What is behind Skin, Hair & Nails
The body's largest organ and its most visible record. Collagen, elastin and barrier lipids degrade on a measurable schedule — and the evidence shows the degradation mechanisms specifically, because that is what the evidence actually witnesses. Evidence A — Human trial evidence.
Tissue structure and remodeling. Evidence A — Human trial evidence.
The transcription factor that commands the body's own antioxidant and detoxification arsenal. Evidence A — Human trial evidence.
The master inflammatory switch — indispensable to defend against threat, corrosive when it never stands down. Evidence B — Preclinical.
Nitric-oxide blood-vessel relaxation and flow. Evidence A — Human trial evidence.
Advanced glycation end-products — the sugar-damaged proteins that stiffen tissue and inflame the vessel wall. Evidence A — Human trial evidence.
Estrogen balance — set largely by the aromatase enzyme that converts androgens into estrogen — shapes reproductive, bone, skin and metabolic health. The aim is healthy balance for the individual, not simply more or less. Evidence A — Human trial evidence.
Dihydrotestosterone — the potent 5α-reductase product that binds the dermal-papilla androgen receptor and drives follicular miniaturization. Evidence A — Human trial evidence.
Keratin plates that record the last six months of systemic health. Direction uncertain: koilonychia is a sign of iron deficiency, not a cause of it, so the arrow may be drawn backwards.
Evidence on these pathways
NF-κB → CD38 NADase. “Regulation of CD38 expression in HASM cells involves the transcription factor NF-κB, and glucocorticoids inhibit this expression through NF-κB-dependent and -independent mechanisms.” — Regulation of the cd38 promoter in human airway smooth muscle cells by TNF-α and dexamethasone. Respiratory Research, 2008, vol 9, 26. doi:10.1186/1465-9921-9-26
NF-κB → COX-2 Induction. “Moreover, the nuclear factor kappa B (NF-κB) inhibitor BAY11‐7085 or the TLR4 neutralizing antibody markedly blocked PM2.5-induced IL-6 and COX-2 expression.” — PM2.5 exposure upregulates pro-inflammatory protein expression in human microglial cells via oxidant stress and TLR4/NF-κB pathway. Ecotoxicology and Environmental Safety, 2024, vol 277, article 116386. doi:10.1016/j.ecoenv.2024.116386
NF-κB → Kynurenine Pathway. “Treatment of vaccinated DCs with pharmacological NF-κB inhibitors ACHP or DHMEQ significantly inhibited IDO1 biosynthesis, suggesting a role for NF-κB signaling in vaccine up-regulation of dendritic cell IDO1.” — Induction of Indoleamine 2, 3-Dioxygenase in Human Dendritic Cells by a Cholera Toxin B Subunit—Proinsulin Vaccine. PLoS ONE, 2015, volume 10, e0118562. doi:10.1371/journal.pone.0118562
NF-κB → Muscle Recovery. “Activation of NF-κB in skeletal muscle leads to degradation of specific muscle proteins, induces inflammation and fibrosis, and blocks the regeneration of myofibers after injury/atrophy.” — Nuclear factor-kappa B signaling in skeletal muscle atrophy. Journal of Molecular Medicine, 2008, volume 86, issue 10, pages 1113-1126. doi:10.1007/s00109-008-0373-8
Formulas that act on these pathways
Acts on 5 of these pathways: Skin Structure & Barrier, Nrf2, NF-κB, Advanced Glycation (AGEs), Nail Health.
Acts on 3 of these pathways: Nrf2, NF-κB, DHT.
Acts on 3 of these pathways: Skin Structure & Barrier, Nrf2, NF-κB.
Acts on 3 of these pathways: Nrf2, NF-κB, Advanced Glycation (AGEs).
Acts on 3 of these pathways: Nrf2, NF-κB, Advanced Glycation (AGEs).
What this page does not claim
This page names the pathways involved and the published evidence on each. It does not claim that any formula treats, cures or prevents Skin, Hair & Nails. A pathway opens here only on graded, published evidence, under a standard fixed before the evidence was gathered, and every figure above carries its grade.
These statements have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat, cure or prevent any disease.