Glutathione and MTHFR

Glutathione and MTHFR

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Katie Stone - Naturopath

Written By:

Katie Stone - Naturopath
Dr. Nare Simonyan - PhD Pharmaceutical Science

Medical Reviewer:

Dr. Nare Simonyan - PhD Pharmaceutical Science
Kari Asadorian - BSN, RN

Edited By:

Kari Asadorian - BSN, RN
Last updated:

The Relationship Between Glutathione, Methylation, and MTHFR

Glutathione synthesis and MTHFR activity involve interconnected but distinct metabolic pathways. MTHFR functions in the folate cycle, where it converts 5,10-methylenetetrahydrofolate into 5-methyltetrahydrofolate (5-MTHF). In a vitamin B12-dependent reaction, 5-MTHF supports the conversion of homocysteine back into methionine.


Glutathione is produced through a different pathway. Homocysteine can enter the vitamin B6-dependent transsulfuration pathway, where it is converted through cystathionine into cysteine. Cysteine then combines with glutamate and glycine to form glutathione. Therefore, the biochemical connection between MTHFR and glutathione involves homocysteine metabolism, but MTHFR does not directly produce or control glutathione.


Methylation is the transfer of a methyl group to another molecule, such as DNA or a protein. These reactions can affect a molecule’s activity, stability or interactions. For example, DNA methylation helps regulate gene expression without changing the underlying DNA sequence, although its effects depend on where methylation occurs within the genome.


One-carbon metabolism is supported by several nutrients and dietary compounds, including folate, riboflavin (vitamin B2), vitamin B6, vitamin B12, methionine, choline and betaine. Deficiencies, certain medical conditions and some medications may affect these pathways.


Common MTHFR variants, particularly C677T, can reduce MTHFR enzyme activity. However, their metabolic effects vary according to genotype, nutritional status and other health factors. A common MTHFR variant alone does not establish that a person has a nutrient deficiency, impaired methylation or low glutathione, and current evidence does not show that these variants directly cause glutathione deficiency.


This article examines the functions of glutathione, its indirect biochemical connection with methylation and MTHFR, and the evidence concerning factors that may influence glutathione status.

What is Glutathione?

Glutathione is a tripeptide made from glutamate, cysteine and glycine. It is often described as the body’s “master antioxidant” because it is an abundant intracellular antioxidant that helps maintain cellular redox balance, both directly and through antioxidant enzymes such as glutathione peroxidases.


GSH refers to reduced glutathione. After participating in antioxidant reactions, it can be converted into oxidized glutathione (GSSG) and subsequently recycled back into GSH.


Glutathione is present in most cells, generally at millimolar intracellular concentrations. The liver contains particularly high levels of glutathione, where it plays an important role in cellular redox balance and the metabolism of certain reactive compounds.1

Glutathione’s main roles include:

  • Neutralizing harmful free radicals and other reactive species 
  • Serving as a reducing substrate for antioxidant enzymes such as glutathione peroxidases  
  • Supporting the recycling of other antioxidants, including vitamin C and, indirectly, vitamin E 
  • Helping neutralize or metabolize certain reactive compounds and drug metabolites, including the reactive acetaminophen metabolite NAPQI 
  • Participating in Phase II detoxification reactions through glutathione conjugation 
  • Binding or conjugating with certain reactive compounds and metals, which may facilitate their metabolism, sequestration or elimination 
  • Regulating cellular proliferation and apoptosis
  • Supporting mitochondrial redox balance and helping protect mitochondrial components, including mitochondrial DNA, from oxidative damage

Essentially, glutathione helps protect cells against reactive oxygen and nitrogen species generated during normal metabolism and in response to certain environmental exposures.2


Newer research suggests that glutathione also has metabolic and signaling functions beyond antioxidant defense. A 2024 mouse study found that liver glutathione synthesis influenced NRF2 signaling, lipogenic enzyme expression and circulating triglyceride levels. However, this was preclinical research and does not demonstrate that glutathione supplementation produces the same effects in humans.3

How Can an MTHFR Gene Mutation Affect Glutathione Levels?

To understand how the MTHFR gene mutation affects glutathione, we first need to understand one-carbon metabolism. This is a series of biochemical reactions that delivers one-carbon units to numerous pathways.


The folate cycle and methionine cycle are two major components of this network required for regulating amino acid homeostasis, including the three amino acids that make up glutathione: cysteine, glycine, and glutamic acid.


Homocysteine produced during the methylation process can be converted to cysteine, which is then combined with two other amino acids (glutamate and glycine) to form glutathione.


The MTHFR enzyme is involved in homocysteine metabolism, but it does not directly transfer a methyl group to methionine. Instead, it converts 5,10-methylenetetrahydrofolate into 5-methyltetrahydrofolate (5-MTHF). In a vitamin B12-dependent reaction catalyzed by methionine synthase, 5-MTHF provides the methyl group used to convert homocysteine back into methionine.4


Methionine is activated to form S-adenosylmethionine (SAM), the principal methyl donor for many reactions in the body. After donating a methyl group, SAM is converted into S-adenosylhomocysteine (SAH), which is then converted into homocysteine. Homocysteine can either be remethylated to regenerate methionine or enter the vitamin B6-dependent transsulfuration pathway.


During transsulfuration, homocysteine is converted into cystathionine and then cysteine. Cysteine is subsequently combined with glutamate and glycine through separate enzyme-catalyzed reactions to produce glutathione. Therefore, cysteine - not glutathione itself - is the direct product derived from the transsulfuration pathway.


MTHFR also catalyzes the conversion of 5,10-methylenetetrahydrofolate into 5-methyltetrahydrofolate, the predominant circulating form of folate. However, common MTHFR variants may reduce MTHFR enzyme activity and influence folate metabolism or homocysteine levels, particularly when folate or riboflavin status is low; they do not typically cause folate deficiency.


Some common MTHFR genotypes, particularly C677T homozygosity, may be associated with higher homocysteine levels, especially when folate or riboflavin status is low.5 However, these variants do not automatically cause low methionine, accumulation of S-adenosylhomocysteine (SAH), reduced S-adenosylmethionine (SAM) or low glutathione.6 Vitamin B12 supports the remethylation of homocysteine to methionine, while methionine can contribute indirectly to cysteine production through the methionine cycle and transsulfuration pathway. Cysteine availability is an important factor in glutathione synthesis.


A 2025 observational study involving 421 Polish adults evaluated glutathione concentrations, vitamin B12 and betaine intake, and several one-carbon metabolism genotypes, including MTHFR. The researchers found that selected nutritional, genetic and glutathione-related measures were associated with diabetes-related metabolic parameters. However, because the study was observational and did not specifically establish a causal relationship between MTHFR and glutathione, it does not demonstrate that a common MTHFR variant directly causes glutathione deficiency.7

What Issues Could Low Glutathione Cause?

Low or altered glutathione status may reduce cellular antioxidant capacity and is associated with greater oxidative stress. However, lower glutathione measurements do not necessarily indicate a clinical deficiency.  Altered glutathione status has been observed in association with cancer, cystic fibrosis and various neurodegenerative, cardiovascular, inflammatory, immune and metabolic conditions. However, these associations do not establish that low glutathione causes these conditions.8


Glutathione also contributes to immune-cell function, including macrophage and T-cell responses.9


A 2023 systematic review of 35 human studies found that blood glutathione generally declined with advancing age. Most brain studies also suggested an age-related decline, although the findings differed among brain regions and studies. These results demonstrate an association between aging and glutathione status but do not prove that low glutathione accelerates aging10. The relationship between glutathione and cancer is more complex. A 2024 retrospective study involving 460 breast cancer patients found that chemotherapy-resistant tumors had higher intracellular glutathione levels. Glutathione administration was also associated with a higher recurrence rate following chemotherapy, although the observational study could not establish causality. Therefore, higher glutathione levels are not necessarily beneficial in every clinical context.11


For this reason, maintenance of adequate glutathione levels may enhance immunocompetence, protect the body from numerous chronic diseases, and improve the ability to recover from illness or physical stress.

How Does Glutathione Impact Methylation?

Experimental studies in cellular and animal models suggest that severe glutathione depletion can alter methionine metabolism, SAM availability and DNA methylation. However, these findings do not establish that ordinary variations in glutathione status impair DNA methylation in humans.12-14 Experimental evidence suggests that glutathione may help protect vitamin B12 from inactivation by certain reactive compounds, although the clinical significance of this interaction in humans remains uncertain. Vitamin B12 functions as a cofactor for methionine synthase, an enzyme connecting the folate and methionine cycles.15,16

How Can Supplementation Help?

The bioavailability of oral glutathione appears to depend on its formulation, dose and duration of use. Although some earlier short-term studies found no significant change in glutathione status, other human trials have reported increased glutathione levels following oral supplementation. A 2026 randomized crossover pilot study involving 14 healthy adults found that a micellar glutathione formulation produced greater systemic glutathione exposure than standard oral glutathione.17 However, this small, formulation-specific study evaluated bioavailability rather than long-term clinical benefits. A small 2015 crossover study also found that sublingual glutathione increased plasma glutathione more effectively than standard oral glutathione or N-acetylcysteine (NAC) in adults with metabolic syndrome.18


 

Cysteine availability can limit glutathione synthesis, and NAC supplies cysteine that the body may use to make glutathione. Glycine is another amino acid required for glutathione production. Recent evidence concerning combined glycine and NAC supplementation, known as GlyNAC, is promising but mixed.19


A small 2023 randomized trial involving 24 older adults found that 16 weeks of GlyNAC supplementation increased glutathione and improved several measures of oxidative stress and metabolic health. However, another randomized trial involving 114 healthy older adults found no overall increase in glutathione following two weeks of GlyNAC. An exploratory subgroup with high oxidative stress and low baseline glutathione appeared to benefit.20 A 2023 systematic review and meta-analysis of 26 controlled clinical trials also found that NAC supplementation increased glutathione and total antioxidant capacity in adults.21 These findings suggest that NAC or GlyNAC may support glutathione production in some populations, particularly when baseline glutathione is low or oxidative demand is high, but the response is not universal.

The B vitamins also play a major role in glutathione synthesis and the metabolism of homocysteine22. Homocysteine may then be converted into cysteine and remethylated into methionine to be used for glutathione. The deficiency of B-vitamins may impair the homocysteine-methionine cycle23, which in turn can lead to reduced glutathione levels. Riboflavin is also a component of the glutathione redox cycle24, and lower riboflavin levels may lead to reduced glutathione.

Folate supplementation may increase methionine and SAM levels25 and, as a result, improve methylation. It has also been suggested that the combination of folate, vitamin B12, and vitamin B6 may improve methylation, increase transsulfuration, and possibly reduce stress.

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  • 3rd-Party Tested for Purity, Potency & Safety
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Frequently Asked Questions about glutathione and MTHFR

Does glutathione lower homocysteine?

Current evidence does not establish that oral glutathione supplementation reliably lowers homocysteine in humans. NAC has reduced homocysteine in some studies, but NAC and glutathione are distinct interventions. Homocysteine levels are also influenced by folate, vitamin B12, vitamin B6, riboflavin, kidney function, medications, genetics and other health factors.26

What are the symptoms of glutathione deficiency?

Low glutathione status does not have a specific, easily recognizable set of symptoms. Severe inherited disorders of glutathione synthesis are rare and may cause hemolytic anemia, metabolic acidosis and neurologic abnormalities. These disorders should not be confused with lower glutathione measurements or common MTHFR variants. Altered glutathione status has been observed in association with aging and several chronic diseases, but these associations do not prove that low glutathione causes those conditions.27

Who should avoid glutathione?

Evidence concerning glutathione supplementation during pregnancy and breastfeeding is limited. People who are pregnant, planning pregnancy or breastfeeding should consult a qualified healthcare professional before using a glutathione supplement. People receiving chemotherapy, managing a medical condition or taking prescription medications should also consult their healthcare professional before supplementation.

What depletes glutathione in the body?

Glutathione can become depleted when oxidative demand exceeds the body’s ability to synthesize and recycle it. Factors that may reduce glutathione status include acetaminophen overdose, chronic excessive alcohol consumption, smoking, certain toxic exposures, severe illness and inadequate availability of amino acids needed for glutathione synthesis. The effect depends on the substance, dose, duration of exposure and individual health status.28-31

Does methylation produce glutathione?

Methylation does not directly produce glutathione. The methionine cycle and transsulfuration pathway are connected through homocysteine. Homocysteine can either be remethylated to methionine or enter transsulfuration to produce cysteine for glutathione synthesis. However, the amount entering each pathway depends on several enzymes, nutrients and regulatory signals and cannot be predicted from MTHFR status or generalized “methylation efficiency” alone.

References

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    https://pubmed.ncbi.nlm.nih.gov/39709466/

  12. Khingkan Lertratanangkoon, Joseph M. Scimeca, Jing-na Wei; "Inhibition of Glutathione Synthesis with Propargylglycine Enhances N-Acetylmethionine Protection and Methylation in Bromobenzene-Treated Syrian Hamsters"; The Journal of Nutrition; 2023 Feb

    https://www.sciencedirect.com/science/article/pii/S0022316623019922

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    https://link.springer.com/article/10.1007/s44371-026-00815-1

  16. William P Watson, Tony Munter, Bernard T Golding; "A new role for glutathione: protection of vitamin B12 from depletion by xenobiotics"; Chem Res Toxicol.; 2004 Dec

    https://pubmed.ncbi.nlm.nih.gov/15606130/

  17. Julia Solnier, Min Du, Yiming Zhang, Yoon Seok Roh, Yun Chai Kuo, Afoke Ibi, Simon Wood, Mary Hardy, Roland J Gahler, Chuck Chang; "A Targeted Metabolomic Assessment of Oral Glutathione Bioavailability and Safety in Humans: A Randomized Crossover Clinical Trial"; Antioxidants (Basel).; 2026 Mar

    https://pubmed.ncbi.nlm.nih.gov/41897500/

  18. Bernard Schmitt, Morgane Vicenzi, Catherine Garrel, Frédéric M Denis; "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 Dec

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  19. Giulia Lizzo, Eugenia Migliavacca, Daniela Lamers, Adrien Frézal, John Corthesy, Gerard Vinyes-Parès, Nabil Bosco, Leonidas G Karagounis, Ulrike Hövelmann, Tim Heise, Maximilian von Eynatten, Philipp Gut; "A Randomized Controlled Clinical Trial in Healthy Older Adults to Determine Efficacy of Glycine and N-Acetylcysteine Supplementation on Glutathione Redox Status and Oxidative Damage"; Front Aging.; 2022 Mar

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  21. Mahsa Mahmoudinezhad, Fatemeh Abbaszadeh, Meysam Zarezadeh, Nazgol Bahreini, Parsa Jamilian, Parmida Jamilian, Alireza Ostadrahimi; "N-acetylecysteine, a powerful agent in the reinforcement of anti-oxidant profile: A systematic review and dose-response meta-analysis of controlled clinical trials"; Clinical nutrition ESPEN; 2023 Apr

    https://pubmed.ncbi.nlm.nih.gov/36963867/

  22. Zorislava Bajic, Tanja Sobot, Ranko Skrbic, Milos P Stojiljkovic, Nenad Ponorac, Amela Matavulj, Dragan M Djuric; "Homocysteine, Vitamins B6 and Folic Acid in Experimental Models of Myocardial Infarction and Heart Failure—How Strong Is That Link?"; Biomolecules; 2022 Apr

    https://pmc.ncbi.nlm.nih.gov/articles/PMC9027107/

  23. Tahniat Rehman, Muhammad Asim Shabbir, Muhammad Inam‐Ur‐Raheem, Muhammad Faisal Manzoor, Nazir Ahmad, Zhi‐Wei Liu, Muhammad Haseeb Ahmad, Azhari Siddeeg, Muhammad Abid, Rana Muhammad Aadil; "Cysteine and homocysteine as biomarker of various diseases"; Food science and nutrition; 2020 Aug

    https://pmc.ncbi.nlm.nih.gov/articles/PMC7500767/

  24. Marziyeh Ashoori, Ahmad Saedisomeolia; "Riboflavin (vitamin B₂) and oxidative stress: a review"; The British journal of nutrition; 2014 Jun

    https://pubmed.ncbi.nlm.nih.gov/24650639/

  25. Imtiaz Hussain Raja Abbasi, Farzana Abbasi, Lamei Wang, Mohamed E Abd El Hack, Ayman A Swelum, Ren Hao, Junhu Yao, Yangchun Cao; "Folate promotes S-adenosyl methionine reactions and the microbial methylation cycle and boosts ruminants production and reproduction"; AMB Express; 2018 Apr

    https://pmc.ncbi.nlm.nih.gov/articles/PMC5913057/

  26. Federico Cacciapuoti; "N-Acetyl-Cysteine supplementation lowers high homocysteine plasma levels and increases Glutathione synthesis in the trans-sulfuration pathway: Beneficial effects on several cardiovascular and neurodegenerative diseases"; Italian Journal of Medicine; 2019 Nov

    https://www.researchgate.net/publication/337611026_N-Acetyl-Cysteine_supplementation_lowers_high_homocysteine_plasma_levels_and_increases_Glutathione_synthesis_in_the_trans-sulfuration_pathway_Beneficial_effects_on_several_cardiovascular_and_neurodege

  27. Nazzareno Ballatori, Suzanne M Krance, Sylvia Notenboom, Shujie Shi, Kim Tieu, Christine L Hammond; "Glutathione dysregulation and the etiology and progression of human diseases"; Biological chemistry; 2009 Mar

    https://pmc.ncbi.nlm.nih.gov/articles/PMC2756154/

  28. Nazzareno Ballatori, Suzanne M Krance, Sylvia Notenboom, Shujie Shi, Kim Tieu, Christine L Hammond; "Glutathione dysregulation and the etiology and progression of human diseases"; Biological chemistry; 2009 Mar

    https://pmc.ncbi.nlm.nih.gov/articles/PMC2756154/

  29. Marta Anna Lech, Monika Leśkiewicz, Kinga Kamińska, Zofia Rogóż, Elżbieta Lorenc-Koci; "Glutathione Deficiency during Early Postnatal Development Causes Schizophrenia-Like Symptoms and a Reduction in BDNF Levels in the Cortex and Hippocampus of Adult Sprague–Dawley Rats"; International journal of molecular sciences; 2021 Jun

    https://pmc.ncbi.nlm.nih.gov/articles/PMC8229148/

  30. Ioannis Zalachoras, Fiona Hollis, Eva Ramos-Fernández, Laura Trovo, Sarah Sonnay, Eveline Geiser, Nicolas Preitner, Pascal Steiner, Carmen Sandi, Laia Morató; "Therapeutic potential of glutathione-enhancers in stress-related psychopathologies"; Neuroscience & Biobehavioral Reviews; 2020 Mar

    https://www.sciencedirect.com/science/article/abs/pii/S0149763419311133

  31. Federico Maria Rubino; "Toxicity of Glutathione-Binding Metals: A Review of Targets and Mechanisms"; Toxics; 2015 Jan

    https://pmc.ncbi.nlm.nih.gov/articles/PMC5634692

Katie Stone - Naturopath

About the Author

Katie is a qualified Naturopath (BNatMed) and freelance writer from New Zealand. She specializes in all things health and wellness, particularly dietary supplements and nutrition. Katie is also a dedicated runner and has completed more half-marathons than she can count!

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