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Accepted Paper:

Association between genetic polymorphism of melanopsin photoreceptor and sleep/wake timing  
Sang-il Lee (Kyushu University) Shigekazu Higuchi (Kyushu University)

Paper short abstract:

Human sleep and circadian rhythm adapt to a 24-hour light/dark cycle. The melanopsin photoreceptor in the retina plays an important role in circadian photoentrainment. We found that melanopsin gene polymorphism is associated with sleep/wake timing.

Paper long abstract:

The human sleep/wake cycle is adjusted by circadian rhythms that adapt to a 24-hour light/dark cycle. The melanopsin photoreceptor in the retina plays an important role in circadian photoentrainment in the natural environment. However, artificial light at night has adverse effects on human sleep and circadian rhythm in modern society. We have already found that melanopsin gene polymorphism is associated with pupillary light response, but the association with sleep/wake timing has remained unclear. A total of 348 healthy Japanese university students participated in this study. The genotypes of rs1079610 (I394T) located in the coding region were analyzed. Bedtime, wake time and midpoint of sleep on weekdays of CC subjects were significantly later than those of TT and TC subjects. We have already found that pupilloconstriction in subjects with the C allele is highly responsive to light. The delayed sleep/wake timing of CC subjects might be a consequence of the high responsiveness to light at night since exposure to light at night induces phase delay. C allele frequency of I394T in the European population is larger than that in the Asian-Japanese and Sub-saharan African populations. High responsiveness to light may be an adaptive trait for a short photoperiod in European people living in high latitude areas. However, our results suggest that high responsiveness to light is a cause of delayed sleep timing in adolescents living under artificial light at night in modern society.

Panel P137
Environment and adaptation in human evolution (JSPA panel) (CLOSED)
  Session 1