The Intersection of Cultural Characteristics and Genetics on the Prevalence of Delayed Sleep Phase Syndrome in Brazilian and Japanese Adults

Abram Estafanous,Karim Sedky,David Bennett Bennett

doi:10.14302/issn.2574-4518.jsdr-20-3161

Abstract

Delayed sleep phase syndrome (DSPS) is a circadian rhythm disorder where individuals experience difficulty modifying the time they go to sleep and wake up in response to environmental changes. The circadian rhythm itself is regulated by a variety of clock genes, and various other genes (e.g., AA-NAT gene, CKIϵ gene) code for proteins that regulate clock genes. Various polymorphisms of the clock gene influencers have been shown to increase susceptibility to DSPS. This paper seeks to examine how certain cultural characteristics (e.g., napping, timing of meals, exposure to artificial light) and the presence of the AA-NAT gene (G619A polymorphism) and the CKIϵ gene (S408N polymorphism) influence the prevalence of DSPS amongst Japanese and Brazilian populations.

Highlights

The circadian rhythm is an intrinsic oscillator of physiological function that results in 24-hour day and night cycles[1]
The studies that this review examined only looked at two polymorphisms – the G619A polymorphism of the AA-NAT gene and the S408N polymorphism of the CKIε gene
We reviewed two studies that examined the prevalence of the AA-NAT gene (G619A polymorphism) among Delayed sleep phase syndrome (DSPS) patients in a Brazilian and Japanese population and two studies that examined the prevalence of the CKIε gene (S408N polymorphism) in a Brazilian and Japanese population

Summary

Introduction

The circadian rhythm is an intrinsic oscillator of physiological function that results in 24-hour day and night cycles[1]. These cycles allow organisms to adapt to changes in the environment, such as changes in light duration[2]. SCN neurons receive light from the retina, and this photic information is converted into chemical information that alters gene expression of SCN neurons[2]. The SCN transmits the rhythmic information it receives, such as the amount of daylight, to cells found elsewhere in the body (e.g., pineal gland) that results in a variety of outputs (e.g., endocrine signals, body temperature changes)[2]. The SCN induces the pineal gland to secrete melatonin. The expression of melatonin is an important regulator of sleep as it correlates with an increase in sleep propensity[5] and decreased sleep onset latency[6]

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