Abstract
Introduction Personalized sleep medicine is an emerging area of research and practice. Recent studies have identified clear inter-individual differences in performance vulnerability to sleep loss. Although clear biomarkers for this vulnerability are not known, new research indicates that genetic influences on sleep and circadian systems may be important. To assess the clnical applicabilty of these findings for diagnosis and treatment of patients with circadian rhythm disorders we summarized the present knowledge and speculate about futural developments. Materials and methods Literature search using PubMed. Results Dim Light melatonin Onset (DLMO) plays a key role in the diagnosis of circadian rhythm sleep disorders. It cannot be predicted by sleep parameters or polymorphisms of clock- or other sleep related genes. For melatonin treatment DLMO is crucial, as this treatment is most effective if administered at a time which is related to the DLMO. Efficacy of melatonin treatment depends not only on its personalized time of administration, but also on the speed of its metabolisation. For slow melatonin metabolisation may pile up daily melatonin levels and consequently stop melatonin efficacy. Melatonin metabolisation is influenced by CYP1A2 gene activity. Several methods to assess Cyp1A2 activity are being developed, using melatonin, coffee, green tea and chocolate as test substances or measuring CYP1A2 polymorphisms. Co-morbidities including ADHD and autism spectrum disorder (ASD) influence circadian sleep rhythm and their response to melatonin treatment. CYP1A2 polymorphisms might be correlated with slow melatonin metabolisation and ASD. Conclusion DLMO, melatonin metabolisation tests and assessment of psychiatric co-morbidity are crucial for effective diagnosis and treatment of circadian rhythm sleep disorders. Further development of techniques to measure melatonin and its metabolisation will increase the clinical applicability. Acknowledgement This is a non-sponsored study.
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