLUTATHIONE INTO YOUR CELLS
Glutathione is made up of three amino acids, glycine, glutamic acid and cysteine. Each cell produces its own GSH according to need within itself.
The determining factor as to how much it can make to ultimately keep levels up to the needed 70% in the active form...is determined by the availability of the amino acid cysteine. The production of cysteine becomes less and less efficient as we get older going into a steady decline by around age 55 onward.
This is just at a time when its most needed to protect our brains and neurological system from syndromes such as Alzheimer's Disease and dementia, which are now becoming more and more common.
Before we go further, let me explain "active" form (technically called the "reduced" form) and "inactive" (technically called the "oxidized" form) forms of glutathione. The active form is the one that can perform all the functions listed above act as a powerful antioxidant, work to combat diseases of aging and a potent player in detoxification. It is often shown in written works as "GSH".
The inactive form is present when GSH has done its work donating electrons and needs to regenerate itself which it can do. Its usually shown as GSSG (lacking the H..because it gave it away to stabilize some other molecule).
In a healthy situation, the percentage of GSH is about 90% with only 10% of Glutathione existing as GSSG. When these ratios change and there is more and more GSSG present, that is when the cell becomes sick, and is vulnerable to attack from toxins and microbes. If GSH falls below 70%...the cells/organ/person is in HUGE trouble!
There is one provison to this situation. If GSH is "used" to clear up a situation from our own metabolism, then it can regenerate itself just fine. HOWEVER if its used to combat "xenobiotics" or toxins from the outside of our bodies, such as chemicals, heavy metals, toxins, etc., then it cant regenerate.
This is where we run into trouble today as our food is not replenishing us the way it should and supplementing for Glutathione is tricky
Glutathione's three major roles in the body are summarized by the letters A-B-C.
- Anti-oxidant- Blood Booster- Cell Detoxifier
Learn more about Glutathione click here
The determining factor as to how much it can make to ultimately keep levels up to the needed 70% in the active form...is determined by the availability of the amino acid cysteine. The production of cysteine becomes less and less efficient as we get older going into a steady decline by around age 55 onward.
This is just at a time when its most needed to protect our brains and neurological system from syndromes such as Alzheimer's Disease and dementia, which are now becoming more and more common.
Before we go further, let me explain "active" form (technically called the "reduced" form) and "inactive" (technically called the "oxidized" form) forms of glutathione. The active form is the one that can perform all the functions listed above act as a powerful antioxidant, work to combat diseases of aging and a potent player in detoxification. It is often shown in written works as "GSH".
The inactive form is present when GSH has done its work donating electrons and needs to regenerate itself which it can do. Its usually shown as GSSG (lacking the H..because it gave it away to stabilize some other molecule).
In a healthy situation, the percentage of GSH is about 90% with only 10% of Glutathione existing as GSSG. When these ratios change and there is more and more GSSG present, that is when the cell becomes sick, and is vulnerable to attack from toxins and microbes. If GSH falls below 70%...the cells/organ/person is in HUGE trouble!
There is one provison to this situation. If GSH is "used" to clear up a situation from our own metabolism, then it can regenerate itself just fine. HOWEVER if its used to combat "xenobiotics" or toxins from the outside of our bodies, such as chemicals, heavy metals, toxins, etc., then it cant regenerate.
This is where we run into trouble today as our food is not replenishing us the way it should and supplementing for Glutathione is tricky
Glutathione's three major roles in the body are summarized by the letters A-B-C.
- Anti-oxidant- Blood Booster- Cell Detoxifier
Learn more about Glutathione click here
What conditions or problems is glutathione used for?
Glutathione peroxidase may help delay the physical effects and problems of aging.
Adequate amounts of Glutathione are needed to help the immune system fight against free-radical damage, infection, and illness.
Glutathione may help prevent or lessen symptoms of conditions like asthma and rheumatoid arthritis.
Learn more about Glutathione click here
Glutathione's three major roles in the body are summarized by the letters A-B-C.
- Anti-oxidant- Blood Booster- Cell Detoxifier
Adequate amounts of Glutathione are needed to help the immune system fight against free-radical damage, infection, and illness.
Glutathione may help prevent or lessen symptoms of conditions like asthma and rheumatoid arthritis.
Learn more about Glutathione click here
Glutathione's three major roles in the body are summarized by the letters A-B-C.
- Anti-oxidant- Blood Booster- Cell Detoxifier
Wednesday, January 16, 2008
Substances that Boost Glutathione Levels and Protect Brain Cells
Taking Glutathione itself as a supplement does not boost cellular Glutathione levels, since it breaks down in the digestive tract before it reaches the cells.
However, intravenous Glutathione therapy and Glutathione precursors or dietary supplements are effective in boosting intracellular levels ofGlutathione.
Intravenous Glutathione Injections:
Intravenous Glutathione injections have been shown to produce amazing and rapid results, in patients with Parkinson's disease. Followingeven a single dosage of intravenous Glutathione, many of the symptoms of Parkinson's disease rapidly improve, often in as little as 15 minutes.
Glutathione Precursors:
In the Alzheimer's study conducted by Welsh GP, Andrew McCaddon, adding theGlutathione precursor, N-acetyl-cysteine (NAC) to a protocol thatlowered homocysteine levels by simple supplementation with B12 and folate, resulted in prompt, striking, and sustained clinical improvement in nearly all the patients.
Cucurmin (turmeric):
Studies have shown that the Indian curry spice, cucurmin, has neuroprotective effects because of its ability to induce the enzyme, hemeoxygenase-1(HO-1), which protects neurons exposed to oxidant stress. Treatment of brain cells called astrocytes, with curcumin, increases expression of HO-1 protein as well as Glutathione S-transferase.
Proc Natl Acad Sci U S A. 2003 Jun 24;100(13):7919-24. Epub 2003 Jun 05.
Am J Geriatr Psychiatry. 2003 Mar-Apr;11(2):246-9
Can Curry Protect Against Alzheimer's?; American Physiological Society (APS) Press Release; 16-Apr-2004
Glutathione's three major roles in the body are summarized by the letters A-B-C.
- Anti-oxidant- Blood Booster- Cell Detoxifier
THE MAX GXL is a PATENTED High Performance Formula which:
Dramatically Raises Your Energy Level
Slows Down The Aging Process
Strengthens Your Immune System
Fights Inflammation and Diseases of Aging
Improves Athletic Performance & Recovery
Detoxifies Your Body
However, intravenous Glutathione therapy and Glutathione precursors or dietary supplements are effective in boosting intracellular levels ofGlutathione.
Intravenous Glutathione Injections:
Intravenous Glutathione injections have been shown to produce amazing and rapid results, in patients with Parkinson's disease. Followingeven a single dosage of intravenous Glutathione, many of the symptoms of Parkinson's disease rapidly improve, often in as little as 15 minutes.
Glutathione Precursors:
In the Alzheimer's study conducted by Welsh GP, Andrew McCaddon, adding theGlutathione precursor, N-acetyl-cysteine (NAC) to a protocol thatlowered homocysteine levels by simple supplementation with B12 and folate, resulted in prompt, striking, and sustained clinical improvement in nearly all the patients.
Cucurmin (turmeric):
Studies have shown that the Indian curry spice, cucurmin, has neuroprotective effects because of its ability to induce the enzyme, hemeoxygenase-1(HO-1), which protects neurons exposed to oxidant stress. Treatment of brain cells called astrocytes, with curcumin, increases expression of HO-1 protein as well as Glutathione S-transferase.
Proc Natl Acad Sci U S A. 2003 Jun 24;100(13):7919-24. Epub 2003 Jun 05.
Am J Geriatr Psychiatry. 2003 Mar-Apr;11(2):246-9
Can Curry Protect Against Alzheimer's?; American Physiological Society (APS) Press Release; 16-Apr-2004
Glutathione's three major roles in the body are summarized by the letters A-B-C.
- Anti-oxidant- Blood Booster- Cell Detoxifier
THE MAX GXL is a PATENTED High Performance Formula which:
Dramatically Raises Your Energy Level
Slows Down The Aging Process
Strengthens Your Immune System
Fights Inflammation and Diseases of Aging
Improves Athletic Performance & Recovery
Detoxifies Your Body
Monday, January 14, 2008
Increasing Tissue Glutathione Levels
It is clear that those with the highest Glutathione levels are likely to live the longest in the best of health. A number of ways have been demonstrated to increase Glutathione (GSH) and the Glutathione enzymes, Glutathione peroxidase (G-Px) and Glutathione reductase (GR).
Several small studies have shown that moderate, prolonged physical exercise increases Glutathione and its related enzyme levels in the blood and skeletal muscles.
Many vitamins and nutritional supplements are also Glutathione boosters. Lipoic acid, pine bark extract (pycnogenol), melatonin, bilberry, grape extract, and turmeric have all been shown to elevate Glutathione. Oral glutamine may also raise tissue Glutathione levels, although there are conflicting reports.
I used to think that oral Glutathione was destroyed in the stomach, and was not effective in raising Glutathione concentrations. However, Dr. Steve Edelson, of the Edelson Center for Environmental and Preventive Medicine in Atlanta, Georgia, kindly sent me a number of articles that convinced me otherwise. These articles demonstrated that about 80 percent of oral Glutathione is absorbed intact, and that the blood levels remain elevated for about three hours (Fig. 6)
Several small studies have shown that moderate, prolonged physical exercise increases Glutathione and its related enzyme levels in the blood and skeletal muscles.
Many vitamins and nutritional supplements are also Glutathione boosters. Lipoic acid, pine bark extract (pycnogenol), melatonin, bilberry, grape extract, and turmeric have all been shown to elevate Glutathione. Oral glutamine may also raise tissue Glutathione levels, although there are conflicting reports.
I used to think that oral Glutathione was destroyed in the stomach, and was not effective in raising Glutathione concentrations. However, Dr. Steve Edelson, of the Edelson Center for Environmental and Preventive Medicine in Atlanta, Georgia, kindly sent me a number of articles that convinced me otherwise. These articles demonstrated that about 80 percent of oral Glutathione is absorbed intact, and that the blood levels remain elevated for about three hours (Fig. 6)
Click here for more about Glutathione and its benefits to our body.
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
Thursday, January 10, 2008
Glutathione and Helicobacter pylori
Helicobacter pylori is the primary cause of gastritis and peptic ulcer disease and can lead to the onset of gastric cancer.
Previous studies have shown that H. pylori infection causes increased production of reactive oxygen species within the gastric mucosa, possibly leading to the H. pylori associated diseases. One group of researchers, after reviewing the medical literature, proposed that the severity of inflammation and damage associated with H. pylori infection is dependent on stomach cells’ ability to counteract the increased reactive oxygen species load.
They hypothesized that Glutathione availability is important in mounting an adequate defense against the reactive oxygen species generated by the H. pylori infection.
The researchers suggested that increasing Glutathione availability could provide a novel method for preventing or reducing the damage caused by Helicobacter pylori. By Kimberly Pryor
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
Previous studies have shown that H. pylori infection causes increased production of reactive oxygen species within the gastric mucosa, possibly leading to the H. pylori associated diseases. One group of researchers, after reviewing the medical literature, proposed that the severity of inflammation and damage associated with H. pylori infection is dependent on stomach cells’ ability to counteract the increased reactive oxygen species load.
They hypothesized that Glutathione availability is important in mounting an adequate defense against the reactive oxygen species generated by the H. pylori infection.
The researchers suggested that increasing Glutathione availability could provide a novel method for preventing or reducing the damage caused by Helicobacter pylori. By Kimberly Pryor
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
Sunday, January 6, 2008
Common symptoms of Diabetes
Symptoms:
*Unusual thirst
*Frequent urination
*Extreme fatigue and weakness
*Blurred vision
*Abdominal pains
*Nausea and vomiting
*Rapid weight loss or gain
*Skin infections
*Impotence
*Fluid retention (especially in legs and feet)
*Poor healing of skin wounds
*Decreased tolerance to cold
*Chronic itching
*Irregular or rapid heart rate
*Dry scaly skin
*Numbness or tingling of fingers and toes
*Extreme hunger pangs
*Hot and sweaty with clammy perspiration
*Heart tremors and palpitations
*Apprehensive with no obvious reason
*Shaky and nervous
*Disoriented, confused, inability to concentrate
*Frequent headaches, dizziness
*Mood changes, irritability
All diabetic symptoms are related to chronically high levels of glucose in the blood, which causes the premature aging of all body parts. So all diabetic symptoms can be explained in terms of what happens to the body as it ages. The branch of science that studies the aging process is called Gerontology and much of what happens to people with uncontrolled diabetes. more...
It is well known that aging is accompanied by a precipitous fall inglutathione levels. Lower glutathione levels are implicated in manydiseases associated with aging including cataracts, Alzheimer's,Parkinson's atherosclerosis and others.Journal of Clinical Epidemiology 47:1021-26, 1994.
Click here to demonstrate to you why glutathione is so important to your health and well-being.
If you have any of the symptoms mentioned above, a family history of diabetes, or are aged 45 or above, contact your doctor or healthcare professional and initiate blood and urine tests for diabetes.
*Unusual thirst
*Frequent urination
*Extreme fatigue and weakness
*Blurred vision
*Abdominal pains
*Nausea and vomiting
*Rapid weight loss or gain
*Skin infections
*Impotence
*Fluid retention (especially in legs and feet)
*Poor healing of skin wounds
*Decreased tolerance to cold
*Chronic itching
*Irregular or rapid heart rate
*Dry scaly skin
*Numbness or tingling of fingers and toes
*Extreme hunger pangs
*Hot and sweaty with clammy perspiration
*Heart tremors and palpitations
*Apprehensive with no obvious reason
*Shaky and nervous
*Disoriented, confused, inability to concentrate
*Frequent headaches, dizziness
*Mood changes, irritability
All diabetic symptoms are related to chronically high levels of glucose in the blood, which causes the premature aging of all body parts. So all diabetic symptoms can be explained in terms of what happens to the body as it ages. The branch of science that studies the aging process is called Gerontology and much of what happens to people with uncontrolled diabetes. more...
It is well known that aging is accompanied by a precipitous fall inglutathione levels. Lower glutathione levels are implicated in manydiseases associated with aging including cataracts, Alzheimer's,Parkinson's atherosclerosis and others.Journal of Clinical Epidemiology 47:1021-26, 1994.
Click here to demonstrate to you why glutathione is so important to your health and well-being.
If you have any of the symptoms mentioned above, a family history of diabetes, or are aged 45 or above, contact your doctor or healthcare professional and initiate blood and urine tests for diabetes.
Glutathione infusion potentiates glucose-induced insulin secretion in aged patients with impaired glucose tolerance
OBJECTIVE: To evaluate the effect of glutathione infusion on beta-cell response to glucose in elderly people with impaired glucose tolerance (IGT).
RESEARCH DESIGN AND METHODS: Ten patients with normal glucose tolerance and 10 patients with IGT were matched for age (mean +/- SE, 72.1 +/- 2.8 vs. 71.0 +/- 3.4 yr), body mass index (23.1 +/- 1.1 vs. 22 +/- 2.1 kg/m2), and sex (6/4 vs. 5/5, men/women) underwent glutathione infusion (10 mg/min) under basal conditions and during 75-g oral glucose tolerance tests and intravenous glucose tolerance tests (0.33 g.kg body wt-1.3 min-1). Patients with IGT were also submitted to euglycemic-hyperinsulemic and hyperglycemic glucose clamps.
RESULTS:In subjects with normal glucose tolerance, glutathione infusion failed to affect beta-cell response to glucose. In contrast, glutathione significantly potentiated glucose-induced insulin secretion in patients with IGT. Furthermore, in the latter group studied by hyperglycemic clamps, glutathione infusion significantly potentiated the beta-cell response to glucose when plasma glucose levels varied between 10 and 15 mM. This effect disappeared at plasma glucose levels greater than 15 mM. No effect of glutathione on insulin clearance and action was observed.
CONCLUSIONS: Glutathione infusion enhances insulin secretion in elderly people with IGT.
G Paolisso, D Giugliano, G Pizza, A Gambardella, P Tesauro, M Varricchio and F D'Onofrio Institute of Geriatric Medicine, First Medical School; University of Naples, Italy.
Click here to demonstrate to you why glutathione is so important to your health and well-being.
RESEARCH DESIGN AND METHODS: Ten patients with normal glucose tolerance and 10 patients with IGT were matched for age (mean +/- SE, 72.1 +/- 2.8 vs. 71.0 +/- 3.4 yr), body mass index (23.1 +/- 1.1 vs. 22 +/- 2.1 kg/m2), and sex (6/4 vs. 5/5, men/women) underwent glutathione infusion (10 mg/min) under basal conditions and during 75-g oral glucose tolerance tests and intravenous glucose tolerance tests (0.33 g.kg body wt-1.3 min-1). Patients with IGT were also submitted to euglycemic-hyperinsulemic and hyperglycemic glucose clamps.
RESULTS:In subjects with normal glucose tolerance, glutathione infusion failed to affect beta-cell response to glucose. In contrast, glutathione significantly potentiated glucose-induced insulin secretion in patients with IGT. Furthermore, in the latter group studied by hyperglycemic clamps, glutathione infusion significantly potentiated the beta-cell response to glucose when plasma glucose levels varied between 10 and 15 mM. This effect disappeared at plasma glucose levels greater than 15 mM. No effect of glutathione on insulin clearance and action was observed.
CONCLUSIONS: Glutathione infusion enhances insulin secretion in elderly people with IGT.
G Paolisso, D Giugliano, G Pizza, A Gambardella, P Tesauro, M Varricchio and F D'Onofrio Institute of Geriatric Medicine, First Medical School; University of Naples, Italy.
Click here to demonstrate to you why glutathione is so important to your health and well-being.
THE EFFECTS OF STREPTOZOTOCIN DIABETES AND DIETARY IRON INTAKE ON CATALASE
THE EFFECTS OF STREPTOZOTOCIN DIABETES AND DIETARY IRON INTAKE ON CATALASE, GLUTATHIONE PEROXIDASE, SUPEROXIDE DISMUTASE AND LIPID PEROXIDATION IN CARDIAC AND SKELETAL MUSCLES OF RATS
Abstract
Catalase, glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) prevent oxygen free radical mediated tissue damage. Diabetes increases and a low dietary intake of iron decreases catalase activity in muscle. Therefore, the combined effects of diabetes and iron deficiency on the free radical scavenging enzyme system and lipid peroxidation were studied. Male, weanling rats were injected with streptozotocin (65 mg/kg, IV) and fed diets containing either 35 ppm iron (Db + Fe) or 8 ppm iron (Db $-$ Fe). Sham injected animals served as iron adequate (C + Fe) or iron deficient (C $-$ Fe) controls. Heart, gastrocnemius (GT), soleus and tibialis anterior (TA) muscles were dissected, weighted and analyzed for catalase, GSH-Px and SOD activities after 3, 6 or 9 weeks on the respective diets. The TBA assay was used to assess lipid peroxidation in the GT muscle. Diabetes elevated catalase activity in all muscles while it had a slight lowering effect on SOD and GSH-Px activities in the GT and TA muscles. In the C $-$ Fe rats, catalase activity declined and remained depressed in all muscles except the heart. There was an elevation in GSH-Px and SOD in the GT muscles of these animals after 6 weeks but not after 9 weeks of consuming the low iron diet. The Db $-$ Fe animals were unable to respond to the diabetic state with catalase activity as high as observed in the Db + Fe rats. Treatment with insulin or iron returned catalase to control levels. The C $-$ Fe animals had significantly lower levels of lipid peroxidation than the other groups at 6 and 9 weeks. Refeeding an iron adequate diet resulted in an increase in lipid peroxidation levels. These studies indicate that skeletal muscle free radical scavenging enzymes are sensitive to metabolic states and that dietary iron influences lipid peroxidation in this tissue.
SYDNEY REBECCA MORROW, THE UNIVERSITY OF TEXAS GRAD. SCH. OF BIOMED. SCI. AT HOUSTON Date: 1987
Click here to demonstrate to you why glutathione is so important to your health and well-being
Abstract
Catalase, glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) prevent oxygen free radical mediated tissue damage. Diabetes increases and a low dietary intake of iron decreases catalase activity in muscle. Therefore, the combined effects of diabetes and iron deficiency on the free radical scavenging enzyme system and lipid peroxidation were studied. Male, weanling rats were injected with streptozotocin (65 mg/kg, IV) and fed diets containing either 35 ppm iron (Db + Fe) or 8 ppm iron (Db $-$ Fe). Sham injected animals served as iron adequate (C + Fe) or iron deficient (C $-$ Fe) controls. Heart, gastrocnemius (GT), soleus and tibialis anterior (TA) muscles were dissected, weighted and analyzed for catalase, GSH-Px and SOD activities after 3, 6 or 9 weeks on the respective diets. The TBA assay was used to assess lipid peroxidation in the GT muscle. Diabetes elevated catalase activity in all muscles while it had a slight lowering effect on SOD and GSH-Px activities in the GT and TA muscles. In the C $-$ Fe rats, catalase activity declined and remained depressed in all muscles except the heart. There was an elevation in GSH-Px and SOD in the GT muscles of these animals after 6 weeks but not after 9 weeks of consuming the low iron diet. The Db $-$ Fe animals were unable to respond to the diabetic state with catalase activity as high as observed in the Db + Fe rats. Treatment with insulin or iron returned catalase to control levels. The C $-$ Fe animals had significantly lower levels of lipid peroxidation than the other groups at 6 and 9 weeks. Refeeding an iron adequate diet resulted in an increase in lipid peroxidation levels. These studies indicate that skeletal muscle free radical scavenging enzymes are sensitive to metabolic states and that dietary iron influences lipid peroxidation in this tissue.
SYDNEY REBECCA MORROW, THE UNIVERSITY OF TEXAS GRAD. SCH. OF BIOMED. SCI. AT HOUSTON Date: 1987
Click here to demonstrate to you why glutathione is so important to your health and well-being
Significance of glutathione-dependent antioxidant system in diabetes-induced embryonic malformations
Hyperglycemia-induced embryonic malformations may be due to an increase in radical formation and depletion of intracellular glutathione (GSH) in embryonic tissues. In the past, we have investigated the role of the glutathione-dependent antioxidant system and GSH on diabetes-related embryonic malformations. Embryos from streptozotocin-induced diabetic rats on gestational day 11 showed a significantly higher frequency of embryonic malformations (neural lesions 21.5 vs. 2.8%, P<0.001; GSH in embryonic tissues of diabetic pregnant rats on day 11 was significantly lower than that of normal rats. The activity of y-glutamylcysteine synthetase (gamma-GCS), the rate-limiting GSH synthesizing enzyme, in embryos of diabetic rats was significantly low, associated with reduced expression of gamma-GCS mRNA. Administration of buthionine sulfoxamine (BSO), a specific inhibitor of gamma-GCS, to diabetic rats during the period of maximal teratogenic susceptibility (days 6-11 of gestation) reduced GSH by 46.7% and increased the frequency of neural lesions (62.1 vs. 21.5%, P<0.01) GSH ester to diabetic rats restored GSH concentration in the embryos and reduced the formation of ROS, leading to normalization of neural lesions (1.9 vs. 21.5%) and improvement in nonneural lesions (26.7 vs. 47.4%) and growth retardation. Administration of insulin in another group of pregnant rats during the same period resulted in complete normalization of neural lesions (4.3 vs. 21.5%), nonneural lesions (4.3 vs. 47.4%), and growth retardation with the restoration of GSH contents. Our results indicate that GSH depletion and impaired responsiveness of GSH-synthesizing enzyme to oxidative stress during organogenesis may have important roles in the development of embryonic malformations in diabetes.
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
Abnormalities of retinal metabolism in diabetes or galactosemia
PURPOSE: Experimental galactosemia and diabetes are known to result in diabetic-like retinopathy in animals, but the mechanism by which the retinopathy develops remains unclear.
Defects of retinal metabolism that are common to galactosemia and diabetes are closely associated with the development of retinopathy and might play a role in the pathogenesis of the retinal disease.
METHODS: Effects of experimental galactosemia on retinal calcium-activated ATPase [(Ca,Mg)-ATPase], sodium-potassium ATPase [(Na,K)-ATPase], glutathione, ATP, and pertinent ions have been compared with the effects of experimental diabetes in rat and dog models of diabetic retinopathy.
RESULTS: Activities of (Ca,Mg)-ATPase and (Na,K)-ATPase were decreased as a result of either experimental galactosemia or diabetes in both the dog and the rat, and the decreases were accompanied by a diminution of reduced glutathione (GSH) in the retina. Ouabain-insensitive ATPase activity in the retina was not significantly reduced by diabetes or galactosemia, suggesting that the observed defects in (Ca,Mg)-ATPase and (Na,K)-ATPase activities were specific. The decrease of retinal GSH levels was associated with an elevated concentration of oxidized glutathione in diabetes but not in galactosemia. Retinal ATP and ion concentrations remained unaffected by experimental galactosemia or diabetes.
CONCLUSIONS: Comparison of two etiologically dissimilar models of diabetic retinopathy (diabetes and galactosemia) has revealed abnormalities of retinal metabolism that are shared by the two models. Further comparisons of retinal metabolism between these two models should reveal additional sequelae of hyperglycemia that are associated with, and that might play a role in, the development of diabetic retinopathy.
TS Kern, RA Kowluru and RL Engerman Department of Ophthalmology and Visual Science, University of Wisconsin- Madison 53706-1532.
Investigative Ophthalmology & Visual Science, Vol 35, 2962-2967, Copyright © 1994 by Association for Research in Vision and Ophthalmology
Defects of retinal metabolism that are common to galactosemia and diabetes are closely associated with the development of retinopathy and might play a role in the pathogenesis of the retinal disease.
METHODS: Effects of experimental galactosemia on retinal calcium-activated ATPase [(Ca,Mg)-ATPase], sodium-potassium ATPase [(Na,K)-ATPase], glutathione, ATP, and pertinent ions have been compared with the effects of experimental diabetes in rat and dog models of diabetic retinopathy.
RESULTS: Activities of (Ca,Mg)-ATPase and (Na,K)-ATPase were decreased as a result of either experimental galactosemia or diabetes in both the dog and the rat, and the decreases were accompanied by a diminution of reduced glutathione (GSH) in the retina. Ouabain-insensitive ATPase activity in the retina was not significantly reduced by diabetes or galactosemia, suggesting that the observed defects in (Ca,Mg)-ATPase and (Na,K)-ATPase activities were specific. The decrease of retinal GSH levels was associated with an elevated concentration of oxidized glutathione in diabetes but not in galactosemia. Retinal ATP and ion concentrations remained unaffected by experimental galactosemia or diabetes.
CONCLUSIONS: Comparison of two etiologically dissimilar models of diabetic retinopathy (diabetes and galactosemia) has revealed abnormalities of retinal metabolism that are shared by the two models. Further comparisons of retinal metabolism between these two models should reveal additional sequelae of hyperglycemia that are associated with, and that might play a role in, the development of diabetic retinopathy.
TS Kern, RA Kowluru and RL Engerman Department of Ophthalmology and Visual Science, University of Wisconsin- Madison 53706-1532.
Investigative Ophthalmology & Visual Science, Vol 35, 2962-2967, Copyright © 1994 by Association for Research in Vision and Ophthalmology
Oxidative Stress and Glutathione Synthesis in Type 2 Diabetes: a Stable Isotope Approach
Many of the complications of diabetes are linked to oxidative damage.
We set out to determine whether the reduced antioxidant capacity (as reflected by glutathione concentration) in type diabetes is due to reduced synthesis or increased consumption of glutathione(GSH), and whether short-term dietary supplementation with glycine and cysteine, precursors of GSH, would improve oxidant status.
2H2-glycine was infused for 7 hours to measure glycine kinetics and red blood cell GSH (RBC-GSH) synthesis in diabetic and euglycemic subjects. These same measurements were repeated in a subset of diabetic subjects after 2 weeks of supplementation with glycine and cysteine, the precursors of glutathione. Lipid hydroperoxide and lymphocyte glutathione concentration were also measured.
Twenty euglycemic subjects and 10 subjects with type 2 diabetes participated in the unsupplemented study.
Authors
Reeds, Peter
Jahoor, Farook
Siripoom, Mckay - BAYLOR COLLEGE/MEDICINE
Morlese, John - UNIV. WEST INDIES
Forrester, Terrence - UNIV. WEST INDIES
Jackson, Alan - ROYAL COLLEGE/PHYSICIANTS
Balasubramanyan, Ashok - BAYLOR COLLEGE/ MEDICINE
We set out to determine whether the reduced antioxidant capacity (as reflected by glutathione concentration) in type diabetes is due to reduced synthesis or increased consumption of glutathione(GSH), and whether short-term dietary supplementation with glycine and cysteine, precursors of GSH, would improve oxidant status.
2H2-glycine was infused for 7 hours to measure glycine kinetics and red blood cell GSH (RBC-GSH) synthesis in diabetic and euglycemic subjects. These same measurements were repeated in a subset of diabetic subjects after 2 weeks of supplementation with glycine and cysteine, the precursors of glutathione. Lipid hydroperoxide and lymphocyte glutathione concentration were also measured.
Twenty euglycemic subjects and 10 subjects with type 2 diabetes participated in the unsupplemented study.
Authors
Reeds, Peter
Jahoor, Farook
Siripoom, Mckay - BAYLOR COLLEGE/MEDICINE
Morlese, John - UNIV. WEST INDIES
Forrester, Terrence - UNIV. WEST INDIES
Jackson, Alan - ROYAL COLLEGE/PHYSICIANTS
Balasubramanyan, Ashok - BAYLOR COLLEGE/ MEDICINE
Hepatic Glutathione Metabolism in Diabetes
Glutathione is important in the regulation of the redox state, and a decline in its tissue level has often been considered to be indicative of increased oxidative stress in diabetes.
In this study of diabetic rats, the level of hepatic glutathione was normal unless food intake was restricted.
Thus, the previous report of a reduction in hepatic glutathione in diabetes is likely to be the result of food deprivation rather than diabetes alone. In contrast to changes characteristic of oxidative stress, the efflux of glutathione in bile from diabetic animals was significantly decreased, whereas hepatic mixed disulfides were unchanged, and the hepatic gamma-glutamyltransferase activity was considerably increased.
These changes were not reproduced by food deprivation. The decrease in biliary excretion of glutathione in diabetes may reflect an attempt to conserve glutathione by activation of the hepatic gamma-glutamyl cycle. We conclude that the disturbances of glutathione metabolism in diabetes are not typical of those seen in oxidative stress or food restriction.
Click here to demonstrate to you why Glutathione is so important to your health and well-being.
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
In this study of diabetic rats, the level of hepatic glutathione was normal unless food intake was restricted.
Thus, the previous report of a reduction in hepatic glutathione in diabetes is likely to be the result of food deprivation rather than diabetes alone. In contrast to changes characteristic of oxidative stress, the efflux of glutathione in bile from diabetic animals was significantly decreased, whereas hepatic mixed disulfides were unchanged, and the hepatic gamma-glutamyltransferase activity was considerably increased.
These changes were not reproduced by food deprivation. The decrease in biliary excretion of glutathione in diabetes may reflect an attempt to conserve glutathione by activation of the hepatic gamma-glutamyl cycle. We conclude that the disturbances of glutathione metabolism in diabetes are not typical of those seen in oxidative stress or food restriction.
Click here to demonstrate to you why Glutathione is so important to your health and well-being.
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
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
Infection and Inflammation, and Chronic Fatigue Syndrome
A theory was published by Dr. Martin L. Pall, a professor of biochemistry and basic medical sciences at Washington State University, in 2001. The theory starts with the observation that infections that precede and may therefore induce Chronic Fatigue Syndrome and related conditions act to induce excessive production of inflammatory cytokines. This initial step activates a series of reactions:
Inflammatory cytokines induce, in turn, nitric oxide synthase (iNOS), which synthesizes excessive amounts of nitric oxide. Nitric oxide reacts with superoxide to produce the potent oxidant peroxynitrite. Peroxynitrite acts via six known biochemical mechanisms to increase the levels of both nitric oxide and superoxide, which react to produce more peroxynitrite. In this way, once peroxynitrite levels are elevated, they may act to continue the elevation, thus producing a self-sustaining vicious cycle. According to the theory, it is this cycle that maintains the chronic symptoms of Chronic Fatigue Syndrome, and it is this cycle, therefore, that must be interrupted to effectively treat this condition (Pall 2001a).
Breaking the chain of inflammation caused by chronic viral infections would require a three-part protocol:
First, the underlying viral infection should be addressed with antiviral supplements (such as ginseng, echinacea, and lactoferrin) and those that shift the Th1:Th2 ratio (such as essential fatty acids and vitamin E).
Second, inflammation should be reduced with anti-inflammatory agents (such as essential fatty acids and curcumin).
Third, the nitric oxide system should be supported with supplements (such as arginine, vitamin B2 [riboflavin], vitamin B3 [niacin], and folate).
Click here to demonstrate to you why Glutathione is so important to your health and well-being
Inflammatory cytokines induce, in turn, nitric oxide synthase (iNOS), which synthesizes excessive amounts of nitric oxide. Nitric oxide reacts with superoxide to produce the potent oxidant peroxynitrite. Peroxynitrite acts via six known biochemical mechanisms to increase the levels of both nitric oxide and superoxide, which react to produce more peroxynitrite. In this way, once peroxynitrite levels are elevated, they may act to continue the elevation, thus producing a self-sustaining vicious cycle. According to the theory, it is this cycle that maintains the chronic symptoms of Chronic Fatigue Syndrome, and it is this cycle, therefore, that must be interrupted to effectively treat this condition (Pall 2001a).
Breaking the chain of inflammation caused by chronic viral infections would require a three-part protocol:
First, the underlying viral infection should be addressed with antiviral supplements (such as ginseng, echinacea, and lactoferrin) and those that shift the Th1:Th2 ratio (such as essential fatty acids and vitamin E).
Second, inflammation should be reduced with anti-inflammatory agents (such as essential fatty acids and curcumin).
Third, the nitric oxide system should be supported with supplements (such as arginine, vitamin B2 [riboflavin], vitamin B3 [niacin], and folate).
Click here to demonstrate to you why Glutathione is so important to your health and well-being
Immune Response to Bacterial and Viral Antigens and Chronic Fatigue Syndrome
There are two different types of T-helper cells that defend against different organisms:
T-helper 1 cells target organisms that invade cells, such as viruses. Interleukin-12 (IL-12) stimulates Th1 activation.
T-helper 2 cells (Th2) target organisms that are found outside of cells. Th2 cells are involved in humoral or antibody-mediated immunity and are triggered by interleukin-10 (IL-10), which is stimulated by bacteria, parasites, toxins, and allergens.
Each of the T-helper cells are activated by different cytokines (see following table). In a healthy condition, there is a balance between Th1 and Th2 activity. When presented with an acute infection, the Th1 system predominates (and Th2 is suppressed). In chronic infections, the Th2 system predominates, leading to antibody production.
Viruses, especially herpes viruses (such as Epstein-Barr virus, cytomegalovirus, and human herpes virus 6), make proteins that mimic IL-10, which activates the immune system and remains untouched by the body's natural defenses.
Addressing the two different types of T-helper cells has been the focus of work by Paul Cheney, M.D. His protocols are designed to stimulate Th1 and inhibit Th2.
According to Dr. Cheney, chronic fatigue patients have activation of T-helper 2 cells (Th2). Th2 activation suppresses T-helper 1 (Th1) activity, particularly cytotoxic T-cells and natural killer (NK) cells, which are the main defense against viruses. In this way the viruses are able to "fool" the immune system.
Several mechanisms can be used to stop the process of Th2 activation:
Enhance natural killer (NK) cell function. Lower interleukin-10 (IL-10) levels, which will reduce Th2 activation. Raise interleukin-12 (IL-12) levels, which stimulate Th1 activation.
An article in the Journal of Clinical Infectious Disease measured NK cell activity in 50 healthy individuals and 20 patients with clinically defined chronic fatigue immune dysfunction syndrome (CFIDS). The patients were divided into three groups based on severity of clinical status. NK cell activity decreased with the increasing severity of the clinical condition (Ojo-Amaize et al. 1994).
Several nutritional supplements, including essential fatty acids, glutathione vitamin A, vitamin E, DHEA, and melatonin, have been found to have beneficial effects on the Th1:Th2 ratio (see the Natural Therapies section).
Click here to demonstrate to you why Glutathione is so important to your health and well-being
T-helper 1 cells target organisms that invade cells, such as viruses. Interleukin-12 (IL-12) stimulates Th1 activation.
T-helper 2 cells (Th2) target organisms that are found outside of cells. Th2 cells are involved in humoral or antibody-mediated immunity and are triggered by interleukin-10 (IL-10), which is stimulated by bacteria, parasites, toxins, and allergens.
Each of the T-helper cells are activated by different cytokines (see following table). In a healthy condition, there is a balance between Th1 and Th2 activity. When presented with an acute infection, the Th1 system predominates (and Th2 is suppressed). In chronic infections, the Th2 system predominates, leading to antibody production.
Viruses, especially herpes viruses (such as Epstein-Barr virus, cytomegalovirus, and human herpes virus 6), make proteins that mimic IL-10, which activates the immune system and remains untouched by the body's natural defenses.
Addressing the two different types of T-helper cells has been the focus of work by Paul Cheney, M.D. His protocols are designed to stimulate Th1 and inhibit Th2.
According to Dr. Cheney, chronic fatigue patients have activation of T-helper 2 cells (Th2). Th2 activation suppresses T-helper 1 (Th1) activity, particularly cytotoxic T-cells and natural killer (NK) cells, which are the main defense against viruses. In this way the viruses are able to "fool" the immune system.
Several mechanisms can be used to stop the process of Th2 activation:
Enhance natural killer (NK) cell function. Lower interleukin-10 (IL-10) levels, which will reduce Th2 activation. Raise interleukin-12 (IL-12) levels, which stimulate Th1 activation.
An article in the Journal of Clinical Infectious Disease measured NK cell activity in 50 healthy individuals and 20 patients with clinically defined chronic fatigue immune dysfunction syndrome (CFIDS). The patients were divided into three groups based on severity of clinical status. NK cell activity decreased with the increasing severity of the clinical condition (Ojo-Amaize et al. 1994).
Several nutritional supplements, including essential fatty acids, glutathione vitamin A, vitamin E, DHEA, and melatonin, have been found to have beneficial effects on the Th1:Th2 ratio (see the Natural Therapies section).
Click here to demonstrate to you why Glutathione is so important to your health and well-being
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