Glutathione Activation

Glutathione is an important tripeptide (ie, made from cysteine, glycine, and glutamic acid) molecule multiple roles from protecting cells from mercury and other toxic metal, to protection from hard alcohol, persistent organic pollutants and more while it’s antioxydant activities. In this Page, i  will delve into Gluthatione’s biological process (Section A) and then zero in on its major benefits (Section B) and conclude on how to activate it (Section C)

Section A

Glutathione Physiology, Production, and Recycling

Glutathione (GSH) is an important antioxidant in plants, animals, fungi, and some bacteria and archaea. Glutathione is capable of preventing damage to important cellular components caused by reactive oxygen species such as free radicals, peroxides, lipid peroxides, and heavy metals. It is a tripeptide with a gamma peptide linkage between the carboxyl group of the glutamate side chain and the amine group of cysteine, and the carboxyl group of cysteine is attached by normal peptide linkage to a glycine. Glutathione is a  found in surprisingly high levels—5 millimolar—concentrations in most cells. This is the same concentration in cells as glucose, potassium, and cholesterol! Considering the high level of metabolic activity required to produce glutathione, such a high level underlines its importance. (Source)

Once oxidized, glutathione can be reduced back by glutathione reductase, using NADPH as an electron donor. The ratio of reduced glutathione to oxidized glutathione within cells is often used as a measure of cellular oxidative stress. (1)

GGT as Measure of Glutathione Need

GGT (gamma-glutamyl transferase) is upregulated in proportion to the need for glutathione such as for the detoxification of POPs. (Source). It provides the rate-limiting cysteine through a catabolic “salvage pathway.” Increases in GGT correlate with many diseases: metabolic syndrome, both fatal and nonfatal coronary heart disease (CHD) events, atherosclerosis, fatty liver, diabetes, cancer, hypertension, and carotid intima-media thickness. (Source) Research also shows a GGT 30 to 40—well within the normal range—is associated with a doubling of the risk of all-cause mortality. (Source).

Section B

 Glutathione’s role in increasing Detoxification and decreasing Inflammation and Oxidative stress

Glutathione is an important detox molecule with multiple roles from protecting cells from mercury and other toxic metals, to protection from hard alcoho and protection from persistent organic pollutants (POPs). Some of Glutathion’s key biological processes are summarized in the latter part of this paragraph. It plays a crucial role in shielding cellular macromolecules from endogenous and exogenous reactive oxygen and nitrogen species. While it directly quenches some free radicals, it deals directly with the causes of oxidative stress such as mercury and POPs. The benefits are as follows: Direct chemical neutralization of singlet oxygen, hydroxyl radicals, and superoxide radicals Cofactor for several antioxidant enzymes Regeneration of vitamins C and E Neutralization of free radicals produced by Phase I liver metabolism of chemical toxins One of approximately 7 liver Phase II reactions, which conjugate the activated intermediates produced by Phase I to make them water soluble for excretion by the kidneys Transportation of mercury out of cells and the brain Regulation of cellular proliferation and apoptosis Vital to mitochondrial function and maintenance of mitochondrial DNA (mtDNA). (Source)  The bottom line is that Glutathione is involved in the detoxification of both xenobiotic and endogenous compounds. It facilitates excretion from cells (Hg, mercury), facilitates excretion from body (POPs, Hg) and directly neutralizes (POPs, many oxidative chemicals). Glutathione facilitates the plasma membrane transport of toxins by at least 4 different mechanisms, the most important of which is formation of glutathione S-conjugates.

Low levels of glutathione and/or transferase activity are also associated with chronic exposure to chemical toxins and an abuse in alcohol, especially hard alcohol and bad quality wine taken in excessive amounts, cadmium exposure, AIDS/HIV, macular degeneration, Parkinson’s disease, and other neurodegenerative disordersGlutathione directly scavenges diverse oxidants: superoxide anion, hydroxyl radical, nitric oxide, and carbon radicals. Glutathione catalytically detoxifies: hydroperoxides, peroxynitrites, and lipid peroxides (2) Another way glutathione protects cells from oxidants is through recycling of vitamins C and E. Glutathione depletion triggers apoptosis, although it is unclear whether it is mitochondrial or cytosol pools of GSH that are the determining factor. (3)

Another importance of glutathione is that its cellular and mitochondrial levels directly are highly associated with health and longevity. Depletion of GSH has been implicated in many chronic degenerative diseases, including, but not limited to the following: Neurodegenerative disorders (Alzheimer’s, Parkinson’s, and Huntington’s diseases, amyotrophic lateral sclerosis, Friedreich’s ataxia) Pulmonary disease (COPD, asthma, and acute respiratory distress syndrome) Immune diseases (HIV, autoimmune disease) Cardiovascular diseases (hypertension, myocardial infarction, cholesterol oxidation) Chronic age-related diseases (cataracts, macular degeneration, hearing impairment, and glaucoma) Liver disease Cystic fibrosis Aging process itself.  (Source)

GSH depletion has also been strongly associated with the diseases and loss of function with aging. A representative study of community-dwelling elderly found that higher glutathione levels were associated with higher levels of physical health, fewer illnesses, and higher levels of self-rated health. (4)

Gluthation’s Longevity Boost Impact

With regard to Longevity medicine,  GSH status has been found to parallel telomerase activity, an important indicator of lifespan. (5). This depletion of GSH also shows up as progressive loss of mitochondrial function due to accumulation of damage to mtDNA(6). The ability of animal species to protect their mtDNA is directly proportional to longevity (7).

Section C

Holistic Techniques to Increase Intracellular and Intramitochondrial Glutathione

Direct administration and promotion of production of glutathione have been used effectively in a wide range of diseases, includuing, but not limited to cancer, accelerated aging, Parkinson’s, peripheral obstructive arterial disease, cystic fibrosis, emphysema, COPD, preterm infants autism, contrast-induced nephropathy, chronic otitis media, lead exposure, nail biting, nonalcoholic fatty liver disease, exercise-induced fatigue, the list is long. Considering how important glutathione is to health, many researchers have looked for ways to increase intracellular and intramitochondrial levels.

The first approach is to decrease the need for glutathione, which means decreasing toxic load, from mercury to POP, hard alcohol etc (Source)

Second step is to the Government’s certified GMO conventional grown toxic food, as conventionally grown foods has been seen to be a major cause to gluthatione depletion (8)

A third step is to provide other antioxidants to decrease oxidative stress. A good example is α-lipoic acid, supplementation of which increases mitochondrial glutathione levels even though ALA is not used in the synthesis or recycling of glutathione. (9)

A fourth step is to directly administer glutathione. This can be done orally, topically, intravenously, intranasally, or in nebulized form or even liposomal. Glutathione administered intravenously, inhaled, and ingested intranasally increases systemic levels. (10) IV glutathione has a short half-life but has shown at least short-term efficacy in several diseases. Oral administration is controversial; while most research shows that oral glutathione does not increase RBC glutathione, there are a few studies that show efficacy. (11)  My opinion is that unmodified oral glutathione is unlikely to consistently elevate cellular levels. Oral and transdermal liposomal glutathione show promise, but research is premature. (12)

The fifth step is to provide specific nutrients to promote glutathione production. As noted above, cysteine availability is the rate-limiting step in the de novo production of glutathione. While oral cysteine does not make it through the digestive track, supplemental cysteine in the form of whey or N-acetylcysteine (NAC) is effective at raising levels. While there is substantial variation, 800 mg/d of NAC will substantially increase glutathione in virtually all patients without side or toxic effects. So the H.M. Institute recomments this posoloty of NAC (to be determined with the patient’s health provider) when chronic dieases sets in, unless the patient opts for chemo. (13)

Starting doses for the first 4 cohorts of 3 subjects were 400, 800, 1600, and 3200 mg/m2/day in divided doses doubled at the end of each month in the absence of toxicity to a final dose of 6400 mg/m2/day. The total planned period on NAC for each subject was 6 months. Pharmacokinetic and pharmacodynamic measurements were carried out at the beginning of the study and at the end of each month. The second stage of the study consisted of a daily dose of 800 mg/m2/day. During this part of the study, NAC in plasma and GSH and oxidized glutathione reductase (GRD) in PBL were measured on day 1 and again at the end of first, second, and sixth month on NAC. Major toxicities were bad taste and gastrointestinal disturbances. The highest nontoxic dose was 800 mg/m2/day in most of the subjects. (Source) 

For the rare patient who reacts to NAC, SAMe can be used. (14) Methionine is not recommended  as it will increase homocysteine. Interestingly, supplementing with NAC (600 mg/d for 4 wk) decreases GGT 25%, suggesting that increasing de novo synthesis decreases the need for GGT recycling. (15) For those looking for a nonsupplemental solution, 500 mL of alcohol-free beer per day raises RBC glutathione 29%! (16) Contrarily to most mainstream and even integrative beliefs, even small amounts of wine can help to increase gluthatione’s anti-oxidant and the microbiome’s favorable role. But quality traditional wine, especially red which is rich in polyphenols that the microbiome cherishes. Wine’s yeast for example was shown to up regulate longevity genes. (Source)

Sixth step: While certain foods like avocados and nuts are high in gluthatione, their bioavailability is not great. On the other hand, mushrooms bioavailability is better. (Source) If only because they are taking in holistically with both its major compounds combined, ergothioneine and glutathione even if cooked.

According to the researchers, who report their findings in a recent issue of Food Chemistry, the amounts of ergothioneine and glutathione in mushrooms vary by species with the porcini species, a wild variety, containing the highest amount of the two compounds among the 13 species tested”. (Source)

Seventh step: Heliotherapy (helio = sunlight) Calcitriol (1,25-dihydroxyvitamin D3), the active metabolite of vitamin D3, after being synthesized from calcifediol in the kidney, increases glutathione levels in the brain and appears to be a catalyst for glutathione production. (Source).  It takes about ten days for the body to process vitamin D3 into calcitriol. (Source). So for those who are in need of Sun therapy or vitamin D2 therapy, a good ten days is recommended.

8 . Increase methylation nutrients.

Vitamins B6, B12 and Folate (also known as B9) are important nutrients in glutathione production. The best food sources of these B vitamins are fish, spinach, asparagus, turnip greens, avocado, sunflower seeds, dark leafy greens, papaya, oranges, cantaloupe, and legumes.

9. Boost Selenium This mineral plays an important role in helping the body both produce and recycle glutathione. The best food sources of selenium are Brazil nuts, sunflower seeds, oatmeal (gluten-free),  and brown rice.

10. Cysteine rich Foods. For those who tolerate dairy well, raw organic milk and raw non-denatured whey protein may be helpful in supplying cysteine, which is considered the most important of the three building blocks of glutathione. The H.M institute generally recommends to avoid dairy, but in certain cases, the benefits may outweigh the risks when it comes to glutathione production and a few other conditions. Cysteine must come from food since our bodies cannot produce it and the two best sources are raw milk and bioactive, non-denatured whey protein. Since heat and cooking destroy the cysteine, it is important that the source is raw.

11. Boost glutamine rich foods and prioritize a Mediterranean and-or vegan type diet, depending on the person’s uniqueness. Glutamine is plentiful in plants and meats but is easily destroyed by heat.  Eating fresh, raw parsley and spinach is a good start.

There are many other examples of foods and holistic procedures to increase glutathione. For example, 83 g/d of almonds increases glutathione in smokers by 16% and decreases their DNA damage by 29%. (17) Other glutathione boosting foods: Garlic Blackstrap molasses Raw red beets Okra Squash Pumpkin seeds Sesame seeds Walnuts Tomato Carrot Dill Mushrooms Shellfish Grapefruit Orange Zucchini Strawberry Quinoa Buckwheatà Spiruline

12. Spices: Turmeric, cinnamon, and cardamom are three spices that are helpful for restoring glutathione levels.

13. Relaxation, sleep and exercises: Minimizing stress is key in preventing depletion of glutathione. Practice stress-reducing activities like deep breathing, meditation, yoga and leisure walking as often as possible. Sometimes a few minutes of stretching and deep breathing before bed can help you wind down, reduce stress hormone production, and contribute to a more restful nights’ sleep.

Sleep is a crucial component in the body’s ability to heal and produce sufficient glutathione. Studies show that glutathione levels were significantly reduced in the brains of sleep-deprived animals, so try to get as much quality sleep as possible and take naps when necessary.

Melatonin is a hormone that is released at night time and acts to regulate sleep. It is a powerful antioxidant that has been shown to increase glutathione levels in the brain, liver, muscle tissue and blood. Sour cherries, especially Montmorency cherries are a great food source of melatonin.

Exercise also boosts glutathione production and improves the body’s ability to detoxify. Start slowly by doing gentle exercise and work your way up to 30 minutes a day of sports or more vigorous exercise such as hiking or biking. Resistance training for 20-40 minutes is also effective and will help increase and maintain lean muscle mass

14. Meditation: And then there is meditation, practitioners have 20% higher levels of glutathione. (18) . These examples suggest that holistic lifestyle is key.

15. Broccoli Sprouts: Induction of phase 2 detoxication enzymes (e.g., glutathione transferases, epoxide hydrolase, NAD(P)H: quinone reductase, and glucuronosyltransferases) is a powerful strategy for achieving protection against carcinogenesis, mutagenesis, and other forms of toxicity of electrophiles and reactive forms of oxygen. Since consumption of large quantities of fruit and vegetables is associated with a striking reduction in the risk of developing a variety of malignancies, it is of interest that a number of edible plants contain substantial quantities of compounds that regulate mammalian enzymes of xenobiotic metabolism. Thus, edible plants belonging to the family Cruciferae and genus Brassica (e.g., broccoli and cauliflower) contain substantial quantities of isothiocyanates (mostly in the form of their glucosinolate precursors) some of which (e.g., sulforaphane or 4-methylsulfinylbutyl isothiocyanate) are very potent inducers of phase 2 enzymes. (Source) 3-day-old sprouts of cultivars of certain crucifers including broccoli and cauliflower contain 10-100 times higher levels of glucoraphanin (the glucosinolate of sulforaphane) than do the corresponding mature plants. Glucosinolates and isothiocyanates can be efficiently extracted from plants, without hydrolysis of glucosinolates by myrosinase (…)  Hence, small quantities of crucifer sprouts may protect against the risk of cancer as effectively as much larger quantities of mature vegetables of the same variety. (Source)

 Bioavailability and supplementation

As we noted, systemic bioavailability of orally consumed glutathione is poor because the molecule, a tripeptide, is the substrate of proteases (peptidases) of the alimentary canal, and due to the absence of a specific carrier of glutathione at the level of cell membrane. (19).

Because direct supplementation of glutathione is not always successful, supply of the raw nutritional materials used to generate GSH, such as cysteine and glycine, may be more effective at increasing glutathione levels. Other antioxidants such as ascorbic acid (vitamin C) may also work synergistically with glutathione, preventing depletion of either. The glutathione-ascorbate cycle, which works to detoxify hydrogen peroxide (H2O2), is one very specific example of this phenomenon.

Additionally,  as we saw, compounds such as N-acetylcysteine (20)  (NAC) and alpha lipoic acid (21) (ALA, not to be confused with the unrelated alpha-linolenic acid) are both capable of helping to regenerate glutathione levels. NAC in particular is commonly used to treat overdose of acetaminophen, a type of potentially fatal poisoning which is harmful in part due to severe depletion of glutathione levels.

S-adenosylmethionine (SAMe), a cosubstrate involved in methyl group transfer, has also been shown to increase cellular glutathione content in persons suffering from a disease-related glutathione deficiency. (22).

Case in Point: Cancer

Low glutathione is commonly observed in wasting and negative nitrogen balance, as seen in cancer, HIV/AIDS, sepsis, trauma, burns, and athletic overtraining. Low levels are also observed in periods of starvation. These effects are hypothesized to be influenced by the higher glycolytic activity associated with cachexia, which result from reduced levels of oxidative phosphorylation. (23)

However, once a tumor has been established, elevated levels of glutathione may act to protect cancerous cellsby conferring resistance to chemotherapeutic drugs. The antineoplastic mustard drug canfosfamide was modelled on the structure of glutathione. So for those patients on  cytotoxic chemo, we don’t recommend taking Glutathione. (24)

Discussion

Glutathione is a simple molecule made up of three amino acids – cysteine, glycine and glutamine. This simple molecule packs a seriously healing punch and is essential for proper immune function, detoxification, and controlling inflammation in the body.

For patients struggling with fatigue and chronic illness, maximizing glutathione is a top priority. Insufficient glutathione prevents the mitochondria (the power house of the cell) from producing ATP which is the primary source of energy for all living cells. Without the ability to make sufficient ATP, we feel exhausted and our body’s ability to heal is greatly reduced.

Not only is glutathione our body’s main antioxidant, protecting our cells from oxidative stress and facilitating energy production, it is the most critical component in our bodies’ detoxification system. It acts like a magnet to grab toxins and free radicals, delivering them into the bile and stool for safe removal from the body. Normally glutathione is recycled in the body, providing continuous protection from oxidative stress or toxicity, but when our bodies accumulate too high a toxic load, this process is inhibited.

 

Conclusion

Strong Bio-availability of glutathione is critical for maintaining health, protecting the body from toxins, and promoting longevity. Fortunately, there is much we can do to optimize glutathione levels including eating mushrooms. In contradistinction from the human, animal and plant Kingdoms, the fungi Kingdom has biologically evolved as a species along side humans, have used these ancestral foods for millions of years, they are easy to pick and eat. Both the French and the Italians are avid mushroom hunters, which may partially explain why they do better than the US in terms of healthy lifespans.

Ch. Joubert (H.M. Institute Director)

Reference and Precision Notes

(1).  Thiol groups are reducing agents, existing at a concentration around 5 mM in animal cells. Glutathione reduces disulfide bonds formed within cytoplasmic proteins to cysteines by serving as an electron donor. In the process, glutathione is converted to its oxidized form, glutathione disulfide (GSSG), also called L-(–)-glutathione.
(2). Marí M, Morales A, Colell A, García-Ruiz C, Fernández-Checa JC. Mitochondrial glutathione, a key survival antioxidant. Antioxid Redox Signal. 2009;11(11):2685–2700. doi: 10.1089/ARS.2009.2695. [PMC free article] [PubMed] [Cross Ref
(3). Marí Marí M, Morales A, Colell A, García-Ruiz C, Fernández-Checa JC. Mitochondrial glutathione, a key survival antioxidant. Antioxid Redox Signal. 2009;11(11):2685–2700. doi: 10.1089/ARS.2009.2695. [PMC free article] [PubMed] [Cross Ref]
(4). Julius M, Lang CA, Gleiberman L, Harburg E, DiFranceisco W, Schork A. Glutathione and morbidity in a community-based sample of elderly. J Clin Epidemiol. 1994;47(9):1021–1026. [PubMed]
(5). Borrás C, Esteve JM, Viña JR, Sastre J, Viña J, Pallardó FV. Glutathione regulates telomerase activity in 3T3 fibroblasts. J Biol Chem. 2004;279(33):34332–34335. [PubMed]
(6). Wei YH, Ma YS, Lee HC, Lee CF, Lu CY. Mitochondrial theory of aging matures—roles of mtDNA mutation and oxidative stress in human aging. Zhonghua Yi Xue Za Zhi (Taipei) 2001;64(5):259–270. [PubMed]
(7). Barja G, Herrero A. Oxidative damage to mitochondrial DNA is inversely related to maximum life span in the heart and brain of mammals. FASEB J. 2000;14(2):312–318. [PubMed]
(8).  Pizzorno J. The path ahead: persistent organic pollutants (POPs)—a serious clinical concern. Integrative Med Clin J. 2013;12(2):8–11. Dr Pissorno is one of the major authorities on Gluthatione, the Happiness Medicine Institute recommends reading him as he has a holistic and naturopathic approach.
(9).  M, Ingersoll RT, Lykkesfeldt J, et al. (R)-alpha-lipoic acid-supplemented old rats have improved mitochondrial function, decreased oxidative damage, and increased metabolic rate. FASEB J. 1999;13(2):411–418. [PubMed]
(10). Buhl R, Vogelmeier C, Critenden M, et al. Augmentation of glutathione in the fluid lining the epithelium of the lower respiratory tract by directly administering glutathione aerosol. Proc Natl Acad Sci U S A. 1990;87(11):4063–4067. [PMC free article] [PubMed]
(11). Allen J, Bradley RD. Effects of oral glutathione supplementation on systemic oxidative stress biomarkers in human volunteers. J Altern Complement Med. 2011;17(9):827–833. [PMC free article] [PubMed]
(12). Kern JK, Geier DA, Adams JB, Garver CR, Audhya T, Geier MR. A clinical trial of glutathione supplementation in autism spectrum disorders. Med Sci Monit. 2011;17(12):CR677–CR682. [PMC free article] [PubMed]
(13). Pendyala L, Creaven PJ. Pharmacokinetic and pharmacodynamic studies of N-acetylcysteine, a potential chemopreventive agent during a phase I trial. Cancer Epidemiol Biomarkers Prev. 1995;4(3):245–251. [PubMed]
(14). Liber CS, Packer L. S-Adenosylmethionine: molecular, biological, and clinical aspects—an introduction. Am J Clin Nutr. 2002;76(5):1148S–1150S. [PubMed]
(15). Pamuk GE, Sonsuz A. N-acetylcysteine in the treatment of non-alcoholic steatohepatitis. J Gastroenterol Hepatol. 2003;18(10):1220–1221. [PubMed]
(16). Martínez Alvarez JR, Bellés VV, López-Jaén AB, Marín AV, Codoñer-Franch P. Effects of alcohol-free beer on lipid profile and parameters of oxidative stress and inflammation in elderly women. Nutrition. 2009;25(2):182–187. [PubMed]
(17). Li N, Jia X, Chen CY, et al. Almond consumption reduces oxidative DNA damage and lipid peroxidation in male smokers. J Nutr. 2007;137(12):2717–2722. [PubMed]
(18). Sharma H, Datta P, Singh A, et al. Gene expression profiling in practitioners of Sudarshan Kriya. J Psychosom Res. 2008;64(2):213–218. [PubMed]
(19). Allen J, Bradley RD (September 2011). “Effects of oral glutathione supplementation on systemic oxidative stress biomarkers in human volunteers”Journal of Alternative and Complementary Medicine17 (9): 827–33. doi:10.1089/acm.2010.0716PMC 3162377 . PMID 21875351. And: Witschi A, Reddy S, Stofer B, Lauterburg BH (1992). “The systemic availability of oral glutathione”. European Journal of Clinical Pharmacology43 (6): 667–9. doi:10.1007/bf02284971PMID 1362956.
(20) “Acetylcysteine Monograph for Professionals – Drugs.com”.
(21).  Zhang J, Zhou X, Wu W, Wang J, Xie H, Wu Z (2017). “Regeneration of glutathione by α-lipoic acid via Nrf2/ARE signaling pathway alleviates cadmium-induced HepG2 cell toxicity”. Environ Toxicol Pharmacol51: 30–37.. PMID 28262510
(22).  Lieber CS (November 2002). “S-adenosyl-L-methionine: its role in the treatment of liver disorders”. The American Journal of Clinical Nutrition76 (5): 1183S–7S. PMID 12418503 :  And: Vendemiale G, Altomare E, Trizio T, Le Grazie C, Di Padova C, Salerno MT, Carrieri V, Albano O (May 1989). “Effects of oral S-adenosyl-L-methionine on hepatic glutathione in patients with liver disease”. Scandinavian Journal of Gastroenterology24 (4): 407–15 PMID 2781235. And Loguercio C, Nardi G, Argenzio F, Aurilio C, Petrone E, Grella A, Del Vecchio Blanco C, Coltorti M (September 1994). “Effect of S-adenosyl-L-methionine administration on red blood cell cysteine and glutathione levels in alcoholic patients with and without liver disease”. Alcohol and Alcoholism29 (5): 597–604. doi:10.1093/oxfordjournals.alcalc.a045589PMID 7811344.
(23).  Dröge W, Holm E (November 1997). “Role of cysteine and glutathione in HIV infection and other diseases associated with muscle wasting and immunological dysfunction”FASEB Journal11 (13): 1077–89. PMID 9367343. AND: Tateishi N, Higashi T, Shinya S, Naruse A, Sakamoto Y (January 1974). “Studies on the regulation of glutathione level in rat liver”Journal of Biochemistry75 (1): 93–103. doi:10.1093/oxfordjournals.jbchem.a130387PMID 4151174.
(24). Balendiran GK, Dabur R, Fraser D (2004). “The role of glutathione in cancer”. Cell Biochemistry and Function. 22 (6): 343–52. doi:10.1002/cbf.1149. PMID15386533.

General References

Vesce, S et al. Acute Glutathione Depletion Restricts Mitochondrial ATP Export in Cerebellar Granule Neurons

Phytochemicals – Sulforaphane

Hayes, JD, McLelland LI. – Glutathione and glutathione-dependent enzymes represent a co-ordinately regulated defence against oxidative stress.

Hyman, M. – Glutathione: The Mother of All Antioxidants

ImmuneHealthScience.com – Glutathione Foods

ImmuneHealthScience.com – How to Raise Glutathione Levels

D’Almeida, Vânia, et al. – Sleep deprivation induces brain region‐specific decreases in glutathione levels

Mandal, A. – What is Oxidative Stress?

Vitamin B12 on Nutri-Facts.org

Harvard School of Public Health Nutrition Source – Three of the B Vitamins: Folate, Vitamin B6, and Vitamin B12

Biswas, SK, et al. – Curcumin Induces Glutathione Biosynthesi

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