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Background: Aluminum neurotoxicity has been implicated in neurodevelopmental disorders, including autism spectrum disorder (ASD). Nonchelation approaches that may influence urinary metal excretion remain largely unexplored. Photobiomodulation (PBM) at 660 nm modulates mitochondrial cytochrome c oxidase activity and cellular bioenergetics, with possible downstream effects on renal physiology. Case: A 5-year-old boy with ASD and a historical elevated urinary aluminum result (220 µg/g creatinine at age 3) underwent serial urine toxic metals testing. Methods: Al, with creatinine by Jaffé reaction. Two baseline specimens preceded pulsed 660 nm PBM initiation. A follow-up specimen was collected January 21, 2026. Intervention: Pulsed 660 nm PBM via multi-diode red laser (Program #1: 9/33/60 Hz, 15 min/session, 3 × /day) on Days 3-8. Specimens collected as consistent first morning voids. Results: Baseline urinary aluminum was stable (10.0 and 9.8 µg/g creatinine; reference <40). After PBM, aluminum rose to 58 µg/g on Day 3 and peaked at 98 µg/g on Day 7. A severely dilute Day 8 specimen was excluded. At two-month follow-up, aluminum remained above reference (49 µg/g). Mercury exceeded reference in all specimens including baseline. Follow-up mercury rose to 8.4 µg/g creatinine with urine pH >8.0. Conclusion: This case describes a temporal increase in urinary aluminum excretion following pulsed 660 nm PBM. Urinary aluminum alone is insufficient to establish systemic mobilization, reduced tissue burden, or clinical benefit. The observation is hypothesis-generating; controlled studies with verified dosimetry and validated outcomes are warranted.
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Zaharakis et al. (2026) studied this question.
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