Psychological Pain as a Risk Factor for Suicidal Ideation: An Ecological Momentary Assessment Study on Inpatients With Depression With and Without Comorbid Borderline Personality Disorder.

Objective: Psychological pain (PP) is a potentially important risk factor for suicide. However, its temporal stability and association with suicidal ideation (SI) remain obscure. Whether PP represents a risk factor for SI independently of depression, anxiety, and hopelessness or is more prominent and temporally unstable in patients with depression and borderline personality disorder (BPD) is also unclear.Methods: From November 2020 to December 2022, psychiatric inpatients with depression without (N = 37) and with (N = 30) BPD were recruited to an ecological momentary assessment (EMA) study, wherein their PP, severity of depression, SI, and hopelessness were assessed 3 times daily using visual analog scales. Multilevel regression models were estimated.Results: Altogether, 4,320 EMA observations were collected. PP correlated with hopelessness (r = 0.417), depression (r = 0.339), and anxiety (r = 0.496), but the between-patient variance of PP remained at 1.26 (95% CI, 1.025-1.533) after controlling for these variables. The within-patient variance of PP was associated with SI (ß = 0.17 [95% CI, 0.12-0.22]) with a magnitude comparable to hopelessness (ß = 0.1 [95% CI, 0.05-0.15]) and depression (ß = 0.12 [95% CI, 0.08-0.17]). Patients with depression and BPD reported higher daily PP and SI (P < .001) and a more prominent within-patient variation in PP.Conclusions: In psychiatric inpatients with depression, besides depression and hopelessness, PP represents an independent risk factor for SI, varying within a timescale of days. Depressive patients with BPD may experience more prominent and temporally unstable PP, likely underlying their higher vulnerability to SI.

A critical review of risk-sensitive foraging.

Foraging is risk sensitive if choices depend on the variability of returns from the options as well as their mean return. Risk-sensitive foraging is important in behavioural ecology, psychology and neurophysiology. It has been explained both in terms of mechanisms and in terms of evolutionary advantage. We provide a critical review, evaluating both mechanistic and evolutionary accounts. Some derivations of risk sensitivity from mechanistic models based on psychophysics are not convincing because they depend on an inappropriate use of Jensen's inequality. Attempts have been made to link risk sensitivity to the ecology of a species, but again these are not convincing. The field of risk-sensitive foraging has provided a focus for theoretical and empirical work and has yielded important insights, but we lack a simple and empirically defendable general account of it in either mechanistic or evolutionary terms. However, empirical analysis of choice sequences under theoretically motivated experimental designs and environmental settings appears a promising avenue for mapping the scope and relative merits of existing theories. Simply put, the devil is in the sequence.

Borderline personality disorder and depression severity predict suicidal outcomes: A six-month prospective cohort study of depression, bipolar depression, and borderline personality disorder.

BACKGROUND: Suicide risk is high in patients with major depressive disorder (MDD), bipolar disorder (BD) and borderline personality disorder (BPD). Whether risk levels of and risk factors for suicidal ideation (SI) and suicide attempts (SA) are similar or different in these disorders remains unclear, as few directly comparative studies exist. The relationship of short-term changes in depression severity and SI is underinvestigated, and might differ across groups, for example, between BPD and non-BPD patients. METHODS: We followed, for 6 months, a cohort of treatment-seeking, major depressive episode (MDE) patients in psychiatric care (original n = 124), stratified into MDE/MDD, MDE/BD and MDE/BPD subcohorts. We examined risks of suicide-related outcomes and their risk factors prospectively. We examined the covariation of SI and depression over time with biweekly online modified Patient Health Questionnaire 9 surveys and analysed this relationship through multi-level modelling. RESULTS: Risk of SA in BPD (22.2%) was higher than non-BPD (4.23%) patients. In regression models, BPD severity was correlated with risk of SA and clinically significant SI. During follow-up, mean depression severity and changes in depression symptoms were associated with SI risk regardless of diagnosis. CONCLUSIONS: Concurrent BPD in depression seems predictive for high risk of SA. Severity of BPD features is relevant for assessing risk of SA and SI in MDE. Changes in depressive symptoms indicate concurrent changes in risk of SI. BPD status at intake can index risk for future SA, whereas depressive symptoms appear a useful continuously monitored risk index.

Social anxiety disorder is a risk factor for alcohol use problems in the National Comorbidity Surveys.

BACKGROUND: According to the self-medication and biopsychosocial models, individuals with social anxiety disorder (SAD) are at increased risk of developing an alcohol use disorder (AUD) as alcohol represents a maladaptive coping mechanism for some sufferers of SAD. The SAD-to-AUD causation was earlier supported in Norwegian longitudinal twin data and later questioned using longitudinal data from the USA. METHODS: We re-analyzed partly the same USA-based data (National Comorbidity Surveys, n = 5001), conducting theoretical and simulation analyses on different formulations of temporality and using real-data Logistic regression analysis to investigate whether baseline SAD was associated with AUD at the follow-up. RESULTS: Upon proper analysis of temporality, SAD preceded AUD. Specifically, SAD was the only one of the seven anxiety disorders that predicted 10-year later AUD after adjusting for all other anxiety disorders and AUD at the baseline (odds ratio was 1.70% and 95% confidence interval 1.12-2.57). SAD was also associated with incident AUD (OR = 1.64, 95% CI = 1.14-2.37). We provide formal, simulation-based, and data-based arguments on how certain flawed models of incidence attenuate the temporal association. CONCLUSIONS: We demonstrated temporality and specificity in SAD-to-AUD association, which are considered signs of causation. We further identified and discussed problems in previous statistical analyses with different conclusions. Our findings add support for models positing causal effects of SAD on AUD, such as the self-medication and biopsychosocial models. The available evidence suggests that treating SAD should incur better chances of preventing AUD compared to treating other anxiety disorders, which lack comparable evidence on causation.

Associations between specific depressive symptoms and psychosocial functioning in psychotherapy.

BACKGROUND: Psychotherapy for depression aims to reduce symptoms and to improve psychosocial functioning. We examined whether some symptoms are more important than others in the association between depression and functioning over the course of psychotherapy treatment. METHODS: We studied associations between specific symptoms of depression (PHQ-9) and change in social and occupational functioning (SOFAS), both with structural equation models (considering liabilities of depression and each specific symptom) and with logistic regression models (considering the risk for individual patients). The study sample consisted of adult patients (n = 771) from the Finnish Psychotherapy Quality Registry (FPQR) who completed psychotherapy treatment between September 2018 and September 2021. RESULTS: Based on our results of logistic regression analyses and SEM models, the baseline measures of depression symptoms were not associated with changes in functioning. Changes in depressed mood or hopelessness, problems with sleep, feeling tired, and feeling little interest or pleasure were associated with improved functioning during psychotherapy. The strongest evidence for symptom-specific effects was found for the symptom of depressed mood or hopelessness. LIMITATIONS: Due to our naturalistic study design containing only two measurement points, we were unable to study the causal relationship between symptoms and functioning. CONCLUSIONS: Changes in certain symptoms during psychotherapy may affect functioning independently of underlying depression. Knowledge about the dynamics between symptoms and functioning could be used in treatment planning or implementation. Depressed mood or hopelessness appears to have a role in the dynamic relationship between depression and functioning.

The p factor of psychopathology and personality in middle childhood: genetic and gestational risk factors.

BACKGROUND: A joint, hierarchical structure of psychopathology and personality has been reported in adults but should also be investigated at earlier ages, as psychopathology often develops before adulthood. Here, we investigate the joint factor structure of psychopathology and personality in eight-year-old children, estimate factor heritability and explore external validity through associations with established developmental risk factors. METHODS: Phenotypic and biometric exploratory factor analyses with bifactor rotation on genetically informative data from the Norwegian Mother, Father, and Child Cohort (MoBa) study. The analytic sub-sample comprised 10 739 children (49% girls). Mothers reported their children's symptoms of depression (Short Moods and Feelings Questionnaire), anxiety (Screen for Anxiety Related Disorders), attention-deficit/hyperactivity disorder inattention and hyperactivity, oppositional-defiant disorder, conduct disorder (Parent/Teacher Rating Scale for Disruptive Behavior Disorders), and Big Five personality (short Hierarchical Personality Inventory for Children). Developmental risk factors (early gestational age and being small for gestational age) were collected from the Medical Birth Registry. RESULTS: Goodness-of-fit indices favored a p factor model with three residual latent factors interpreted as negative affectivity, positive affectivity, and antagonism, whereas psychometric indices favored a one-factor model. ADE solutions fitted best, and regression analyses indicated a negative association between gestational age and the p factor, for both the one- and four-factor solutions. CONCLUSION: Correlations between normative and pathological traits in middle childhood mostly reflect one heritable and psychometrically interpretable p factor, although optimal fit to data required less interpretable residual latent factors. The association between the p factor and low gestational age warrants further study of early developmental mechanisms.

Direction of dependence analysis for pre-post assessments using non-Gaussian methods: a tutorial.

OBJECTIVE: We introduced methods for solving causal direction of dependence between variables observed in pre- and post-psychotherapy assessments, showing how to apply them and investigate their properties via simulations. In addition, we investigated whether changes in depressive symptoms drive changes in social and occupational functioning as suggested by the phase model of psychotherapy or vice versa, or neither. METHOD: As a Gaussian (normal-distribution) model is unidentifiable here, we used an identifiable linear non-Gaussian structural vector autoregression model, conceptualizing instantaneous effects as during-psychotherapy causation and lagged effects as pre-treatment predictors of change. We tested six alternative estimators in six simulation settings that captured different real-world scenarios, and used real psychotherapy data from 1428 adult patients (Finnish Psychotherapy Quality Registry; assessments on Patient Health Questionnaire-9 and Social and Occupational Functioning Assessment Schedule). RESULTS: The methodology was successful in identifying causal directions in simulated data. The real-data results provided no evidence for single direction of dependence, suggesting shared or reciprocal causation. CONCLUSIONS: A powerful new tool was presented to investigate the process of psychotherapy using observational data. Application to patient data suggested that depression symptoms and functioning may reciprocate or reflect third variables instead of one predominantly driving the other during psychotherapy.

Measurement Invariant but Non-Normal Treatment Responses in Guided Internet Psychotherapies for Depressive and Generalized Anxiety Disorders.

Assessment of treatment response in psychotherapies can be undermined by lack of longitudinal measurement invariance (LMI) in symptom self-report inventories, by measurement error, and/or by wrong model assumptions. To understand and compare these threats to validity of outcome assessment in psychotherapy research, we studied LMI, sum scores, and Davidian Curve Item Response Theory models in a naturalistic guided internet psychotherapy treatment register of 2,218 generalized anxiety disorder (GAD) patients and 3,922 depressive disorder (DD) patients (aged ≥16 years). Symptoms were repeatedly assessed by Generalized Anxiety Disorder Assessment-7 (GAD-7) or Beck Depression Inventory. The symptom self-reports adhered to LMI under equivalence testing, suggesting sum scores are reasonable proxies for disorder status. However, the standard LMI assumption of normally distributed latent factors did not hold and inflated treatment response estimates by 0.2 to 0.3 standard deviation units compared with sum scores. Further methodological research on non-normally distributed latent constructs holds promise in advancing LMI and mental health assessment.

Feasibility of generic, short, and easy-to-use assessment of psychological distress during psychotherapy: Longitudinal measurement invariance of CORE-10 and -OM.

Objective: While the CORE-10 inventory for Clinical Outcome Routine Evaluation has shown good psychometric properties in cross-sectional assessment, the feasibility of generic, short, and easy-to-use longitudinal assessment of a broadband construct such as the targeted "general psychological distress" remains to be psychometrically demonstrated. Therefore, we investigated longitudinal measurement invariance (LMI) of CORE-10. For comprehensiveness, we also analyzed its parent inventory, CORE-OM. Method: We investigated the LMI of pre- and post-therapy CORE-10 and -OM assessments in a naturalistic treatment register of 1715 patients' short psychotherapies, testing whether the construct of "psychological distress" remained the same across the treatments. Results: We observed good psychometric properties and no violations of LMI for CORE-10 in chi-squared equivalence tests, nor in effect-size-based evaluations. Only the highly sensitive chi-squared difference tests detected LMI violations but these had little practical influence. The CORE-OM data did not fit well with factorial models but this was cross-sectional rather than a genuinely longitudinal (LMI-related) issue. Conclusions: CORE-10 appeared a structurally valid measure of general psychological distress and suitable for longitudinal assessment, whereas the CORE-OM had a less clear factorial structure. Regarding psychometrics, these findings support the use of CORE-10 in longitudinal assessment during psychotherapy and do not support CORE-OM.

Continuity of genetic and environmental influences on clinically assessed major depression from ages 18 to 45.

BACKGROUND: Studies on the stability of genetic risk for depression have relied on self-reported symptoms rather than diagnoses and/or short follow-up time. Our aim is to determine to what degree genetic and environmental influences on clinically assessed major depressive disorder (MDD) are stable between age 18 and 45. METHODS: A population-based sample of 11 727 twins (6875 women) born between 1967 and 1991 was followed from 2006 to 2015 in health registry data from primary care that included diagnoses provided by treating physicians. Individuals with schizophrenia or bipolar disorder (n = 163) were excluded. We modelled genetic and environmental risk factors for MDD in an accelerated longitudinal design. RESULTS: The best-fitting model indicated that genetic influences on MDD were completely stable from ages 18 to 45 and explained 38% of the variance. At each age, the environmental risk of MDD was determined by the risk at the preceding observation, plus new environmental risk, with an environmental correlation of +0.60 over 2 years. The model indicated no effects of shared environment and no environmental effects stable throughout the observational period. All long-term stability was therefore explained by genetic factors. CONCLUSIONS: Different processes unfolded in the genetic and environmental risk for MDD. The genetic component is stable from later adolescence to middle adulthood and accounted for nearly all long-term stability. Therefore, molecular genetic studies can use age-heterogenous samples when investigating genetic risk variants of MDD. Environmental risk factors were stable over a short span of years with associations rapidly decreasing and no evidence of permanent environmental scarring.

Longitudinal Associations of Explosive and Adventurous Temperament Profiles With Character Development: The Modifying Effects of Social Support and Attachment.

OBJECTIVE: The aim of this study was to examine (a) whether adventurous and explosive temperament profiles (presumed precursors of antisocial and borderline personality) are associated with character traits over a 15-year follow-up and (b) whether social support and attachment security modify the relationship between temperament profiles and character development. METHODS: 2,028 subjects of the Young Finns study completed the Temperament and Character Inventory, the Multidimensional Scale of Perceived Social Support, and the Relationship Questionnaire at 3 assessment points between 1997 and 2012. RESULTS: Both explosive and adventurous temperament profiles seemed to predispose individuals to have less mature personalities; that is, these profiles were consistently associated with lower cooperativeness (P < .001), and explosive temperament also with lower self-directedness (P < .001), over the entire follow-up period. These relationships did not vary significantly at the individual level and were sustained after controlling for age, gender, and socioeconomic status. However, the presence of high social support and secure attachment was found to decrease the likelihood that explosive temperament would lead to an immature adulthood character (P < .001). In contrast, persons with the adventurous temperament were likely to have a more mature character under low social support and an immature one under high experienced social support (P < .05). CONCLUSIONS: Individuals with the explosive temperament benefit from high social support and secure attachment. From the point of view of the therapy process, this knowledge might be of importance. In contrast, individuals with the adventurous temperament were able to direct their behavior better in social environments that were not likely to support their basic temperaments.

Testing Genetic and Environmental Associations Between Personality Disorders and Cocaine Use: A Population-Based Twin Study.

Until now, data have not been available to elucidate the genetic and environmental sources of comorbidity between all 10 DSM-IV personality disorders (PDs) and cocaine use. Our aim was to determine which PD traits are linked phenotypically and genetically to cocaine use. Cross-sectional data were obtained in a face-to-face interview between 1999 and 2004. Subjects were 1,419 twins (µage = 28.2 years, range = 19-36) from the Norwegian Institute of Public Health Twin Panel, with complete lifetime cocaine use and criteria for all 10 DSM-IV PDs. Stepwise multiple and Least Absolute Shrinkage and Selection Operator (LASSO) regressions were used to identify PDs related to cocaine use. Twin models were fitted to estimate genetic and environmental associations between the PD traits and cocaine use. In the multiple regression, antisocial (OR = 4.24, 95% CI [2.66, 6.86]) and borderline (OR = 2.19, 95% CI [1.35, 3.57]) PD traits were significant predictors of cocaine use. In the LASSO regression, antisocial, borderline, and histrionic were significant predictors of cocaine use. Antisocial and borderline PD traits each explained 72% and 25% of the total genetic risks in cocaine use, respectively. Genetic risks in histrionic PD were not significantly related to cocaine use. Importantly, after removing criteria referencing substance use, antisocial PD explained 65% of the total genetic variance in cocaine use, whereas borderline explained only 4%. Among PD traits, antisocial is the strongest correlate of cocaine use, for which the association is driven largely by common genetic risks.