Glutathione

GLUTATHIONE

$4.95

HELPS PREVENT SERIOUS CHRONIC ILLNESS

One of the MOST POWERFUL antioxidants

Scientific RESEARCHCONFIRMS

effectiveness

magazine presents

GLUTATHIONEby LISE ALSCHULER, ND, FABNO

magazine presents

Copyright © 2009 by Lise Alschuler, ND, FABNO and Active Interest Media, Inc.

All rights reserved. No part of this booklet may be reproduced, stored in an electronic retrieval system, or transcribed in any form or by any means, electronic or mechanical, including photocopying and recording, without the prior written permission of the publisher, except for the inclusion of quotations in a review.

Published by:Active Interest Media, Inc.300 N. Continental Blvd., Suite 650El Segundo, CA 90245

This booklet is part of the Better Nutrition Healthy Living Guide series. For more information, visit www.betternutrition.com. Better Nutrition magazine is available at fine natural health stores throughout the United States. Design by Aline Design: Bellingham, Wash.

The information in this booklet is for educational purposes only and is not recommended as a means of diagnosing or treating an illness. All health matters should be supervised by a qualified healthcare professional. The publisher and the author(s) are not responsible for individuals who choose to self-diagnose and/or self-treat.

GLUTATHIONE

CONTENTSChapter One: Sound The Alarm—Electron Robbery ..4

Chapter Two: Antioxidant Protection ............................. 10

Chapter Three: Health Applications ..................................14

Chapter Four: The Glutathione Rich Lifestyle ........... 20

Chapter Five: Increasing Glutathione Production ...24

Chapter Six: Glutathione Supplementation ................27

Selected References ....................................................................31

4 G L U T A T H I O N E

Chapter One

Sound The Alarm–Electron Robbery

G L U T A T H I O N E 5

“ Aging is the progressive accumulation of diverse, deleterious changes with time that increase the chance of disease and death. The basic chemical process underlying aging was first advanced by the free radical theory of aging in 1954: the reaction of active free radicals, normally produced in the organisms, with cellular constituents initiates the changes associated with aging.”

—Denham Harmon, M.D., Ph.D., originator of the free radical theory of disease and aging

Are you feeling rusty? Perhaps you should be since every process that occurs in the human body—from breathing to eating to moving our limbs—creates oxidation. While breathing, eating

and moving are certainly essential to life, they also generate oxidative stress in the form of reactive oxygen molecules—so-called free radicals. In fact, the very process of creating energy within our cells produces reactive oxygen molecules. These free radicals, like the polluting exhaust from an automobile, are the unfortunate by-products of our own cellular engines. Free radicals, if left unchecked, will exert tremendous damage to our tis-sues. In fact, the existence of free radicals and their oxidative damage is at the core of aging and of chronic disease.

The process of free radical-induced tissue damage is mimicked in nature in the corrosion of metals. When iron is exposed to moisture in the air, rust forms. This rust is the result of iron molecules donating electrons to the reactive oxygen molecules in air. This changes the structure of the remaining iron molecules, creating a brown, brittle metal which flakes off. We refer to this altered form of iron as rust. In a sense, unchecked free radical damage in our own bodies is akin to causing our organs and tissues to rust!

This process begins with the production of energy in our cells. Within each of one of our cells there is a small, but powerful mitochondria. Mitochondria are like the batteries of our cells because this is where energy is produced. Within the inner membrane of the mitochondria, oxygen is used to produce energy as ATP, the universal currency of energy


= proton; this molecule has 8 protons

= electron; this molecule has 2 in its inner ring and 5 in its outer ring. A neutral, non-reactive molecule would have a total of 8 electrons to balance the 8 protons.

= missing electron making this molecule a reactive free radical

Free Radical Molecule


in our body. The process used to make ATP uses electrons from oxygen molecules and is, most simply, a process of transferring electrons from one molecule to another. In doing this, some oxygen molecules are left missing an electron. These electron-hungry oxygen molecules become free radicals. Free radicals have at least one unpaired electron in their outer orbit, essentially giving it an electrical charge. Free radicals are very unstable and react quickly with other compounds, in order to steal an electron. The stolen electron fills the outer ring of the oxygen molecule, allowing it to regain its electrical stability. Free radicals are so greedy for an electron that they literally rip electrons off of other molecules. This violent electron robbery leaves the victim molecule missing an electron in its outer orbit. The victim, in turn, becomes a free radical and it too rips an electron off of a nearby molecule. When these molecules are part of our bodily tissue—for instance, the molecules that comprise the inner membrane of the mitochondria—the rapid fire chain of electron robbery will, over time, cause injury to the membrane. If this injury isn’t repaired, it will ultimately damage the DNA and impair the mitochondrial pro-duction of energy. Energy is required to fuel other cellular processes crit-ical to our healthy survival. When energy production is impaired, the cellular production of proteins needed for cell repair, cell growth, and cellular communication declines. The loss of these critical cellular func-tions leads to the development of chronic diseases. In fact, almost every chronic illness known to humankind has been linked in some measure to free radical-induced tissue damage. If the damage is extensive enough, the energy demands of the body exceed its supply. Combining this lack of cellular energy with free-radical damage speeds up the aging process.

Conditions Linked to Oxidative Stress Cardiovascular disease, stroke

Cancer

Neurodegenerative diseases (Parkinson’s, Alzheimer’s)

Diabetes

Cataracts, macular degeneration

Human immunodeficiency virus (HIV), hepatitis B

Asthma, chronic obstructive pulmonary disease (COPD)

Psychiatric diseases (schizophrenia, bipolar disorder)

Inflammatory diseases and disorders

Aging


Producing energy is not the only cause of free radicals. Tobacco is one of the worst offenders. Each puff of cigarette smoke contains over 1,000 free radicals. Imagine the load of free radicals that enter the body of a pack-a-day smoker! In addition to cigarette smoke, there are many other sources of environmentally-derived free radicals. Industrial pollutants generate free radicals and contribute to associated free-radical tissue dam-age. Free radicals are found in diesel fuel exhaust, in the hydrocarbons, ozone and nitrous oxide from carbon-based fuel exhaust, in pesticides, and herbicides. We are also exposed to free radicals when we eat food out of plastic containers (particularly if these containers have been heated) due to the phthalates in plastic. Phthalates are mainly used as plasticizers (substances added to plastics to increase their flexibility). Ionizing radia-tion also generates free radicals. This is, in fact, the way in which radiation is used to destroy cancerous tumors.

Ultraviolet radiation from the sun causes oxidative damage to our skin which manifests as wrinkles, age spots, and even skin cancer. Alcohol metabolized in the liver turn into free radical compounds. This is one of the reasons why excessive and prolonged alcohol ingestion is linked with liver disease, neurological diseases, and cancer. Digestion generates free radicals as this energy-intensive process breaks down food particles. Satu-rated fat and trans fats are potent dietary sources of free radicals. Exercise

Oxidative Damage to Cells and Tissues

Reactive Oxygen Species (ROS)

DiseasesAging

Protein Damage Cell Functioning& Signaling

DNA Damage & Mutation

LipidPeroxidation


also generates free radicals in our muscles as energy production increases to meet the demands on the working muscles. There is no escaping free radical exposure—we produce them and we encounter them in the envi-ronment every minute of every day.

While this may seem like a dismal state of affairs, it should be pointed out that free radicals are not always bad. The destructive nature of free radicals is an exceptionally useful way to destroy foreign invaders and mutated cells. Our immune cells use free radicals to destroy infected and cancerous cells. Certain immune cells carry specialized vesicles containing hydroxyl radicals. When these immune cells encounter an infected or damaged cell, they inject the contents of this vesicle into the target cell. The infected and mutated cells don’t stand much of a chance in the face of this free radical onslaught.

Free radicals are also helpful, somewhat ironically, in the prevention of certain chronic diseases such as cancer and heart disease. When a cell sustains damage to its DNA, it must be either repaired or destroyed (the process of cellular self-destruction is called apoptosis). In the presence of damage, free radicals in the cell initiate cell repair pathways. If the damage cannot be repaired, these free radicals induce apoptotic pathways.

These examples illustrate the breathtaking wisdom of living organisms. We have found a way to utilize some of the most destructive compounds that our tissues will ever encounter to our advantage! Alas, despite this ingenious use of free radicals for our benefit, by and large, free radicals are more harmful than helpful. The world we live in, the diets we consume, and the advanced age of our population (our cells and our DNA becomes more vulnerable to damage as we age) have left us far out-gunned by free radicals. The chain of electron robbery constantly threatens our vitality and longevity. Thankfully, there are ways to avert this destruction. The main way to stop free radical electron robbery is to bring in the sheriff molecules known as antioxidants.

Free radicals are also helpful, somewhat ironically, in the prevention of certain chronic diseases such as cancer and heart disease.


Chapter 2

Antioxidant ProtectionThe ability to rapidly extinguish oxidative stress is clearly essential

to our health. This is where antioxidants come to the rescue! Anti-oxidants are compounds whose primary function in the body is

to quench free radicals and prevent oxidative stress to our tissues. Anti-oxidants are compounds that are able to donate electrons to the greedy electron-poor free radical molecules. When our body has sufficient anti-oxidant capacity, we are able to neutralize and eliminate free radicals and, in so doing, relieve oxidative stress. Our antioxidant defense sys-tem is built out of a number of different antioxidant compounds, each with different abilities to quench free radicals. These compounds work together to provide the greatest defense. There are two broad categories of antioxidants—those which are produced within our body (endoge-nous antioxidants) and those which we consume (exogenous antioxi-dants). Both types are critical, although endogenous antioxidants are more powerful.

Some of the antioxidants that we make are large enzymatic molecules like superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx). These compounds are enzymes and their production is increased in response to oxidative stress. Other endogenous antioxidants include smaller compounds like thiols (such as alpha lipoic acid), ubiquinone (coenzyme Q10), and uric acid. These molecules respond less dynamically to acute oxidative stress and instead exert consistent antioxidative actions. Antioxidant enzymes work as a team to neutralize free radicals. Going back to our sheriff metaphor, SOD is the first sheriff to step into the gun fight with a free radical robber. SOD fires the first shot and wounds the free radical, transforming it into a less harmful oxygen-based free radical. The next two sheriffs, catalase and glutathione peroxidase then step in and fin-ish the job, converting the oxygen-based free radical into harmless water and oxygen. The smaller antioxidants such as alpha lipoic acid could be thought of as the sheriff’s deputies and they are essential in providing com-plete defense. Alpha-lipoic acid, for instance, is able to regenerate glutathi-one (as well as vitamins E and C) after a show-down with a free radical.


Fruits and vegetables are jam-packed with

antioxidants, which is why a diet high in these foods over

a lifetime is consistently correlated with lowered risk

of major chronic diseases.


This cooperation between antioxidants is essential to replace the electrons that antioxidant compounds give to free radicals to neutralize them.

Exogenous antioxidants include compounds such as vitamin C (ascorbic acid), vitamin E (tocopherols and tocotrienols), carotenes, flavonoids, and phenols. The richest sources of dietary antioxidants are fruits and vegetables. In fact, fruits and vegetables are jam-packed with antioxidants, which is why a diet high in these foods over a lifetime is consistently correlated with lowered risk of major chronic diseases. A very large study of over 100,000 participants that was conducted out of the Harvard School of Public Health found that total fruit and vegetable intake was inversely associated with the risk of major chronic diseases, especially cardiovascular disease. At least five servings of fruits and vegetables daily lowered the risk of cardiovascular disease by 12 percent. The more colorful the fruits and vegetables are, the more antioxidants you are eating. The compounds that give the colors to fruits and vegetables are known as phenols and flavonoids, with different ones creating different colors. Thus, eating a variety of colorful fruits and vegetables will ensure a variety of these potent antioxidants.

Many consider glutathione to be the most important of our body’s antioxidants, especially since it is found in every cell of the body.

Dietary antioxidants are one way to augment the antioxidant defense system of your body. Another way to accomplish this goal is to supple-ment with selected antioxidants. Not all antioxidants are amenable to supplementation, particularly the large molecule enzyme antioxidants. It has taken many years and much science to develop oral supplements of compounds such as glutathione that are absorbable and that increase the antioxidative potential of the body.

What is The Role of Glutathione?Many consider glutathione (also known as GSH) to be the most

important of our body’s antioxidants, especially since it is found in every cell of the body. It is composed of three amino acids—glutamaic


acid, cysteine, and glycine—and it has numerous functions within our cells. Glutathione is found throughout the body and is especially con-centrated in the liver.

Inside the cell, glutathione acts as the primary antioxidant against free radicals produced by toxic chemicals and viruses. It also plays an essen-tial role in the liver’s detoxification process by binding detoxified reactive molecules into non-reactive compounds that can then be excreted. This powerful antioxidant is also involved in DNA repair. Glutathione preserves the structure and function of key cellular proteins and helps to transport amino acids across the cell membrane. It also boosts our immunity.

The role of GSH as an antioxidant is extremely important. It is able to trade electrons in such a way as to regenerate itself and other antioxidants into their active forms. Glutathione is produced within our cells; the amount produced is dependent upon the availability of cysteine, one of its component amino acids. When the cellular concentration of glutathi-one reaches a certain level, the cell will not produce more until the level goes down. Despite being the most common antioxidant within cells, glutathione deficiency does occur. Deficiency is linked with several dis-eases and presumably replenishing glutathione in individuals with these diseases may beneficial.

Role of Glutathione in Detoxification

Detoxified products

Detoxified products

Detoxified products

Glutathione Peroxidases

(GPXs)

Glutathione S-transfereses

(GSTs)

Lipids

GSH

free radicalsROS

Peroxides

toxins, drugs, carcinogens


Chapter 3

Health Applications

G lutathione deficiency has been linked to many chronic diseases. Diseases such as Alzheimer’s disease, Parkinson’s disease, schizo-phrenia, bipolar disorder, hepatitis, cystic fibrosis, HIV infection

and AIDS, cancer, heart disease, stroke, macular degeneration, asthma, COPD, and diabetes are all linked to oxidative damage and glutathione deficiency. Glutathione deficiency allows oxidative damage to accelerate the progression of these conditions. Let’s take a closer look at some of these health conditions.

Alzheimer’s disease and Parkinson’s disease are both conditions that typically affect older adults. Both of these conditions are the result of oxi-dative damage. One of the underlying biochemical events in Parkinson’s disease is the depletion of glutathione in affected neurons. This depletion allows oxidative stress to create mitochondrial dysfunction, and finally neuronal cell death. Pre-clinical studies have shown that herbal sources of glutathione reverse this mitochondrial oxidative damage and prevent neu-ronal cell death. Some drugs developed to treat Parkinson’s disease work, in large part, by increasing glutathione levels and glutathione activity in nerve tissue. Alzheimer’s disease is another neurological condition that is the result of oxidative damage. Oxidative stress increases myloid-beta peptides in the brain. These peptides are involved in the disease process of Alzheimer’s. Neurons with depleted glutathione are much more suscep-tible to oxidation and the buildup of myloid-beta peptides. Adequate glu-tathione can exert preventive actions and has a role in the management of both Parkinson’s and Alzheimer’s disease.

Various psychiatric conditions are also made worse by oxidative dam-age. Brain glutathione levels are decreased in schizophrenia, a disorder that often is chronic and resistant to treatment. A six month randomized, multicenter, double-blind, placebo-controlled study looked at the safety and effectiveness of oral n-acetyl cysteine (NAC) as a source of glutathione in 140 adults with schizophrenia. The study found that taking NAC was a safe and moderately effective strategy for raising glutathione and, in doing so, improving the response to medication in chronic schizophrenia.

The role of oxidative stress in bipolar disorder has become increasingly recognized as an important factor in this illness. People with active bipo-lar disorder have unregulated glutathione activity which is thought to be a compensatory response to the high oxidative stress. Unfortunately,


if these individuals’ glutathione stores become depleted, their bipolar symptoms are likely to worsen. Glutathione depletion is a very real possi-bility in people with bipolar disorder as some people with this condition attempt to ‘self-medicate’ their symptoms with excessive alcohol or sugar consumption. They may also be prone to tobacco addiction. All of these activities strain glutathione reserves, and, over time, will contribute to glu-tathione deficiency. In turn, this deficiency will aggravate the symptoms of bipolar disorder.

The development of various cancers has also been linked to glutathione deficiency. The risk of oral cancer is reduced by more than 50 percent in individuals with the highest blood levels (>5.9mmol/g Hb) of glutathi-one compared to those with the lowest levels (<4.9mmol/g Hb). A similar association has been found for pharyngeal cancer. Men and women who consumed the greatest daily amount of glutathione in their diet (50 to 242 mg) had a more than 50 percent reduction in their risk of develop-ing pharyngeal cancer compared to those with the lowest intake (5mg -33mg). Low levels of glutathione have also been linked to the develop-ment of cancers of the colon, prostate, breast, and bladder.

Viral diseases are closely linked to glutathione deficiency. People

with hepatitis, HIV infection, and AIDS characteristically have low glutathione levels.

Chronic oxidative stress and the depletion of endogenous antioxidants play a key role in the development of chronic obstructive pulmonary dis-ease (COPD) and asthma. High oxidative stress coupled with low antioxi-dant levels increases the risk of developing bronchial asthma and COPD. It can also make these chronic conditions worse, primarily because of a decrease in glutathione activity. This may also explain why certain people with asthma are vulnerable to having asthma attacks from heavy exercise. Exercise creates significant oxidative stress. In asthmatics whose glutathi-one levels are depleted, this additional oxidative event can be enough to trigger an attack. A similar phenomenon is seen in people with COPD. Systemic inflammation and oxidative stress are associated with muscle wasting and muscle dysfunction in people with COPD, particularly when their glutathione stores are used up.


Viral diseases are closely linked to glutathione deficiency. People with hepatitis, HIV infection, and AIDS characteristically have low glutathione levels. The role of antioxidants in the course of these viral infections can seem confusing. Initially, infection with these viruses requires immune cell destruction via oxidative damage. Additionally, some of the anti-viral medications used to treat these diseases stimulate the oxidative processes in order to destroy the virally infected cells. Thus, an oxidative immune response is needed, not an antioxidant defense. However, as hepatitis and AIDS viral diseases progress, their symptoms are mediated by oxidative damage. Hepatitis C infection, for example, significantly lowers vitamin C and glutathione levels. To make matters worse, treatment with ribavi-rin (a commonly used anti-viral medication for hepatitis) further reduces the activity of glutathione peroxidase (and superoxide dismutase). Thus, both the infection and its treatment elevate oxidative stress in hepatitis. This elevated oxidative stress, in turn, causes the much feared liver fibro-sis and ultimately cirrhosis that can occur as a result of chronic hepatitis. Oxidative stress is also implicated in many of the disease manifestations of AIDS such as dementia, muscle wasting, opportunistic infections, can-cers and liver dysfunction. Glutathione depletion is, unfortunately, com-monly found in people with AIDS. Addressing their crippled antioxidant defense system is critical to reducing the myriad of symptoms that this disease causes.

Glutathione status is closely tied to the progression and severity of diabetes. In fact, most of the damage associated with diabetes is oxida-tive damage. High levels of circulating glucose (blood sugar) presents a significant oxidative challenge to the body. In poorly controlled diabet-ics, elevated blood sugars react with protein amino acids to form reac-tive proteins. These compounds (advanced glycation end products) create oxidative damage to blood vessels, namely in the eyes and in the kidney. Unless interrupted, this damage will ultimately lead to blindness and to renal failure. Adding insult to injury is the fact that many diabetics will, over time, develop a glutathione deficiency. One study of adolescents with poorly controlled type 1 diabetes mellitus found these individuals to have significant depletion of blood glutathione. This depletion occurs because glutathione is required to mitigate the oxidative damage. Unfortunately, consumption of glutathione-rich foods and even glutathione precursors such as n-acetyl cysteine may not raise glutathione levels in diabetics. This may be because diabetics have impaired ability to utilize these precursors to make glutathione.

Macular degeneration is another condition that is the result of oxi-dative damage, and a condition that is responsive to glutathione. Age-related macular degeneration is the most common cause of vision loss in


Glutathione deficiency allows oxidative damage to

accelerate the progression of many chronic diseases.


people over 50 years old. Macular degeneration occurs as yellow deposits called drusen accumulate between the retinal pigment epithelium and the underlying choroid layer of the eye. Over time, drusen accumulation can result in vision loss in the center of the visual field (the macula). One fac-tor influencing the progression of this disease is oxidation and glutathi-one deficiency. Given the high exposure to sunlight and to oxygen in the air, the eye is particularly prone to oxidative damage. Antioxidant protec-tion is of critical importance in maintaining eye health. Retinal deteriora-tion occurs when there is an insufficient level of the free radical scavenger glutathione. Oxidative mechanisms are considered to contribute to the aging changes that underlie age-related macular degeneration. Individuals with glutathione deficiency are particularly at risk for the development of macular degeneration.

Oxidative stress is now recognized as a key event in the development of coronary artery diseases such as atherosclerosis. An initial oxidative injury to a blood vessel triggers a healing response which involves cre-ating a cholesterol-rich cap over the area of injury. Unfortunately, this healing response can perpetuate itself and ultimately lead to the buildup of fatty plaque deposits on the artery wall. The plaques can become large enough to block the flow of blood. Also, over time, portions of these plaques harden and can break off, forming a thrombus (blood clot). A thrombus can lodge itself in a blood vessel and impede the flow of blood through that vessel. Once blood flow is blocked, the tissues that require that blood will be deprived of nutrients and oxygen. When arterial block-age happens in a vessel supplying blood to the brain, a stroke can result. When blood vessel occlusion happens in an artery supplying a portion of the heart, a heart attack occurs. Obviously these are very serious con-sequences of cardiovascular disease, which, for many individuals could be avoided.

Cardiovascular disease is largely a preventable disease. Since oxidative injury to the blood vessel is the initial step in cardiovascular disease, it only makes sense that sufficient antioxidant defense is necessary to deter the damage. The role of glutathione in this protection is important. One clinical study showed that low dose NAC (a precursor to glutathione) effectively reduces myocardial oxidative stress in patients undergoing coronary bypass surgery. Glutathione-based antioxidation also plays a key role in helping to prevent the neurological consequences of ischemic stroke (lack of blood supply to affected areas of the brain). When alpha-lipoic acid, a precursor to glutathione, is given to stroke victims, improve-ment in their neurological function is noted. Glutathione thus plays an important role in both the tolerance to ischemia and in the prevention of ischemic stroke.


Cystic fibrosis is a genetic condition, characterized by thick mucus build-up in the lungs as well as other organs such as bile ducts and intes-tines. People with cystic fibrosis suffer from difficulty breathing, pneu-monia, and numerous other illnesses. The role of glutathione in cystic fibrosis cannot be overstated. Glutathione production and secretion by lung cells is impaired in cystic fibrosis. Lack of glutathione leads to free radical-induced chronic inflammation and infection. Several studies have investigated the use of inhaled glutathione as a treatment for cystic fibro-sis. Glutathione inhalation improves lung capacity and results in greater ease of breathing. Inhaled glutathione therapy is well tolerated by people with cystic fibrosis and appears to have minimal to no side effects.

Aging is associated with a depletion of glutathione. Oxidative tissue dam-age, particularly to the mitochondria, is now a widely accepted explanation for aging. Intracellular glutathione is one of the most important antioxi-dants to prevent this oxidative aging process. Various animal studies have found that aged animals have lower glutathione levels in all of their major organs than young animals. This decline in tissue glutathione is associated with a decline in the function of those organs. This same phenomenon has been observed in adults. People with chronic kidney disease have very low levels of glutathione in their kidneys and, as the kidney damage progresses, the ability of the kidney cells to make glutathione decreases even further. This creates a vicious cycle of continued kidney damage.

As we age, our production of glutathione decreases in all cells. Sixty-year olds have significantly less glutathione in their blood than 20-year olds. Also, as we age, we may inadvertently do things which empty out our glutathione stores. Many older people experience various body aches and pains and turn to anti-inflammatory medications for relief. Unfortunately, frequent use of acetaminophen (Tylenol), a commonly used anti-inflam-matory, depletes glutathione. A low glutathione level in older adults wors-ens their health status in many more ways than experiencing pain. Older people with deficient glutathione feel unhealthy overall. This is because the decline in antioxidant protection associated with aging is coupled with the effects of cumulative oxidative damage from a lifetime of exposure to free radicals. The net result is chronic disease and poor health.

The health problems reviewed in this chapter are all conditions which are worsened by free radical-caused oxidative damage. Glutathione is the most prevalent antioxidant in our cells. When glutathione levels become depleted, our cells are even more vulnerable to the ravages of oxidative damage. While the majority of glutathione in our body is made within our cells, in cases of glutathione depletion, boosting glutathione levels from exogenous sources may be necessary.


Chapter 4

The Glutathione-Rich Lifestyle

The majority of glutathione in our body is created within our cells. As I’ve mentioned, glutathione is made by combining three amino acids: glutamic acid, cysteine, and glycine. According to researchers

at Emory University, levels of glutathione vary over the course of the day. Glutathione levels are the highest for about six hours after each meal. Our lowest level of glutathione is in the morning before our first meal. While healthy children and young adults tend to have sufficient glutathione, production of this critical nutrient decreases as we age. Once we reach the age of 45, we begin to produce less glutathione—and we produce less and less as we continue to age. Given this decline, and the multiple health conditions associated with a glutathione deficiency, it is important for adults to compensate for this decreased production by supplementing glutathione in their diet and in the form of supplements. While supple-ments can be an efficient way to increase glutathione stores, creating a glu-tathione-rich foundation with diet and lifestyle will fortify this important antioxidant defense system. Many of the foods that increase glutathione stores do so by providing cells with these precursors to glutathione. Some lifestyle activities have also been found to increase the rate of glutathione production in your body.

Food Sources of GlutathioneGlutathione is found in a variety of foods, particularly fruits, vegetables,

and meats. Foods rich in glutathione include asparagus, spinach, garlic, avocado, squash, zucchini, potatoes, melons, grapefruit, strawberries, and peaches. Some foods contain other compounds which trigger the body’s production of glutathione. For instance, cyanohydroxybutene increases glutathione production and is found in broccoli, cauliflower, Brussels sprouts and cabbage. Herbs such as turmeric, cinnamon, and cardamom contain flavonoid compounds which increase glutathione. Selenium, found in Brazil nuts, meat, and seafood, is also needed to make glutathi-one. Eating just one to two Brazil nuts daily supplies enough selenium for most people. Alpha lipoic acid will increase the production of gluta-thione and it is found in red meat, organ meats (such as liver), and yeast


(particularly Brewer’s yeast). In addition, the B vitamin riboflavin, found in sunflower seeds, spinach, and avocados, is a precursor co-factor for glutathione. Glutathione production depends on its sulphur-containing amino acid, cysteine. Eggs and garlic are good sources of sulphur-contain-ing amino acids. Whey protein is also rich in sulphur-containing amino acids. Undenatured whey protein is a non-heated product that provides intact sulphur-containing amino acids, such as cysteine.

As discussed in the previous chapter, cystic fibrosis is a chronic inflam-matory lung condition caused by a glutathione deficiency in the face of oxidative stress. In a trial of twenty-one individuals with cystic fibrosis, supplementation with whey protein powder increased glutathione levels. These patients took 10 g of whey protein isolate or casein placebo twice a day for three months. Glutathione levels were measured in the patients’ lymphocytes (a type of white blood cell). The people supplementing with whey protein experienced a 46.6 percent increase in their lymphocyte glu-tathione levels. Those supplementing with casein did not see any change. This study demonstrated that dietary supplementation with a whey-based product can increase glutathione levels in cystic fibrosis.

Another randomized placebo-controlled clinical trial studied the use of a fermented food made from fruit, nuts, and vegetables rich in poly-phenols on the immune system in healthy volunteers. By the end of the four-week study, the researchers noted that eating the fermented food significantly enhanced intracellular glutathione levels in all of the white blood cells. In other words, boosting glutathione with this functional food also boosted immunity.

Selenium, found in Brazil nuts, meat, and seafood,

is also needed to make glutathione. Eating just

one to two Brazil nuts daily supplies enough selenium for

most people.


While there are many foods that increase glutathione, there are also some foods that decrease glutathione. Foods like cereal, bread, tea, coffee, and dairy products not only lack glutathione, they destroy it.

Food is an important way to increase glutathione production in the body. There are a variety of foods that provide glutathione or glutathione precursors making it possible for everyone to find some way to enhance the glutathione with their diet. If diet isn’t enough, there are lifestyle options as well.

Lifestyle And GlutathioneYoga and glutathione? As odd as it may sound, the practice of yoga

increases our body’s production of glutathione. This was nicely demon-strated in a recent clinical trial. This study was conducted on healthy male volunteers from the Indian Navy who were divided into two groups—a yoga group and a control group. The yoga group was trained in yoga for six months. The yoga schedule consisted of prayers, asana, pranayama, and meditation. The control group practiced routine physical training exercise, also for six months. Glutathione levels increased significantly (p < 0.05) in the yoga group over the control group after completion of training.

Another way to augment the antioxidant defense system of our body and to protect our glutathione stores is by spending time every day with our body in contact with the earth. The earth is a vast and continuous source of electrons. Free radicals, the cause of oxidative damage, are desperate for

Nutrient to Increase Food Sources

Glutathione Asparagus, spinach, garlic, avocado, squash, zucchini, potatoes, melons, grapefruit, strawberries, and peaches

Seleniuim Brazil nuts, meat, and seafood

Cyanohydroxybutene Broccoli, cauliflower, Brussels sprouts, and cabbage

Alpha lipoic acid Red meat, organ meats (such as liver), and yeast (particularly Brewer’s yeast)

Riboflavin Sunflower seeds, spinach, and avocado

Cysteine Eggs, garlic, and whey protein

Flavonoids Turmeric, cinnamon, and cardamom


electrons. Instead of spending regular time in contact with this enormous source of electrons, we have insulated ourselves from it. One of the worse consequences of modern living is our lack of physical contact with the earth. Most of us spend our days insulated in our rubber soled shoes and living in buildings, sometimes several stories off of the ground. Very few individuals take their shoes and socks off and put their feet on the earth every day. If they did, their bodies would experience an influx of electrons and antioxidant effects. This influx, in turn, would spare our beleaguered antioxidants such as glutathione.

The practice of yoga increases

our body’s production of glutathione.


Chapter 5Increasing Glutathione Production

I f you think you might benefit from glutathione supplementation, you may be interested in first determining if you are low in glutathione. Unfortunately, testing for glutathione is not easy. There are some tests

which purport to measure the glutathione in red blood cells. The problem with these tests is that the blood drawn from the person is transported in a test tube to the central lab and then analyzed some time later. Glu-tathione is a strong antioxidant, but the blood that surrounds it is easily damaged by oxidation as soon as the test tubes are exposed to light. As glutathione soaks up the free radicals formed by this oxidative damage, the amount of glutathione in the red blood cells decreases. This makes these blood tests generally inaccurate. If one has access to a laboratory that can draw the blood and immediately process it for glutathione, the results are more accurate. Additionally, some laboratories offer an assessment of the glutathione detoxification pathway in the liver as part of a detoxification panel. Insufficient glutathione detoxification indicates glutathione defi-ciency. Other laboratories offer urine tests which measure urinary organic acids that provide an indirect assessment of glutathione status. Still other specialized laboratory tests offer a measurement of glutathione function in lymphocytes which may indicate bodily glutathione stores. Although none of these tests are considered the gold standard for evaluating glutathione status, they each provide some indication of overall glutathione levels.

According to John P. Richie, Jr., PhD, professor of Public Health Sci-ences and Pharmacology at Penn State University College of Medicine, glutathione depletion is common and levels can vary substantially from one person to another. He says, “Laboratory findings clearly indicate that oral glutathione supplementation is an efficient means to maintaining optimal glutathione levels.”

The reality is that most of us are somewhat deficient in glutathione—particularly if we are over the age of 45. Certainly, on older individual with one or more of the diseases discussed in Chapter 3 is very likely to be deficient in glutathione. The standard Western diet is devoid of gluta-thione thanks largely to the high amounts of processed foods it contains. As a result, dietary intake of glutathione-rich foods among Americans is low. Studies have found that Americans only consume from 3 to 150 mg


of glutathione per day—and the average intake is 35 mg per day. Optimal intake of glutathione is more than 250 mg per day, so it is easy to see why the average American is deficient in glutathione if the only source is food. This, coupled with decreasing glutathione production as we age, leaves most of us glutathione deficient. Additionally, because glutathione is naturally low in the morning, among people with insufficient overall glutathione, the early morning represents a time of very low glutathione. This translates into a window of vulnerability to oxidative insult. Aug-menting glutathione with supplements, particularly in the morning, may reduce this risk.

The reality is that most of us are somewhat deficient in glutathione—particularly if we are over the age of 45.


Supplements to Increase GlutathioneN-acetyl cysteine: One way to increase glutathione levels is to supple-

ment with glutathione precursors. One of the most effective of these sup-plements is N-acetyl-cysteine (NAC). NAC is derived from the amino acid l-cysteine, and is a precursor to glutathione. NAC is quickly metabolized into glutathione once it enters the body. It has been shown to increase glutathione levels in numerous scientific studies and clinical trials. Of note, NAC is approved by the FDA for the treatment of acetaminophen overdose. Acetaminophen depletes glutathione and rapid depletion as the result of overdose is the cause of the life threatening damage to the liver. NAC is typically taken in doses between 250 mg and 1,500 mg and is well tolerated.

Alpha lipoic acid: Another supplement that will increase glutathione is alpha-lipoic acid (ALA). ALA has demonstrated benefit in a number of diseases including diabetes, drug-induced heart damage, kidney disease, glaucoma, and poorly-healing wounds. It has been studied in doses rang-ing from 300 mg to 1,200 mg daily, although doses above 1,200 mg can cause nausea, vomiting, and dizziness. ALA should not be taken by people with hypothyroidism, thiamine deficiency or concurrently with chemo-therapy drugs unless under medical supervision.

Milk thistle: Milk thistle, or Silymarin officinalis, is an herb that exerts potent antioxidant effects, especially in the liver. A group of flavonoids in milk thistle, collectively referred to as silymarin, is responsible for the antioxidant effects. One of the most important ways milk thistle protects the liver is by preventing the depletion of glutathione. By preserving glu-tathione stores, milk thistle can protect the liver from many industrial toxins such as carbon tetrachloride, as well as alcohol and even the very poisonous Amanita mushroom. Milk thistle supplements are often stan-dardized to contain 70 to 80 percent silymarin. Dosages ranging from 160 to 800 mg of a standardized extract have been studied in the treatment of hepatitis and diabetic cirrhosis. Milk thistle is generally well tolerated and without side effects.

Other nutrients: Other nutrients which help to raise the level of glu-tathione in the body can be supplemented individually. These nutrients include choline, pycnogenol (pine bark extract), vitamin B12, and sele-nium. In addition, supplementation with vitamins C and E will increase glutathione levels. All of these nutrients have other health benefits so, depending upon the health conditions you may have, different supple-ments may be more appropriate.


Chapter 6

Glutathione Supplementation

While supplementing glutathione precursors as a means to increase tissue levels of glutathione can be effective, this does not always work. For instance, numerous studies using NAC to

increase glutathione levels in individuals with COPD failed to show higher concentrations of glutathione in the blood or the lungs, even at doses of 1,800 mg daily. Various aerosol preparations of glutathione have been developed as a way to raise glutathione levels, primarily in the lung. While glutathione levels do increase, glutathione disulfide or oxidized glutathi-one levels increase as well. Glutathione disulfide can be problematic in people with COPD or asthma because this compound increases bronchi-ole constriction, which, in turn, compromises airflow. Furthermore, and rather disappointingly, aerosolized glutathione in some studies has failed to decrease oxidation in the lung.

An alternative way to augment tissue glutathione levels is to supple-ment directly with glutathione. Many healthcare professionals assert that directly supplementing glutathione will not result in increased tissue levels. Because glutathione is a large molecule composed of three amino acids, these individuals believe that glutathione is too big to be absorbed through the intestine and into the blood. Instead, it has been said that orally ingested glutathione is broken down in the intestines and in the liver, and the component amino acids are either eliminated or perhaps used for a variety of other purposes. The truth about what happens to orally administered glutathione appears to be much more complex.

For many years, we have known that dietary glutathione can be absorbed intact in the rat through the upper part of the intestine. Some of orally administered glutathione is, in fact, broken apart into its three main com-ponents (glutamic acid, cysteine and glycine) by a specific enzyme secreted by the intestinal cells. These components are then absorbed into the intes-tinal cell and are re-assembled back into glutathione inside the intestinal cell. The re-assembled glutathione is then either used as an antioxidant within the intestinal cell or is excreted into the blood and transported through the blood to other tissues. Another portion of ingested gluta-thione is transported across the intestinal wall into the blood by specific


transporters in the intestinal cells. This intact glutathione is then distrib-uted to other tissues. In rats, both of these processes occur independently of one another and simultaneously. These animal studies show that the specific transport of glutathione across the intestine is less energy depen-dent, faster and more efficient. This same glutathione transport system has also been observed in human intestinal cells. In fact, the majority of different cell types in the body utilize this transport system to bring glu-tathione from the blood to the inside of cells. The existence of this gluta-thione transporter in human intestinal cells facilitates efficient absorption of glutathione from the intestines into the blood stream. The presence of this same transporter on the cells in other organs, in turn, facilitates the absorption of glutathione into the tissues where it is needed to combat oxidative stress.

This process of glutathione absorption was eloquently demonstrated in a mouse model of cystic fibrosis. In the lung, the glutathione trans-porter protein is known as the cystic fibrosis transmembrane conduc-tance regulator (CFTR) protein. People with cystic fibrosis have a genetic defect in CFTR and are therefore unable to obtain sufficient glutathione in their lung cells. This leaves their lungs unprotected against environmen-tal agents including ozone, particulate matter, nitrogen oxides, cigarette smoke, and microbes. People without cystic fibrosis have very high con-centrations of CFTR in both their lung epithelium and in their intestines as a natural defense against the many inhaled and ingested oxidants.

The importance of CFTR was demonstrated in a study with mice which showed that taking glutathione orally resulted in a rapid increase of gluta-thione in the blood (within 30 minutes) and in the lung (within 60 min-utes). But, when the mice had the CFTR gene removed, glutathione levels did not increase in their blood or lungs. This experiment illustrates the importance of this glutathione transporter protein in the rapid systemic distribution of glutathione.

Other studies have demonstrated the active transport of glutathione across the intestines and into distant organs in animals. In these stud-ies, the brain, kidney, lung, skin, and heart have all been found to have increased glutathione concentrations after the subjects were given oral glutathione. Animal studies have also found that orally administered glu-tathione significantly reduces the development of oxidative diseases such as colon and tongue cancers.

Despite this compelling data, proof of the wide-spread tissue distribu-tion from orally-administered glutathione in humans is yet to be con-firmed. The only human study on oral glutathione found that a dose of 3 gm of glutathione failed to increase the concentrations of glutathione,


cysteine or glutamate in the blood even four hours after the oral ingestion of the glutathione. It should be pointed out, however, that the dose used in this study is much lower than the doses used in the successful animal studies. This human study dose was the equivalent of 50 mg/kg versus the equivalent dose used in animal studies of 100 to 300 mg/kg. Additional human dosage studies are clearly needed. In the meantime, there is sug-gestive evidence that oral glutathione is a reasonable way to provide glu-tathione to the body. “Oral glutathione supplementation is an effective means to enhancing glutathione and protecting against oxidative stress,” concludes Penn State professor, Dr. Richie. “The effectiveness of oral GSH supplementation at increasing blood GSH levels has been documented in humans and controlled clinical trials are underway to better delineate the protective properties of oral GSH supplementation in healthy adults.”

While the most effective daily dose is unknown, preclinical data sug-gests that fairly high levels of this supplement are necessary to produce significant increases in tissue levels of glutathione. Without the guid-ance of human trial data, dosage recommendations for glutathione range from 100 mg to 3,000 mg daily. Too much supplemental glutathione could worsen the body’s own production of glutathione. It would seem most prudent to utilize as many diverse ways of increasing glutathione as possible. Including glutathione-rich foods in the daily diet, avoiding

Coupled with the natural decline of our most prevalent

antioxidant, glutathione, tissue oxidation and the subsequent

diseases seems inevitable—unless we take charge of our

health and commit ourselves to diligently strengthening

our antioxidant defenses.


glutathione-destroying foods, and supplementing with both glutathione precursors and glutathione itself may be an effective strategy to appropri-ately increase tissue glutathione levels. It is also important to remember that the need for glutathione appears to be the greatest in the morning before the first meal of the day, an optimal time for supplementation.

Setria® is a widely studied glutathione ingredient that is available in several different natural health products. This reduced, concentrated pure form of L-glutathione is made available through Kyowa Hakko Bio Co Ltd., a world leader in the development, manufacturing, and marketing of pharmaceuticals, nutraceuticals, and food products.

In general, glutathione appears to be a safe supplement. There have been no reported adverse reactions to supplemental glutathione taken orally, inhaled, used intramuscularly or intravenously. However, people with cancer should not supplement with glutathione because, theoreti-cally, it may stimulate the growth of existing cancerous tumors. Doses of 3 g of oral glutathione have been used experimentally with no adverse effects. The long-term effects of glutathione supplementation at any level are unknown. Glutathione is not recommended for children and is unlikely to be of benefit to young adults.

Final ThoughtsThe seemingly inevitable march of aging seems fraught with degenera-

tive diseases and ill health. This unhealthy aging is, for the most part, the result of accumulating oxidative damage. Free radicals produced during the normal course of the activities of daily living combined with those produced from environmental pollutants slowly but surely overwhelm our body’s antioxidative defenses. Coupled with the natural decline of our most prevalent antioxidant, glutathione, tissue oxidation and the subse-quent diseases seems inevitable—unless we take charge of our health and commit ourselves to diligently strengthening our antioxidant defenses. Including glutathione-rich foods in our diet, spending time in contact with the earth, and supplementing with glutathione precursors and gluta-thione itself will help to rebuild our antioxidant protection. Although we may not be able to reverse aging, we can certainly help ourselves age with more health and vitality.


Selected ReferencesAndreazza AC, Kauer-Sant’anna M, Frey BN, et al. Oxidative stress markers in bipolar disorder: a meta-analysis. Journal of Affective Disorders 111(2-3):135-44, Dec 2008.

Aw TY, Wierzbicka G, Jones DP. Oral glutathione increases tissue glutathione in vivo. Chemico-Biological Interactions 80:89-97, 1991.

Berk M, Copolov D, Dean O, et al. N-acetyl cysteine as a glutathione precursor for schizophrenia--a double-blind, randomized, placebo-controlled trial. Biological Psychiatry 1;64(5):361-8, Sep 2008.

Darmaun D, Smith SD, Sweeten S, et al. Poorly controlled type 1 diabetes is associated with altered glutathione homeostasis in adolescents: apparent resistance to N-acetylcysteine supplementation. Pediatrics Diabetes 9(6):577-82, Dec 2008.

Favilli F, Marraccini P, Iantomasi T, et al. Effect of orally administered glutathione on glutathione levels in some organs of rats: role of specific transporters. British Journal of Nutrition 78:293-300, 1997.

Flagg EW, Coates RJ, Jones DP, et al. Dietary glutathione intake and the risk of oral and pharyngeal cancer. American Journal of Epidemiology 139(5):453-65, Mar 1994.

Fleming JE, Miquel J, Benschk G. Age-dependent changes in mitochondria. Molecular Biology of Aging. Plenum, New York, 143-155, 1985.

Franco R, Schoneveld OJ, Pappa A, et al. The central role of glutathione in the pathophysiology of human diseases. Archives of Physiology and Biochemistry 113(4-5):234-58, Oct-Dec 2007.

Grey V, Mohammed SR, Smountas AA, et al. Improved glutathione status in young adult patients with cystic fibrosis supplemented with whey protein. Journal of Cystic Fibrosis 2(4):195-8, Dec 2003.

Gumral N, Naziroglu M, Ongel K, et al. Antioxidant enzymes and melatonin levels in patients with bronchial asthma and chronic obstructive pulmonary disease during stable and exacerbation periods. Cell Biochemistry and Function 27(5):276-83, Ju 2009.

Hagen TM, Wierzbicka GT, Sillau AH, et al. Bioavailability of dietary glutathione: effect on plasma concentration. American Journal of Physiology. 259: G524-9, 1990.

Harman, D. Free radical theory of aging: an update: increasing the functional life span. Annals of the New York Academy of Science 1067:10-21, May 2006.

Hung HC, Joshipura KJ, Jiang R, et al. Fruit and vegetable intake and risk of major chronic disease. Journal of the National Cancer Institute 96(21):1577-84, Nov 2004.

Hunjan MK and DF Evered, Absorption of glutathione from the gastro-intestinal tract. Biochimica et biophysica acta. 815:184-8, 1985.

Iantomasi T, Favilli F, Marraccini P, et al. Glutathione transport system in human small intestine epithelial cells. Biochimica et biophysica acta.1330:274-83, 1997.

Jagatha B, Mythri RB, Vali S, et al. Curcumin treatment alleviates the effects of glutathione depletion in vitro and in vivo: therapeutic implications for Parkinson’s disease explained via in silico studies. Free Radical Biology & Medicine. Mar 1, 2008.

Jones, DP, et al. Oral administration of glutathione (GSH) increases plasma GSH concentration in humans. FASEB J 3:A1250, 1989.

Julius M, Lang CA, Gleiberman L, et al. Glutathione and morbidity in a community-based sample of elderly. Journal of Clinical Epidemiology 47(9):1021-6, Sep 1994.


Kariya C, Leitner H, Min E, et al. A role for CFTR in elevation of glutathione levels in the lung by oral glutathione administration. American Journal of Physiology–Lung Cellular and Molecular Physiology. 292:L1590-7, 2007.

Köksal H, Rahman A, Burma O, et al. The effects of low dose N-acetylcysteine (NAC) as an adjunct to cardioplegia in coronary artery bypass surgery. Anadolu kardiyoloji dergisi 8(6):437-43, Dec 2008.

Lin CC, Yin MC. Vitamins B depletion, lower iron status and decreased antioxidative defense in patients with chronic hepatitis C treated by pegylated interferon alfa and ribavirin. Clinical Nutrition 28(1):34-8 Feb 2009.

Oschman JL. Perspective: assume a spherical cow: the role of free or mobile electrons in bodywork, energetic and movement therapies. Journal of Bodywork and Movement Therapies 12(1):40-57, Jan 2008.

Marc RE, Jones BW, Watt CB, et al. Extreme retinal remodeling triggered by light damage: implications for age related macular degeneration. Molecular Vision 14:782-806, Apr 2008.

Melo JB, Sousa C, Garção P, et al. Galantamine protects against oxidative stress induced by amyloid-beta peptide in cortical neurons. European Journal of Neuroscience 29(3):455-64, Feb 2009.

Richie JP Jr, Kleinman W, Marina P, et al. Blood iron, glutathione, and micronutrient levels and the risk of oral cancer. Nutrition & Cancer 60(4):474-82, 2008.

Schoen C, Schulz A, Schweikart J, et al. Regulatory effects of a fermented food concentrate on immune function parameters in healthy volunteers. Nutrition 25(5):499-505, May 2009.

Sinha S, Singh SN, Monga YP, et al. Improvement of glutathione and total antioxidant status with yoga. Journal of Alternative and Complementary Medicine 13(10):1085-90 Dec 2007.

Schwartz, JL, Shklar, G. Glutathione inhibits experimental oral carcinogenesis, p53 expression, and angiogenesis. Nutr Cancer 26:229-36, 1996.

Valavanidis A, Fiotakis K, Vlachogianni T. Airborne particulate matter and human health: toxicological assessment and importance of size and composition of particles for oxidative damage and carcinogenic mechanisms. Journal of Environmental Science and Health. Part C, Environmental Carcinogenesis & Ecotoxicology Reviews. 26(4):339-62, Oct-Dec 2008.

Vazquez-Chona F, Vaughan DK, Organisciak DT, et al.The systemic availability of oral glutathione. European Journal of Clinical Pharmacology. 43: 667–669, 1992.

Wang Y, Zhang L, Moslehi R, et al. Long-term garlic or micronutrient supplementation, but not anti-Helicobacter pylori therapy, increases serum folate or glutathione without affecting serum vitamin B-12 or homocysteine in a rural Chinese population. Journal of Nutrition 139(1):106-12; Jan 2009.

Zachara BA, Gromadzinska J, Zbrog Z, et al. Selenium supplementation to chronic kidney disease patients on hemodialysis does not induce the synthesis of plasma glutathione peroxidase. Acta biochimica Polonica 56(1):183-7, 2009.

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This booklet provides a comprehensive picture of one of the most complex, yet important, nutrients available. Author and clinician Lise Alschuler, ND, reveals that glutathione

deficiency has been linked to some of the most debilitating diseases of our time including Alzheimer’s, Parkinson’s, hepatitis, cystic fibrosis, cancer, heart disease, asthma, diabetes, and others. Dr. Alschuler explains, “Glutathione deficiency allows oxidative damage to accelerate the progression of these conditions.” She shows readers how they can shore up their stores of glutathione through a combination of diet, lifestyle, and dietary supplements.

THE SUPREME ANTIOXIDANT

Lise Alschuler, ND, FABNO, is a naturopathic physician with board certification in naturopathic oncology. She practices naturopathic oncology at Naturopathic Specialists, LLC, in Scottsdale, Ariz. Dr. Alschuler has authored many articles in professional and popular press publications and is the coauthor of the Definitive Guide to Cancer: An Integrative Approach to Prevention, Treatment and Healing. She currently serves as president of the American Association of Naturopathic Physicians.

ABOUT THE AUTHOR OF THIS BOOKLET

GLUTATHIONE

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Glutathione

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Transcript of Glutathione