CYP1A2 is a liver enzyme that metabolizes caffeine and also contributes to melatonin breakdown. Genetic variants (e.g., rs762551) determine whether a person is a 'fast' or 'slow' metabolizer. Slow metabolizers clear caffeine more slowly, leading to prolonged stimulant effects that can disrupt sleep onset and quality. Additionally, CYP1A2's role in melatonin metabolism suggests a possible direct influence on the sleep-wake cycle, though evidence for this is primarily mechanistic. Observational studies link slow CYP1A2 genotype with higher caffeine sensitivity and poorer sleep, but confounding factors like habitual intake and other genes (e.g., ADORA2A) play a role. The current evidence is moderate: it relies on pharmacokinetic principles and small association studies rather than large randomized trials. A DNA test can indicate your metabolizer status, but it cannot diagnose sleep disorders. Sleep is multifactorial; genetics is just one piece of the puzzle.
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