Depletes CoQ10. This medication is commonly used for Diabetes
Sulfonylureas, a class of anti-diabetic drugs, have been found in research to significantly deplete Coenzyme Q10 (COQ10). This nutrient may be beneficial to individuals with diabetes as it is found to assist: high blood pressure, decrease triglycerides, improve HDL cholesterol, and provide glycemic control.
Pelton R. Coenzyme Q10: A Miracle Nutrient Advances in Understanding. Integr Med (Encinitas). 2020 Apr;19(2):16-20. PMID: 33041702; PMCID: PMC7482328.Miyake Y, Shouzu A, Nishikawa M, et al. Effect of treatment with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors on serum coenzyme Q10 in diabetic patients. Arzneimittelforschung. 1999;49(4):324-329. Pelton R, LaValle J, Hawkins EB, et al. Drug Induced Nutrient Depletion Handbook. Hudson, OH:LexiComp, Inc.;2001:409. Berger W. Incidence of severe side effects during therapy with sulfonylureas and biguanides. Horm Metab Res Suppl. 1985;15:111-115.
Ubiquinol/Ubiquinone — 50mg of each
CoQ10 deficiency can present in infancy as a severe encephalomyopathy or multisystemic mitochondrial disease, with features such as hypotonia, developmental delay, intractable seizures, lactic acidosis, cardiomyopathy, and failure to thrive. Reports of infantile‑onset multisystem CoQ10 deficiency describe very early presentations, sometimes in the neonatal period, with rapid neurologic deterioration and involvement of brain, heart, kidney, and liver, and many affected children die in the first months or years of life despite intensive care. The important clinical point is that, although outcomes are often poor in the most severe cases, some infants and young children show neurologic improvement or stabilization when CoQ10 deficiency is recognized early and high‑dose CoQ10 supplementation is started promptly, which is why this diagnosis is considered a treatable cause of infantile encephalomyopathy
CoQ10 is a key mitochondrial antioxidant, and circulating levels are often reduced in people with chronic kidney disease and chronic heart failure, where deficiency is linked to greater oxidative stress and poorer organ function. In CKD cohorts, lower CoQ10 levels correlate with increased cardiovascular risk, and supplementation has been reported to improve markers such as proteinuria, mitochondrial function, and oxidative stress, with some studies suggesting better preservation of kidney function over time. In patients with chronic heart failure, trials such as Q-SYMBIO have shown that CoQ10 supplementation can improve cardiac function parameters and significantly reduce major adverse cardiovascular events, cardiovascular mortality, and heart‑failure–related hospitalizations.