Fatigue Pathophysiology is the scientific study of the underlying biological, cellular, and molecular mechanisms that precipitate the subjective experience of profound, persistent, and often disabling fatigue that is unresponsive to conventional rest. This complex domain investigates the multi-systemic failures contributing to this state, including mitochondrial dysfunction, chronic neuroinflammation, and persistent neuroendocrine dysregulation. Identifying the specific dysfunctional pathways is paramount for developing effective, targeted clinical interventions.
Origin
The term is a synthesis of the clinical symptom “fatigue” and the scientific discipline “pathophysiology,” which examines how disease processes disrupt normal bodily function. It represents a crucial shift from viewing chronic fatigue as purely psychological to recognizing it as a measurable, biologically based clinical syndrome with distinct molecular signatures.
Mechanism
Key mechanisms often involve compromised Adenosine Triphosphate (ATP) production due to measurable mitochondrial impairment and chronic, low-grade immune activation leading to elevated pro-inflammatory cytokines. These cytokines directly interfere with central nervous system function and neurotransmitter balance. Furthermore, hormonal imbalances, particularly HPA axis dysregulation and subtle thyroid axis impairment, contribute by disrupting cellular metabolic rate and energy substrate utilization, perpetuating a state of systemic energy deficit.
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