Glutathione, the Master Antioxidant
Share this post
Does supplementation really increase glutathione levels?
Scientists have been trying to understand the aging process for, well, ages. One thing we know for sure is that oxidative stress plays a major role in the aging process, and a powerful antioxidant known as glutathione helps fight that oxidative stress.,
Oxidative stress is a process that occurs within our cells and tissues similar to the process that causes apples to turn brown or oils to go rancid. Cells produce metabolic byproducts known as reactive oxygen species (ROS). The term “reactive” means that these forms of oxygen can react with (bind to) proteins, lipids, and/or DNA, causing them to become oxidized. Excessive oxidation can cause permanent damage to cell structure and function, eventually leading to cell death.,,
When cell death occurs in the brain, it may increase the risk of neurodegenerative diseases, including Alzheimer’s and Parkinson’s.,,, In the heart, cell damage can increase the risk of heart disease.,, And that’s not all: oxidative stress is also associated with lung disease, non-alcoholic fatty liver disease (NAFLD),, high blood pressure, diabetes,, glaucoma, macular degeneration, and viral and mycobacterial infections.,,,
A decline in GSH levels contributes to oxidative stress, and it’s abundantly clear that GSH levels decline with age.
This is why glutathione (GSH), the master antioxidant in human cells, is vitally important. The beneficial effects of GSH are a result of its direct ROS scavenger action as well as its ability to support the activity of GSH-peroxidase, a selenium-containing enzyme that defends against peroxides, a form of ROS.
A decline in GSH levels contributes to oxidative stress, and it’s abundantly clear that GSH levels decline with age.,, Low GSH levels are also associated with vitamin D deficiency, and vitamin D supplementation may not correct vitamin D deficiency unless GSH is first restored. Smoking,,, alcohol use, eating an unhealthy diet, exposure to environmental and air pollutants,, , and use of certain medications also deplete GSH and increase oxidative stress.
For all these reasons, some scientists have suggested that increasing cellular levels of GSH may help preserve health and slow the aging process. The key question then becomes: is it possible to increase the body’s GSH levels?
N-acetylcysteine: a glutathione precursor
GSH is made from the amino acids cysteine, glycine, and glutamine. Low levels of cysteine within cells can thus limit the ability of cells to make their own GSH during times of oxidative stress., A supplement known as N-acetylcysteine (NAC), which is metabolized to cysteine following absorption, can supply the cysteine required for the synthesis of GSH. NAC can thus often correct GSH depletion and reduce oxidative stress.
Clinically, NAC may be used to counteract acetaminophen toxicity. Acetaminophen, a common pain reliever, is metabolized in the liver to a highly toxic substance, abbreviated NAPQI. Detoxification of NAPQI requires high concentrations of GSH, and the resulting depletion of GSH stores can cause permanent liver damage. Acetaminophen-induced liver damage can be prevented by administering NAC.
NAC also has shown clinical benefits in cases of acute kidney, heart, and brain damage, all of which are associated with oxidative stress.,, GSH has direct effects against mycobacteria, such as tuberculosis (M. tuberculosis), and NAC has thus been suggested as an adjuvant to the standard medical treatments for tuberculosis infections.,
Oxidative stress is a major feature of Alzheimer’s disease (AD). A reduction in GSH has been detected selectively in the brain regions affected by AD pathology and correlated with the extent of cognitive impairments. NAC supplementation has been shown to have positive effects in animal models of AD, including improvements in memory.,, A preliminary study showed that administration of NAC daily (50 mg/kg/day) for 6 months resulted in favorable changes in some cognitive symptoms in individuals with AD.
It’s worth noting that NAC is not a powerful antioxidant in its own right: its strength lies in the replenishment of GSH in deficient cells, and it is thus likely to be ineffective in cells replete in GSH. The efficacy of NAC also depends on the activity of enzymes for the synthesis of GSH. NAC is therefore not effective in all cases.,,
Does glutathione supplementation work?
The human body produces GSH, but GSH is also present in the diet. Some of the richest food sources of GSH are spinach, avocado, asparagus, and okra. Because the intestines contain an enzyme that degrades GSH, however, some researchers believe that oral intake of GSH does not increase GSH levels in the body. One study published in 1992 stated that a single oral dose of GSH had no impact on plasma GSH levels after 4.5 hours. A 2011 study also reported that GSH supplementation had no effect on red blood cell GSH levels after one month. These negative results, however, may be more indicative of the limitations of the techniques used to assess blood GSH than of the actual GSH concentrations.
Long-term oral administration of glutathione is an effective means of enhancing body stores of glutathione.
In contrast, more recent studies have shown that supplemental GSH can boost GSH levels in the body.,, GSH has been shown to be absorbed in the intestine and rapidly transferred to red blood cells and the liver. In a randomized, double-blind, placebo-controlled trial, healthy adults were given either 250 mg GSH, 1,000 mg GSH, or placebo daily for six months; both dosages increased blood GSH levels compared to a placebo. In the 1,000 mg GSH group, the level of GSH increased by up to 30-35% in blood and up to 260% in buccal (cheek) cells, a highly significant result. The researchers conclude, “Altogether, these findings are consistent with previous pre-clinical studies and indicate that long-term oral administration of glutathione is an effective means of enhancing body stores of glutathione.”
In animal studies, GSH supplementation was shown to increase blood, heart, and brain levels of GSH;,, protect the brain against oxidative stress;, protect the intestines against fasting-induced stress; and reverse the age-associated decline in immune responsiveness. GSH also was shown to reduce the toxicity of acetaminophen;, in fact, one study suggests that GSH may be even more effective than NAC at the same dose.
GSH supplementation in humans also has measurable effects. In one study, participants’ natural killer cell activity was enhanced more than twofold after three months of GSH supplementation (1,000 mg per day). In a pilot study of individuals with NAFLD, GSH supplementation at a dose of 300 mg per day for four months led to a significant decrease in alanine aminotransferase (ALT), a liver enzyme, suggesting a reduction in liver damage. In addition, a liposomal formulation of GSH was shown to boost immune responses against M. tuberculosis and HIV.,
A supplemental form of GSH known as S-acetylglutathione has been shown to be more bioavailable than the standard, non-acetylated form of GSH., Just as NAC is a precursor of cysteine, S-acetylglutathione is a precursor of GSH that is well absorbed in the gut and more stable in plasma.,,
In sum, GSH supplementation can help restore the body’s GSH levels in times of need – including conditions of oxidative stress and aging. Data suggests that the S-acetylglutathione form may be more effective in this regard than non-acetylated glutathione.
What about other antioxidants?
Glutathione may be the “master” antioxidant, but it’s not the only antioxidant! The word “antioxidant” refers to a general common action, but antioxidants are in fact distinct chemical entities with different means of achieving their effects.
Antioxidants can be found in certain botanicals, foods, and beverages., Along with vitamins C and E, examples of natural products with antioxidant (and other) health-benefiting properties include (but are not limited to) silymarin (milk thistle);, curcumin (from turmeric);, alpha lipoic acid;, melatonin;, CoQ10;, resveratrol;, sulforaphane; and berberine. When considering antioxidant supplementation, it is important to select the substance with the right profile, based on the nutritional and health status of each person and their individual needs.
 Wu G, et al. Glutathione metabolism and its implications for health. J Nutr. 2004 Mar;134(3):489-92.
 Franco R, et al. The central role of glutathione in the pathophysiology of human diseases. Arch Physiol Biochem. 2007 Oct-Dec;113(4-5):234-58.
 Smeyne M, Smeyne RJ. Glutathione metabolism and Parkinson’s disease. Free Radic Biol Med. 2013 Sep;62:13-25.
 Hohn A, et al. Happily (n)ever after: aging in the context of oxidative stress, proteostasis loss and cellular senescence. Redox Biol. 2017 Apr;11:482-501.
 Childs BG, et al. Cellular senescence in aging and age-related disease: from mechanisms to therapy. Nat Med. 2015 Dec;21(12):1424-35.
 Saharan S, Mandal PK. The emerging role of glutathione in Alzheimer’s disease. J Alzheimers Dis. 2014;40(3):519-29.
 Mandal PK, et al. Brain glutathione levels–a novel biomarker for mild cognitive impairment and Alzheimer’s disease. Biol Psychiatry. 2015 Nov 15;78(10):702-10.
 Mischley LK, et al. Glutathione as a biomarker in Parkinson’s disease: associations with aging and disease severity. Oxid Med Cell Longev. 2016;2016:9409363.
 Fang C, et al. The interrelation between reactive oxygen species and autophagy in neurological disorders. Oxid Med Cell Longev. 2017;2017:8495160.
 Usal A, et al. Decreased glutathione levels in acute myocardial infarction. Jpn Heart J. 1996 Mar;37(2):177-82.
 Tsuru R, et al. Redox imbalance in patients with coronary artery disease showing progression of atherosclerotic lesions. J Cardiol. 2006 Oct;48(4):183-91.
 Kumar D, et al. Oxidative stress and apoptosis in heart dysfunction. Herz. 2002 Nov;27(7):662-8.
 Singh S, et al. Evaluation of oxidative stress and antioxidant status in chronic obstructive pulmonary disease. Scand J Immunol. 2017 Feb;85(2):130-7.
 Li L, et al. A Western diet induced NAFLD in LDLR(-/)(-) mice is associated with reduced hepatic glutathione synthesis. Free Radic Biol Med. 2016 Jul;96:13-21.
 Sacco R, et al. Glutathione in the treatment of liver diseases: insights from clinical practice. Minerva Gastroenterol Dietol. 2016 Dec;62(4):316-24.
 Robaczewska J, et al. Role of glutathione metabolism and glutathione-related antioxidant defense systems in hypertension. J Physiol Pharmacol. 2016 Jun;67(3):331-7.
 Lagman M, et al. Investigating the causes for decreased levels of glutathione in individuals with type II diabetes. PLoS One. 2015 Mar 19;10(3):e0118436.
 Rosales-Corral S, et al. Diabetes and Alzheimer disease, two overlapping pathologies with the same background: oxidative stress. Oxid Med Cell Longev. 2015;2015:985845.
 Aslan M, et al. Oxidative and nitrative stress markers in glaucoma. Free Radic Biol Med. 2008 Aug 15;45(4):367-76.
 Sun Y, et al. Glutathione depletion induces ferroptosis, autophagy, and premature cell senescence in retinal pigment epithelial cells. Cell Death Dis. 2018 Jul 9;9(7):753.
 Morris D, et al. Glutathione synthesis is compromised in erythrocytes from individuals with HIV. Front Pharmacol. 2014 Apr 11;5:73.
 Allen M, et al. Mechanisms of control of Mycobacterium tuberculosis by NK cells: role of glutathione. Front Immunol. 2015 Oct 5;6:508.
 Guerrero CA, Acosta O. Inflammatory and oxidative stress in rotavirus infection. World J Virol. 2016 May 12;5(2):38-62.
 Staal FJ, et al. Intracellular glutathione levels in T cell subsets decrease in HIV-infected individuals. AIDS Res Hum Retroviruses. 1992 Feb;8(2):305-11.
 Rushworth GF, Megson IL. Existing and potential therapeutic uses for N-acetylcysteine: the need for conversion to intracellular glutathione for antioxidant benefits. Pharmacol Ther. 2014 Feb;141(2):150-9.
 Neal M, Richardson JR. Time to get personal: a framework for personalized targeting of oxidative stress in neurotoxicity and neurodegenerative disease. Curr Opin Toxicol. 2018 Feb;7:127-32.
 Samiec PS, et al. Glutathione in human plasma: decline in association with aging, age-related macular degeneration, and diabetes. Free Radic. Biol. Med. 1998;24:699-704.
 Meng J, et al. The decay of redox-stress response capacity is a substantive characteristic of aging: revising the redox theory of aging. Redox Biol. 2017 Apr;11:365-374.
 Alvarez JA, et al. Vitamin D status is independently associated with plasma glutathione and cysteine thiol/disulphide redox status in adults. Clin Endocrinol (Oxf). 2014 Sep;81(3):458-66.
 Jain SK, et al. Glutathione stimulates vitamin D regulatory and glucose-metabolism genes, lowers oxidative stress and inflammation, and increases 25-hydroxy-vitamin D levels in blood: a novel approach to treat 25-hydroxyvitamin D deficiency. Antioxid Redox Signal. 2018 Dec 10;29(17):1792-1807.
 Faux SP, et al. The role of oxidative stress in the biological responses of lung epithelial cells to cigarette smoke. Biomarkers. 2009 Jul;14 Suppl 1:90-6.
 Rahman I, MacNee W. Lung glutathione and oxidative stress: implications in cigarette smoke-induced airway disease. Am J Physiol. 1999 Dec;277(6):L1067-88.
 Moriarty SP, et al. Oxidation of glutathione and cysteine in human plasma associated with smoking. Free Radic Biol Med. 2003 Dec 15;35(12):1582-8.
 Bailey SM, et al. Chronic ethanol consumption alters the glutathione/glutathione peroxidase-1 system and protein oxidation status in rat liver. Alcohol Clin Exp Res. 2001 May;25(5):726-33.
 Noeman SA, et al. Biochemical study of oxidative stress markers in the liver, kidney and heart of high fat diet induced obesity in rats. Diabetol Metab Syndr. 2011 Aug 3;3(1):17.
 Biswas SK, Rahman I. Environmental toxicity, redox signaling and lung inflammation: the role of glutathione. Mol Aspects Med. 2009 Feb-Apr;30(1-2):60-76.
 Fiorito G, et al. Oxidative stress and inflammation mediate the effect of air pollution on cardio- and cerebrovascular disease: a prospective study in nonsmokers. Environ Mol Mutagen. 2018 Apr;59(3):234-46.
 Li N, et al. Ultrafine particulate pollutants induce oxidative stress and mitochondrial damage. Environ Health Perspect. 2003 Apr;111(4):455-60.
 Sekhar R, et al. Reversing aging: preventing age-related decline in glutathione and mitochondrial function increases longevity. Innov Aging. 2018 Nov;2(Suppl 1):887.
 McCarty MF, DiNicolantonio JJ. An increased need for dietary cysteine in support of glutathione synthesis may underlie the increased risk for mortality associated with low protein intake in the elderly. Age (Dordr). 2015 Oct;37(5):96.
 Go YM, Jones DP. Redox theory of aging: implications for health and disease. Clin Sci (Lond). 2017 Jun 30;131(14):1669-88.
 Athersuch TJ, et al. Paracetamol metabolism, hepatotoxicity, biomarkers and therapeutic interventions: a perspective. Toxicol Res (Camb). 2018 Mar 6;7(3):347-57.
 Song JW, et al. Double-blinded, randomized controlled trial of N-acetylcysteine for prevention of acute kidney injury in high risk patients undergoing off-pump coronary artery bypass. Nephrology (Carlton). 2015 Feb;20(2):96-102.
 Mahmoud KM, Ammar AS. Effect of N-acetylcysteine on cardiac injury and oxidative stress after abdominal aortic aneurysm repair: a randomized controlled trial. Acta Anaesthesiol Scand. 2011 Sep;55(8):1015-21.
 Senanayake MP, et al. N-acetylcysteine in children with acute liver failure complicating dengue viral infection. Ceylon Med J. 2013 Jun;58(2):80-2.
 Teskey G, et al. The synergistic effects of the glutathione precursor, NAC and first-line antibiotics in the granulomatous response against Mycobacterium tuberculosis. Front Immunol. 2018 Sep 12;9:2069.
 Cao R, et al. Characterizing the effects of glutathione as an immunoadjuvant in the treatment of tuberculosis. Antimicrob Agents Chemother. 2018 Oct 24;62(11).
 Arimon M, et al. Oxidative stress and lipid peroxidation are upstream of amyloid pathology. Neurobiol Dis. 2015 Dec;84:109-19.
 daCosta M, et al. N-acetylcysteine treatment attenuates the cognitive impairment and synaptic plasticity loss induced by streptozotocin. Chem Biol Interact. 2017 Jun 25;272:37-46.
 Reyes RC, et al. Neuronal glutathione content and antioxidant capacity can be normalized in situ by N-acetyl cysteine concentrations attained in human cerebrospinal fluid. Neurotherapeutics. 2016 Jan;13(1):217-25.
 Fu AL, et al. Protective effect of N-acetyl-L-cysteine on amyloid beta-peptide-induced learning and memory deficits in mice. Brain Res. 2006 Sep 13;1109(1):201-6.
 Adair JC, et al. Controlled trial of N-acetylcysteine for patients with probable Alzheimer’s disease. Neurology. 2001 Oct 23;57(8):1515-7.
 Morris D, et al. Glutathione supplementation improves macrophage functions in HIV. J Interferon Cytokine Res. 2013 May;33(5):270-9.
 Jones DP, et al. Glutathione in foods listed in the National Cancer Institute’s Health Habits and History Food Frequency Questionnaire. Nutr Cancer. 1992;17(1):57-75.
 Witschi A, et al. The systemic availability of oral glutathione. Eur J Clin Pharmacol. 1992;43(6):667-9.
 Allen J, Bradley RD. Effects of oral glutathione supplementation on systemic oxidative stress biomarkers in human volunteers. J Altern Complement Med. 2011 Sep;17(9):827-33.
 Richie JP Jr, et al. Randomized controlled trial of oral glutathione supplementation on body stores of glutathione. Eur J Nutr. 2015 Mar;54(2):251-63.
 Kovacs-Nolan J, et al. In vitro and ex vivo uptake of glutathione (GSH) across the intestinal epithelium and fate of oral GSH after in vivo supplementation. J Agric Food Chem. 2014 Oct 1;62(39):9499-506.
 Park EY, et al. Increase in the protein-bound form of glutathione in human blood after the oral administration of glutathione. J Agric Food Chem. 2014 Jul 2;62(26):6183-9.
 Aw TY, et al. Oral glutathione increases tissue glutathione in vivo. Chem Biol Interact. 1991;80(1):89-97.
 Ghosh S, et al. Cardiomyocyte apoptosis induced by short-term diabetes requires mitochondrial GSH depletion. Am J Physiol Heart Circ Physiol. 2005 Aug;289(2):H768-76.
 Yabuki Y, Fukunaga K. Oral administration of glutathione improves memory deficits following transient brain ischemia by reducing brain oxidative stress. Neuroscience. 2013 Oct 10;250:394-407.
 Kahl A, et al. Critical role of flavin and glutathione in complex I-mediated bioenergetic failure in brain ischemia/reperfusion injury. Stroke. 2018 May;49(5):1223-31.
 Uchida H, et al. Protective effects of oral glutathione on fasting-induced intestinal atrophy through oxidative stress. World J Gastroenterol. 2017 Sep 28;23(36):6650-64.
 Furukawa T, et al. Reversal of age-associated decline in immune responsiveness by dietary glutathione supplementation in mice. Mech Ageing Dev. 1987 Apr;38(2):107-17.
 Trenti T, et al. Plasma glutathione level in paracetamol daily abuser patients. Changes in plasma cysteine and thiol groups after reduced glutathione administration. Toxicol Lett. 1992 Dec;64-5.
 Saito C, et al. Novel mechanisms of protection against acetaminophen hepatotoxicity in mice by glutathione and N-acetylcysteine. Hepatology. 2010 Jan;51(1):246-54.
 Honda Y, et al. Efficacy of glutathione for the treatment of nonalcoholic fatty liver disease: an open-label, single-arm, multicenter, pilot study. BMC Gastroenterol. 2017 Aug 8;17(1):96.
 Islamoglu H, et al. Effects of ReadiSorb L-GSH in altering granulomatous responses against Mycobacterium tuberculosis infection. J Clin Med. 2018 Mar 1;7(3):40.
 Ly J, et al. Liposomal glutathione supplementation restores Th1 cytokine response to Mycobacterium tuberculosis infection in HIV-infected individuals. J Interferon Cytokine Res. 2015 Nov;35(11):875-87.
 Vogel JU, et al. Effects of S-acetylglutathione in cell and animal model of herpes simplex virus type 1 infection. Med Microbiol Immunol. 2005 Jan;194(1-2):55-9.
 Fanelli S, et al. Oral administration of S-acetyl-glutathione: impact on the levels of glutathione in plasma and in erythrocytes of healthy volunteers. Int J Clin Nutr Diet. 2018;4(2):134.
 Cacciatore I, et al. Prodrug approach for increasing cellular glutathione levels. Molecules. 2010 Mar 3;15(3):1242-64.
 Fraternale A, et al. Inhibition of murine AIDS by pro-glutathione (GSH) molecules. Antiviral Res. 2008 Feb;77(2):120-7.
 Bast A, Haenen GRMM. Nutritional antioxidants: it is time to categorize. In: Lamprecht M, editor. Antioxidants in Sport Nutrition. Boca Raton (FL): CRC Press/Taylor & Francis; 2015.
 Gülçin İ. Antioxidant activity of food constituents: an overview. Arch Toxicol. 2012 Mar;86(3):345-91.
 Xu DP, et al. Natural antioxidants in foods and medicinal plants: extraction, assessment and resources. Int J Mol Sci. 2017 Jan 5;18(1):96.
 Valenzuela A, et al. Selectivity of silymarin on the increase of the glutathione content in different tissues of the rat. Planta Med. 1989 Oct;55(5):420-2.
 Singhal NK, et al. Melatonin or silymarin reduces maneb- and paraquat-induced Parkinson’s disease phenotype in the mouse. J Pineal Res. 2011 Mar;50(2):97-109.
 Pulido-Moran M, et al. Curcumin and health. Molecules. 2016 Feb 25;21(3):264.
 Khanizadeh F, et al. Combination therapy of curcumin and alendronate modulates bone turnover markers and enhances bone mineral density in postmenopausal women with osteoporosis. Arch Endocrinol Metab. 2018 Aug;62(4):438-45.
 Mousavi SM, et al. Effect of alpha-lipoic acid supplementation on lipid profile: a systematic review and meta-analysis of controlled clinical trials. Nutrition. 2018 Aug 23;59:121-30.
 Rochette L, et al. Alpha-lipoic acid: molecular mechanisms and therapeutic potential in diabetes. Can J Physiol Pharmacol. 2015 Dec;93(12):1021-7.
 Reiter R, et al. Mitochondria: central organelles for melatonin′ s antioxidant and anti-aging actions. Molecules. 2018;23(2):509.
 Botham KM, et al. The emerging role of disturbed CoQ metabolism in nonalcoholic fatty liver disease development and progression. Nutrients. 2015 Dec 1;7(12):9834-46.
 Potgieter M, et al. Primary and secondary coenzyme Q10 deficiency: the role of therapeutic supplementation. Nutr Rev. 2013 Mar;71(3):180-8.
 Bird JK, et al. Cardiovascular and antiobesity effects of resveratrol mediated through the gut microbiota. Adv Nutr. 2017 Nov 15;8(6):839-49.
 Mousavi SM, et al. Resveratrol supplementation significantly influences obesity measures: a systematic review and dose-response meta-analysis of randomized controlled trials. Obes Rev. 2018 Dec 5.[In Press]
 Jiang X, et al. Chemopreventive activity of sulforaphane. Drug Des Devel Ther. 2018 Sep 11;12:2905-13.
 Ma X, et al. The pathogenesis of diabetes mellitus by oxidative stress and inflammation: its inhibition by berberine. Front Pharmacol. 2018 Jul 27;9:782.
Share this post
Marina MacDonald, MS, PhD
Gut Microbiota Diversity in the Young and Old
A factor in disease conditions and aging? In recent decades, there has been an explosion of information regarding the role that the human microbiota plays in both health and disease. Projects such as the National Institutes of Health Human Microbiome Project, and similar collaborative efforts in other countries, have focused on the collection of…
Does the Paleo Diet Really Work?
A critical review of the evidence One of the most controversial diets in recent times is the Paleolithic (“Paleo”) diet, also known as the Stone Age diet. The Paleo diet seeks to address 21st century ills by revisiting the way humans ate during the Paleolithic era, more than 2 million years ago. As a…
How many psychotherapists does it take to change a light bulb? None. The light bulb has to want to change itself. This joke makes light of a prevailing truth about human psychology: the most powerful shifts happen when we are ready to lean in and change ourselves. There are all kinds of incentives out…
Breaking Bad: Homocysteine and Aging
The role of B vitamins in cardiovascular and neurological health “If I’d known I was going to live this long, I’d have taken better care of myself.” – Eubie Blake, American composer, upon reaching the age of 100 By now it’s widely known that high blood cholesterol levels can be harmful to our health….
Fighting Fatty Liver, Part 1 of 2
How the gut, microbes, inflammation, and diet affect the liver, and what to do about it The fatty liver epidemic Sedentary lifestyles, nutrient-poor diets, chemical exposures, and an excess of sugar and refined foods are wreaking havoc on and in our bodies more than ever before. And the effects aren’t just cosmetic – beyond…
The Beauty of “Beasty Bits”
Glandular products for advanced support What is Glandular Therapy? When it comes to the matter of the endocrine glands and the hormones they produce, modern medicine has done well in isolating and synthesizing in the lab the very hormones we produce in our bodies. Whether it’s the insulin injected by a Type I diabetic,…
Subscribe for Updates
- Botanicals (57)
- GI Health (53)
- Healthy Aging (122)
- Immune Support (41)
- In The News (42)
- Kids Health (21)
- Stress and Relaxation (50)
- Video (9)
- Vitamins & Minerals (52)
Latest Issue of FOCUS Newsletter Available Now!
About Nutrition In Focus
Subscribe for Updates
Contents of this website are for the purpose of information and education only,
and not a guide to diagnosis or treatment of a particular disorder or its symptoms.
Copyright©2018-2021 Allergy Research Group®. All Rights Reserved.