Mitochondrial

A research-based comparison of NMN and NR as NAD+ precursors — covering the salvage pathway, Brenner and Yoshino human trial data, bioavailability debate, sublingual NMN, dose protocols, cost in the Australian market, and how to test NAD+ levels.

CoQ10 (ubiquinone) and ubiquinol are two forms of the same mitochondrial cofactor. This clinical review covers bioavailability data, age-related conversion decline, statin depletion, and evidence-based dosing for practitioners.

A systematic comparison of NAD+ precursors — NMN vs NR vs niacin vs NMN riboside — covering mechanisms, bioavailability, clinical trial data, dosing, and what naturopathic practitioners need to know in 2026.

Mitochondrial-derived peptides (MDPs) are a recently characterised class of signalling molecules encoded in the mitochondrial genome that act as systemic stress signals. This overview covers the known MDPs — humanin, MOTS-c, SHLP2 — their receptor targets, and what the mitokine concept means for understanding mitochondria as endocrine organs.

NAD+ is a coenzyme central to mitochondrial energy metabolism whose decline with age activates the sirtuin longevity pathway deficit. This article covers the NAD+/NADH ratio as a metabolic signal, how sirtuins read it, and what the preclinical data on NAD+ precursors reveals about the sirtuin-PARP competition that determines whether the cell repairs or ages.

MOTS-c is a 16-amino acid peptide encoded within the mitochondrial 12S rRNA gene that translocates to the nucleus during metabolic stress, activating AMPK and the folate-methionine cycle to restore metabolic homeostasis. This article covers its discovery, nuclear translocation mechanism, and what the exercise and metabolic stress data reveals about its role in adaptation.

Humanin and small humanin-like peptides (SHLPs 1–6) are mitochondrial-derived peptides encoded in the 16S rRNA gene. This review examines their cytoprotective, metabolic, and longevity-associated mechanisms.

SS-31 (elamipretide) is a tetrapeptide that selectively concentrates in the inner mitochondrial membrane through electrostatic interaction with cardiolipin, restoring electron transport chain efficiency and reducing mitochondrial ROS production. This article covers the cardiolipin biology, the targeting mechanism, and what the preclinical data shows across cardiac, renal, and neurological models.