Poor tolerance to shift work linked to genes: study

Scientists have identified genetic factors that influence our tolerance to shift work, an advance that may explain why some people can not handle constant disruptions to their daily rhythm.
Covering the entire genome, the study discovered that a common variation in the melatonin receptor 1A (MTNR1A) gene is linked to the job-related exhaustion experienced by shift workers.
Shift work often disrupts the circadian rhythm, which can lead to sleep disorders and daytime fatigue.
The study, led by Tiina Paunio from the University of Helsinki in Finland, involved shift workers from many different lines of work.
The differences in the job-related exhaustion reported by employees were contrasted with genetic differences in their entire genome.

The link to the melatonin receptor gene was discovered in a group of 176 shift workers.

The study also established that the risk variation of the melatonin receptor 1A (MTNR1A) gene is probably related to the methylation of DNA in the regulatory sequence of the MTNR1A gene as well as the weaker expression of the MTNR1A gene.
The methylation of DNA is one of the epigenetic mechanisms regulating the functioning of the genome, influenced by not only by variations in DNA sequence, but also environmental factors such as fluctuations in the circadian rhythm.
As it results in a smaller number of melatonin receptors, the risk variant of the gene can cause weaker natural melatonin signalling, one of the regulatory mechanisms in stabilising the circadian rhythm.

The influence of the risk variant of the MTNR1A gene may explain the degree to which light exposure at night disrupts the circadian rhythm of shift workers.
"The variant we have now discovered can only explain a small part of the variation between individuals, and it cannot be used as a basis to determine a person's tolerance to shift work," Paunio said.
The study was published in the journal Sleep.