Andrew Huberman talks with mitochondria researcher Dr. Jared Rutter (University of Utah, HHMI) about how mitochondria generate cellular energy, regulate cell growth and division, and link to aging and cancer. The conversation frames metabolism as an emergent property of trillions of individual mitochondria-containing cells.
Listen →In mice, opioids and methamphetamine (but not natural rewards) trigger calcium influx through the mitochondrial calcium uniporter in dopamine-releasing nerve terminals, fueling the rapid ATP production that sustains drug-driven dopamine surges. Blocking this mitochondrial calcium channel genetically or pharmacologically reduced drug-induced dopamine release and addictive behavior without disrupting normal reward processing, pointing to it as a possible addiction drug target.
Read source →A new nanobody-based delivery system precisely targets healthy donor mitochondria to damaged neurons, cardiac cells, and other specific cell types — rescuing degenerating neurons in both a human optic-nerve-atrophy cell model and mice. Still preclinical, but a concrete step toward treating primary mitochondrial diseases like TK2 deficiency.
Read source →Dr. Martin Picard (Columbia) explains how mitochondria translate behavior, psychology, and mindset into cellular energy production, and how exercise, nutrition, sleep, and stress reduction measurably affect mitochondrial function and aging markers.
Listen →Dr. Martin Picard (Columbia) explains how mitochondria translate behavior, psychology, and mindset into cellular energy production, and how exercise, nutrition, sleep, and stress reduction measurably affect mitochondrial function and aging markers.
Listen →In a placebo-controlled RCT of 50 healthy middle-aged adults, 1,000 mg/day of urolithin A for 4 weeks expanded naive, less-exhausted CD8+ T cells and measurably increased mitochondrial biogenesis within those immune cells — a rare case of a supplement showing a measurable immune-aging effect this quickly. Conducted with the Buck Institute for Research on Aging.
Read source →The cardiolipin-targeting peptide SS-31/elamipretide became the first approved therapy for Barth syndrome, based on >45% improvement in knee extensor muscle strength in the Phase 2 TAZPOWER trial — a landmark for the whole mitochondrial-peptide class.
Read source →Huberman and Attia dig into the NAD+ pathway, comparing NAD, NMN, and NR supplementation, routes of administration, and what the clinical literature actually supports for longevity.
Listen →López-Otín, Blasco, Partridge, Serrano & Kroemer expand the hallmarks of aging from 9 to 12, including mitochondrial dysfunction — and map how each hallmark reinforces the others.
Read source →A 4-month, placebo-controlled RCT (NCT03464500) found ~12% gains in muscle strength and improved mitochondrial biomarkers (lower plasma acylcarnitines and CRP) from the mitophagy-activating postbiotic Urolithin A.
Read source →In transgenic mouse models, the mitochondrial-derived peptide MOTS-c boosted intrinsic muscle mitochondrial bioenergetics and lowered ROS-related oxidative damage — requiring both PGC-1α and AMPK signalling, without increasing raw mitochondrial volume. Animal data only; a human Phase 2a trial (MOTS-MET) for prediabetes began enrolling in 2026.
Read source →An evergreen research hub tracking the evidence base for Urolithin A as a mitophagy-inducing postbiotic, updated as new studies land.
Read source →A 2026 Nature Metabolism review of how mitophagy, biogenesis, and mitochondrial network dynamics change with age, and what that means for healthspan interventions targeting mitochondrial quality rather than just quantity.
Read source →This PRISMA systematic review pooled 113 studies (33 human, 80 rodent) on NAD+-boosting compounds like NR and NMN. It found rodent studies often showed metabolic and mitochondrial benefits, but in humans, oral NR/NMN reliably raised NAD+-related biomarkers while effects on real functional and health outcomes were mixed or null, and no outcomes trials existed yet for IV/wellness-clinic NAD+ infusions.
Read source →Mitrix Bio is manufacturing donor mitochondria in bioreactors and infusing them into paying patients at Right to Try clinics in Texas, California, and Florida — including a 91-year-old physicist as one of its first two patients. No peer-reviewed efficacy data exists yet. Included as a development worth watching, not a recommendation — this is an unregulated, direct-to-consumer offering with an N of 2.
Read source →Using bioinformatic and protein-docking analysis, researchers compared the mitochondrial-derived peptide humanin across mammals with different oxidative-stress profiles (deep-diving cetaceans, high-metabolism shrews, long-lived primates). Species under greater oxidative stress carried more structurally stable humanin variants, suggesting evolution has tuned the peptide's protective function and offering a template for designing humanin-based therapeutic analogs.
Read source →This narrative review synthesizes mechanistic and preclinical evidence that the supplement PQQ activates mitochondrial biogenesis pathways (CREB, PGC-1a, TFAM) and protects against oxidative injury, applying that evidence to skin aging and recovery after aesthetic procedures. The authors note the dermatology-specific human evidence base is still thin relative to the preclinical mechanism data.
Read source →This narrative review examines how heat acclimation protocols alter mitochondrial biogenesis and bioenergetic function across cell, rodent, and human studies, and links those subcellular changes to exercise performance gains. The authors propose a heat-acclimation protocol designed to maximize mitochondrial adaptation and flag open questions for future research.
Read source →Preclinical work showing MOTS-c, an mtDNA-encoded peptide, restores mitochondrial respiration and energy homeostasis in a type 2 diabetic cardiac model — building the mechanistic case for its "exercise mimetic" reputation.
Read source →A deep dive into Zone 2 training dose, frequency, and duration, and how it drives mitochondrial biogenesis and oxidative capacity.
Listen →A masterclass on energy system pathways, fuel sources, exercise training zones, and mitochondrial function as both a diagnostic and treatment target for metabolic health.
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