Randomized Clinical Trial of How Long-Term Glutathione Supplementation Offers Protection from Oxidative Damage and Improves HbA1c in Elderly Type 2 Diabetic Patients
What this study found
Glutathione supplementation improved redox status and reduced oxidative DNA damage, and it was well tolerated. In the DG arm, GSH increased significantly over 6 months (Cohen's d = 1.01; p < 0.001), GSSG also increased (Cohen's d = 0.61; p < 0.001), and 8-OHdG decreased significantly (Cohen's d = -1.07; p < 0.001). HbA1c fell in both groups overall, but the between-group difference was small and not significant (Cohen's d = -0.16; p > 0.05). In the elderly subgroup, HbA1c reduction was significantly greater with glutathione than with anti-diabetic therapy alone (Cohen's d = -0.41; p < 0.05),…
- Study & population
- Randomized clinical trial in adults with type 2 diabetes receiving anti-diabetic treatment in Pune, India.
- Intervention
- Oral glutathione, 500 mg once daily for 6 months, was given in addition to ongoing anti-diabetic therapy.
- Key limitation
- The main glycemic benefit was modest overall, with no significant between-group HbA1c advantage in the full diabetic cohort.
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Open PDFOriginal abstract
Complications in type 2 diabetes (T2D) arise from hyperglycemia-induced oxidative stress. Here, we examined the effectiveness of supplementation with the endogenous antioxidant glutathione (GSH) during anti-diabetic treatment. A total of 104 non-diabetic and 250 diabetic individuals on anti-diabetic therapy, of either sex and aged between 30 and 78 years, were recruited. A total of 125 diabetic patients were additionally given 500 mg oral GSH supplementation daily for a period of six months. Fasting and PP glucose, insulin, HbA1c, GSH, oxidized glutathione (GSSG), and 8-hydroxy-2-deoxy guanosine (8-OHdG) were measured upon recruitment and after three and six months of supplementation. Statistical significance and effect size were assessed longitudinally across all arms. Blood GSH increased (Cohen’s d = 1.01) and 8-OHdG decreased (Cohen’s d = −1.07) significantly within three months (p < 0.001) in diabetic individuals. A post hoc sub-group analysis showed that HbA1c (Cohen’s d = −0.41; p < 0.05) and fasting insulin levels (Cohen’s d = 0.56; p < 0.05) changed significantly in diabetic individuals above 55 years. GSH supplementation caused a significant increase in blood GSH and helped maintain the baseline HbA1c overall. These results suggest GSH supplementation is of considerable benefit to patients above 55 years, not only supporting decreased glycated hemoglobin (HbA1c) and 8-OHdG but also increasing fasting insulin. The clinical implication of our study is that the oral administration of GSH potentially complements anti-diabetic therapy in achieving better glycemic targets, especially in the elderly population.