Depletes CoQ10. This medication is commonly used for Diabetes
Biguanide (anti-diabetic) drugs have been found in scientific evidence to decrease serum levels of coenzyme Q10. Type 2 diabetes can increase oxidative stress in the body, weakening its defenses and potentially harming cells. CoQ10, a powerful antioxidant, plays a crucial role in protecting cells from this damage. CoQ10 supplementation may help restore these levels, potentially improving mitochondrial function and protecting the kidneys from damage.
Sourris KC, Harcourt BE, Tang PH, Morley AL, Huynh K, Penfold SA, Coughlan MT, Cooper ME, Nguyen TV, Ritchie RH, Forbes JM. Ubiquinone (coenzyme Q10) prevents renal mitochondrial dysfunction in an experimental model of type 2 diabetes. Free Radic Biol Med. 2012 Feb 1;52(3):716-723.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. Kishi T, et al. Bioenergetics in clinical medicine. XI. Studies on CoQ and diabetes mellitus. J Med 1976;7: 307-321.
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.
CoQ10 deficiency has been identified as a potentially reversible cause of steroid‑resistant nephrotic syndrome and glomerular nephropathy, particularly in children and young adults with genetic defects in CoQ10 biosynthesis. In reported series, affected patients often present with heavy proteinuria and progressive kidney dysfunction that fail to respond to standard steroid therapy, but genetic testing sometimes reveals mutations in CoQ10‑related genes (such as COQ2, COQ6, or ADCK4). The encouraging part is that in a subset of these cases, early and sufficiently dosed CoQ10 supplementation has been associated with reduced proteinuria and stabilization or partial improvement of kidney function, making it an important, treatable consideration in otherwise unexplained steroid‑resistant nephrotic syndrome.
In some children and young adults, primary CoQ10 deficiency has been linked to hypertrophic cardiomyopathy (HCM), where the heart muscle becomes abnormally thick and stiff despite the absence of more common causes like longstanding hypertension. Case series and reports describe patients with genetically confirmed CoQ10 biosynthetic defects who develop HCM alongside other mitochondrial features such as exercise intolerance, muscle weakness, or neurologic symptoms, and cardiac imaging often shows concentric or asymmetric left ventricular hypertrophy. The hopeful aspect is that early recognition and CoQ10 supplementation have, in some documented cases, led to improved cardiac function or stabilization of wall thickness over time, making CoQ10 deficiency a particularly important and potentially treatable consideration in otherwise unexplained or familial‑appearing HCM.