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Antidepressant medication (ADM)-only, psychotherapy-only, and their combination are the first-line treatment options for major depressive disorder (MDD). Previous meta-analyses of randomized controlled trials (RCTs) established that psychotherapy and combined treatment were superior to ADM-only for MDD treatment remission or response. The current meta-analysis extended previous ones by determining the comparative efficacy of ADM-only, psychotherapy-only, and combined treatment on suicide attempts and other serious psychiatric adverse events (i.e. psychiatric emergency department [ED] visit, psychiatric hospitalization, and/or suicide death; SAEs). Peto odds ratios (ORs) and their 95% confidence intervals were computed from the present random-effects meta-analysis. Thirty-four relevant RCTs were included. Psychotherapy-only was stronger than combined treatment (1.9% v. 3.7%; OR 1.96 [1.20–3.20], p = 0.012) and ADM-only (3.0% v. 5.6%; OR 0.45 [0.30–0.67], p = 0.001) in decreasing the likelihood of SAEs in the primary and trim-and-fill sensitivity analyses. Combined treatment was better than ADM-only in reducing the probability of SAEs (6.0% v. 8.7%; OR 0.74 [0.56–0.96], p = 0.029), but this comparative efficacy finding was non-significant in the sensitivity analyses. Subgroup analyses revealed the advantage of psychotherapy-only over combined treatment and ADM-only for reducing SAE risk among children and adolescents and the benefit of combined treatment over ADM-only among adults. Overall, psychotherapy and combined treatment outperformed ADM-only in reducing the likelihood of SAEs, perhaps by conferring strategies to enhance reasons for living. Plausibly, psychotherapy should be prioritized for high-risk youths and combined treatment for high-risk adults with MDD.

Scar theory proposes that heightened depression and anxiety precede and predict worse cognitive functioning outcomes, whereas the vulnerability theory posits the opposite pathway. However, most investigations on this topic have been cross-sectional, precluding causal inferences. Thus, we used cross-lagged prospective network analyses to facilitate causal inferences in understanding the relations between psychopathology and cognitive functioning components. Racially-diverse midlife women ( = 1816) participated in the Study of Women's Health Across the Nation at two time-points, spanning one year apart. Five psychopathology (anxiety severity, depressed mood, somatic symptoms, positive affect, interpersonal problems) and four cognitive functioning nodes (working memory (WM), processing speed (PS), facial recognition (FCR), and verbal memory (VRM)) were assessed. All analyses adjusted for age, menopausal status, estradiol, and follicle-stimulating hormones. Contemporaneous networks yielded notable inverse between-node relations ( ) between interpersonal problems and reduced FCR and PS, and between depressed mood and lower FCR, VRM, or PS. Nodes that had the highest likelihood to bridge other constructs were positive affect, anxiety severity, WM, and VRM. Temporal networks produced edges consistent with the scar ( . vulnerability) hypotheses. Higher somatic symptoms were related to reduced PS and WM, and greater depressed mood was correlated with lower future PS and WM. Also, higher anxiety severity coincided with decreased future PS and WM. Greater positive affect was associated with stronger future PS, FCR, and WM. Also, positive affect had the strongest relations with other nodes. Findings suggest the importance of targeting symptoms and cognitive functioning simultaneously.

The cognitive model (Hirsch & Mathews, 2012) and attentional control theory (Eysenck & Derakshan, 2011) postulate that compromised executive function (EF) and other cognitive constructs are negatively linked to increased excessive and uncontrollable worry, the core symptom of generalized anxiety disorder (GAD). However, the prospective link between neuropsychological constructs and GAD are not well understood. A nationally representative sample of 2605 community-dwelling adults whose average age was 55.20 (s.d. = 11.41, range 33-84; 56.31% females) participated at baseline and 9-year follow-up. Baseline neuropsychological function and symptoms were measured using the Brief Test of Adult Cognition by Telephone and Composite International Diagnostic Interview - Short Form. Multivariate Poisson and negative binomial regression analyses were conducted with 11 baseline covariates entered simultaneously: age, gender, years of formal education, perceived control, hypertension/diabetes, body mass index, exercise status, as well as GAD severity, panic disorder severity, and depression severity. Those with baseline GAD were also removed. Lower Time 1 composite global cognition z-score independently predicted higher Time 2 GAD severity and diagnosis [odds ratio (OR) 0.60, 95% confidence interval (CI) 0.40-0.89, p = 0.01]. Poor inhibition, set-shifting, working memory (WM) updating, inductive reasoning, and global cognition sequentially forecasted heightened GAD. However, processing speed, verbal WM, verbal fluency, and episodic memory did not predict future GAD. Global cognition, inductive reasoning, inhibition, set-shifting, and WM updating EF impairments may be distal risk factors for elevated GAD nearly a decade later.

Scar models posit that heightened anxiety and depression can increase the risk for subsequent reduced executive function (EF) through increased inflammation across months. However, the majority of past research on this subject used cross-sectional designs. We therefore examined if elevated generalized anxiety disorder (GAD), major depressive disorder (MDD), and panic disorder (PD) symptoms forecasted lower EF after 20 months through heightened inflammation. Community-dwelling adults partook in this study ( = 614; = 51.80 years, 50% females). Time 1 (T1) symptom severity (Composite International Diagnostic Interview - Short Form), T2 (2 months after T1) inflammation serum levels (C-reactive protein, fibrinogen, interleukin-6), and T3 (20 months after T1) EF (Brief Test of Adult Cognition by Telephone) were assessed. Structural equation mediation modeling was performed. Greater T1 MDD and GAD (but not PD) severity predicted increased T2 inflammation (Cohen's = 0.21-1.92). Moreover, heightened T2 inflammation forecasted lower T3 EF ( = -1.98 to -1.87). T2 inflammation explained 25-32% of the negative relations between T1 MDD or GAD and T3 EF. T1 GAD severity predicting T3 EF via T2 inflammation path was stronger among younger ( . older) adults. Direct effects of T1 MDD, GAD, and PD forecasting decreased T3 EF were found ( = -2.02 to -1.92). Results remained when controlling for socio-demographic, physical health, and lifestyle factors. Inflammation can function as a mechanism of the T1 MDD or GAD-T3 EF associations. Interventions that successfully treat depression, anxiety, and inflammation-linked disorders may avert EF decrements.

Vulnerability theories propose that suboptimal levels of lipid markers and proinflammatory proteins predict future heightened depression. Scar models posit the reverse association. However, most studies that tested relationships between non-specific immune/endocrine markers and depression did not separate temporal inferences between people and within-person and how different immunometabolism markers related to unique depression symptoms. We thus used cross-lagged prospective network analyses (CLPN) to investigate this topic. Community midlife women ( = 2224) completed the Center for Epidemiologic Studies-Depression scale and provided biomarker samples across five time-points spanning 9 years. CLPN identified significant relations ( ) among components ( ) of depression (depressed mood, somatic symptoms, interpersonal issues), lipid markers [insulin, fasting glucose, triglycerides, low-density lipoprotein-cholesterol (LDL), high-density lipoprotein-cholesterol (HDL)], and proinflammatory proteins [C-reactive protein (CRP), fibrinogen], within and across time-points. All models adjusted for age, estradiol, follicle-stimulating hormone, and menopausal status. In within-person temporal networks, higher CRP and HDL predicted all three depression components ( = 0.131-2.112). Increased LDL preceded higher depressed mood and interpersonal issues ( somatic symptoms) ( = 0.251-0.327). Elevated triglycerides predicted more somatic symptoms ( depressed mood and interpersonal problems) ( = 0.131). More interpersonal problems forecasted elevated fibrinogen and LDL levels ( = 0.129-0.331), and stronger somatic symptoms preceded higher fibrinogen levels ( = 0.188). Results supported both vulnerability and scar models. Long-term dysregulated immunometabolism systems, social disengagement, and related patterns are possible mechanistic accounts. Cognitive-behavioral therapies that optimize nutrition and physical activity may effectively target depression.

Affective neuroscience and scar theories propose that increased excessive worry, the hallmark symptom of generalized anxiety disorder (GAD), predicts future declines in executive functioning (EF). However, the preponderance of cross-sectional designs used to examine between-person chronic worry-EF relationships has blocked progress on understanding their potentially causal within-person associations. Accordingly, this study used bivariate dual latent change score (LCS) models to test whether within-person increased GAD severity might relate to future reduced EF. Community-dwelling adults (N = 2581, 46 years on average, s.d. = 11.40, 54.71% female) were assessed for GAD symptom severity (Composite International Diagnostic Interview-Short Form) across three waves, spaced about 9 years apart. Three aspects of EF [inhibition, set-shifting, and mixing costs (MCs; a measure related to common EF)], were assessed with stop-and-go switch tasks. Participants responded to 20 normal and 20 reverse single-task block trials and 32 mixed-task switch block trials. EF tests were administered at time 2 (T2) and time 3 (T3), but not at time 1 (T1). After controlling for T1 depression, LCS models revealed that within-person increased T1 - T2 GAD severity substantially predicted future reduced T2 - T3 inhibition and set-shifting (both indexed by accuracy and latency), and MC (indexed by latency) with moderate-to-large effect sizes (|d| = 0.51-0.96). Results largely support scar theories by offering preliminary within-person, naturalistic evidence that heightened excessive worry can negatively predict future distinct aspects of cognitive flexibility. Effectively targeting pathological worry might prevent difficulties arising from executive dysfunction.

BackgroundThe COVID-19 pandemic could affect college students’ mental health. We examined screening rates for psychological disorders before and during the pandemic.MethodsUndergraduates were surveyed before (n = 3643) or during the pandemic (n = 4970). Logistic regression adjusting for participant demographics was conducted.ResultsFrequencies of depression [OR 1.32, 95% CI (1.17, 1.48)], alcohol use disorder [OR 1.70, 95% CI (1.50, 1.93)], bulimia nervosa/binge-eating disorder [OR 1.54, 95% CI (1.28, 1.85)], and comorbidity [OR 1.19, 95% CI (1.04, 1.35)] were greater during (vs. before) the pandemic. Frequencies of posttraumatic stress disorder were lower during the pandemic [OR 0.86, 95% CI (0.75, 0.98)]. The upward trend in alcohol use disorder was stronger among women than men [OR 1.47, 95% CI (1.18, 1.83)]. The upward trend in depression was stronger among Black students than White students [OR 1.72, 95% CI (1.19, 2.49)]. Anxiety disorders, insomnia, anorexia nervosa, and suicidality showed no significant trends.ConclusionsDepression, alcohol use disorder, bulimia nervosa/binge-eating disorder, and comorbidity were higher, whereas posttraumatic stress disorder was lower during the pandemic. Women and Black students could face especially heightened risk for alcohol use disorder and depression, respectively, during the pandemic.

Scar and vulnerability models assert that increased psychopathology may predict subsequent executive functioning (EF) deficits (and vice versa) over protracted timescales, yet most prior work on this topic has been cross-sectional. Thus, we tested the within- and between-person relations between EF, depression, and anxiety. Older adult participants (n = 856) were assessed across four waves, approximately 2 years apart. Performance-based EF and caregiver-rated symptom measures were administered. Bivariate latent change score and random-intercept cross-lagged panel models were conducted. Within persons, random-intercept cross-lagged panel models revealed that prior greater depression forecasted lower subsequent EF, and vice versa (d = -0.292 vs. -0.292). Bivariate dual latent change score models showed that within-person rise in depression predicted EF decreases, and vice versa (d = -0.245 vs. -0.245). No within-person, cross-lagged, EF-anxiety relations emerged. Further, significant negative between-person EF-symptom relations were observed (d = -0.264 to -0.395). Prospective, within-person findings offer some evidence for developmental scar and vulnerability models.

Theory and research indicated that executive functioning (EF) correlated with, preceded, and stemmed from worry in generalized anxiety disorder (GAD). The present secondary analysis (Zainal & Newman, 2023b) thus determined whether EF domains mediated the effect of a 14-day (5 prompts/day) mindfulness ecological momentary intervention (MEMI) against a self-monitoring control (SM) for GAD. Participants ( = 110) diagnosed with GAD completed self-reported (Attentional Control Scale, GAD Questionnaire, Perseverative Cognitions Questionnaire) and performance-based tests (Letter-Number Sequencing, Stroop, Trail Making Test-B, Verbal Fluency) at baseline, post-treatment, and one-month follow-up (1MFU). Causal mediation analyses determined if pre-post changes in EF domains preceded and mediated the effect of MEMI against SM on pre-1MFU changes in GAD severity and trait repetitive negative thinking (RNT). MEMI was more efficacious than SM in improving pre-post inhibition ( = -2.075, 95% [-3.388, -0.762], = .002), working memory ( = 0.512, 95% [0.012, 1.011], = .045), and set-shifting ( = -2.916, 95% [-5.142, -0.691], = .010) but not verbal fluency and attentional control. Within groups, MEMI but not SM produced improvements in all examined pre-post EF outcomes except attentional control. Only pre-post improvements in inhibition mediated the effect of MEMI against SM on pre-1MFU reductions in GAD severity ( = -0.605, 95% [-1.357, -0.044], = .030; proportion mediated = 7.1%) and trait RNT ( = -0.024, 95% [-0.054, -0.001], = .040; proportion mediated = 7.4%). These patterns remained after conducting sensitivity analyses with non-linear mediator-outcome relations. Optimizing MEMI for GAD might entail specifically boosting inhibition plausibly by augmenting it with dialectical behavioral therapy, encouraging high-intensity physical exercises, and targeting negative emotional contrast avoidance.