Introduction:
The Trier social stress test (TSST) is well established to induce psychological stress
in human experiments. So far the effect of TSST, performed in the late evening, on
sleep and on stress hormone secretion before sleep onset was not examined. The corticotropin
releasing hormone receptor type 1 (CRH R1) gene encodes the CRHR1 receptor. This protein
is essential in the activation of the stress response of the hypothalamo-pituitary-adrenocortical
(HPA) system. Variants of the single nucleotide polymorphism (SNP) rs110402 of the
CRHR1 gene were shown to influence the risk to develop depression after childhood
maltreatment. This risk is elevated in homozyguous C carriers of this SNP, whereas
TT carriers appear to be more resilient to this risk. We examined the effect of TSST
on sleep and HPA hormones and whether this effect is influenced by the CRHR 1 genotype.
Methods:
52 male healthy volunteers, 20 to 30 years old, without any history of childhood trauma
or any other risk of psychiatric disorder in their own and family history, were selected
for their CRHR1 genotype. According to randomized schedule 31 CC and 21 TT carriers
underwent two sessions, separated by one week. Each session consisted of one night
of adaptation and one polysomnography (PSG, 23.00 to 07.00) in our sleep laboratory.
Before PSG subjects were either exposed to a TSST from 22.30 to 22.40 or underwent
a control setting without stress. Mental stress before and after TSST was assessed
by visual analogue scale. Saliva for later analysis of cortisol and cortisone was
collected four times between 20.00 and 22.55.
Results:
The TT carriers showed significantly higher cortisol reactivity compared to the CC.
Cortisone increased without effect of genotype. The perceived stress was inversely
to the cortisol reactivity for the CC carriers significantly higher than for the TT
carriers. Analysis of polysomnography showed reduced time spent in rapid eye movement
(REM) sleep, elevated percentage of wakefulness during sleep period time and prolonged
sleep onset latency after TSST compared to baseline irrespective of genotype.
Conclusion:
Our findings suggest that psychosocial stress by TSST stimulates HPA hormone secretion
and impairs sleep. The changes of subjectively perceived stress and of cortisol levels
were influenced by CRHR1 genotype. Interestingly healthy CC carriers without history
of childhood maltreatment show elevated mental stress and reduced cortisol response
after TSST. Changes of cortisone and of sleep after TSST were independent of CRHR1
genotype.
