This paper revisits the pioneering contributions of John Nash Ott, a mid-20th-century photobiologist whose innovative time-lapse photography and controlled animal experiments demonstrated significant physiological and behavioral disruptions caused by artificial lighting deficient in full-spectrum wavelengths. Long regarded as anecdotal or inadequately explained, Ott's observations are reexamined here through the modern frameworks of redox biology and ferroptosis, providing a cohesive mechanistic explanation that bridges historical insights with cutting-edge science. Grounded in the Iron Trap Hypothesis, the analysis posits that spectral imbalances from unnatural light sources impair circadian entrainment, diminish NAD⁺ and melatonin synthesis, and attenuate Nrf2/HO-1 signaling pathways. These perturbations culminate in the sequestration of reactive iron species within tissues, precipitating lipid peroxidation, mitochondrial dysfunction, and ferroptosis—an iron-dependent, non-apoptotic cell death modality increasingly linked to prevalent conditions such as neurodegeneration, cardiovascular disease, and neurodevelopmental disorders. By synthesizing Ott's empirical findings with recent redox-focused studies (2024–2025), this paper reframes his work as a visionary antecedent rather than an anomaly, illuminating the interplay between environmental light exposure, iron homeostasis, and biological coherence. It establishes a novel interdisciplinary paradigm at the intersection of photobiology, environmental health, and oxidative stress research, with implications for preventive strategies in light-polluted modern environments. Keywords: John Nash Ott, ferroptosis, Iron Trap Hypothesis, redox biology, photobiomodulation, circadian disruption, Nrf2/HO-1 signaling, mitochondrial dysfunction, neurodegeneration, full-spectrum light.