CYP1A2's role in sleep is indirect, primarily through caffeine metabolism. CYP1A2 is the main enzyme that breaks down caffeine in the liver. Individuals with a slow CYP1A2 variant (e.g., *1F/*1F) metabolize caffeine more slowly, leading to a longer half-life. This can impair sleep quality if caffeine is consumed in the afternoon or evening, as it remains active longer, blocking adenosine receptors. However, the provided context contains no direct evidence linking CYP1A2 to sleep regulation itself. The evidence is mechanistic, based on pharmacokinetics, not clinical sleep studies. A CYP1A2 genetic test may indicate caffeine sensitivity, but not sleep disorders per se. Other factors like sleep hygiene, stress, and clock gene variants are more relevant. Caution against overinterpretation: CYP1A2 is not a sleep gene.
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