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Mitochondria supply the energy needed for organ function, movement, and recovery from stress. Protecting their function is therefore relevant to healthy aging. Mitochondrial care should address both avoidable injury and the potential of targeted nutrient treatment. This narrative review examines environmental stressors, medications across 14 therapeutic groups, and selected nutrient interventions. Its central message is that preventing deficiency and optimizing function are different objectives. Higher doses improve outcomes in some cofactor-responsive disorders; a small study in adult-onset mitochondrial myopathy also reported improved muscle performance. These findings justify testing whether greater nutrient availability can overcome impaired transport, utilization, or increased metabolic demand in other patients. The I-OM functional-dose hypothesis proposes that selected metabolic constraints may respond to exposures above conventional replacement doses. Author-recorded ranges define research questions rather than validated mitochondrial prescriptions. Published intervention results, author-proposed ranges, and documented adverse exposures are distinguished; unresolved historical claims are segregated in the appendix. The highest dose reported is not necessarily the most effective dose or a safe ceiling. Vitamin D concentrations likewise require interpretation alongside calcium metabolism, renal function, and clinical outcomes. The proposed approach combines exposure reduction, essential nutrient adequacy, and individualized investigation of higher-dose nutrition, guided by measurable functional benefit and harm. This framework supports a more active research agenda for mitochondrial health and healthy longevity; it does not establish a universal supplement regimen or demonstrate extension of human lifespan.
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Richard Z. Cheng (2026) studied this question.
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