What is behind Inflammation & Pain
Chronic low-grade inflammation in peripheral tissue — vessel wall, myocardium, follicle, joint. Evidence B — Preclinical.
A cytokine with two faces. Chronically elevated it is a core inflammaging marker; acutely released from contracting muscle it is a myokine with metabolic benefit. Same molecule, opposite meaning by context. Evidence B — Preclinical.
The master inflammatory switch — indispensable to defend against threat, corrosive when it never stands down. Evidence B — Preclinical.
An inducible enzyme switched on by inflammatory signaling. Evidence A — Human trial evidence.
The NLRP3 inflammasome — a sensor of cellular stress that ignites sterile, damage-driven inflammation. Evidence A — Human trial evidence.
The transcription factor that commands the body's own antioxidant and detoxification arsenal. Evidence A — Human trial evidence.
A master inflammatory messenger of the immune system.
Evidence on these pathways
IL-6 → Systemic Inflammation. “IL-6 is the chief stimulator of the production of most acute phase proteins [8], whereas the other implicated cytokines influence subgroups of acute phase proteins.” — Interleukin-6 and chronic inflammation. Arthritis Research & Therapy, 2006, volume 8, Suppl 2, S3. doi:10.1186/ar1917
NLRP3 Inflammasome → Caspase-1. “The NLRP3 inflammasome is a critical component of the innate immune system that mediates caspase-1 activation and the secretion of proinflammatory cytokines IL-1β/IL-18 in response to microbial infection and cellular damage.” — The NLRP3 Inflammasome: An Overview of Mechanisms of Activation and Regulation. International Journal of Molecular Sciences, 2019, 20(13), 3328. doi:10.3390/ijms20133328
NLRP3 Inflammasome → Osteoarthritis. “Mechanistically, ERK5 interacted with the PYD domain of NLRP3 and mediated NLRP3 phosphorylation at serine 198, which facilitated mature inflammasome assembly, triggered pyroptosis and subsequently exacerbated OA progression.” — Inhibition of ERK5 activity ameliorates osteoarthritis by suppressing NLRP3 inflammasome-mediated chondrocyte pyroptosis. Bone Research; 2026; volume 14; article number 95. doi:10.1038/s41413-026-00573-x
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
Formulas that act on these pathways
Acts on 6 of these pathways: Systemic Inflammation, IL-6, NF-κB, COX-2 Induction, NLRP3 Inflammasome, Nrf2.
Acts on 5 of these pathways: Systemic Inflammation, IL-6, NF-κB, NLRP3 Inflammasome, Nrf2.
Acts on 5 of these pathways: Systemic Inflammation, IL-6, NF-κB, COX-2 Induction, NLRP3 Inflammasome.
Acts on 5 of these pathways: Systemic Inflammation, IL-6, NF-κB, NLRP3 Inflammasome, Nrf2.
Acts on 5 of these pathways: Systemic Inflammation, IL-6, NF-κB, NLRP3 Inflammasome, Nrf2.
Acts on 4 of these pathways: Systemic Inflammation, IL-6, NF-κB, Nrf2.
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 Inflammation & Pain. 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.