Low-grade chronic inflammation in ageing patients quietly sensitises pain receptors and disrupts mitochondrial energy production. This results in a clinical constellation often seen in older adults:

• Persistent, nonspecific muscle or joint pain

• Reduced physical resilience and easy fatigability

• Non-restorative sleep and heightened sensory sensitivity

• “Idiopathic” fatigue that doesn’t respond to conventional therapies

Emerging biomedical evidence highlights a bidirectional relationship: inflammation impairs mitochondrial function → lower ATP output → more reactive oxygen species (ROS) → further inflammation → more mitochondrial damage. This vicious cycle underpins syndromes like fibromyalgia, chronic fatigue, and frailty.