Systemic redox imbalance in neurodegeneration: How industrial metabolic disruption and colonial health legacies drive cellular dysfunction

Indigenous systems (e.g., Amazonian *ayahuasca* ceremonies, Tibetan *tummo* practices) treat redox imbalance as a symptom of spiritual and ecological disconnection, using plant-based therapies that enhance mitochondrial efficiency. Modern science validates these approaches: curcumin (turmeric) and resveratrol (grapes) modulate ROS via Nrf2 pathways, yet Indigenous knowledge is excluded from funding and citation networks. The erasure of these traditions reflects a colonial epistemology that dismisses non-Western metabolic insights as 'anecdotal'.

The 19th-century 'disease of civilisation' debate (e.g., George Beard’s neurasthenia) parallels today’s redox crisis, linking industrialisation to neural degeneration via dietary and environmental toxins. Colonial medical systems prioritised acute infectious disease treatment over chronic metabolic disorders, creating lasting disparities in neurodegeneration research and care. The 1950s discovery of mitochondrial DNA damage by ROS was foreshadowed by Indigenous observations of 'soul loss' in dementia, yet Western science only now acknowledges these patterns.

Cross-culturally, redox imbalance is framed as a rupture between human and ecological systems: Māori link it to *mauri* (life force) depletion from land exploitation, while Chinese medicine ties it to *qi* stagnation from environmental pollution. African diasporic traditions use *bush medicine* (e.g., *Sutherlandia frutescens*) to restore mitochondrial function, with clinical trials showing efficacy in reducing ROS. These parallels suggest a universal metabolic response to ecological disruption, yet Western science treats them as isolated phenomena.

Scientific consensus confirms ROS as a driver of neurodegeneration via lipid peroxidation, protein aggregation, and mitochondrial DNA damage, but the field lacks integration of environmental epigenetics and transgenerational toxic exposure. Studies show glyphosate and microplastics disrupt redox homeostasis, yet research funding prioritises drug development over pollution regulation. The 'mystery' of ROS formation stems from reductionist cell biology that ignores systemic interactions between diet, microbiome, and xenobiotics.

Artistic traditions encode redox imbalance as a metaphor for societal decay: Dante’s *Inferno* maps neural chaos to industrial pollution, while African griot oral histories link cognitive decline to colonial land theft. Modern neuroaesthetics research shows that art therapy (e.g., mandala drawing) reduces oxidative stress via parasympathetic activation, yet this is dismissed as 'subjective'. Spiritual practices like Sufi *dhikr* or Hindu *pranayama* enhance mitochondrial efficiency through breathwork, a mechanism validated by studies on CO₂-induced ROS modulation.

Future scenarios must model neurodegeneration as a convergence of industrial metabolic disruption, climate-induced toxin release, and healthcare inequities. Projections suggest a 300% increase in Alzheimer’s by 2050 if agrochemical use and urban pollution continue unchecked, disproportionately affecting Global South populations. Scenario planning should include Indigenous land stewardship models (e.g., *milpa* systems) and circular economy policies to reduce mitochondrial toxic load.

Marginalised communities bear disproportionate redox burdens: Black Americans have higher ALS rates due to lead exposure from redlining, while Indigenous peoples face mitochondrial damage from uranium mining (e.g., Navajo Nation). Global South researchers (e.g., in Nigeria or India) document environmental epigenetics in neurodegeneration but lack funding to publish in high-impact journals. Their insights—such as the role of aflatoxins in ALS—are sidelined in favour of Western genetic determinism.