The CLOCK gene (Circadian Locomotor Output Cycles Kaput) is a core component of the human circadian clock. Together with other clock genes (e.g., PER, CRY), it regulates the 24‑hour sleep‑wake cycle, hormone secretion (melatonin, cortisol), and metabolic rhythms. Disrupted CLOCK function – due to genetic variants or chronic misalignment (e.g., shift work, late light exposure) – can shift chronotype (e.g., extreme eveningness) and impair sleep quality, often manifesting as daytime fatigue, reduced alertness, and poor recovery. Evidence comes mainly from animal models and genome‑wide association studies (GWAS), which show modest but reproducible links between CLOCK polymorphisms (e.g., rs1801260) and sleep traits. However, effect sizes are small, and lifestyle factors (light, meal timing, stress) dominate. A DNA test for CLOCK variants can indicate a genetic tendency toward a certain sleep pattern, but it cannot diagnose fatigue. For a thorough assessment, sleep diaries, actigraphy, and clinical work‑up (e.g., for sleep apnea, iron deficiency) are essential. MyBody‑X includes CLOCK variants in its panels, but the practical value for explaining fatigue is limited.
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