Summary
This narrative review synthesises evidence on how persistent cellular stress from lifestyle factors (psychological stress, sleep disruption, hypercaloric intake, physical inactivity) drives failure of adaptive homeostatic mechanisms, leading to chronic non-communicable diseases. The authors propose a unifying model wherein chronic pathology emerges from cumulative failure of cellular resilience systems—including redox regulation, proteostasis, mitochondrial quality control, autophagy, and DNA damage response—rather than isolated organ-specific defects. The review highlights circadian rhythm disruption and hypothalamic-pituitary-adrenal axis overactivation as central to this process, and identifies sleep optimisation, stress reduction, and metabolic regulation as mechanistically grounded preventive interventions.
Regional applicability
The mechanisms described are universal to human physiology and thus applicable to United Kingdom populations. The lifestyle risk factors identified (chronic stress, poor sleep, overconsumption, sedentariness) are highly prevalent in high-income countries including the UK, making the proposed prevention strategies relevant to UK public health policy and individual clinical practice.
Key measures
Biochemical mechanisms of cellular stress adaptation; oxidative damage; protein misfolding; mitochondrial dysfunction; low-grade inflammation; genomic instability; hypothalamic-pituitary-adrenal axis activity; glymphatic clearance; DNA repair capacity
Outcomes reported
The review examines how cellular homeostasis mechanisms (redox regulation, proteostasis, mitochondrial quality control, autophagy, DNA damage response) fail under sustained lifestyle stress, contributing to chronic disease development. It emphasises circadian and neuroendocrine regulation as key factors in cellular resilience and identifies sleep, stress reduction, and metabolic regulation as prevention strategies.
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