Nitric Oxide decline is a multi-factorial process rooted in cellular aging. The primary culprit is the progressive dysfunction of eNOS (endothelial nitric oxide synthase)—the enzyme responsible for producing NO—which becomes less efficient with age. Simultaneously, oxidative stress intensifies as environmental aggressors and natural metabolic processes generate free radicals that destroy NO molecules faster than they can be synthesized. The endothelial cells where NO production occurs also deteriorate over time, becoming damaged by chronic inflammation and glycation, further compromising their ability to manufacture adequate NO. Additionally, essential cofactors like BH4 (tetrahydrobiopterin) become depleted, while inhibitory compounds such as ADMA accumulate, directly blocking the enzymatic pathways needed for NO synthesis. The result is a compounding effect: less NO is produced, more is destroyed, and the cellular infrastructure required for its creation steadily weakens—manifesting visibly as reduced circulation, impaired collagen production, and the gradual loss of skin vitality.
