Anti-aging

Ashwagandha (Withania somnifera) has accumulated strong clinical trial evidence for cortisol reduction, testosterone support, and stress adaptation. This practitioner-level review covers mechanisms, trials, dosing, and safety.

Rhodiola rosea (Arctic root) modulates the stress response via salidroside and rosavins. This review covers clinical trial data on fatigue, cognitive performance, cortisol, and exercise adaptation.

A clinician-to-patient framework covering autophagy mechanisms (mTOR/AMPK), types (macroautophagy, mitophagy), fasting protocols (16:8, 24h, 5:2), autophagy-inducing compounds (spermidine, resveratrol, berberine), and clinical cautions: for naturopathic practice.

Senescent cells accumulate with age and drive chronic inflammation through the SASP. Here's the current evidence on senolytics (compounds that selectively clear senescent cells) including quercetin, dasatinib, fisetin, and navitoclax, from early-phase clinical trials.

Growth hormone secretagogues stimulate endogenous pulsatile GH release rather than replacing it, preserving the physiological pulse architecture that exogenous GH overrides. This article covers somatotroph biology, the IGF-1 axis, the difference between secretagogue and exogenous GH pharmacology, and what the longevity and body composition data shows.

Epigenetic clocks measure biological age through DNA methylation patterns at specific CpG sites, and several peptide interventions have produced measurable clock reversals in preclinical and early clinical research. This article covers how the Horvath, GrimAge, and DunedinPACE clocks work, what they measure, and what the Yamanaka factor and peptide intervention data means for ageing biology.

Partial cellular reprogramming using Yamanaka factors (Oct4, Sox2, Klf4, c-Myc) transiently reverses epigenetic age in somatic cells without inducing pluripotency. This review examines the mechanistic basis, key experimental findings, and the distinction between full and partial reprogramming.

Cellular senescence (the irreversible arrest of damaged cells) drives tissue inflammation and age-related pathology through the SASP. This review examines peptide-based senolytic strategies targeting senescent cell survival pathways.

GHK-Cu (glycyl-L-histidyl-L-lysine copper complex) is an endogenous tripeptide that declines with age and activates over 4,000 genes involved in collagen synthesis, wound repair, anti-inflammatory signalling, and antioxidant defence. This article covers the copper binding chemistry, the TGF-β and decorin pathway interactions, and the skin and wound healing data.