Glutathione Human Clinical Research: What the Evidence Shows

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Glutathione is often sold as the body's master antioxidant, but a catchy label is not proof that a capsule, lozenge or injection helps people. This page weighs glutathione human clinical research on its merits: what randomized trials measured, what they found, where they disagree, and how much confidence each finding deserves. If you have wondered whether swallowing glutathione even raises your levels, whether any of it improves health outcomes, or whether intravenous use is justified, the sections below answer those questions with traceable sources and plain-language caveats.

Executive evidence summary

The short version, graded honestly:

• Raising blood glutathione by mouth is unsettled. One 6-month randomized trial found increases of roughly 30–35% in several blood compartments at 1,000 mg/day. A 4-week trial at 500 mg twice daily found no significant change. A 2025 meta-analysis of randomized trials found no statistically significant pooled difference in erythrocyte or plasma glutathione.
• Liposomal and sublingual products each rest on very small studies (12 and 20 participants), so conclusions are preliminary.
• Almost every positive result is a surrogate marker (blood glutathione, immune assays, melanin index). Evidence that glutathione prevents or treats a disease is lacking in the sources reviewed.
• Skin lightening: small oral and topical trials suggest a possible effect on melanin index in sun-exposed skin, but a systematic review called the evidence inconclusive.
• Intravenous glutathione for cosmetic purposes lacks convincing efficacy data, and regulators have warned about adverse effects.
• Overall certainty ranges from low to very low for every outcome examined (see the grading table).

The research question behind glutathione human clinical research

Glutathione (GSH) is a tripeptide the body makes from cysteine, glutamate and glycine, and it is central to redox balance and immune function. Cell and animal work shows it matters biologically. That is mechanism, not clinical proof, and nothing here uses laboratory data to support claims of human benefit.

The clinical question is structured in three tiers:

1. Bioavailability: does a given formulation raise glutathione in human blood or tissue?
2. Biomarker effects: does it change oxidative stress or immune markers?
3. Clinical outcomes: does it improve how people feel, function or progress with a disease?

A yes at tier 1 does not imply a yes at tier 3, which is why this page keeps them apart.

How the evidence was identified and selected

This is a structured evidence review, not a PRISMA-compliant systematic review. Sources were located through targeted web and PubMed-indexed searches in October 2026, with priority given to randomized controlled trials (RCTs), then controlled or pilot studies, then systematic reviews and meta-analyses. Reviews were used to cross-check trial findings, not to replace them.

Inclusion rules: human participants only; glutathione itself (not precursors such as N-acetylcysteine or GlyNAC) as the intervention; formulation and route reported separately. Where I could verify a study's design, sample size, dose and results from the abstract or full text, they are reported. Where I could not, the table says not extracted rather than guessing. Several additional trials are listed by design only for that reason.

Because the search was not exhaustive, absence of a study here does not mean it does not exist. Readers should treat this page as a map and check primary papers before relying on any figure.

Oral glutathione: does it raise body stores?

For years, the prevailing view was that oral glutathione is broken down in the gut. Early human work, such as a 1992 study of the systemic availability of oral glutathione (Witschi et al.), is generally cited as showing no meaningful rise in blood levels after a single large dose. Verify the exact dose and sample against the full text before quoting it.

The positive trial. Richie and colleagues ran a 6-month randomized, double-blind, placebo-controlled trial in 54 non-smoking healthy adults (about three-quarters women, mean age around 47) comparing 250 mg/day, 1,000 mg/day and placebo. Blood glutathione rose after 1, 3 and 6 months at both doses relative to baseline. At 6 months in the high-dose group, glutathione increased by roughly 30–35% in erythrocytes, plasma and lymphocytes and by about 260% in cheek (buccal) cells. In the low-dose group, whole blood rose about 17% and erythrocytes about 29%. The oxidized-to-reduced glutathione ratio fell in whole blood, and levels returned toward baseline after a 1-month washout, which suggests ongoing intake is needed to maintain any rise.

The null trial. Allen and Bradley randomized 40 healthy adults to 500 mg twice daily or placebo for 4 weeks. They reported no significant change in oxidative stress biomarkers, including glutathione status.

Pooled evidence. A 2025 systematic review and meta-analysis (Mangkalopakorn et al.) identified five eligible RCTs and pooled three. The standardized mean difference was 0.74 (95% CI −0.44 to 1.91; P = 0.22) for erythrocyte glutathione and 0.44 (95% CI −0.21 to 1.09; P = 0.19) for plasma glutathione. The authors concluded supplementation did not significantly raise levels, while noting that higher doses and longer durations might.

Why the discrepancy? Plausible explanations include dose and duration (4 weeks versus 6 months), small samples, differing assay methods, and which blood compartment was measured. The wide confidence intervals mean the meta-analysis could not rule out a benefit or no benefit. This is an inconsistent literature, not a settled one.

Liposomal glutathione and sublingual forms

Do not assume findings for one formulation apply to another.

Liposomal glutathione. Sinha and colleagues conducted a 1-month pilot in 12 healthy adults given 500 or 1,000 mg/day of liposomal glutathione. Samples were taken at baseline and after 1, 2 and 4 weeks. Glutathione increased in whole blood, erythrocytes, plasma and peripheral blood mononuclear cells. Natural killer (NK) cell cytotoxicity rose by up to 400% at 2 weeks and lymphocyte proliferation by up to 60%. Plasma 8-isoprostane fell by 35% and the oxidized:reduced glutathione ratio by 20%. The authors reported no differences between dose groups but acknowledged limited statistical power, and described the findings as preliminary. The abstract does not describe a placebo arm; confirm in the full text.

Sublingual glutathione. Schmitt and colleagues ran a randomized crossover study in 20 volunteers with metabolic syndrome, comparing N-acetylcysteine, conventional oral glutathione and a novel sublingual glutathione across 21-day periods. They concluded the sublingual form was superior for raising glutathione. This is a single, small trial in one population, and the product developer's role should be checked in the paper.

Neither study measured a patient-important clinical outcome.

Intravenous glutathione: efficacy and safety evidence

Intravenous (IV) use has grown in cosmetic clinics, yet the evidence base is thin. A review in the Indian Journal of Dermatology, Venereology and Leprology concluded that there is no evidence proving IV glutathione's skin-lightening efficacy, and noted that adverse effects led the Philippine Food and Drug Administration to issue a public warning against off-label uses such as skin lightening. A 2026 critical narrative review similarly judged current evidence too limited to justify routine IV use for cosmetic skin lightening and called for adequately powered RCTs and longer safety studies.

Small IV studies in conditions such as Parkinson's disease and peripheral artery disease exist in the wider literature but were not extracted for this page. IV administration bypasses the digestive tract and carries risks (infusion reactions, infection, product quality) that oral supplements do not, so oral safety data cannot be extrapolated to injections.

Glutathione supplement trials by health outcome

Immune function and oxidative stress

Both Richie (NK cytotoxicity roughly doubled in the high-dose group at 3 months, in a subset of participants) and Sinha (up to 400% at 2 weeks) reported immune-assay changes. These are laboratory markers measured in small subsets or small samples, and no study reviewed here showed fewer infections or better health. Allen and Bradley, by contrast, found no change in oxidative stress markers, and Søndergård (below) found no change in muscle oxidative stress markers. Evidence of benefit on oxidative stress is therefore mixed.

Skin pigmentation

The Dilokthornsakul systematic review (2019) examined trials in healthy volunteers using oral glutathione at 250–500 mg/day and one topical 2% oxidized glutathione product. Oral 500 mg/day and the topical product reduced melanin index in sun-exposed skin; no significant differences appeared in sun-protected skin. The authors judged the evidence inconclusive because of study quality and inconsistent findings. Trials by Arjinpathana and Asawanonda (2012) and Weschawalit and colleagues (2017) are among the primary studies; their full details were not extracted here. Melanin index is a cosmetic surrogate, and durability after stopping is unknown.

Insulin sensitivity and type 2 diabetes

Søndergård and colleagues randomized 20 obese men (10 with type 2 diabetes) to 1,000 mg/day oral glutathione or placebo for 3 weeks. Insulin sensitivity, measured by the gold-standard hyperinsulinemic-euglycemic clamp, increased significantly in the glutathione group. Muscle glutathione rose numerically (19%) without a change in the glutathione:disulfide ratio, and markers of oxidative stress did not change. The study is intriguing but tiny and short.

Kalamkar and colleagues reported a pragmatic trial in roughly 200 Indian patients with type 2 diabetes, described as a case-control cohort design despite the trial label in the title. The authors report improved glutathione stores, lower 8-OHdG and lower HbA1c, particularly in patients over 55. The non-standard design raises risk-of-bias concerns, and the duration and exact dose were not extracted here. A separate registered trial (NCT06313164) evaluated an enhanced oral glutathione product in 250 patients with diabetes (217 completed); its report describes HbA1c and insulin variations not consistently reaching statistical significance.

Liver disease

Lai and colleagues randomized 61 patients with cirrhosis to oral glutathione 500 mg/day, vitamin B6 or placebo for 12 weeks, with extended follow-up (median 984 days). Neither treatment produced statistically significant effects on oxidative stress or antioxidant capacity indicators during the intervention period. Honda and colleagues reported an open-label, single-arm, multicenter pilot in non-alcoholic fatty liver disease; with no control group, it cannot establish efficacy, and its results were not extracted here.

Other conditions

Oral reduced glutathione in children with cystic fibrosis (Visca et al., 2015) and inhaled glutathione in cystic fibrosis (Calabrese et al., 2015, a randomized single-blind trial) have been studied. I did not extract their results, so no claim is made. Parkinson's disease evidence is covered only through a narrative review and is not graded here.

Human studies table

Columns follow the requested structure. NE = not extracted or not verified from the sources reviewed.

Study (year)	Design	N	Participants	Formulation	Dose / route	Duration	Primary outcomes	Main findings	Adverse events	Major limitations	Link
Richie et al. (2015)	RCT, double-blind, placebo-controlled	54	Healthy non-smoking adults, ~41 women, mean age ~47	Oral reduced GSH (Setria brand)	250 or 1,000 mg/day, oral	6 months + 1-month washout	GSH in blood, erythrocytes, plasma, lymphocytes, buccal cells	+30–35% blood compartments and +260% buccal cells at 1,000 mg/day; GSSG:GSH ratio fell; NK activity ~2x in a subset; returned to baseline after washout	NE	Small sample; surrogate endpoints; immune assays in subset; product-company involvement	doi:10.1007/s00394-014-0706-z
Allen & Bradley (2011)	RCT, double-blind, placebo-controlled	40	Healthy adults without acute or chronic disease	Oral reduced GSH	500 mg twice daily, oral	4 weeks	Systemic oxidative stress biomarkers incl. GSH status	No significant changes in biomarkers or GSH status	NE	Short duration; small sample; healthy population	doi:10.1089/acm.2010.0716
Sinha et al. (2018)	1-month pilot (placebo arm not described in abstract)	12	Healthy adults	Liposomal GSH	500 or 1,000 mg/day, oral	4 weeks	GSH in blood compartments; immune and oxidative markers	GSH increased; NK cytotoxicity up to +400%; 8-isoprostane −35%; no dose difference	NE	Tiny pilot; low power; surrogates; controls unclear	doi:10.1038/ejcn.2017.132
Schmitt et al. (2015)	Randomized crossover	20	Adults with metabolic syndrome	Oral GSH vs sublingual GSH vs NAC	NE	21-day periods	GSH levels, oxidative stress markers	Authors report sublingual form superior for GSH supplementation	NE (safety assessed)	Single small trial; surrogates; funding NE	PMC4536296
Søndergård et al. (2021)	RCT, double-blind, placebo-controlled	20	Obese men, 10 with type 2 diabetes	Oral GSH	1,000 mg/day, oral	3 weeks	Insulin sensitivity (clamp)	Insulin sensitivity increased; muscle GSH +19% (numerical); oxidative markers unchanged	NE	Very small; short; all male	PMID 33740389
Kalamkar et al. (2022)	Pragmatic trial, case-control cohort design	~200	Indian adults with type 2 diabetes	Oral GSH	NE	NE	Blood GSH, 8-OHdG, HbA1c	Reported better GSH stores, lower 8-OHdG and HbA1c, esp. over 55	NE	Non-standard design; confounding risk	PMC9137531
Lai et al. (2020)	RCT, double-blind, placebo-controlled	61	Patients with cirrhosis	Oral GSH vs vitamin B6 vs placebo	500 mg/day, oral	12 weeks (+ median 984-day follow-up)	Oxidative stress and antioxidant capacity indicators	No significant effects during intervention	NE	Small; surrogate endpoints	doi:10.3390/nu12071978
Dilokthornsakul et al. (2019)	Systematic review	NE	Healthy volunteers	Oral GSH, topical oxidized GSH	250–500 mg/day oral; 2% topical	Varied	Skin melanin index	Brighter sun-exposed skin at 500 mg/day oral and topical; none in sun-protected skin; judged inconclusive	NE	Study quality; inconsistent findings	PMID 30895708
Mangkalopakorn et al. (2025)	Systematic review and meta-analysis	5 RCTs (3 pooled)	Mixed	Oral GSH	Varied	Varied	Erythrocyte and plasma GSH	No significant pooled difference	NE	Few trials; high risk of bias in selective reporting; wide CIs	doi:10.59796/jcst.V15N1.2025.90
Arjinpathana & Asawanonda (2012); Weschawalit et al. (2017); Honda et al. (2017); Visca et al. (2015); Calabrese et al. (2015)	Various	NE	Various	Various	NE	NE	NE	Identified, not extracted	NE	NE	See references

Study design quality and risk of bias

Only some listed studies are randomized, double-blind and placebo-controlled (Richie, Allen, Søndergård, Lai). Others are pilots, crossovers or non-standard cohorts. The meta-analysis authors rated most included trials as low risk or having some concerns, but high risk for selective reporting because many outcomes and assays were measured. Common weaknesses are small samples, short durations, reliance on surrogate outcomes, and multiple outcomes with limited correction for multiplicity.

Participants, dose, duration and endpoints

• Participants: mostly healthy adults, with smaller trials in metabolic syndrome, obesity/type 2 diabetes and cirrhosis. Results in healthy people should not be assumed to apply to patients, children or older adults.
• Dose and form: oral doses ranged from 250 mg/day to 1,000 mg/day; the Allen trial used 1,000 mg/day in two divided doses. These are the doses studied, not recommendations. Liposomal, sublingual and IV products behave differently and were tested in separate, small studies.
• Duration: from 3 weeks to 6 months, with one cirrhosis follow-up extending years. Long-term outcome data are absent.
• Endpoints: nearly all primary endpoints were biomarkers. Insulin sensitivity by clamp is a more physiologic measure but still intermediate.

Statistical versus clinical significance

A statistically significant 30% rise in a blood level is a laboratory finding. It becomes clinically meaningful only if it translates into outcomes people notice, such as fewer infections or better glycemic control, and sustained benefit has not been shown. NK cytotoxicity doubling in a subset is an assay result, not disease protection. The melanin-index change is measurable but its cosmetic importance and durability are uncertain. Conversely, a non-significant pooled result with wide confidence intervals does not prove glutathione does nothing; it shows imprecision.

Funding and conflicts of interest

The Richie trial tested Kyowa Hakko's Setria glutathione, and the company publicized the results in press materials. That does not invalidate the work, but readers should read the paper's funding and disclosure statements. Funding statements for the other studies were not extracted here. Several liposomal and sublingual products are commercial, so industry involvement should be checked for each. Independent replication of the positive oral and liposomal findings would materially strengthen confidence.

Consistency across trials

Consistency is limited. Oral glutathione raised blood levels in a 6-month trial but not in a 4-week trial, and the pooled estimate was imprecise. Immune and oxidative-stress findings point in different directions across studies. Skin trials lean positive in sun-exposed sites but vary by product and site. The insulin-sensitivity signal comes from one 20-person trial and a design-limited cohort. No outcome has been replicated across multiple independent, adequately powered RCTs.

Systematic reviews and meta-analyses

• Mangkalopakorn et al. (2025): no significant pooled change in erythrocyte or plasma glutathione across three RCTs; authors suggest higher dose and longer duration may matter.
• Dilokthornsakul et al. (2019): possible brightening of sun-exposed skin; overall evidence inconclusive.
• Narrative reviews (2016 and 2026): both caution that evidence for IV and cosmetic use is limited and call for larger, longer, better-controlled trials.

Evidence grading

Grades use GRADE terminology (high, moderate, low, very low) and consider risk of bias, inconsistency, imprecision, indirectness and publication bias. They are my judgment from the sources reviewed, not an official GRADE assessment.

Outcome	Certainty	Reasoning
Oral GSH raises blood GSH (healthy adults)	Low	One positive 6-month RCT, one null 4-week RCT, non-significant meta-analysis; imprecise and inconsistent
Liposomal GSH raises blood GSH	Very low	One 12-person pilot; control arm unclear; very imprecise
Sublingual GSH raises blood GSH	Very low	One 20-person crossover in one population
Immune markers (NK activity etc.)	Very low	Surrogate, subset or tiny samples; no clinical immune outcome
Oxidative stress markers	Low to very low	Mixed: reductions in two studies, null in others
Skin lightening (oral/topical)	Low to very low	Small trials, cosmetic surrogate, inconsistent; review inconclusive
Insulin sensitivity / HbA1c	Very low	Tiny RCT plus design-limited cohort; short follow-up
Liver outcomes (cirrhosis biomarkers)	Low	One null RCT of 61 patients; surrogates only
IV GSH efficacy (cosmetic)	Very low / insufficient	No adequate efficacy evidence in sources reviewed; safety warnings
Prevention or treatment of any disease	Not supported	No adequate clinical-outcome trials reviewed

Because mechanistic plausibility and a few preliminary studies cannot raise certainty, none of these outcomes is graded moderate or high.

Safety and medical responsibility

In the studies summarized by a Mahidol University drug information service (a secondary source), no serious adverse effects were reported for oral glutathione; reported events included dizziness, back pain, flushing, loose stools, bloating, constipation and weight gain, and no study had used more than 1,000 mg/day. Many trials I reviewed did not report adverse events in the abstracts, so safety data were largely not extracted. Long-term safety is poorly characterized. Oral and IV risks differ, and IV use outside a medically supervised indication is particularly concerning given the regulatory warnings noted above. People who are pregnant or breastfeeding, have asthma, liver or kidney disease, take medicines or are considering chemotherapy-adjacent products should speak with a qualified healthcare professional; this page cannot offer individualized advice.

Limitations and evidence gaps

• Few trials, mostly under 100 participants, with short durations.
• Heavy reliance on surrogate endpoints.
• Inconsistent formulations, assays and sampling compartments.
• Limited reporting of adverse events and funding in the extracted material.
• Potential publication bias, since small positive supplement trials are more likely to be published.
• Several trials (skin, liver, cystic fibrosis, Parkinson's disease) were identified but not extracted in this review.
• Needed next: adequately powered, independent, placebo-controlled RCTs with clinical endpoints, head-to-head formulation comparisons and long-term safety follow-up.

Bottom-line interpretation

Human evidence shows that glutathione supplementation can change some biomarkers in some trials, but results are inconsistent, samples are small and clinical benefit is unproven. Oral glutathione may raise blood levels at around 1,000 mg/day over months, yet a meta-analysis could not confirm this. Liposomal and sublingual forms are promising but under-tested. IV use for cosmetic purposes lacks solid supporting evidence. The responsible conclusion is cautious interest, not confident claims.

Frequently asked questions

Does oral glutathione raise glutathione levels in humans? Sometimes. A 6-month RCT reported 30–35% increases in several compartments at 1,000 mg/day, while a 4-week RCT and a pooled analysis did not show significant increases.

Is liposomal glutathione better absorbed? Early data in 12 people are encouraging, but there is no robust head-to-head comparison with other oral forms in large trials.

Does glutathione treat or prevent disease? The reviewed evidence does not support that claim. Trials measured mostly biomarkers.

Does glutathione lighten skin? Small trials suggest a possible effect on sun-exposed skin melanin index, but a systematic review called the evidence inconclusive.

Is intravenous glutathione safe and effective? Efficacy evidence for cosmetic use is lacking, and regulators have warned about adverse effects.

Conclusion

Glutathione human clinical research is real but early. The strongest finding is a possible rise in blood glutathione with higher-dose, longer oral use; the weakest link is any proof of patient-important benefit. If you are considering a glutathione product, discuss it with a clinician, and treat claims that exceed the evidence above with skepticism.

References

Links and identifiers below were checked against abstracts, PubMed/PMC pages or the reference list of the 2025 meta-analysis. Items marked * should be verified against full text before publication.

1. Richie JP Jr, Nichenametla S, Neidig W, Calcagnotto A, Haley JS, Schell TD, Muscat JE. Randomized controlled trial of oral glutathione supplementation on body stores of glutathione. Eur J Nutr. 2015;54(2):251–263. https://doi.org/10.1007/s00394-014-0706-z
2. 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. https://doi.org/10.1089/acm.2010.0716
3. Sinha R, Sinha I, Calcagnotto A, Trushin N, Haley JS, Schell TD, Richie JP Jr. Oral supplementation with liposomal glutathione elevates body stores of glutathione and markers of immune function. Eur J Clin Nutr. 2018;72(1):105–111. https://doi.org/10.1038/ejcn.2017.132 (PMID 28853742)
4. Schmitt B, et al. Effects of N-acetylcysteine, oral glutathione (GSH) and a novel sublingual form of GSH on oxidative stress markers: a comparative crossover study. Redox Biol. 2015. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4536296/ *
5. Søndergård SD, Cintin I, Kuhlman AB, et al. The effects of 3 weeks of oral glutathione supplementation on whole body insulin sensitivity in obese males with and without type 2 diabetes: a randomized trial. Appl Physiol Nutr Metab. 2021;46(9):1133–1142. https://doi.org/10.1139/apnm-2020-1099 (PMID 33740389)
6. Kalamkar S, Acharya J, Kolappurath Madathil A, et al. Randomized clinical trial of how long-term glutathione supplementation offers protection from oxidative damage and improves HbA1c in elderly type 2 diabetic patients. Antioxidants. 2022;11(5):1026. https://doi.org/10.3390/antiox11051026
7. Lai CY, Cheng SB, Lee TY, Hsiao YF, Liu HT, Huang YC. Impact of glutathione and vitamin B-6 in cirrhosis patients: a randomized controlled trial and follow-up study. Nutrients. 2020;12(7):1978. https://doi.org/10.3390/nu12071978
8. Witschi A, Reddy S, Stofer B, Lauterburg BH. The systemic availability of oral glutathione. Eur J Clin Pharmacol. 1992;43(6):667–669. https://doi.org/10.1007/BF02284971 *
9. Arjinpathana N, Asawanonda P. Glutathione as an oral whitening agent: a randomized, double-blind, placebo-controlled study. J Dermatolog Treat. 2012;23(2):97–102. https://doi.org/10.3109/09546631003801619 *
10. Weschawalit S, Thongthip S, Phutrakool P, Asawanonda P. Glutathione and its antiaging and antimelanogenic effects. Clin Cosmet Investig Dermatol. 2017;10:147–153. https://doi.org/10.2147/CCID.S128339 *
11. Dilokthornsakul W, Dhippayom T, Dilokthornsakul P. The clinical effect of glutathione on skin color and other related skin conditions: a systematic review. J Cosmet Dermatol. 2019;18(3):728–737. PMID 30895708
12. Mangkalopakorn P, Segsarnviriya C, Keeratipranon M, Maiprasert M. Glutathione levels after glutathione supplementation: a systematic review and meta-analysis. J Curr Sci Technol. 2025;15(1):90. https://doi.org/10.59796/jcst.V15N1.2025.90
13. Sonthalia S, Daulatabad D, Sarkar R. Glutathione as a skin whitening agent: facts, myths, evidence and controversies. Indian J Dermatol Venereol Leprol. 2016;82:262–272. https://ijdvl.com/?p=4842 * (confirm author list)
14. Critical narrative review of glutathione for skin lightening via intravenous, oral and topical routes (2026). https://doi.org/10.25122/jml-2026-0054 * (author list not extracted)
15. Honda Y, Kessoku T, Sumida 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;17:96. https://doi.org/10.1186/s12876-017-0652-3
16. Visca A, Bishop CT, Hilton S, Hudson VM. Oral reduced L-glutathione improves growth in pediatric cystic fibrosis patients. J Pediatr Gastroenterol Nutr. 2015;60(6):802–810. https://doi.org/10.1097/MPG.0000000000000738
17. Calabrese C, Tosco A, Abete P, et al. Randomized, single blind, controlled trial of inhaled glutathione vs placebo in patients with cystic fibrosis. J Cyst Fibros. 2015;14(2):203–210. https://doi.org/10.1016/j.jcf.2014.09.014
18. Mahidol University Drug Information Unit. Q&A on oral glutathione safety (secondary source). https://pharmacy.mahidol.ac.th/dic/qa_full.php?id=4989
19. ClinicalTrials.gov NCT06313164. Impact of oral glutathione on oxidative damage and HbA1c in type 2 diabetes. https://clinicaltrials.gov/study/NCT06313164

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Editorial note before publishing: originality was not run through a plagiarism checker, so no similarity score is claimed. Please run one, verify the starred references and the items marked NE against primary papers, and have a qualified reviewer sign off. Word count is approximately 3,900.