How is "Caffeine Sensitivity during Sleep Deprivation" encoded by the genome?
Caffeine is a major stimulant most available worldwide and is found in more than 60 plants, including coffee beans, tea leaves, and cacao pods. In addition to natural caffeine, health professionals often use synthetic caffeine to counteract sleep loss-related neurobehavioral impairment, increase alertness, and decrease subjective sleepiness. Recent studies showed individual differences in cognitive responses to sleep deprivation and caffeine consumption/administration based on genetics, sleep, and circadian influences.
Despite the many laboratory studies individual's responses to total sleep deprivation (TSD), there is little data available on the influence of combined polymorphisms and the effects of caffeine administration. It has been reported that it is particularly the SNP rs1800629 of TNF-α that determines a level of resilience to being impaired due to TSD, whereas no significant association was found with ADORA2A, PER3, TLR4, and a gene polymorphism located in the MHC nearby that of TNFα, DQB1*0602. The same group recently showed no interaction of TNFα genotype with the beneficial effect of caffeine (200 or 300 mg) on performance during TSD.
This study aimed to evaluate the influence of four SNPs and caffeine effects on wakefullness and function by using a psychomotor vigilance test (PVT) and subjective sleepiness in healthy subjects. A total of 37 subjects, including regular caffeine consumers (247 ± 23 mg per day) completed the study. In caffeine (2 × 2.5 mg/kg/24 h, twice a day) or placebo-controlled conditions, subjects performed a computer-based version of the 10-min PVT and reported sleepiness every six hours (Karolinska sleepiness scale (KSS)) during TSD. In the PVT, subjects were instructed to respond by clicking the left mouse button as soon as the visual stimulus appeared without making false starts. The inter-stimulus interval was randomized between 2 and 10s. The reaction time (RT) is quantified in milliseconds for a 1 s period and the response was regarded as valid if RT was ≥ 100 ms. Results are expressed as the number of lapses (RTs > 500 ms) and speed. Genotyping for four SNPs, including rs1800629 in the TNF-α gene was performed. Results showed that caffeine significantly lowered the number of lapses compared with the placebo condition. In A allele carriers for rs1800629 showed a significant caffeine effect at four PVT timing (8-h of awakening duration, 20-h, 26-h, and 32-h), while this is present at two PVT timing (14-h and 32-h) in G/G genotype carriers. This suggests that carriers of allele A benefit more from the stimulating effect of caffeine than G/G.
These results on PVT lapses partly contradict those of Satterfield et al. (2015), who did not find interaction with caffeine administration. In their study, subjects had to abstain from caffeine only for the week prior to each laboratory experiment. In contrast, these subjects maintained their usual caffeine consumption until the experiment to be as close as possible to real-life conditions. Moreover, there was no significant difference in habitual caffeine consumption between TNF-α genotypes in our subjects. Thus, in Satterfield et al. (2015), researchers of the current study can suggest that regular caffeine consumers may have experienced withdrawal symptoms that may have altered their neurobehavioral response to sleep deprivation. If you would like to know more about this research, you can read the study here:
https://pubmed.ncbi.nlm.nih.gov/33920292/
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