Muzaffer Kaser

Background: Healthcare workers experience disproportionately high rates of depression, anxiety, and post-traumatic stress compared with the general population. Within the NHS, work-related stress and mental health–related sickness absence has increased over the past decade, a trend intensified by COVID-19. Mental health support offers are patchy across the UK, and the evidence base around interventions is scarce. The Staff Mental Health Service (SMHS) provides rapid, confidential support for NHS staff across Cambridgeshire and Peterborough. In this study, we report an economic evaluation of this dedicated service. Aims: To assess costs and patient outcomes associated with SMHS treatment, compared with local NHS Talking Therapies (TT) support. Method: A model-based cost–consequence analysis comparing two treatment pathways: SMHS or TT, versus TT only. Routinely collected service data and survey responses informed a decision-tree model estimating costs (2022/23 £GBP), clinical outcomes (PHQ-9 and GAD-7 scores), and quality-adjusted life years (QALYs). Additional analyses examined service waiting times and productivity losses. Results: Costs per patient were slightly higher for SMHS or TT (£614 versus £553), resulting in an incremental cost-effectiveness ratio of £7,126/QALY. Treatment at either SMHS or TT yielded greater improvements in mental health outcomes than TT alone, with mean score reductions of 4.2 versus 2.8 (PHQ-9), and 4.6 versus 2.7 (GAD-7). Median waiting times were substantially shorter at SMHS versus TT from referral to assessment (14 versus 17 days), referral to treatment (22 versus 51 days), and assessment to first treatment (7 versus 30 days; all p<0.001). Productivity losses during waiting periods were lower for SMHS, with an estimated value of £2,018 per patient. Conclusions: The SMHS offers a clinically effective and cost-effective model of support for NHS staff, delivering greater improvements in mental health symptoms, substantially shorter waiting times, and reduced productivity losses at only modest additional cost compared with TT. These findings provide early evidence that specialist services for healthcare workers represent good value for money and support continued investment in specialist staff mental health provision within the NHS.

Background: Psychiatric disorders are increasingly conceptualised as heterogeneous categories with transdiagnostic underlying mechanisms that cut across multiple diagnoses and vary within a single diagnosis. Inflammation induced by psychosocial stress is one particularly potent example: previous research suggests that inflammatory profiles may correspond to symptom subgroups rather than traditional diagnostic categories. However, robust identification of transdiagnostic symptoms linked to specific inflammatory profiles remains rare. In this study, we examined the relationship between inflammatory profiles (at baseline and after a stress induction) and transdiagnostic symptom dimensions in females, who show higher prevalence of stress-related disorders such as anxiety and depression. Methods: A modest but relatively homogenous healthy female sample, between the ages of 18 and 35, was recruited (N=26). We obtained venous blood samples, at baseline and after a combined physiological and social stress induction, to measure full blood counts, plasma cytokines and peripheral blood mononuclear cells (PBMCs; for cell stimulation and intracellular flow cytometry analysis). Participants completed a battery of psychiatric self-report questions, from which we modelled three transdiagnostic factor scores. Finally, we used Bayesian regressions to evaluate the predictive contribution of transdiagnostic factors to inflammatory markers (at baseline and stress-induced), as well as to the principal components of inflammatory measures (derived from a principal component analysis (PCA) of the inflammatory data). Results: We identified specific relationships between inflammatory profiles and transdiagnostic symptom dimensions. Higher scores on a ‘social withdrawal’ factor were associated with greater baseline neutrophil (95% highest density interval (HDI) = [0.06, 1.32]; BF ₁₀ = 2.92) and monocyte counts (95% HDI = [0.29, 1.46]; BF ₁₀ = 19.08), whereas higher ‘anxious-depression’ scores were associated with a lower baseline monocyte count (95% HDI = [−0.96, −0.02]; BF ₁₀ = 1.81) and a greater inflammatory response to stress (e.g., change in neutrophil scores from pre- to post stress induction: (95% HDI = [0.18, 2.14]); BF ₁₀ = 5.66). We also found evidence for an association between the ‘social withdrawal’ factor and an immune principal component most strongly weighted by monocytes, basophils, and IL-6 (95% HDI = [−1.14, −0.01]; BF ₁₀ = 1.88). Conclusions: We find preliminary evidence that different transdiagnostic psychiatric symptom dimensions map onto specific inflammatory profiles, both at baseline and after a stress induction. This represents a proof-of-principle for the use of data-driven and hypothesis-driven approaches to identify and link transdiagnostic factors with inflammatory changes, which may be of use to future studies with larger, clinical populations, or for testing in the context of stratified interventions.

Young people with childhood adversity (CA) were at increased risk to experience mental health problems during the COVID-19 pandemic. Pre-pandemic research identified high-quality friendship support as a protective factor that can buffer against the emergence of mental health problems in young people with CA. This longitudinal study investigated friendship buffering effects on mental health symptoms before and at three timepoints during the pandemic in 102 young people (aged 16–26) with low to moderate CA. Multilevel analyses revealed a continuous increase in depression symptoms following the outbreak. Friendship quality was perceived as elevated during lockdowns and returned to pre-pandemic baseline levels during reopening. A stress-sensitizing effect of CA on social functioning was evident, as social thinning occurred following the outbreak. Bivariate latent change score modeling revealed that before and during the pandemic, young people with greater friendship quality self-reported lower depression symptoms and vice versa. Furthermore, sequential mediation analysis showed that high-quality friendships before the pandemic buffered depression symptoms during the pandemic through reducing perceived stress. These findings highlight the importance of fostering stable and supportive friendships in young people with CA and suggest that through reducing stress perceptions high-quality friendships can mitigate mental health problems during times of multidimensional stress.

Introduction COVID-19-related social isolation and stress may have significant mental health effects, including post-traumatic stress, anxiety and depression. These factors are thought to disproportionately affect populations at risk of psychopathology, such as adolescents with a history of childhood adversity (CA). Therefore, examining which factors may buffer the impact of COVID-19-related stress and isolation in vulnerable adolescents is critical. The Resilience After the COVID-19 Threat (REACT) study assesses whether emotion regulation capacity, inflammation and neuroimmune responses to stress induced in the laboratory prior to the pandemic predict responses to COVID-19-related social isolation and stress in adolescents with CA. We aim to elucidate the mechanisms that enable vulnerable adolescents to maintain or regain good mental health when confronted with COVID-19. Methods and analysis We recruited 79 adolescents aged 16–26 with CA experiences from the Resilience After Individual Stress Exposure study in which we assessed emotion regulation, neural and immune stress responses to an acute stress task. Our sample completed questionnaires at the start of the UK lockdown (‘baseline’; April 2020) and three (July 2020) and 6 months later (October 2020) providing crucial longitudinal information across phases of the pandemic progression and government response. The questionnaires assess (1) mental health, (2) number and severity of life events, (3) physical health, (4) stress perception and (5) loneliness and friendship support. We will use multilevel modelling to examine whether individual differences at baseline are associated with responses to COVID-19-related social isolation and stress. Ethics and dissemination This study has been approved by the Cambridge Psychology Research Ethics Committee (PRE.2020.037). Results of the REACT study will be disseminated in publications in scientific peer-reviewed journals, presentations at scientific conferences and meetings, publications and presentations for the general public, and through social media.

Cognitive dysfunction in depression is associated with poorer clinical outcomes and interference with psychosocial functioning. However, most treatments for depression do not specifically target cognition. Neurocognitive deficits such as memory and concentration problems tend to persist after mood symptoms recover. Improving cognition in depression requires a better understanding of the brain systems implicated in depression. A comprehensive approach is warranted for refined ways to assess and treat cognitive dysfunction in depression.

Impairments in mismatch negativity (MMN) generation have been consistently reported in patients with schizophrenia. However, underlying oscillatory activity of MMN deficits in schizophrenia and the relationship with cognitive impairments have not been investigated in detail. Time-frequency power and phase analyses can provide more detailed measures of brain dynamics of MMN deficits in schizophrenia. 21 patients with schizophrenia and 21 healthy controls were tested with a roving frequency paradigm to generate MMN. Time-frequency domain power and phase-locking (PL) analysis was performed on all trials using short-time Fourier transforms with Hanning window tapering. A comprehensive battery (CANTAB) was used to assess neurocognitive functioning. Mean MMN amplitude was significantly lower in patients with schizophrenia (95% CI 0.18 - 0.77). Patients showed significantly lower EEG power (95% CI -1.02 - -0.014) in the ~4-7 Hz frequency range (theta band) between 170 and 210 ms. Patients with schizophrenia showed cognitive impairment in multiple domains of CANTAB. However, MMN impairments in amplitude and power were not correlated with clinical measures, medication dose, social functioning or neurocognitive performance. The findings from this study suggested that while MMN may be a useful marker to probe NMDA receptor mediated mechanisms and associated impairments in gain control and perceptual changes, it may not be a useful marker in association with clinical or cognitive changes. Trial-by-trial EEG power analysis can be used as a measure of brain dynamics underlying MMN deficits which also can have implications for the use of MMN as a biomarker for drug discovery.