Feb 24, 2026SIRT3 and Mitochondrial Integrity: NAD-Dependent Deacetylase, Caloric Restriction Mimicry, and ActivatorsSIRT3 is the primary mitochondrial sirtuin — a NAD-dependent deacetylase that regulates ATP synthesis, ROS detoxification, and fatty acid oxidation. Its activity declines with age and NAD+ depletion. Activators include honokiol, urolithin A, and exercise, though human trial data is thin.
Feb 18, 2026CoQ10 and Mitochondrial Function: Age-Related Decline and Clinical EvidenceCoQ10 declines with age and statin exposure. Human evidence is strongest in heart failure and statin-associated muscle symptoms, while prevention use in healthy adults remains less certain.
Feb 17, 2026SIRT3 Activators in Early Clinical Development: Mitochondrial Targets for AgingSIRT3 is a mitochondrial deacetylase linked to energy efficiency and oxidative stress resistance. Novel small-molecule SIRT3 activators are in preclinical development; human efficacy data does not yet exist.
Feb 8, 2026Mitochondria and Aging: Bioenergetics, ROS, Fission/Fusion Dynamics, and Intervention TargetsMitochondrial dysfunction is a central hallmark of aging. ATP production efficiency declines, ROS production increases, and the balance of fission (fragmentation) and fusion (elongation) shifts unfavorably. This article explains the biology and maps interventions — from CoQ10 to urolithin A — to specific mitochondrial nodes.
Feb 5, 2026Mitochondrial Health Stack: CoQ10, PQQ, Carnitine, ALA, and Urolithin A — Synergies and EvidenceA comprehensive mitochondrial support protocol addresses electron transport (CoQ10), fatty acid transport (carnitine), biogenesis (PQQ, urolithin A), and antioxidant protection (ALA). Each supplement addresses a different node in mitochondrial biology. Stacking rationale is strong, though direct synergy evidence in humans is limited.
Jan 8, 2026Urolithin A and Mitophagy: Direct Supplementation vs Pomegranate, Evidence ReviewUrolithin A is the most clinically studied mitophagy activator in humans. Amazentis trials show improved muscle function and mitochondrial biomarkers in older adults. Diet alone rarely produces adequate levels.