Liposomal Glutathione
Research

GLUTATHIONE DEPLETION HAS AN IMPORTANT ROLE IN THE PATHOLOGY OF COVID-19.


The NIH has published a study showing glutathione (GSH) is deficient in individuals with Covid-19(12). The latest study from the NIH shows "a major reduction in intracellular glutathione levels was observed in PBMC lysates from COVID-19 patients compared to Healthy Controls (HCs) (Figure 4I)". It was interesting to observe that the deficiency persisted for at least 50 days after acute symptoms even in individuals who had mild to moderate infection (Figure 7H)(12).

The title of a 2020 article sums up the role of glutathione in Covid-19: “Deficiency of Glutathione as the Most Likely Cause of Serious Manifestations and Death in COVID-19 Patients”(1). This paper has been corroborated by two clinical studies published in September & December, 2021 showing deficiency of glutathione (GSH) is associated with increased severity of Covid-19 (2, 3). The data in the first paper(2) reveals decreased levels of total GSH (tGSH) were associated with an increased risk of severe COVID-19 infection. The reduced (active) GSH (rGSH) level showed a negative association with D-dimer levels. This means as GSH goes down,  clotting goes up. The article stated, “GSH appears to be an important factor to oxidative damage prevention as the infection progresses. This suggests the potential clinical efficacy of correcting glutathione metabolism as an adjunct therapy for COVID-19”(2).

In 2020 Dr. Timothy Guilford, science advisor for Your Energy Systems, LLC,  which designed and distributes ReadiSorb® Liposomal Glutathione co-authored a paper(4) and addendum(5) discussing the loss of glutathione during Covid-19 infection: “Glutathione Supplementation as an Adjunctive Therapy in COVID-19”. A summary is posted below.

Four clinical studies document the safety and efficacy of ReadiSorb® Liposomal Glutathione (RLG) in restoring glutathione in adults(6-8)  and children(9). The studies were conducted in individuals with conditions with low glutathione such as HIV(6, 7), Type 2 Diabetes Mellitus (T2DM)(8), and autism(9).

The ReadiSorb® Liposomal Glutathione clinical studies were preceded by cell studies demonstrating that ReadiSorb® Liposomal Glutathione will restore glutathione levels and macrophage immune defense 1,000 times more effectively than N-acetyl cysteine (NAC)(10, 11). The study showed that NAC required an amount 1,000 times larger than ReadiSorb® Glutathione to achieve the same result(10, 11).

Scientific Summary: 

paper (4) and addendum (5) discuss the loss of glutathione during Covid-19 infection. During infection with Covid-19, loss of GSH begins with the attachment of the S protein to cells. Once infection starts, severe acute respiratory syndrome (SARS) coronaviruses contain a protein (N protein) that helps the virus replicate. N protein programs infected cells to produce immune hormones (cytokines) known as IL-6 and TGF-beta. IL-6 depletes GSH in cells including lung cells and TGF-beta is well characterized to compromise GSH production.  Both IL-6 and TGF-beta have been shown in clinical studies to predict a more severe progression of Covid-19 symptoms. This information may explain why Covid-19 has led to severe illness in certain individuals, especially those with conditions associated with low GSH, such as diabetes (Addendum 3.9).

 
Footnotes
  1. Polonikov A. Endogenous Deficiency of Glutathione as the Most Likely Cause of Serious Manifestations and Death in COVID-19 Patients. ACS Infect Dis. 2020. PMCID: PMC7263077. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7263077/
  2. Kryukov EV, Ivanov AV, Karpov VO, Vasil’evich Alexandrin V, Dygai AM, Kruglova MP, et al. Association of Low Molecular Weight Plasma Aminothiols with the Severity of Coronavirus Disease 2019. Oxid Med Cell Longev. 2021;2021:9221693. https://doi.org/10.1155/2021/9221693
  3. Kumar P, Osahon O, Vides DB, Hanania N, Minard CG, Sekhar RV. Severe Glutathione Deficiency, Oxidative Stress and Oxidant Damage in Adults Hospitalized with COVID-19: Implications for GlyNAC (Glycine and N-Acetylcysteine) Supplementation. Antioxidants. 2022;11(1):50. https://www.mdpi.com/2076-3921/11/1/50
  4. Guloyan V, Oganesian B, Baghdasaryan N, Yeh C, Singh M, Guilford F, et al. Glutathione Supplementation as an Adjunctive Therapy in COVID-19. Antioxidants (Basel). 2020;9(10). https://www.ncbi.nlm.nih.gov/pubmed/32992775
  5. Venketaraman V, Guilford F. Depletion of Glutathione in Covid-19. Scholarly Community Encyclopedia Antioxidants (Basel). 2020 https://encyclopedia.pub/6357
  6. Ly J, Lagman M, Saing T, Singh MK, Tudela EV, Morris D, et al. Liposomal Glutathione Supplementation Restores TH1 Cytokine Response to Mycobacterium tuberculosis Infection in HIV-Infected Individuals. J Interferon Cytokine Res. 2015;35(11):875-87. PMCID: 4642835. http://www.ncbi.nlm.nih.gov/pubmed/26133750
  7. Valdivia A, Ly J, Gonzalez L, Hussain P, Aing T, Islamoglu H, et al. Restoring cytokine balance in HIV Positive Individuals with Low CD4 T Cell Counts. AIDS Res Hum Retroviruses. 2017. http://www.ncbi.nlm.nih.gov/pubmed/28398068
  8. To K, Cao R, Yegiazaryan A, Owens J, Nguyen T, Sasaninia K, et al. Effects of Oral Liposomal Glutathione in Altering the Immune Responses Against Mycobacterium tuberculosis and the Mycobacterium bovis BCG Strain in Individuals With Type 2 Diabetes. Front Cell Infect Microbiol. 2021;11:657775. PMCID: PMC8211104. https://www.frontiersin.org/articles/10.3389/fcimb.2021.657775/full
  9. 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):CR677-82. http://www.ncbi.nlm.nih.gov/pubmed/22129897
  10. Morris D, Guerra C, Khurasany M, Guilford F, Saviola B, Huang Y, et al. Glutathione supplementation improves macrophage functions in HIV. J Interferon Cytokine Res. 2013;33(5):270-9. http://www.ncbi.nlm.nih.gov/pubmed/23409922
  11. Lagman M, Ly J, Saing T, Kaur Singh M, Vera Tudela E, Morris D, et al. Investigating the Causes for Decreased Levels of Glutathione in Individuals with Type II Diabetes. PLoS One. 2015;10(3):e0118436. http://www.ncbi.nlm.nih.gov/pubmed/25790445
  12. Lage SL, Amaral EP, Hilligan KL, Laidlaw E, Rupert A, Namasivayan S, et al. Persistent Oxidative Stress and Inflammasome Activation in CD14highCD16? Monocytes From COVID-19 Patients. Front Immunol. 2022;12. https://www.frontiersin.org/article/10.3389/fimmu.2021.799558