What is behind Heart & Circulation
Blood pressure — the force of blood against the vessel wall, a master cardiovascular gauge. Evidence A — Human trial evidence.
Nitric-oxide blood-vessel relaxation and flow. Evidence A — Human trial evidence.
The master inflammatory switch — indispensable to defend against threat, corrosive when it never stands down. Evidence B — Preclinical.
The cell's master energy sensor — when fuel runs low it ignites fat-burning, glucose uptake and mitochondrial renewal while standing down growth. Evidence A — Human trial evidence.
The transport and handling of fats, not simply their level. Particle number, size and oxidation state carry more predictive weight than total cholesterol — a distinction the mainstream number obscures. Evidence A — Human trial evidence.
The heart as a pump and as a tissue that remodels. Evidence A — Human trial evidence.
Structural change of the heart muscle — wall thickening and fibrous scarring laid down in response to sustained load.
The heart muscle cell — attacked by the virus, then by the defense against it. Evidence A — Human trial evidence.
Cardiac excitation-contraction coupling — the calcium cycling that every inotrope and every physiological lever ultimately works through. Evidence A — Human trial evidence.
Evidence on these pathways
AMPK → Insulin Sensitivity. “In model systems, sustained decreases in AMPK activity accompany IR, whereas AMPK activation increases insulin sensitivity.” — AMPK, insulin resistance, and the metabolic syndrome. The Journal of Clinical Investigation, 2013, volume 123, issue 7, pages 2764-2772. doi:10.1172/JCI67227
Blood Pressure → Cardiovascular Health. “The randomised, double-blind, placebo-controlled Systolic Hypertension in Europe trial (Syst-Eur 1) proved that blood pressure (BP) lowering therapy starting with nitrendipine reduces the risk of cardiovascular complications in elderly patients with isolated systolic hypertension.” — How well can blood pressure be controlled? Progress report on the Systolic Hypertension in Europe Follow-Up Study (Syst-Eur 2). Current Controlled Trials in Cardiovascular Medicine, 2001, 2(6), 298–306 (the DOAJ record prints the issue and pages; the present-day BioMed Central page shows the journal as Trials, article 298). doi:10.1186/cvm-2-6-298
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
Formulas that act on these pathways
Acts on 6 of these pathways: Blood Pressure, NF-κB, AMPK, Lipid Metabolism, Cardiac Remodeling, Calcium Handling.
Acts on 3 of these pathways: NF-κB, AMPK, Lipid Metabolism.
Acts on 3 of these pathways: NF-κB, AMPK, Lipid Metabolism.
Acts on 3 of these pathways: NF-κB, AMPK, Lipid Metabolism.
Acts on 3 of these pathways: NF-κB, AMPK, Lipid Metabolism.
Acts on 3 of these pathways: NF-κB, AMPK, Lipid Metabolism.
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 Heart & Circulation. 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.