RESUMEN
OBJECTIVES: We review studies of whether cortisol levels following psychosocial stress exposure differ between patients with psychosis and healthy control subjects. METHODS: Original research published between 1993 and February 2019 was included in the literature search. Studies that used experimentally induced psychosocial stress and reported stress response measures of plasma or saliva cortisol levels in patients at any stage of illness (i.e. high risk, first episode and chronic phase) were included. RESULTS: A total of 17 studies were included. Although there was evidence of inconsistencies in measures, we observed moderate evidence of an association with stress-induced cortisol blunting response across studies. CONCLUSIONS: This review highlights recent evidence of blunting of cortisol response following experimentally induced psychosocial stress. While there was some evidence of this blunted response across illness types and stages, the strongest evidence was observed for those with chronic schizophrenia. Due to the low number of studies, in particular in bipolar disorder, much work is still needed to accurately characterise the biological effects of stress in psychosis.
Asunto(s)
Hidrocortisona/sangre , Trastornos Psicóticos/metabolismo , Esquizofrenia/sangre , Estrés Psicológico/metabolismo , Trastorno Bipolar/sangre , Enfermedad Crónica , Femenino , Humanos , Sistema Hipotálamo-Hipofisario/fisiología , Masculino , Sistema Hipófiso-Suprarrenal/fisiología , Trastornos Psicóticos/psicología , Riesgo , Saliva/metabolismo , Estrés Fisiológico/fisiologíaRESUMEN
Attention-deficit/hyperactivity disorder (ADHD) is a common, highly heritable neurodevelopmental disorder. Genetic loci have not yet been identified by genome-wide association studies. Rare copy number variations (CNVs), such as chromosomal deletions or duplications, have been implicated in ADHD and other neurodevelopmental disorders. To identify rare (frequency ≤1%) CNVs that increase the risk of ADHD, we performed a whole-genome CNV analysis based on 489 young ADHD patients and 1285 adult population-based controls and identified one significantly associated CNV region. In tests for a global burden of large (>500 kb) rare CNVs, we observed a nonsignificant (P=0.271) 1.126-fold enriched rate of subjects carrying at least one such CNV in the group of ADHD cases. Locus-specific tests of association were used to assess if there were more rare CNVs in cases compared with controls. Detected CNVs, which were significantly enriched in the ADHD group, were validated by quantitative (q)PCR. Findings were replicated in an independent sample of 386 young patients with ADHD and 781 young population-based healthy controls. We identified rare CNVs within the parkinson protein 2 gene (PARK2) with a significantly higher prevalence in ADHD patients than in controls (P=2.8 × 10(-4) after empirical correction for genome-wide testing). In total, the PARK2 locus (chr 6: 162 659 756-162 767 019) harboured three deletions and nine duplications in the ADHD patients and two deletions and two duplications in the controls. By qPCR analysis, we validated 11 of the 12 CNVs in ADHD patients (P=1.2 × 10(-3) after empirical correction for genome-wide testing). In the replication sample, CNVs at the PARK2 locus were found in four additional ADHD patients and one additional control (P=4.3 × 10(-2)). Our results suggest that copy number variants at the PARK2 locus contribute to the genetic susceptibility of ADHD. Mutations and CNVs in PARK2 are known to be associated with Parkinson disease.