Salivary cortisol in early psychosis: New findings and meta-analysis

Chaumette, Boris; Kébir, Oussama; Mam-Lam-Fook, Célia; Morvan, Yannick; Bourgin, Julie; Godsil, Bill P.; Plaze, Marion; Gaillard, R.; Jay, Thérèse M.; Krebs, Marie‐Odile

doi:10.1016/j.psyneuen.2015.10.007

Cited by 78 publications

(60 citation statements)

References 63 publications

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“…Help-seeking individuals (16–30 years) consecutively referred to the Adolescent and Young Adults Assessment Centre (Service Hospitalo-Universitaire, Hôpital Sainte-Anne, Paris, France) between 2009 and 2013 were enrolled in the ICAAR collaborative study promoted by Sainte-Anne Hospital as already described. 7 Inclusion criteria were alterations in global functioning (Social and Occupational Functioning Assessment Scale score <70) during the past year that were associated with psychiatric symptoms and/or subjective cognitive complaints. Exclusion criteria included manifest symptoms of psychosis, pervasive developmental or bipolar disorders and individuals with other established diagnoses, such as obsessive-compulsive disorder (fulfilling Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria).…”

Section: Methodsmentioning

confidence: 99%

Methylomic changes during conversion to psychosis

et al. 2016

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The onset of psychosis is the consequence of complex interactions between genetic vulnerability to psychosis and response to environmental and/or maturational changes. Epigenetics is hypothesized to mediate the interplay between genes and environment leading to the onset of psychosis. We believe we performed the first longitudinal prospective study of genomic DNA methylation during psychotic transition in help-seeking young individuals referred to a specialized outpatient unit for early detection of psychosis and enrolled in a 1-year follow-up. We used Infinium HumanMethylation450 BeadChip array after bisulfite conversion and analyzed longitudinal variations in methylation at 411 947 cytosine–phosphate–guanine (CpG) sites. Conversion to psychosis was associated with specific methylation changes. Changes in DNA methylation were significantly different between converters and non-converters in two regions: one located in 1q21.1 and a cluster of six CpG located in GSTM5 gene promoter. Methylation data were confirmed by pyrosequencing in the same population. The 100 top CpGs associated with conversion to psychosis were subjected to exploratory analyses regarding the related gene networks and their capacity to distinguish between converters and non-converters. Cluster analysis showed that the top CpG sites correctly distinguished between converters and non-converters. In this first study of methylation during conversion to psychosis, we found that alterations preferentially occurred in gene promoters and pathways relevant for psychosis, including oxidative stress regulation, axon guidance and inflammatory pathways. Although independent replications are warranted to reach definitive conclusions, these results already support that longitudinal variations in DNA methylation may reflect the biological mechanisms that precipitate some prodromal individuals into full-blown psychosis, under the influence of environmental factors and maturational processes at adolescence.

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Section: Methodsmentioning

confidence: 99%

Methylomic changes during conversion to psychosis

et al. 2016

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“…Overall, a majority of studies has demonstrated abnormalities in cortisol secretion in CHR samples compared to HC (133). In a large sample of 256 CHR patients and 141 HC, the CHR group exhibited significantly higher mean diurnal salivary cortisol levels (134).…”

Section: Mechanisms Of Trauma and Stress In The Chr Populationmentioning

confidence: 99%

The Role of Trauma and Stressful Life Events among Individuals at Clinical High Risk for Psychosis: A Review

et al. 2017

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The experience of childhood trauma (CT) and stressful life events (SLEs) is associated with subsequent development of a variety of mental health conditions, including psychotic illness. Recent research identifying adolescents and young adults at clinical high risk (CHR) for psychosis allows for prospective evaluation of the impact of trauma and adverse life events on psychosis onset and other outcomes, addressing etiological questions that cannot be answered in studies of fully psychotic or non-clinical populations. This article provides a comprehensive review of the current emerging literature on trauma and adverse life events in the CHR population. Up to 80% of CHR youth endorse a lifetime history of childhood traumatic events and victimization (e.g., bullying). Several studies have shown that the experience of CT predicts psychosis onset among CHR individuals, while the literature on the influence of recent SLEs (e.g., death of a loved one) remains inconclusive. Multiple models have been proposed to explain the link between trauma and psychosis, including the stress-vulnerability and stress-sensitivity hypotheses, with emphases on both cognitive processes and neurobiological mechanisms (e.g., the hypothalamic–pituitary–adrenal axis). Despite the preponderance of CHR individuals who endorse either CT or SLEs, no clinical trials have been conducted evaluating interventions for trauma in CHR youth to date. Furthermore, the current process of formal identification and assessment of trauma, SLEs, and their impact on CHR youth is inconsistent in research and clinical practice. Recommendations for improving trauma assessment, treatment, and future research directions in the CHR field are provided.

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“…There appears to be significant variability in the stress-response system as a function of underlying psychopathology. Increased basal cortisol levels have been noted in youth at ultra-high risk for psychosis, while cortisol response to acute stress is blunted compared to healthy controls (Chaumette et al 2016; Pruessner et al 2013). Elevated salivary cortisol has been reported in children with 22q11.2DS.…”

Section: Introductionmentioning

confidence: 99%

Working Memory Impairments in Chromosome 22q11.2 Deletion Syndrome: The Roles of Anxiety and Stress Physiology

Sanders

Hobbs

Stephenson

et al. 2017

J Autism Dev Disord

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Stress and anxiety have a negative impact on working memory systems by competing for executive resources and attention. Broad memory deficits, anxiety, and elevated stress have been reported in individuals with chromosome 22q11.2 deletion syndrome (22q11.2DS). We investigated anxiety and physiological stress reactivity in relation to visuospatial working memory impairments in 20 children with 22q11.2DS and 32 typically developing (TD) children ages 7 to 16. Children with 22q11.2DS demonstrated poorer working memory, reduced post-stress respiratory sinus arrhythmia recovery, and overall increased levels of cortisol in comparison to TD children. Anxiety, but not physiological stress responsivity, mediated the relationship between 22q11.2DS diagnosis and visuospatial working memory impairment. Findings indicate that anxiety exacerbates impaired working memory in children with 22q11.2DS.

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Salivary cortisol in early psychosis: New findings and meta-analysis

Cited by 78 publications

References 63 publications

Methylomic changes during conversion to psychosis

Methylomic changes during conversion to psychosis

The Role of Trauma and Stressful Life Events among Individuals at Clinical High Risk for Psychosis: A Review

Working Memory Impairments in Chromosome 22q11.2 Deletion Syndrome: The Roles of Anxiety and Stress Physiology

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