NOS1 is the human gene that encodes neuronal nitric oxide synthase (nNOS), an enzyme that produces nitric oxide (NO) from the amino acid arginine. NO is a short‑lived signaling gas that modulates vascular smooth muscle relaxation, microvascular blood flow, and some cellular signaling cascades. The rs1879417 site is a single nucleotide polymorphism (SNP) located in or near the NOS1 locus identified in population genetic studies. rs1879417 does not diagnose a condition but serves as an inherited marker of variation in NO‑related biology. It has emerged in genome‑wide and candidate‑gene analyses as a variant that can correlate with differences in expression or regulation of NOS1 and with physiological traits tied to vascular reactivity and hemodynamic patterns. As a stable genomic marker, it provides lifelong context for other dynamic biomarkers measured in blood and urine.

For a genetic marker like rs1879417, “higher” or “lower” refers to presence of alleles previously associated with relatively greater or lesser NOS1 activity or regulation in population studies. Presence of an allele associated with reduced NOS1 expression or function may correlate with patterns suggesting weaker nitric‑oxide signaling, which can influence vascular tone, microvascular responsiveness, or interactions with inflammatory and oxidative stress pathways. Conversely, an allele linked to higher NOS1 activity may associate with comparatively stronger NO signaling and related vascular responses. Interpretation requires the full Cardio Zoomer profile: genetic predispositions are one piece of the picture and should be read alongside lipid, inflammatory, metabolic, endothelial, and oxidative stress markers to understand overall cardiovascular‑related biology and risk patterns.

Cardio Zoomer includes NOS1 – rs1879417 to capture inherited variation in nitric‑oxide biology that can modify vascular tone and interact with lipid, inflammatory, and oxidative pathways. As a stable genetic clue, it helps clinicians interpret why an individual’s dynamic biomarkers and physiological patterns may differ from population averages, supporting more personalized risk mapping and targeted follow‑up testing strategies.