Tuesday, February 12, 2008

Biological Theories

Wear-and-Tear theory
Aging associated changes are the result of chance damage accumulating over time.

Accumulative-Waste Theory
The buildup in cells of waste products that presumably interferes with metabolism.

Autoimmune Theory
Aging results from gradual decline of the body’s autoimmune system.

Cross-Linkage Theory
Aging results from accumulation of cross-linked compounds interfering with normal cell function.

Free-Radical Theory
Free radicals (unstable and highly reactive organic molecules) cause cell damage that results in symptoms we associate with Aging

Cellular Theory
Aging can be explained by structural and functional changes in the cells of an organism.

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Theories of Aging

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Activity Theory

The more active people are the more likely they will be happy.

Continuity Theory

With aging people will tend to maintain the same habits, personalities, and life style that they have developed in earlier years.

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Effects of Aging on Health

Cognitive Effects
Beginning in the thirties is point in the aging process when it is typical to experience cognitive declines. However it is possible to maintain normal cognitive function into old age. Many elderly have memories as sharp or even sharper than their younger counterparts. Semantic or general knowledge memory including vocabulary and definitions remain steady or even increase.

Emotional Effects
Aging typically produces and improvement in emotional intelligence. This is because with age we typically are better able to manage and regulate our emotions. The exception is usually related to health and wellness deficiencies, disease states, or prolonged stress.

Successful Ageing
The Golden Years have been termed "successful ageing" as early as the 1950s and was popularized in the late 80s. The terminology has sparked a debate as to what is “normal ageing" which would have a high risk of illness and "successful ageing" with low risk of disability and high cognitive and physical functioning.

Successful ageing would consist of three components:
1. Low probability of disease or disability

2. High mental and physical function capacity

3. Active engagement with life Alternatively, terms such as "healthy ageing," "optimal ageing" have been proposed.

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The Ultimate Anti-aging Treatment

To facilitate anti aging requires understanding aging. With this knowledge making the changes in life style and diet that can enhance the anti aging process.

Aging
In health care, Ageing or aging in the human body refers to the deterioration of the body the longer we live.

There are social, cognitive, cultural, and economic effects that result from and are effects of Aging. These can affect the way we live our lives, the quality of life we have and the way society views us. One of the ways we care for aging is anti aging treatments.

The Aging population is an important issue in many nations, especially those North of the equator. Thus, age has in influence on the functioning of the society we live in.

In science and biology, Aging is divided into cellular and organism Aging.

The Aging of an organism is is often noted by the declining ability to respond to stress, increased imbalanced homeostasis and increased risk of disease. Some researchers are treating aging as disease. As such, it is considered treatable.

Diet has been shown to play a large role in the anti aging promotion. Dietary intake is considered in a number of ways including nutrient intake, quantity of intake and toxic exposure.

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The Ear Nose Throat Eyes Connection

Glutathione plays an important role in our ear nose throat eyes (ENT) health.

The primary way everything enters our body both good and bad is through the ear nose throat eyes. Actually our eyes are a secondary portal of entry.

The things entering can be good such as breathing, sound and food. It can also be potentially damaging to the body. These include toxins, bacteria's, viruses, and carcinogens. It would only seem natural that the human body would have a defense systems to protect the points of entry.

The good news...it does. It is called the immune system. It is a formidable military force. The strongest front line defense is the marine like tripeptide glutathione. It is not only in each cell, it is in the respiratory tract lining fluid (RTLF). Glutathione is the main antioxidant in this fluid.

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The Upper Respiratory Tract

It depletes with age

The weakest point of the human body would be the place of greatest risk of attack by infection and toxins. Glutathione is the primary defense for the nose and throat.

General Otolaryngology
LaryngitisParotitis (inflammation of the parotid gland)
Pharyngitis (inflammation of the pharynx producing symptoms similar to tonsillitis)
Sleep apneaSnoringTonsillitis (inflammation of tonsils producing pain)
odynophagia (painful swallowing fever etc)
HyperthyroidismThyroid cancer
Sore throat
Strep throat
Esophageal cancer

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The Optimum Level of Antioxidants

The epidemiological evidence and the guidelines of the National Cancer Institute and the National Research Council/National Academy of Sciences suggest that at least two fruits and three vegetables per day is a desirable intake.

Since ascorbate, tocopherol, and ß-carotene supplements are inexpensive and high doses are remarkably non-toxic, there is a school that believes that supplements, in addition to a diet containing recommended levels of fruits and vegetables, are desirable.

There is suggestive, but inadequate epidemiological and biochemical evidence bearing on the question. What is clear is that fruits and vegetables contain many necessary micronutrients in addition to antioxidants, some of which also can prevent mutations. Folic acid, for example, is required for the synthesis of the nucleotides in DNA.

Inadequate intake has been shown to cause chromosome breaks and increased cancer and birth defects. Folate deficiency may be a risk factor for myocardial infarction as well. Niacin is required for making poly (ADP-ribose), a component of DNA repair. Other micronutrients are also likely to be part of our defense systems.

The U.S. Recommended Daily Allowances (RDAs) for ascorbate and tocopherol intake--there is no guideline for [[beta]]-carotene independent of its provitamin A activity--are not adequate for several reasons:

1) The amount recommended, e.g., 60 mg/day for ascorbate, is primarily for avoiding an observable deficiency syndrome, e.g., scurvy, and is not necessarily the amount for optimum lifetime health, which is usually not known.

2) A recommended blood level of each antioxidant, e.g., 60 uM ascorbate, would be a more desirable standard. People vary considerably in the intake required to keep their blood level adequate. A smoker, for example, needs to take in several times as much ascorbate as a non-smoker to keep the blood level the same.

Infections may also cause an oxidative stress that leads to antioxidant depletion by activating phagocytic cells. The observation that antioxidant inadequacy is associated with oxidative damage to DNA of the germ line as well as somatic cells, emphasizes the urgency of defining adequate blood levels.

Since only 9% of Americans, and fewer in most other countries, are eating five fruits and vegetables per day, there is a great opportunity to improve health by increasing consumption.

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Oxidant stress, Birth defects, and Childhood Cancer

Oxidative lesions in sperm DNA are increased 250% when levels of dietary ascorbate is insufficient to keep seminal fluid ascorbate to an adequate level. A sizable percentage of the U.S. population ingest inadequate levels of dietary ascorbate, particularly single males, the poor, and smokers. The oxidants in cigarette smoke deplete the antioxidants in plasma. Smokers must eat two to three times more ascorbate than non-smokers to achieve the same level of ascorbate in blood, but they rarely do.

In a comparison of sperm from smokers and nonsmokers Viczian found that the number of sperm and the percent of mobile sperm decrease significantly in smokers, and this decrease is dependent on the dose and duration of smoking.

Paternal smoking, in particular, appears to increase the risk of birth defects and childhood cancer in their offspring. One expects, and finds, a much larger contribution to the germ line mutation rate from the father than the mother, age of the father being an important risk factor. Thus, inadequate diets (and smoking) of fathers appear to result not only in damage to their own DNA but to the DNA of their sperm, an effect that may reverberate down future generations.

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Antioxidants and Brain Dysfunction

Biochemical studies suggest that oxidation may be important in a number of brain pathologies. The few epidemiological studies are consistent with a protective effect of fruits and vegetables or antioxidants in a number of neurological pathologies, including brain ischemia, Parkinsons disease (PD), and familial amyotrophic lateral sclerosis (FALS), a degenerative disorder of motor neurons .

Ischemic episodes liberate iron, an important catalyst in oxygen radical forming reactions; iron chelators reduce neuron loss following this trauma. In individuals suffering from Parkinson's disease, oxidative DNA damaged is elevated within brain regions rich in dopaminergic neurons (E. Övervik, J. Sanchez-Ramos and B. Ames, unpublished). The most convincing evidence so far for a link between neurological disorders and oxygen radical formation is the strong association found between FALS and mutations in the Cu/Zn superoxide dismutase gene, suggesting that oxygen radicals might be responsible for the selective degeneration of motor neurons occurring in this fatal disease.

The protective role of superoxide dismutase against brain injury due to ischemia is supported by the finding that its overproduction is protective in a transgenic mouse model. Based on the similar protective effects against ischemia induced brain injury by inhibition of nitric oxide formation, and the recent evidence implicating these two radical species in cytotoxicity of neuronal cells, it would appear that peroxynitrite, a powerful oxidant formed from the combination of superoxide anion radical and nitric oxide, plays an important role in neuronal injury following ischemia and reperfusion.

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Antioxidants and Cataracts

Cataract removal is the most common operation in the U.S. (1.2 million per year) with costs of over 3 billion dollars.

Taylor has recently reviewed the impressive evidence that cataracts have an oxidative etiology and that dietary antioxidants can prevent their formation in humans. Five epidemiological studies that have examined the effect of dietary antioxidants on cataracts show strong preventative effects of ascorbate, tocopherol, and carotenoids. Those individuals taking daily supplements of ascorbate or tocopherol had about one-third the risk.

Smoking, a severe oxidative stress, is a major risk factor for cataracts and radiation, an oxidative mutagen, is well-known to cause cataracts.

Eye proteins show an increased level of methionine sulfoxide with age and proteins in human cataracts have over 60 percent of their methionine residues oxidized. Pregnant mice depleted of Glutathione, the main sulfhydryl antioxidants in cells, produce offspring with cataracts. The most promising preventative strategy against cataracts appears to be to increase dietary antioxidants and to decrease smoking.

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Monday, February 11, 2008

Antioxidants, and the Immune System

The proliferation of T and B cells, natural killer cells, and lymphokine activated killer cells that are required to mount an effective defense against pathogens and tumor cells appear to be inhibited markedly with age and upon exposure to oxidants. These effects can, in part, be counteracted in elderly individuals by dietary antioxidant supplementation. While the endogenous sources of oxidants that lead to the suppression of lymphocyte dependent immunity are not known, in vitro studies have demonstrated that polymorphonuclear leucocytes and macrophages, both can inhibit proliferation of various lymphocyte subpopulations through the production of reactive oxygen intermediates and the prostaglandin metabolite PGE2 as well as from nitric oxide.

This suggests that conditions that involve infiltration of polymorphonuclear leucocytes and macrophages (i.e., chronic inflammatory diseases), could result in compromised lymphocyte function. The suppressive effects of macrophages on mitogen induced lymphocyte proliferation can be reversed partially by thiol reagents, catalase or indomethacin, or by NG-monomethyl-L-arginine, a competitive inhibitor of nitric oxide synthesis.

The age associated decrease in cell mediated immunity may be due to a decreased level of certain small molecule antioxidant and antioxidant enzymes that accompany the aging process.

Calorie restriction, a dietary regimen that increases maximal lifespan in rodents also enhances T lymphocyte responsiveness possibly by slowing the rate of thymus involution and by boosting the level of cellular antioxidant defenses.

Antioxidants and cardiovascular disease

A major development in cardiovascular disease research is the finding that oxidation reactions play a central role in atherogenesis and that in epidemiological studies cardiovascular disease is associated with low plasma concentrations of ascorbate, tocopherol and ß-carotene.

A wealth of evidence suggests that oxidative modification of apolipoprotein B100 plays a key role in LDL recognition and that LDL uptake by scavenger receptors in macrophages leads to foam cell formation and atheroschlerotic plaques.

Apolipoprotein B100 can be altered by reactive products of lipid peroxidation that causes a net decrease in positive charge, a modification that leads to its recognition by the scavenger receptors. The beneficial effects of dietary Antioxidants is also strengthened by animal and biochemical studies.

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Antioxidants and Cancer

A critical factor in mutagenesis is cell division. When the cell divides, an unrepaired DNA lesion can give rise to a mutation. Thus an important factor in mutagenesis, and therefore carcinogenesis, is the cell division rate in the precursors of tumor cells. Stem cells are important as precursor cells in cancer because they are not on their way to being discarded. Increasing their cell division rate would increase mutation. As expected, there is little cancer in non-dividing cells. Such diverse agents as chronic infection high levels of particular hormones, or chemicals at doses that cause cell death result in increased cell division and therefore an increased risk for cancer.

Oxidants form one important class of agents that stimulate cell division. This may be related to the stimulation of cell division that occurs during the inflammatory process accompanying wound healing. Antioxidants therefore can decrease mutagenesis, and thus carcinogenesis, in two ways:

by decreasing oxidative DNA damage and by decreasing cell division. Of great interest is the understanding of mechanisms by which tocopherol and carotenoids can prevent cell division

There is an increasing literature on the protective role of dietary tocopherol, ascorbate, and ß-carotene in lowering the incidence of a wide variety of human cancer.

Antioxidants can counteract the induction of cancer in rodents by a variety of carcinogens. Two of the major causes of cancer, cigarette smoke and chronic inflammation, both appear to involve oxidants in their mechanism of action.

Almost all of the epidemiological studies that examined the relation between Antioxidant levels and cigarette-induced lung cancer showed a statistically significant protective effect of Antioxidants.

Antioxidants inhibit much of the pathology of cigarette smoke in rodents.

Inflammatory reactions release large amounts of NO, a radical, nitrosating agent, and indirect mutagenic oxidant. Ascorbate inhibits nitrosation under physiological conditions.

Antioxidants help to protect against the carcinogenic effects of chronic inflammation, as discussed above.

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Dietary antioxidants

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.

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Antioxidants Protect Against Disease

Many defense mechanisms within the organism have evolved to limit the levels of reactive oxidants and the damage they inflict. Among the defenses are enzymes such as superoxide dismutase, catalase, and glutathione peroxidase. The glutathione S-transferases inactivate reactive electrophilic mutagens, including the aldehyde products of lipid peroxidation.

There are also many structural defenses such as sequestering H202 generating enzymes in peroxisomes and chelating any free iron or copper salts in transferrin and ferritin or ceruloplasmin to avoid Fenton chemistry. Superoxide, however, can release iron from ferritin.

Oxidized DNA is repaired by a series of glycosylases that are specific for particular oxidized bases and possibly by non-specific excision repair enzymes. In the absence of cell division these oxidative lesions are removed from DNA quite effectively and the mutation rate is kept to a minimum. Oxidized proteins are degraded by proteases. Lipid hydroperoxides are destroyed by glutathione peroxidase.

Almost all of these defenses appear to be inducible, as are most other types of defenses, i.e., the amounts increase in response to damage. There is a large literature showing that cells respond to low levels of radiation, an oxidative mutagen, by inducing antioxidant defenses that help to protect them against mutation by high levels of radiation.

There is a tradeoff however, since the induction of these defenses makes the cell more sensitive to alkylating mutagens.

In addition to the protective effects of endogenous enzymatic antioxidant defenses, consumption of dietary antioxidants appears to be of great importance. Fruits and vegetables, the main source of antioxidants in the diet, are associated with a lowered risk of degenerative diseases. Block and her colleagues have recently reviewed 172 studies in the epidemiological literature that relate, with great consistency, the lack of adequate consumption of fruits and vegetables to cancer incidence.

The quarter of the population with low dietary intake of fruits and vegetables compared to the quarter with high intake has double the cancer rate for most types of cancer (lung, larynx, oral cavity, esophagus, stomach, colon and rectum, bladder, pancreas, cervix, and ovary). Data on the types of cancer known to be associated with hormone levels are not as consistent and show less protection by fruits and vegetables: for breast cancer the protective effect was about 30%. There is also literature on the protective effect of fruit and vegetable consumption on heart disease and stroke. Only 9% of Americans eat five servings of fruits and vegetables per day, the intake recommended by the National Cancer Insitute and the National Research Council. European countries with low fruit and vegetable intake (e.g., Scotland) are generally in poorer health and have higher rates of heart disease and cancer than countries with high intake (e.g., Greece).

The cost of fruits and vegetables is an important factor in discouraging consumption. Poorer people spend a higher percentage of their income on food, eat less fruits and vegetables, and have shorter life expectancy than wealthier people. A major contributor to health in this century was synthetic pesticides which markedly decreased the cost of food production and ensured that most of the crops planted would be eaten by humans rather than insects. Synthetic pesticide residues do not appear to be a significant cause of cancer.

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Aging is slowed by calorie or protein restriction

In rodents a calorie restricted diet, significantly increases lifespan, decreases reproduction, and markedly decreases cancer rates.

It has been suggested that Darwinian fitness in animals is increased by the delay of reproductive function during periods of low food availability and that the saved resources are invested in maintenance of the body until food resources are available for successful reproduction.

Protein restriction appears to have the same effects on rodents as calorie restriction, though it is less well-studied. An understanding of mechanisms for this marked effect on aging and cancer is becoming clearer and may in good part be due to reduced oxidative damage.

The suggestion that maintenance functions are enhanced in calorie-restricted rats thus resulting in less oxidative damage is supported by the findings of more efficient DNA repair, better coupled mitochondrial respiration and a delay in the age-dependent decline of antioxidant defenses.

The higher level of antioxidant defenses could also account for the enhanced immune response in restricted animals. We have recently shown that either calorie or protein restriction decreases the rate of accumulation of oxidized protein that accompanies aging in rats and preliminary results suggest a decrease in preneoplastic foci and oxidative lesions in DNA as well.

Thus, the overall effect of these enhanced maintenance activities appears to be a reduction in oxidative damage to DNA and protein, a decrease in DNA and protein lesions, and a decrease in somatic mutations. Markedly lower mitotic rates are observed in a variety of tissues in calorie restricted compared to ad libitum fed rodent, which may also contribute to the decrease in tumor incidence.

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*Dietary restriction activates the pituitary adrenocorticotropic axis resulting in a decrease in the release of reproductive and mitogenic hormones. Decreases in mitogenic hormones such as insulin, TSH, growth hormone, estrogen, and prolactin decrease the likelihood of hormone-induced cancers, as has been shown in various animal studies. This is consistent with suppression of mitogenic hormones and decreased proto-oncogene expression. The lowered incidence of mammary tumors observed in calorie-restricted rats has been attributed to reduced circulating levels of the mammotropic hormones estrogen and prolactin.

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Aging and Dietary Restriction

Evolutionary biologists have argued that aging is inevitable because of several tradeoffs. One tradeoff is that a considerable proportion of an animal's resources is devoted to reproduction at a cost to maintenance, which means that the maintenance of somatic tissues is less than that required for indefinite survival. Of the vast array of maintenance processes that are necessary to sustain normal function in somatic cells, those that defend the cell against metabolism derived oxidants are likely to play an important role.

Metabolism has costs: oxidants by-products of normal energy metabolism extensively damage DNA, proteins, and other molecules in the cell, and this damage accumulates with age.

Another tradeoff is that nature selects for many genes that have immediate survival value, but that may have long term deleterious consequences. The oxidative burst from phagocytic cells, for example, protects against death from bacterial and viral infections, but contributes to DNA damage, mutation, and cancer.

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Tobacco, cancer, and heart disease

Smoking, which we and others argue is a major oxidative stress in addition to a source of mutagens, contributes to about one-third of U.S. cancer, about one-quarter of U.S. heart disease and, about 400,000 premature deaths per year in the U.S..

Tobacco is a major global cause of cancer, but it causes even more deaths by other diseases. Tobacco will cause about 3 million deaths per year worldwide in the l990s and will, at present rates of smoking, cause about l0 million deaths per year a few decades from now.

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Thursday, February 7, 2008

Chronic infection, inflammation and cancer

Leucocytes and other phagocytic cells combat bacteria, parasites, and virus-infected cells by destroying them with NO, O2. H2O2 a powerful oxidant mixture. These oxidants protect humans from immediate death from infection, but cause oxidative damage to DNA and mutation thereby contributing to the carcinogenic process.

Antioxidants appear to inhibit some of the pathology of chronic inflammation

Chronic infections contribute to about one-third of the world's cancer. Hepatitis B and C viruses infect about 500 million people, mainly in Asia and Africa, and are a major cause of hepatocellular carcinoma.

Another major Chronic infections is schistosomiasis, which is caused by a parasitic worm that is widespread in China and Egypt. The Chinese worm lays its eggs in the colon, producing inflammation that often leads to colon cancer. The Egyptian worm lays eggs in the bladder, promoting bladder cancer.

Opisthorchis viverrini and Chlonorchis sinensis are liver flukes that infect millions of people in China, Thailand, Laos, and Malaysia. These worms cause chronic inflammation of the biliary tract and markedly increase the risk for developing cholangiocarcinoma.

Helicobacter pylori bacteria, which infect the stomachs of over one-third the world population, appear to be the major cause of stomach cancer, ulcers, and gastritis.

In wealthy countries the disease is usually asymptomatic, which indicates that the effects of inflammation are at least partially suppressed, possibly in part, by adequate levels of dietary Antioxidants.

chronic inflammation resulting from noninfectious sources also to various pathological conditions leading to cancer. For example, chronic inflammation due to asbestos exposure may be in good part the reason it is a significant risk factor for cancer of the lung.

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Sources and Effects of Oxidants

Four endogenous sources appear to account for most of the oxidants produced by cells:

1) As a consequence of normal aerobic respiration, mitochondria consume molecular oxygen, reducing it by sequential steps to produce H20. Inevitable by-products of this process, as stated above, are O2.-, H202, and .OH. About l012 oxygen molecules are processed by each rat cell daily, and the leakage of partially reduced oxygen molecules is about 2%, yielding about 2x1010 superoxide and hydrogen peroxide molecules per cell per day.

2) Phagocytic cells destroy bacteria or virus-infected cells with an oxidative burst of NO, O2.-, H2O2, and [[macron]]OCl. Chronic infection by viruses, bacteria, or parasites, results in a chronic phagocytic activity and consequent chronic inflammation, which is a major risk factor for cancer. Chronic infections are particularly prevalent in third world countries.

3) Peroxisomes, which are organelles responsible for degrading fatty acids and other molecules, produce H202 as a byproduct, which is then degraded by catalase. Evidence suggests that, under certain conditions, some of the peroxide escapes degradation, resulting in its release into other compartments of the cell and in increased oxidative DNA damage.

4) Cytochrome P450 enzymes in animals constitute one of the primary defense systems against natural toxic chemicals from plants, the major source of dietary toxins. The induction of these enzymes, prevent acute toxic effects from foreign chemicals, but also results in oxidant by-products that damage DNA (Park, J.-Y. K. and Ames, B.N., unpublished).

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Three exogenous sources may significantly increase the large endogenous oxidant load.

1) The oxides of nitrogen (NOx) in cigarette smoke (about 1000 ppm) cause oxidation of macromolecules, and deplete antioxidant levels. This is likely to contribute significantly to the pathology of smoking. Smoking is a risk factor for heart disease as well as a wide variety of cancers in addition to lung cancer.

2) Iron (and copper) salts promote the generation of oxidizing radicals from peroxides (Fenton chemistry). Men who absorb significantly more than normal amounts of dietary iron due to a genetic defect (hemochromatosis disease) are at an increased risk for both cancer and heart disease. It has therefore been argued that too much dietary copper or iron, particularly heme iron (which is high in meat), is a risk factor for cardiovascular disease and cancer in normal men

3) Normal diets contain plant food with large amounts of natural phenolic compounds, such as chlorogenic and caffeic acid, that may generate oxidants by redox cycling .

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Oxidation and Damage to DNA, Protein, and Lipids

Oxidative damage to DNA, proteins and other macromolecules accumulates with age and has been postulated to be a major, but not the only, type of endogenous damage leading to aging. Superoxide(O2.-), hydrogen peroxide (H2O2), and hydroxyl radical (.OH), which are mutagens produced by radiation, are also by-products of normal metabolism. Lipid peroxidation gives rise to mutagenic lipid epoxides, lipid hydroperoxides, lipid alkoxyl and peroxyl radicals, and enals ([[alpha]], ß-unsaturated aldehydes). Singlet oxygen, a high energy and mutagenic form of oxygen, can be produced by transfer of energy from light, the respiratory burst from neutrophils, or lipid peroxidation.

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Animals have numerous antioxidants defenses, but since these defenses are not perfect, some DNA is oxidized. Oxidatively damaged DNA is repaired by enzymes that excise the lesions, which are then excreted in the urine. We have developed methods to assay several of these excised damaged bases in the urine of rodents and humans almost all of which appear as the free base from repair by glycosylases. We estimate that the number of oxidative hits to DNA per cell per day is about l00,000 in the rat and about l0,000 in the human. DNA repair enzymes efficiently remove most, but not all, of the lesions formed. Oxidative lesions in DNA accumulate with age, so that by the time a rat is old (2 years) it has about two million DNA lesions per cell, which is about twice that in a young rat. Mutations also accumulate with age . For example, the somatic mutation frequency in human lymphocytes, of which the contribution of oxidative DNA lesions is unknown, is about nine times greater in elderly people than in neonates. The importance of oxidative DNA lesions in cancer and aging is underscored by the existence of specific repair glycosylases that excise these lesions from DNA. In the case of 8-hydroxy-2'-deoxyguanosine, a lesion formed from oxidative damage to guanine residues in DNA, loss of a specific glycosylase activity leads to an appreciable increase in the spontaneous mutation rate, indicating the intrinsic mutagenic potential of this DNA lesion. Many other oxidative DNA lesions are likely to be important as well.

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Mitochondrial DNA (mtDNA) from rat liver has more than ten times the level of oxidative DNA damage than does nuclear DNA from the same tissue. This increase may be due to a lack of mtDNA repair enzymes, lack of histones protecting mtDNA, and the proximity of mtDNA to oxidants generated during oxidative phosphorylation. The cell defends itself against this high rate of damage by a constant turnover of mitochondria, thus presumably removing those damaged mitochondria that produce increased oxidants. Despite this turnover, oxidative lesions appear to accumulate with age in mtDNA at a higher rate than in nuclear DNA.

Oxidative damage could also account for the mutations in mtDNA that accumulate with age

Endogenous oxidants also damage proteins. Stadtman and his colleagues have shown that the proteolytic enzymes that hydrolyze oxidized proteins are not sufficient to prevent an age-associated accumulation of oxidized proteins. In two human diseases associated with premature aging, Werner's syndrome and progeria, oxidized proteins accumulate at a much higher rate than is normal. Fluorescent age pigments, which are thought to be due in part to cross-links between protein and lipid peroxidation products, also accumulate with aging.

Oxidants, Antioxidants, and the Degenerative Diseases of Aging

Metabolism, like other aspects of life, involves trade-offs. Oxidant by-products of normal metabolism cause extensive damage to DNA, protein, and lipid. We argue that this damage (the same as that produced by radiation) is a major contributor to aging and to degenerative diseases of aging such as cancer, cardiovascular disease, immune system decline, brain dysfunction and cataracts. Antioxidant defenses against this damage include ascorbate, tocopherol and carotenoids. Fruits and vegetables are the principal source of ascorbate and carotenoids and are one source of tocopherol. Low dietary intake of fruits and vegetables doubles the risk of most types of cancer as compared to high intake and also markedly increases the risk of heart disease and cataracts. Since only 9% of Americans eat the recommended five servings of fruits and vegetables per day the opportunity for improving health by improving diet is great.

The degenerative diseases associated with aging include cancer, cardiovascular disease, immune system decline, brain dysfunction, and cataracts. The functional degeneration of somatic cells during aging appears, in good part, to contribute to these diseases. The relationship between cancer and age in various mammalian species illustrates this point. Cancer increases with about the fifth power of age in both short-lived species, such as rats, and in long-lived species, such as humans.

Thus a marked decrease in age-specific cancer rates has accompanied the marked increase in life span that has occurred in 60 million years of mammalian evolution: i.e., cancer rates are high in a two year old rat, but low in a two year old human. One important factor in longevity appears to be basal metabolic rate, which is about seven times higher in a rat than a human and which could markedly affect the level of endogenous oxidants and other mutagens produced as by-products of metabolism. The level of oxidative DNA damage appears to be roughly related to metabolic rate in a number of mammalian species (cancer/mutation/endogenous DNA adducts/oxygen radicals)

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By Bruce N. Ames*, Mark K. Shigenaga, and Tory M. Hagen

Antioxidants May Reduce Harmful Complications Of Diabetes

SAN FRANCISCO, CA -- April 20, 1998 -- Duke University Medical Center researchers have found that the depletion of body chemicals called antioxidants may increase the risk of complications from the most common form of diabetes.

The scientists recommend that diabetics take antioxidants supplements, such as vitamin C or E, to help stave off or even forestall the hallmark complications of diabetes, including blindness, kidney failure, amputation and even death.

antioxidants neutralise oxygen free radicals, highly-reactive chemicals that are the potentially-destructive by-products of the body's process of turning food into energy. Normally, the body produces enough antioxidants of its own to keep the reactive oxygen from causing damage.

"We were able to show that patients with poor control of their diabetes who were beginning to show signs of complications had depleted their store of antioxidants ," said Duke researcher Dr. Emmanuel Opara. "Further, we found a significant correlation between high blood-sugar levels and depletion of antioxidants . It appears that this depletion is a major risk factor for developing complications and that antioxidants supplements could lower this risk."

Opara presented his studies yesterday at Experimental Biology `98, the annual scientific meeting of the Federation of American Societies for Experimental Biology (FASEB).
The researchers studied 50 similar people with Type II diabetes -- also known as non-insulin-dependent or adult-onset diabetes. In this form of the disease, insulin produced in the body is unable to trigger the lowering of high blood sugar. Type II diabetes afflicts about 90 percent of the estimated 10.7 million Americans diagnosed with the disease and the 5.4 million believed to have undiagnosed cases, according to the Centers for Disease Control and Prevention.

Insulin is the hormone that normally regulates the level of sugar (glucose) in the blood and is produced by cells in the pancreas. Insulin is secreted when the level of blood glucose rises -- as after a meal.

All diabetic patients in the study were taking only drugs referred to as sulfonylureas, which increase the sensitivity of receptors to insulin throughout the body. Half the patients exhibited microalbuminuria, the excretion of tiny amounts of protein in the urine that is considered a precursor of kidney disease, while the other half did not. T

he researchers took blood samples from all 50 patients, as well as a control group of 20 similar people without diabetes and determined levels of antioxidantsin their blood.
"We found that the non-diabetics' ability to defend against damage from the oxygen free radicals was almost twice that of those patients exhibiting microalbuminuria," Opara explained. "And while the difference between the two diabetic groups was not as pronounced, the difference was still statistically significant. Also, antioxidants depletion correlated with high blood sugar after meals only in the group with microalbuminuria."

The researchers determined antioxidants levels by a new chemical assay developed at King's College in England that enabled them to measure all known antioxidants in the blood and to obtain a more global picture of the body's total antioxidants capacity, Opara said. Other assays are only specific for individual antioxidants.

Using the newly-developed assay, the scientists rated the ability of the non-diabetics to defend against Free radicals damage at 2.7, compared with 1.4 for those with microalbuminuria and 1.7 for the diabetics without microalbuminuria.

Though the exact mechanism of action of the oxygen Free radicals is not yet clear, these findings confirm in humans earlier animal studies of the chemicals' role in damage in diabetes, Opara said. Previous Duke studies by Opara have shown that vitamin E can delay the development of diabetes in obese rats with Type II diabetes and that the depletion of the antioxidants Glutathione caused diabetes in another rat model.

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"The results we've been seeing in our animal studies are now being borne out in humans,” Opara said. "I recommend that since the body has many antioxidants , diabetics should take a number of these agents, including vitamins C and E and Glutathione."

The diabetic patients involved in the current study come from Egypt, and their samples were brought to Duke by E. Abdel-Rahman, one of Opara's collaborators.

Glutathione Deficiency Predicts Poor Survival In HIV Subjects

Glutathione (GSH) deficiency in patients with HIV infection is a strong predictor of poor survival,according to a report published in today's issue of the Proceedings of the National Academy of Sciences.

Stanford University researchers have also discovered that, when used in combination with CD4 cell counts, Glutathione levels can provide a more accurate means of tracking the progression of HIV disease.

Dr. Leonard A. Herzenberg and colleagues in Stanford, California, report the results of in vitro studies in which they evaluated blood samples from 204 HIV-positive patients. They found subjects with Glutathione deficiency had a markedly decreased survival 2-3 years after baseline data collectionwhen compared with subjects without Glutathione deficiency.

Patients with CD4 T cell counts below 200 per microliter also had lower Glutathione levels compared with subjects in earlier stages of HIV infection.

According to Dr. Herzenberg, this study shows for the first time that people with HIV who have lower Glutathione levels have a much lower probability of surviving over the course of three years than do people with normal Glutathione levels. He has presented preliminary reports of these findings at recent meetings.

Dr. Herzenberg also found that Glutathione levels were replenished following oral administration of the glutathione, which suggests a potential intervention to relieve this impairment. If these findings can be replicated, Dr. Herzenberg writes, "...they will provide the foundation for the use of N-acetylcysteine as an inexpensive, nontoxic adjunct therapy for HIV/AIDS, potentially valuable even in remote locations where only minimal medical supervision is available."

Dr. Herzenberg's group believes that HIV-positive subjects should avoid excessive exposure to UV irradiation, alcohol and drugs, such as acetaminophen, which are known to deplete Glutathione levels. And, based on these findings, Dr. Herzenberg and others have asked the FDA to require drug companies to include labeling on products known to deplete Glutathione because of the potential hazard to HIV-positive patient.

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The Role of Glutathione in Eye Care

TYPICALLY the need for reading glasses comes on in the 40s or 50s. The common cause of this is a loss of flexibility in the eye's lens.

The fact that it is a common occurrence does not mean that it cannot be treated if treated soon enough.

Equally important is that the process of decline is also associated with the development of cataracts and general declines in overall health, so one basic treatment helps the body's overall health.

***Note that there might possibly be other problems, and consulting with a physician is always wise where critical health concerns are an issue.

A shortage of the amino acid Glutathione is the primary culprit in the eye decline noted above.

Glutathione slows down the breakdown of DNA within the lens. It protects certain proteins in the lens from oxidizing. It aids in the transport of calcium, potassium, and sodium into the lens.

Declines in these are all contributors to the decline in the health of the lens, its increasing rigidity, and the develoment of cataracts.

Supplementation of Glutathione will resolve the problem -- if done soon enough after the decline in vision is noted. Increasing the Glutathione level in the eye may actually restore some flexibility.

However, if the lens is too rigid, reversing the damage is not possible. At least, though, further decline and develoment of cataracts may be prevented.

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Glutathione helps to support the proper functioning

Glutathione helps to support the proper functioning of your immune system , and will improve immune system already in retreat.

Glutathione acts as an powerful antioxidant and Free radicals scavenger, thereby protecting our DNA and RDA from damage due to many environmental factors.

Glutathione acts as the regulator of other powerful antioxidant.

Glutathione acts as a detoxifying agent, removing foreign objects, chemicals and toxins from the body. As you age, your levels of Glutathione are depleted, thereby allowing the aging process to accelerate.

Levels of Glutathione can be sucessfully improved by taking a high quality nutritional supplement!

***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
http://www.healthline.com/galecontent/glutathione

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Cysteine, Glutamic Acid and Glycine- immune system

Glutathione is a tri-peptide composed of three amino acids: Cysteine, Glutamic Acid and Glycine.

Glutathione and the enzymes it forms, such as GTH peroxidase, are essential to all life and are found in tissues of virtually all plants and animals. GTH is present in all human cells, with the highest levels found in the liver, the lenses of the eyes, pancreas, spleen and kidneys.

Glutathione acts as a powerful antioxidant, a key protector against all types of pollution and is effective in preventing aging. It protects DNA and RNA from free-radical damage.

Glutathione also protects against cellular peroxidation caused by exposure to pesticides, plastics, benzene and carbon tetrachloride, as well as heavy metals, cigarette smoke, smog, drugs, solvents, dyes, phenols and nitrates.

Glutathione works to inhibit the formation of free radicals, dangerous agents that suppress the immune system and promote the formation of mutagens and carcinogens.

Free radicals also speed up the aging process, and it is due to this powerful antioxidant activity that Glutathione is considered useful in the prevention and treatment of a wide range of degenerative diseases.

Studies at the Louisville School of Medicine have clearly shown that Glutathione possesses the unique ability to slow the aging process. While Glutathione aids in the protection of all cells and membranes, a study at Harvard Medical School found that Glutathione is especially able to enhance immune system cells, protecting against damage from radiation and helping to reduce the side effects of chemotherapy and x-rays and alcohol. As a detoxifier of metals and drugs, Glutathione also aids in the treatment of blood and liver disorders.

As individuals grow older, Glutathione levels drop, and the ability to detoxify free radicals decreases.

It can protect against cadmium, copper, and acetaminophen (the active agent in Tylenol) toxicity. Glutathione aids the liver in detoxification, slows the aging process, helps the cardiovascular and immune system, and is helpful in preventing or treating many other health conditions.

Supplementation may prevent, or be helpful with, the following conditions:
Aging
Alcoholism
Asthma
Atherosclerosis (heart disease)
Cancer
Cataracts
Dizziness
Hepatitis
Immunodepression (immune function)
Infertility (male)
Memory Loss (Alzheimer's disease, dementia)
Osteoarthritis
Parkinson's Disease
Peptic Ulcers

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Wednesday, February 6, 2008

Inflammation, Free Radicals, and Cytokines

Although acute Inflammation is an important immune system response, chronic inflammation has also been linked to many diseases, including heart disease. Besides the pro-Inflammation cytokines, Inflammation may be related to the overproduction of free radicals (Janeway CA et al 1999).

A free radical is an atom or group of atoms (i.e., a molecule) with unpaired electrons. Free radicals are extremely unstable and react easily with other molecules, thereby changing their chemical composition. Oxygen is especially susceptible to free radical formation. The free radicals derived from oxygen are known as reactive oxygen species, or oxidants.

When the body has increased levels of reactive oxygen species (i.e., when it is experiencing oxidative stress), widespread damage may result. At high concentrations free radicals can damage fats, proteins, and nucleic acids. They can also cause cell death, gene mutations, and cancer ( Moslen MT 1994). Several diseases may be the result of cellular and genetic damage caused by free radicals, including several immune disorders ( Moslen MT 1994).

In order to reduce the damage caused by elevated free radicals and cytokines (which are both part of the natural immune system), the body fights back by producing antioxidants and hormones such as cortisol to suppress the immune system (Grimble RF 1996). Antioxidants are valuable because they pair with unstable free radicals, thereby limiting the damage free radicals can inflict on other cells.

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Phagocytic cells

Phagocytic cells engulf foreign cells and destroy them. The phagocytic cells are white blood cells and include neutrophils, eosinophils, and macrophages; they have short lives and must be continually replenished by the body. Neutrophils and macrophages are a very important aspect of the innate defenses of the body (Janeway CA et al 1999; Beers MB 2004).


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More study:
Polymorphonuclear leukocytes isolated from chicken peritoneal exudates have been found to catalyze cyanide-insensitive stimulation of respiration and the hexose monophosphate shunt upon exposure to heat-inactivated Staphylococcus aureus.

However, there was no demonstrable formate oxidation concomitant with phagocytosis in either the presence or absence of exogenous catalase. Moreover, chicken polymorphonuclear leukocytes failed to oxidize scopoletin concomitant with phagocytosis in the presence of horseradish peroxidase. While oxygen uptake was increased 2- to 3-fold by the stimulus of phagocytosis, the oxidation of [1-(14)C]glucose was increased approximately 20-fold.

The cells contain two mechanisms, a Glutathione reductase-Glutathione peroxidase system and an NADPH-NAD+ transhydrogenase, each of which is present in sufficient capacity to accommodate the enhanced shunt activity.

Although chicken polymorphonuclear leukocytes were found to possess a substantial capacity to catalyze the cyanide-insensitive oxidation of either NADH or NADPH, the total or specific activities of such processes were not demonstrably affected by phagocytosis.

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Inflammation and fever

Inflammation is a nonspecific response to infection or tissue injury. The four signs of the inflammatory response are redness, swelling, heat, and pain.

Inflammation begins when cells release certain cytokines, including interleukin (IL)-1, IL-6, and tumor necrosis factor-alpha (TNF-alpha ) (Janeway CA et al 1999; Beers MB 2004).

Inflammation is a process by which the body’s white blood cells and chemicals protect us from infection and foreign substances such as bacteria and viruses.

In some diseases, however, the body’s defense system (immune system) inappropriately triggers an Inflammation response when there are no foreign substances to fight off. In these diseases, called autoimmune diseases, the body’s normally protective immune system causes damage to its own tissues. The body responds as if normal tissues are infected or somehow abnormal.

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Physical and chemical barriers

The body's first lines of defense are the skin and mucous membranes, which prevent the entrance of many pathogens.

There are many secondary barriers.

For example, tears, sweat, and saliva combat some bacteria, and the hydrochloric acid and protein-digesting enzymes secreted by the stomach are lethal to many, but not all, pathogens (Janeway CA et al 1999; Beers MB 2004).

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The Immune System

The immune system is an elegant and complex set of components that combine to fight disease, infections, and various pathogens. A healthy immune system distinguishes organisms in the body as “self” or “non-self.” An intact immune response identifies pathogens as “non-self” and rapidly destroys them. A depressed immune system, by contrast, will allow invading organisms to flourish.

Furthermore, when the immune system mistakenly recognizes a “self” cell as “non-self” and mounts an immune response, the result is an autoimmune disorder such as rheumatoid arthritis.

In general, the body has two primary defense mechanisms: natural immunity and acquired immunity. Natural immunity is the “first responder” to an attack. The natural immune response relies on various white blood cells and physical barriers to block or immediately attack any foreign invader and attempt to destroy it.

Acquired immunity, on the other hand, involves antibodies that are created in response to specific foreign antigens. This sort of response requires a few days for the body to recognize the invader and manufacture antibodies against it. Once the body has manufactured a particular antibody for a specific invader, the immune system response is faster and more effective the next time that invader appears (Janeway CA et al 1999; Beers MB 2004).

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Dietary supplement helps to keep immune system balanced

Stanford researchers have found that giving patients who are infected with the human immunodeficiency virus (HIV) a daily dose of a dietary supplement can boost their levels of Glutathione­ a nutrient essential for proper functioning of the immune system. Restoring glutathione levels to those found in healthy people may help HIV-infected patients fight the AIDS-causing virus and fend off other diseases.

"The importance here is that Glutathione is a central component of all cells, and Glutathione deficiency is associated with poor prognosis in many, many diseases," said Leonore (Lee) Herzenberg, PhD, professor of genetics. She is senior author of a paper describing the new study, published in the October 1 issue of the European Journal of Clinical Investigation.

Lee Herzenberg and her colleagues conducted a clinical trial in which 31 HIV-infected patients were given daily doses of N-acetylcysteine (NAC) ­ a substance that is turned into Glutathione in the body. Thirty others were given a benign sugar pill. At the start of the trial all patients had Glutathione deficiency ­ some patients had only half the amount found in healthy people. At the end of the two-month trial, those taking NAC had increased the amount of Glutathione in their bodies to near-normal levels.

"What we've proven is that giving people NAC replenishes the Glutathione stores," said Lee Herzenberg.

At the completion of the eight-week trial, most patients chose to take NAC for the following six months while the researchers continued monitoring the safety of the supplement. They found that patients suffered no ill effects that could be attributed to daily NAC ingestion.

Glutathione is not an anti-retroviral drug, stressed genetics professor Leonard (Len) Herzenberg, PhD. It does not decrease the amount of virus in patients' blood or increase their number of virus-fighting T cells, but it does restore the immune system, the researchers said.
Previous findings by the Herzenbergs and others show that T cells perform better in HIV-infected patients when their Glutathione levels are replenished. Reversal of Glutathione deficiency is also associated with improvement in many other diseases including diabetes, influenza and cystic fibrosis.

"The level of Glutathione is tightly regulated in cells. If nature has gone to the trouble of maintaining those levels, logic says it should be restored to that level if you can," said Lee Herzenberg. "It's like a vitamin deficiency. Any vitamin deficiency would immediately be corrected, and we believe that this is equivalent to a vitamin deficiency."

The Herzenberg team hopes that the benefits of maintaining normal Glutathione levels will encourage people suffering from long-term diseases to avoid lifestyle factors that deplete Glutathione, such as exposure to ultraviolet light and alcohol consumption. They also recommend limited use of acetaminophen ­ the active ingredient in common painkillers such as Tylenol ­ because the risk of liver damage is increased for those with low Glutathione levels.
The Herzenbergs are confident that the new findings will speed the introduction into the U.S. market of medicinal-quality NAC that AIDS patients and others can take to maintain normal Glutathione levels. BY KRISTIN WEIDENBACH

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Raised Glutathione Levels Help Balance Immune System

Researchers from Germany and the US have found that Glutathione can boost the natural antioxidant system of the body.

The body carries many antioxidant defense systems, but inside cells a small protein called glutathione is crucial. Glutathione is essential for the function of immune cells, which protect us from viral and bacterial infections.

In people with immune deficiency, glutathione levels fall well below the normal levels in blood and immune cells. Restoring glutathione levels to those found in healthy people is likely to help immune deficient patients.

Two studies have recently been published with research backing up the claims that Glutathione helps fight disease, one in the European Journal of Clinical Investigation, from Stig Froland in Oslo, Norway, and the other by Leonore and Leonard Herzenberg, a husband and wife team from Stanford, California. The results of their work showed that glutathione levels could indeed be restored in AIDS patients and that this may improve the outlook for these patients.

Herzenberg and colleagues conducted a clinical trial in which 31 HIV-infected patients were given daily doses of Glutathione — and 30 others were given a benign sugar pill. According to the study published in the October 1 issue of the European Journal of Clinical Investigation, those taking Glutathione had increased the amount of glutathione in their bodies to near-normal levels at the end of the two-month trial.

“The importance here is that glutathione is a central component of all cells, and glutathione deficiency is associated with poor prognosis in many, many diseases,” said Herzenberg. “What we’ve proven is that giving people Glutathione replenishes the glutathione stores.”

The authors of the report concluded that “Glutathione offers useful adjunct therapy to increase protection against oxidative stress, improve immune system function and increase detoxification of acetaminophen and other drugs. These findings suggest Glutathione therapy could be valuable in other clinical situations in which there is GSH deficiency.”

“It is important to realize that these results are the culmination of over 10 years of research.” states Frank Staal, an immunologist from Rotterdam, The Netherlands, who worked in this field for many years. “The groups of Droge and Herzenberg were the first to demonstrate that Glutathione is low in AIDS and that this defect contributes to poor immune cell function." ImmuneSupport.com

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Sunday, February 3, 2008

Rehabilitation therapy- Parkinson’s disease

Rehabilitation therapy enhances the lives of people with Parkinson’s disease. A program of physical therapy and occupational therapy can help people learn movement strategies:

How to roll over and get out of bed more easily
How to rise from a chair or get out of a car


Therapists sometimes suggest simple devices to assist with daily activities, such as:
Shower grab bars
Shower stools
Elevated toilet seats

Occupational therapists and physical therapists have experience finding ways to help people button shirts, cook and generally keep their lives going. They know about special kinds of utensils that help keep food on a spoon or a fork. Even people with serious tremor, slowness or rigidity can use these utensils to feed themselves without making a mess.

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Parkinsonism

Any person who has the signs and symptoms characteristic of Parkinson’s disease is said to have parkinsonism, but not every person with parkinsonism has Parkinson’s disease, it's only one of the possibilities.

Patients and their families need to understand parkinsonism, because some 20 to 25 percent of people diagnosed with Parkinson’s disease will eventually be discovered to have some other form of parkinsonism.

Parkinsonism may look like Parkinson’s disease, but over time it does not act like it.
For this reason, if you have been diagnosed with Parkinson’s disease it is important to see a neurologist who has experience diagnosing and treating this disorder.

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Parkinson's Disease Diagnosis

It is difficult to diagnose Parkinson’s disease in the early stages. Early on, Parkinson’s disease is diagnosed almost primarily by its symptoms, and studies indicate that physicians make an incorrect initial diagnosis of Parkinson’s disease in between 10% and 40% of cases. Blood tests are not helpful for diagnosis.

Parkinson’s disease is just one of several neurologic movement disorders that produce similar symptoms.

It is important that the physician you are seeing has experience with all of the different disorders that can masquerade as Parkinson’s disease.

In some of these diseases people quickly become totally disabled; in others, the disease progresses extremely slowly; and in yet others, illness is chronic (always present) and may have more severe symptoms as time goes on. Because the natural history, or progression, of these diseases varies greatly, proper diagnosis is crucial. People need to know which disease they have.

The Neurologic Examination
When performing a neurologic examination to evaluate a patient with a movement disorder, the doctor takes a medical history and performs a physical examination. The doctor asks the patient and the family members or friends about symptoms and observes the patient, asking him or her to walk around the room, sit down, stand up, turn around, and so on.

Diagnostic Tests
Unfortunately, there is no diagnostic test that can confirm Parkinson’s disease. Laboratory testing of the blood of patients with the symptoms typical of Parkinson’s disease only rarely uncovers any abnormality.

Electroencephalograms (EEGs) record some aspects of brain electrical activity, but they are not effective in spotting Parkinson’s disease.

Important Roles of Glutathione
Fight against oxidative cell damage (Free Radicals)Protein SynthesisAmino Acid transportCellular detoxificationImmune system enhancementEnzyme activationFight InflammationATP (energy) production

Our cells are constantly under attack by Free Radicals, which can cause a reduction of our cells ability to function optimally.

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Parkinson Disease Symptom

The following table lists some of the early signs and symptoms of Parkinson’s disease:
-Change in facial expression (staring, lack of blinking)
-Failure to swing one arm when walking
-Flexion (stooped) posture
-"Frozen" painful shoulder
-Limping or dragging of one leg
-Numbness, tingling, achiness or discomfort of the neck or limbs
-Softness of the voice
-Subjective sensation of internal trembling
-Resting tremor

The characteristic symptoms of moderate Parkinson's disease can be remembered with the acronym TRAP:
T
Tremor
Involuntary trembling of the limbs
R
Rigidity
Stiffness of the muscles
A
Akinesia
Lack of movement or slowness in initiating and maintaining movement
P
Postural instability
Characteristic bending or flexion of the body, associated with difficulty in balance and disturbances in gait

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Cause of Parkinson Disease

Although Parkinson’s disease can occur from viral infections or exposure to environmental toxins, such as pesticides (gardeners and farmers are more prone to Parkinson's disease).

The causes of the majority of cases are not well known. Scientists suspect that oxidative damage to neurons in the substantia nigra could well be one of the major causes, particularly due to the depletion of the antioxidants glutathione.

People who sustain substantial head injuries face an increased risk of developing Parkinson’s disease years later.

The cause of Parkinson's disease is unknown.

Many researchers believe that several factors combined are involved: free radicals, accelerated aging, environmental toxins, and genetic predisposition.

It may be that free radicals—unstable and potentially damaging molecules that lack on electron—are involved in the degeneration of dopamine-producing cells.

Free radicals add an electron by reacting with nearby molecules in a process called oxidation, which can damage nerve cells.

Chemicals called antioxidants normally protect cells from oxidative stress and damage. If antioxidative action fails to protect dopamine-producing nerve cells, they could be damaged and, subsequently, Parkinson’s disease could develop.

Dysfunctional antioxidative mechanisms are associated with older age as well, suggesting that the acceleration of age-related changes in dopamine production may be a factor.

Exposure to an environmental toxin, such as a pesticide, that inhibits dopamine production and produces free radicals and oxidation damage may be involved.

Treatment for Parkinson’s disease

The nutritional treatment for Parkinson’s disease is still an uncharted territory.

The most promising approach appears to be the use of antioxidant to slow the oxidation and damage to the substantia nigra.

It’s possible that additional nutritional approaches may be found in the future. Those who exercise regularly early in their adult life have a lower risk of Parkinson’s disease.

Over the past few decades, doctors have made important advances in the treatment of Parkinson’s disease with pharmaceutical medicines.

Improving the Antioxidant SystemOf all the nutritional treatments available for Parkinson’s disease, antioxidant appear to be the most promising choices to prevent or slow the progression of this condition.

Individuals whose diets include plenty of healthy foods containing antioxidant are less likely to develop Parkinson’s disease.

Patients should consume foods, such as fruits and vegetables, that contain glutathione or can help produce it.

Cyanohydroxybutene, a chemical found in broccoli, cauliflower, Brussels sprouts and cabbage, is also thought to increase glutathione levels.

High intake of dairy products may lead to a higher incidence of Parkinson’s disease.

The following antioxidant may be helpful in addition to standard pharmaceutical therapy.

Your health practitioner may also suggest intravenous, intramuscular, or aerosol administration of glutathione supplements for increased effectiveness.

Glutathione -powerful antioxidant found within every cell

Glutathione - or L Glutathione - is a powerful antioxidant found within every cell. Glutathione plays a role in nutrient metabolism, and regulation of cellular events (including gene expression, DNA and protein synthesis, cell growth, and immune response.

This antioxidant, made from the combination of three amino acids cysteine, glutamate, and glycine, forms part of the powerful natural antioxidant glutathione peroxidase which is found in our cells.

Glutathione peroxidase plays a variety of roles in cells, including DNA synthesis and repair, metabolism of toxins and carcinogens, enhancement of the immune system, and prevention of fat oxidation.

However, glutathione is predominantly known as an antioxidant protecting our cells from damage caused by the free radical hydrogen peroxide.

Glutathione also helps the other antioxidants in cells stay in their active form.

Brain glutathione levels have been found to be lower in patients with Parkinson’s disease.

Parkinson's Disease

Parkinson’s disease is a common neurological condition afflicting about 1 percent of men and women over the age of seventy. In Parkinson’s disease, a small region in the brain, called the substantia nigra, begins to deteriorate. The neurons of the substantia nigra use the brain chemical dopamine. With the loss of dopamine, tremors begin and movement slows. Despite current drug therapies, Parkinson’s disease remains a progressive and incurable condition. Many patients with Parkinson’s disease may also suffer from age related cognitive decline or have some of the symptoms of Alzheimer’s disease.