Relationship between genetic polymorphisms of cytokines and self-reported sleep complaints and habitual caffeine consumption.

Sleep Med

Unité Fatigue et Vigilance, Institut de Recherche Biomédicale des Armées (IRBA), 91223, Brétigny-sur Orge, France; Université Paris Cité, VIFASOM, (UPR 7330 Vigilance, Fatigue, Sommeil et Santé Publique), Paris, France.

Published: January 2023

Pro-inflammatory cytokines are involved in sleep-wake regulation and are associated with caffeine consumption. This is a cross-sectional study in 1023 active French workers investigating associations between self-reported sleep complaints (>3months) and total sleep time (TST) with nine single-nucleotide-polymorphisms (SNPs) including pro-inflammatory cytokines, according to caffeine consumption. Participants were characterized as low, moderate and high (0-50, 51-300, and >300 mg/day) caffeine consumers. After adjusting the odd ratios (OR) for age, gender, and smoking, the risk of sleep complaints was higher in subjects with genetic mutations in tumor necrosis factor alpha (TNF-α, rs 1800629) (ORa [95%CI] = 1.43 [1.07-1.92] for both G/A and A/A aggregate genotypes) or interleukin-1 beta (IL-1β, rs1143627) (ORa = 1.61 [1.08-2.44] for homozygous A/A genotype), and the risk was higher when subjects carry the mutations in TNF-α plus IL-1β regardless of caffeine consumption. When stratified with caffeine consumption, the risk of sleep complaints was higher in TNF-α A allele carriers in high caffeine consumers, and in homozygous A/A genotype of IL-1β in moderate and high consumers. None of the nine SNPs influence TST, with the exception of the mutation on CYP1A2 and only when stratified with caffeine consumption. Our results also indicated more caffeine side-effects when carrying mutation on IL1β. This study showed that polymorphisms in TNF-α and/or IL-1β influenced sleep complaints but did not influence total sleep time. This suggests that management of sleep complaints, which can be addressed by clinical interventions, should consider the influence of the genetic profile of pro-inflammatory cytokines.

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Source
http://dx.doi.org/10.1016/j.sleep.2022.10.013DOI Listing

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