Collections · Evidence-graded
Mitochondrial Support
Compounds that repair, energize, and protect the cellular powerhouse
How it works
Mitochondrial dysfunction — declining ATP output, increased ROS generation, impaired fission/fusion dynamics, and accumulated mtDNA damage — is a primary hallmark of aging. Multiple compounds address different nodes: electron transport chain support (CoQ10), mitophagy induction (urolithin A), NRF2-mediated antioxidant defense (sulforaphane), cofactor support (ALA, glycine), and NAD+ repletion (NR).
Evidence overview
A curated set of compounds with the strongest evidence for supporting mitochondrial function, biogenesis, or quality control. Spans CoQ10 (ETC cofactor), urolithin A (mitophagy), sulforaphane (NRF2), alpha-lipoic acid (co-factor + antioxidant), epicatechin (PGC-1α biogenesis), NR, and the GlyNAC glutathione pair.
The mitochondrial electron carrier that declines with age and statin use — with cardiovascular trial support.
A mitochondrial cofactor active in both fat and water — the only antioxidant that regenerates glutathione, vitamin C, and vitamin E simultaneously.
A gut-derived metabolite that triggers mitophagy — with human trials on muscle and mitochondrial function.
The most potent known NRF2 activator, from broccoli, with human trials in cancer chemoprevention and neuroprotection.
The dark chocolate flavonoid linked to myostatin inhibition, cardiovascular protection, and mitochondrial biogenesis in human trials.
The leading NMN alternative — a direct NAD+ precursor with multiple RCTs confirming it safely raises NAD+ levels in humans.
A conditionally essential amino acid that becomes deficient with age and suppresses mTORC1 — extended median lifespan 28% in NIH mice studies.
A glutathione-restoring amino-acid pair with promising small trials on oxidative stress and aging markers.
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