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.

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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.

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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

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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.

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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

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

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.

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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

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).

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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).

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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).

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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.

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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).

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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).

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Chronic Viral Infections and Chronic Fatigue Syndrome

Symptoms of Chronic Fatigue Syndrome resemble a postviral state and for this reason chronic viral conditions have been thought to contribute to Chronic Fatigue Syndrome in some patients.

Several viruses have been associated with Chronic Fatigue Syndrome, including (Manian 1994):
Herpes virus, particularly human herpes virus 6 (HHV-6)
Epstein-Barr virus (a herpes virus which causes infectious mononucleosis)
Cytomegalovirus (a herpes virus)
Coxsackie viruses B1 and B4

If you are infected with a chronic, energy-depleting virus, there are conventional and alternative therapies that may be of help.

It should be noted that most individuals have been exposed to pathogenic viruses that can be reactivated by adverse environmental conditions and cause chronic fatigue and other diseases.
Studies indicate that the Epstein-Barr virus may be suppressed with bilberry extract (anthocyanins), curcumin, carotenoids, and chlorophylls.

The exact doses of these natural plant extracts that might be effective against Epstein-Barr have yet to be determined.

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Possible Causes of Chronic Fatigue Syndrome

~Chronic Viral Infections
~Infection and Inflammation
~Role of the Endocrine System in Chronic Fatigue Syndrome
~Chemical Sensitivity
~Metal Sensitivity
~Oxidative Stress
~Side Effects of Chronic Fatigue Syndrome

~~~The causes of Chronic Fatigue Syndrome are as yet undetermined, but studies have shown that multiple nutrient deficiencies, food intolerance, or extreme physical or mental stress may trigger chronic fatigue. Studies have also indicated that Chronic Fatigue Syndrome may be activated by the immune system, various abnormalities of the hypothalamic-pituitary axes, or by the reactivation of certain infectious agents in the body. Some Chronic Fatigue Syndrome patients were found to have low levels of PBMC beta-endorphin and other neurotransmitters. Thyroid deficiency may also be a contributing factor in Chronic Fatigue Syndrome (refer to the Thyroid Deficiency protocol to find out how to determine if you are deficient in thyroid hormone production).

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Glutathione and Cancer

We urge you to look into how glutathione has proven to be an effective treatment of cancer, in fact there is a product that will give your body the building blocks it needs to manufacture it's own glutathione (GSH), that has a method of use patent as a treatment for cancer.

Cancer causing polychlorinated biphenyls (PCBs) have been found to alter levels of glutathione compounds in experiments, which may alter the body's resistance to certain types of cancer.

Glutathione deficiencies have been linked to many forms of cancer.- Prevents cancerous tissue- Suppresses tumor growth- Eliminates carcinogen- acids - Retards oxidative stress- Prevents wasting disease- Eases side effects of chemotherapy and radiotherapy

Glutathione three major roles in the body are summarized by the letters A-B-C.
- Anti-oxidant
- Blood Booster
- Cell Detoxifier

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Glutathione as a dietary antioxidant, prevention of cancer and other chronic diseases.

There is increasing evidence that antioxidant nutrients may have important health benefits. While the antioxidant glutathione can be synthesized in the body, the amount present in the diet may also be of significance to health, particularly in the prevention of cancer and other chronic diseases.

Investigations of the relationship between dietary glutathione and disease risk will require a database on the glutathione contents of foods. The report summarized here presents data on the glutathione content of 134 commonly consumed foods

In general, dairy products, cereals, and breads were found to be low in glutathione. Freshly prepared meats were high in glutathione, and vegetables and fruits contained moderate to high amounts. Most forms of processing, except freezing, appeared to reduce the glutathione content of foods. The effects of processing were great enough to suggest that individuals who usually consume canned or bottled foods may have substantially lower glutathione intakes than those who customarily eat fresh or frozen foods.

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New Findings on the Role of Glutathione in Cancer

Cancer cells and normal cells are known to respond differently to nutrients and drugs that affect glutathione status.

a lot of studies have shown that tumor cells have increased levels of glutathione levels, which confers resistance to chemotherapy drugs.

One of the challenges of cancer therapy is how to deplete tumor cells of glutathione, so as to make them more vulnerable to the effects of chemotherapy drugs, while at the same time allowing normal cells to remain relatively unaffected by chemotherapeutic drugs.

A number of new findings have emerged that take into consideration the role of glutathione in pathways that promote programmed cell death (apoptosis) in cancer cells.

A German study has reported that glutathione (GSH) plays a critical role in cellular mechanisms that result in cell death. The study found that cancer cells resistant to apoptosis had higher intracellular GSH levels.

Depletion of glutathione in these tumor cells made them more vulnerable to the effects of anticancer drugs or the gene that promotes apoptosis (CD95 or APO-1/Fas). The researchers concluded that apoptosis resistance in tumor cells depends, at least in part, on intracellular GSH levels.

In another study conducted in Spain, researchers found that lowering GSH concentration may be convenient not only for the efficiency of chemotherapy, but also to induce a rather fast and direct apoptosis mechanism in tumor cells.

Based on that premise that the glutathione-S-transferase enzyme is expressed at high levels in many tumors, researchers at the Fox Chase Cancer Center in Pennsylvania, went on to design a novel prodrug (PABA/NO).

The glutathione-s-transferase in tumor cells converts PABA/NO to lethal nitric oxide, resulting in death of the tumor cell. The prodrug was shown to have antitumor effects in an animal model for human ovarian cancer.

In the fourth study, Polish researchers found that ingesting a selenium supplement is beneficial, as a supportive element in chemotherapy.

Selenium is a co-factor of the enzyme glutathioneperoxidase [GSH-P(x)] and was found to significantly increase the activity of GSH-P(x) in patients reciving the supplement.
A previous clinical study by the same researchers recommended the administration of selenium in patients with ovarian cancer undergoing multi-drug chemotherapy.

Another interesting study by researchers in Texas showed that your chances of surviving a type of brain cancer, called primary malignant glioma, could depend on the type of glutathione-s-transferase (GST) gene you were born with.

Having a combination of a two specific variants of GST (germ-line GSTP1*A/*A and GSTM null genotype) confers a survival advantage in some types of brain cancers, but also comes with an increased risk of adverse events related to chemotherapy.

There is compelling evidence to suggest a crucial role for glutathione and substances that target glutathione metabolism in the prevention and treatment of cancer.

Undenatured whey protein is one of the natural foods known to selectively deplete cancer cells of their glutathione, thus making them more susceptible to such cancer treatments as radiation and chemotherapy.

For a complete report on the research on undenatured whey protein and cancer see the report glutathione (GSH) and Whey Protein in Cancer.
http://www.1whey2health.com/cancer_glutathione.htm

Note: The information here is not provided by medical professionals and is not intended as a substitute for medical advice. Please consult your physician before beginning any course of treatment.

References:
http://ezinearticles.com/?New-Findings-on-the-Role-of-Glutathione-in-Cancer&id=19231