Predictors of increased affective symptoms and suicidal ideation during the COVID-19 pandemic: results from a large-scale study of 14 271 Thai adults

Background Increasing data suggest emergent affective symptoms during the COVID-19 pandemic. Objectives To study the impact of the COVID-19 pandemic on affective symptoms and suicidal ideation in Thai adults. Methods The Collaborative Outcomes Study on Health and Functioning during Infection Times uses non-probability sampling (chain referring and voluntary response sampling) and stratified probability sampling to identify risk factors of mental health problems and potential treatment targets to improve mental health outcomes during pandemics. Findings Analysing 14 271 adult survey participants across all four waves of the COVID-19 pandemic in Thailand, covering all 77 provinces from 1 June 2020 to 30 April 2022, affective symptoms and suicidality increased during COVID-19 pandemic. Affective symptoms were strongly predicted by pandemic (feelings of isolation, fear of COVID-19, loss of social support, financial loss, lack of protective devices) and non-pandemic (female sex, non-binary individuals, adverse childhood experiences (ACEs), negative life events, student status, multiple mental health and medical conditions, physical pain) risk factors. ACEs, prior mental health conditions and physical pain were the top three risk factors associated with both increased affective symptoms and suicidal ideation during the COVID-19 pandemic. Partial least squares analysis showed that ACEs were the most important risk factor as they impacted most pandemic and non-pandemic risk factors. Clinical implications Rational policymaking during a pandemic should aim to identify the groups at highest risk (those with ACEs, psychiatric and medical disease, women, non-binary individuals) and implement both immediate and long-term strategies to mitigate the impact of ACEs, while effectively addressing associated psychiatric and medical conditions

Results of Linear SVM and Random Forest Models.

<p>Results of Linear SVM and Random Forest Models.</p

Correlation matrix between the Consortium to Establish a Registry for Alzheimer’s disease test results and age and education in healthy controls.

<p>Correlation matrix between the Consortium to Establish a Registry for Alzheimer’s disease test results and age and education in healthy controls.</p

Mean (SE) z scores of Consortium to Establish a Registry for Alzheimer’s disease tests in normal controls, nondeficit and deficit schizophrenia patients and patients with amnestic mild cognitive impairment (MCI).

<p>TrueWLRecall: Word List Recall, Delayed, true recall; FalseWLRecall: Word List Recall, Delayed, false recall (WL False Recall); CorrectWLRecognition: WL Recognition Correct Yes response; NoWLRecognition: Word List Recognition Correct No response; WLRecognition: sum of Correctand No WLRecognition.</p

Results of multivariate general linear model analyses with the Consortium to Establish a Registry for Alzheimer’s disease (CERAD) tests results as dependent variables and diagnosis as primary explanatory variable, while adjusting for age, sex and education.

<p>Shown are the model-generated marginal means (SE) of the z-scores of all CERAD tests.</p

Mean (SE) z scores of Consortium to Establish a Registry for Alzheimer’s disease tests in normal controls, nondeficit and deficit schizophrenia patients and patients with amnestic mild cognitive impairment (MCI).

<p>WLcorrect1: Trial 1 (WLM correct 1); WLcorrect2: Trial 2 (WLM correct 2); WLcorrect3: Trial 3 (WLM correct 3); WLM: Word List Memory, total score.</p

The Endogenous Opioid System in Schizophrenia and Treatment Resistant Schizophrenia: Increased Plasma Endomorphin 2, and κ and μ Opioid Receptors Are Associated with Interleukin-6

Background: activation of the immune-inflammatory response system (IRS) and the compensatory immune-regulatory system (CIRS) plays a key role in schizophrenia (SCZ) and treatment resistant SCZ. There are only a few data on immune and endogenous opioid system (EOS) interactions in SCZ and treatment resistant SCZ. Methods: we examined serum &beta;-endorphin, endomorphin-2 (EM2), mu-opioid (MOR) and kappa-opioid (KOR) receptors, and interleukin (IL)-6 and IL-10 in 60 non responders to treatment (NRTT), 55 partial RTT (PRTT) and 43 normal controls. Results: serum EM2, KOR, MOR, IL-6 and IL-10 were significantly increased in SCZ as compared with controls. &beta;-endorphin, EM2, MOR and IL-6 were significantly higher in NRTT than in PRTT. There were significant correlations between IL-6, on the one hand, and &beta;-endorphin, EM2, KOR, and MOR, on the other, while IL-10 was significantly correlated with MOR only. A large part of the variance in negative symptoms, psychosis, hostility, excitation, mannerism, psychomotor retardation and formal thought disorders was explained by the combined effects of EM2 and MOR with or without IL-6 while increased KOR was significantly associated with all symptom dimensions. Increased MOR, KOR, EM2 and IL-6 were also associated with neurocognitive impairments including in episodic, semantic and working memory and executive functions. Conclusion: the EOS contributes to SCZ symptomatology, neurocognitive impairments and a non-response to treatment. In SCZ, EOS peptides/receptors may exert CIRS functions, whereas increased KOR levels may contribute to the pathophysiology of SCZ and EM2 and KOR to a non-response to treatment