The effect of dietary intake of the antioxidants ascorbate, tocopherol, and carotenoids is difficult to disentangle by epidemiological studies from other important vitamins and ingredients in fruits and vegetables.
Nevertheless, several arguments suggest that the antioxidants content of fruits and vegetables is a major contributor to their protective effect.
1) Biochemical data, discussed above shows that oxidative damage is massive and is likely to be the major endogenous damage to DNA, proteins, and lipids.
2) Studies showing that oxidative damage to sperm DNA is increased when dietary ascorbate is insufficient
3) Epidemiological studies and intervention trials on prevention of cancer and heart disease in people taking antioxidants supplements are suggestive, though larger studies need to be done. Clinical trials using antioxidants will be the critical test for many of the ideas.
4) Studies on oxidative mechanisms and epidemiology on antioxidants protection for individual degenerative diseases.
Small molecule dietary antioxidants such as Vitamin C (ascorbate), Vitamin E (tocopherol), and carotenoids have generated particular interest as anticarcinogens and as defenses against degenerative diseases. Most carotenoids have antioxidants activity, particularly against singlet oxygen and many, including ß-carotene, can be metabolized to Vitamin A (retinal)
We have called attention to a number of previously neglected physiological antioxidants including urate, bilirubin, carnosine, and ubiquinol. Ubiquinone (CoQ10), for example, is the critical small molecule for transporting electrons in mitochondria for the generation of energy. Its reduced form, ubiquinol, is an effective antioxidants in membranes.
Optimal levels of dietary ubiquinone/ubiquinol could be of importance in many of the
degenerative diseases.
Click here for more about Glutathione and its benefits to our body.
Showing posts with label Cancer cells. Show all posts
Showing posts with label Cancer cells. Show all posts
Monday, February 11, 2008
Tuesday, January 15, 2008
Glutathione in cancer biology and therapy
The Glutathione (GSH ) content of cancer cells is particularly relevant in regulating mutagenic mechanisms, DNA synthesis, growth, and multidrug and radiation resistance.
In malignant tumors, as compared with normal tissues, that resistance associates in most cases with higher GSH levels within these cancer cells. Thus, approaches to cancer treatment based on modulation of GSH should control possible growth-associated changes in GSH content and synthesis in these cells. Despite the potential benefits for cancer therapy of a selective GSH-depleting strategy, such a methodology has remained elusive up to now.
Metastatic spread, not primary tumor burden, is the leading cause of cancer death. For patient prognosis to improve, new systemic therapies capable of effectively inhibiting the outgrowth of seeded tumor cells are needed.
Interaction of metastatic cells with the vascular endothelium activates local release of proinflammatory cytokines, which act as signals promoting cancer cell adhesion, extravasation, and proliferation.
Recent work shows that a high percentage of metastatic cells with high GSH levels survive the combined nitrosative and oxidative stresses elicited by the vascular endothelium and possibly by macrophages and granulocytes. ?-Glutamyl transpeptidase overexpression and an inter-organ flow of GSH (where the liver plays a central role), by increasing cysteine availability for tumor GSH synthesis, function in combination as a metastatic-growth promoting mechanism.
The present review focuses on an analysis of links among GSH, adaptive responses to stress, molecular mechanisms of invasive cancer cell survival and death, and sensitization of metastatic cells to therapy. Experimental evidence shows that acceleration of GSH efflux facilitates selective GSH depletion in metastatic cells.
Estrela JM; Ortega A; Obrador EDepartment of Physiology, University of Valencia, Valencia, Spain.
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
In malignant tumors, as compared with normal tissues, that resistance associates in most cases with higher GSH levels within these cancer cells. Thus, approaches to cancer treatment based on modulation of GSH should control possible growth-associated changes in GSH content and synthesis in these cells. Despite the potential benefits for cancer therapy of a selective GSH-depleting strategy, such a methodology has remained elusive up to now.
Metastatic spread, not primary tumor burden, is the leading cause of cancer death. For patient prognosis to improve, new systemic therapies capable of effectively inhibiting the outgrowth of seeded tumor cells are needed.
Interaction of metastatic cells with the vascular endothelium activates local release of proinflammatory cytokines, which act as signals promoting cancer cell adhesion, extravasation, and proliferation.
Recent work shows that a high percentage of metastatic cells with high GSH levels survive the combined nitrosative and oxidative stresses elicited by the vascular endothelium and possibly by macrophages and granulocytes. ?-Glutamyl transpeptidase overexpression and an inter-organ flow of GSH (where the liver plays a central role), by increasing cysteine availability for tumor GSH synthesis, function in combination as a metastatic-growth promoting mechanism.
The present review focuses on an analysis of links among GSH, adaptive responses to stress, molecular mechanisms of invasive cancer cell survival and death, and sensitization of metastatic cells to therapy. Experimental evidence shows that acceleration of GSH efflux facilitates selective GSH depletion in metastatic cells.
Estrela JM; Ortega A; Obrador EDepartment of Physiology, University of Valencia, Valencia, Spain.
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
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
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.
Click here to demonstrate to you why Glutathione is so important to your health and well-being
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.
Click here to demonstrate to you why Glutathione is so important to your health and well-being
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).
Click here to demonstrate to you why Glutathione is so important to your health and well-being
~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).
Click here to demonstrate to you why Glutathione is so important to your health and well-being
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
Learn more...
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
Learn more...
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.
Click here for more information
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.
Click here for more information
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
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
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