Clinical psychology is a young science. Psychological suffering remains extensive, with core scientific issues the subject of ongoing study and debate. Clinical practice depends on the research base for elucidating etiology, systematic improvements in provision of mental health care, improvements in public health, and credibility with clients and the larger public. Science-oriented training programs endeavor to develop students into independent scientists, clinicians, and/or administrators who produce knowledge and translate it to improve clinical care. Existing training standards accommodate programs with a heavy clinical focus and little to no research training. To accelerate scientific progress, these standards must also accommodate increased scientific and research training by reducing generalist requirements and increasing curricular flexibility for students. On net, these changes would allow clinical psychologists more opportunities to work at the level of the clinic, system, policy, or laboratory and thereby accelerate scientific discovery and translation to understand and reduce mental health burdens in our society, all while existing programs, including practitioner-oriented programs, may continue to flourish.

Although chronic pain is a major risk factor for suicidal behaviors, the shared genetic underpinnings of these phenotypes are poorly understood. This study leveraged genome-wide association data to examine the shared genetic architecture between multidimensional pain (MP), capturing broad genetic liability to chronic pain (n = 1,235,695), and suicidal behaviors, including suicide attempt (SA, n = 787,974) and suicide death (SD, n = 18,223). Integrative cross-trait genetic analyses revealed substantial polygenic overlap between MP and both suicidal behaviors, and identified 76 (244 genes) and 10 (27 genes) distinct shared loci for SA and SD, respectively. The genes mapped to the shared SA loci were enriched in neuronal and synaptic pathways, and integration of multi-omics data further prioritized 10 genes, providing convergent molecular context relevant to the neurobiological and behavioral pathways implicated in the association between pain liability and SA. Mendelian randomization analyses supported a potential causal relationship between MP and both suicidal behaviors, with asymmetric bidirectional effects for MP and SA. Mediation analyses further indicated that 14 health-related traits, including psychological and substance-related behaviors, partially mediated the association between MP and SA. Together, these findings reveal shared genetic architecture between MP and suicidal behaviors, with the association partially mediated by convergent neurobiological and potentially modifiable behavioral pathways relevant to prevention and therapeutic efforts.

Objective: Cancer survivors, defined as those living with or beyond a cancer diagnosis, experience more than double the prevalence of psychopathology when compared to the general population. Categorical diagnostic systems, such as the Diagnostic and Statistical Manual of Mental Disorders (DSM), remain dominant in psycho-oncology despite concerns about reliability, validity, and clinical utility for this population. Dimensional frameworks, such as the Hierarchical Taxonomy of Psychopathology (HiTOP), offer a more precise alternative; however, they have not yet been widely applied in cancer survivors. Accordingly, the objective of this research was to examine the applicability of HiTOP to cancer survivors. Methods: Data from 1,389 participants in 28 countries (n=728 cancer survivors; n=661 community/psychiatric) were collected using the 405-item HiTOP-SR, alongside demographic, clinical, and cancer-specific measures. The HiTOP-SR normative sample (n=780) was also used. Analyses included parametric, non-parametric, and factor analytic approaches. Results: All HiTOP-SR scales demonstrated strong homogeneity and reliability in cancer survivors. Cancer survivors showed significant elevations across Internalising and Somatoform spectra, with current cancer associated with additional elevations in domains of Thought Disorder and components of Disinhibited and Antagonistic psychopathology. An 11-factor model was developed and supported for both cancer and community/psychiatric samples, though the magnitudes of the factor loadings sometimes varied between samples. External validity was strong with theoretically aligned associations. Conclusion: The HiTOP-SR appears reliable within cancer survivors and provides utility in quantifying a broad array of psychopathology experienced. The results highlight the potential applicability and utility of HiTOP to improve cancer research and clinical practice in psycho-oncology.

Background Diagnosis in psychiatry faces familiar challenges. Validity and utility remain elusive, and confusion regarding the fluid and arbitrary border between mental health and illness is increasing. The mainstream strategy has been conservative and iterative, retaining current nosology until something better emerges. However, this has led to stagnation. New conceptual frameworks are urgently required to catalyze a genuine paradigm shift.Methods We outline candidate strategies that could pave the way for such a paradigm shift. These include the Research Domain Criteria (RDoC), the Hierarchical Taxonomy of Psychopathology (HiTOP), and Clinical Staging, which all promote a blend of dimensional and categorical approaches.Results These alternative still heuristic transdiagnostic models provide varying levels of clinical and research utility. RDoC was intended to provide a framework to reorient research beyond the constraints of DSM. HiTOP began as a nosology derived from statistical methods and is now pursuing clinical utility. Clinical Staging aims to both expand the scope and refine the utility of diagnosis by the inclusion of the dimension of timing. None is yet fit for purpose. Yet they are relatively complementary, and it may be possible for them to operate as an ecosystem. Time will tell whether they have the capacity singly or jointly to deliver a paradigm shift.Conclusions Several heuristic models have been developed that separately or synergistically build infrastructure to enable new transdiagnostic research to define the structure, development, and mechanisms of mental disorders, to guide treatment and better meet the needs of patients, policymakers, and society.

OBJECTIVE:Personality traits such as conscientiousness and emotional stability are consistently linked with better metabolic health, but there is limited evidence on the etiology of these associations and their robustness across the life-span. METHODS:Therefore, we estimated phenotypic, genetic, and unique environmental associations of traits indexed by the Multidimensional Personality Questionnaire in early-to-middle adulthood (mean age = 38.3 years) with BMI, waist circumference, high-density lipoprotein cholesterol, C-reactive protein, triglycerides, and glycated hemoglobin in older adulthood (mean age = 70.4 years) using the Minnesota Twin Registry sample (n = 950). RESULTS:Traits that indexed emotional instability in midlife, such as alienation and stress reactivity, were significant predictors of several metabolic outcomes late in life (bivariate |r| ≤ 0.22), whereas negative associations with traits related to conscientiousness (e.g., control, constraint, achievement) tended to be more modest. For most traits that were phenotypically associated, we observed significant genetic correlations. Additionally, alienation and stress reactivity had weak-to-moderate unique environmental correlations with BMI, waist circumference, and C-reactive protein (re = 0.10-0.29). CONCLUSIONS:These results are consistent with an etiology of declining metabolic health into old age involving the propensity toward negative affective experiences decades prior, further validating the health relevance of individual differences in personality.

Polygenic indexes (PGIs) - DNA-based predictors of individual phenotypes - have become essential tools across biomedical and social sciences. We introduce Version 2 of the Polygenic Index Repository, which expands phenotype coverage from 47 to 61, increases the number of participating datasets from 11 to 20, and adopts a more consistent and improved methodology for PGI construction. For 16 phenotypes, we leverage summary statistics from an updated GWAS meta-analysis with greater statistical power compared to the original release, thereby improving the PGI's predictive power. To improve power for family-based analyses, we provide imputed parental PGIs in all datasets with first-degree relatives and offer a framework for interpreting results from analyses that control for parental PGIs. We illustrate the utility of parental PGIs using two applications: (1) comparing PGI associations with and without parental PGI controls for all phenotypes in two Repository datasets with family data, and (2) for BMI and diastolic blood pressure, exploring the contribution of causal versus non-causal components of PGI associations to the imperfect portability of PGIs across subgroups within a genetic ancestry. Collectively, the updates enhance predictive performance, broaden the Repository's scope, and introduce novel resources that reduce confounding bias and improve interpretability.

Racial differences in the prevalence of mild cognitive impairment (MCI) and Alzheimer’s Disease and related dementia (ADRD) are well documented in aging populations. Using data from a large longitudinal study of adults, Black-White disparities in mild cognitive impairment (MCI) were estimated and putative mediators of Black-White disparities in cognitive function were examined. The prevalence of MCI was determined algorithmically for Black and White adults, and longitudinal indicators of income, educational attainment, and interpersonal discrimination were used to conduct a parallel mediation analysis of Black-White disparities in executive function and episodic memory. As expected, there was a statistically significant racial disparity in the prevalence of MCI, such that MCI was more prevalent among Black adults (6.4%) than White adults (3.0%), which was statistically significant according to Fisher’s exact test ( OR = 2.20, p = .041). Continuous distributions of executive function, episodic memory, and general cognition also differed significantly for Black and White adults (range of Cohen’s d = [0.38, 0.76], p-values < .01), as did putative mediators of Black-White disparities in cognitive outcomes, including income, educational attainment, and exposure to discrimination (range of Cohen’s d = [0.26, 1.07], p-values < .01). Parallel mediation analyses indicated that household income, educational attainment, and interpersonal discrimination were all statistically significant (p-values < .005) mediators of Black-White disparities. Approximately 1/3 of the observed Black-White disparity in executive function, episodic memory, and general cognition was accounted for by racial group differences in income, education, and cumulative exposure to interpersonal discrimination, which included lack of support from coworkers and supervisors. Conversely, the remaining 2/3 of the Black-White racial disparity was neither explained by group differences in income, education, nor exposure to discrimination. Future research should focus on identifying additional socioeconomic and modifiable interpersonal factors that account for Black-White disparities in cognitive dysfunction and mild cognitive impairment in aging populations.

Attention-deficit/hyperactivity disorder (ADHD) in adults involves inattention, hyperactivity, and impulsivity, often accompanied by emotional dysregulation and significant functional impairment. Although stimulant medication effectively reduces core symptoms, its impact on broader psychosocial functioning is less consistent. Personality pathology, varying in severity and expression, may account for this variability. This naturalistic study examined how dimensional models of personality pathology influence symptomatic and functional outcomes during pharmacological treatment for adult ADHD. A total of 246 adults (66% women; mean age = 33.5 years) completed assessments of general personality dysfunction, maladaptive personality traits, ADHD symptoms, and functional impairment. Linear mixed-effects models showed that individuals with higher levels of personality dysfunction and maladaptive traits were more functionally impaired and demonstrated less symptomatic improvement during treatment. General personality dysfunction predicted greater functional impairment and higher ADHD symptom burden, while maladaptive domains - particularly Negative Affectivity, Detachment, and Psychoticism - were strongly linked to functional impairment. In contrast, Disinhibition was the only domain meaningfully related to ADHD symptom burden, consistent with its overlap with core ADHD features. Stimulant dosage and treatment duration showed only modest associations with functional change. These findings indicate that personality pathology substantially constrains the effectiveness of pharmacological treatment in adults with ADHD. Higher impairment and limited functional gains among individuals with pronounced personality dysfunction suggest that medication alone is insufficient to improve adaptive functioning. Integrated, personality-informed interventions addressing both neurocognitive and personality-based mechanisms may therefore be required to achieve lasting recovery in everyday life. Keywords: ADHD; Adult ADHD; Pharmacotherapy; Stimulant Medication; Dimensional Personality Pathology; Personality Dysfunction; Functional Impairment

Objectives: Non-adherence to medication is common in the adult ADHD clinical group. The goal of this pre-registered study was to examine whether the DSM-5 Alternative Model of Personality Disorder (AMPD), generality personality dysfunction (LPFS-BF 2.0) or maladaptive personality traits (PID-5), can predict time to premature discontinuation of pharmacological treatment beyond other known factors. Methods: A sample of 284 adult patients with ADHD (60.6% female; Mage = 32.31 years) were investigated for medication adherence from 2018 to 2023, using time-to-event analytic methods. Results: Of the sample, 54 were found to have discontinued treatment prematurely without consulting their physician. Interestingly this group was prescribed considerably lower doses before discontinuation than adhering patients. General personality dysfunction and maladaptive antagonistic personality traits are implicated in varying degrees, with the specific maladaptive personality facets Intimacy Avoidance and Deceitfulness (PID-5) significantly predicting time to premature discontinuation of ADHD medication beyond other known reasons for non-adherence. Conclusions: The broader implication is that the emerging personality pathology models hold promise to predict non-adherence in the adult ADHD population.

Low educational attainment is recognized as a modifiable risk factor for dementia. Despite the commonly accepted notion that greater educational attainment confers lower dementia risk, few family-based studies have investigated the causal bases for the association. Using data from seven twin samples from Sweden, Denmark, Australia, and the US participating in the IGEMS (Interplay of Genes and Environment in Multiple Studies) consortium ( N = 60,027, 10.92% with dementia), we tested whether twins who achieve higher education than their co-twins have lower risk of dementia. The primary analysis applied a multilevel between-within regression framework, supported by descriptive statistics of within-pair differences. Results confirmed an overall association between educational attainment and dementia risk, such that individuals with higher educational attainment had less likelihood of developing dementia (phenotypic regression coefficient = -0.68, p <.0001). Within twin pairs, however, twins who achieved greater education than their co-twins did not uniformly show lower dementia risk (within-family regression coefficient = -0.07, p =.0983, while between-family regression coefficient = -0.98, p <.0001). Taken together, the pattern of results shows that the effect of educational attainment on dementia risk is largely attributable to genetic influences in common to educational attainment and dementia, although there are also contributions from environmental influences shared between members of the same family. Results were similar in men and women. These findings add to the literature by using a co-twin control design to address possible reasons that low educational attainment is associated with greater dementia risk.

Background Childhood adversity has been associated with increased peripheral inflammation in adulthood. However, not all individuals who experience early adversity develop these inflammatory outcomes. Separately, there is also a link between various internalizing emotional distress conditions (e.g. depression, anxiety, and fear) and inflammation in adulthood. It is possible the combination of adult emotional distress and past childhood adversity may be uniquely important for explaining psychopathology-related immune dysfunction at midlife.Methods Using data from the Midlife in the United States (MIDUS) study (n = 1255), we examined whether internalizing, defined as past 12-month emotional distress symptomatology and trait neuroticism, moderated associations between childhood adversity and heightened inflammation in adulthood. Using latent variable modeling, we examined whether transdiagnostic or disorder-specific features of emotional distress better predicted inflammation.Results We observed that childhood adversity only predicted adult inflammation when participants also reported adult internalizing emotional distress. Furthermore, this moderation effect was specific to the transdiagnostic factor of emotional distress rather than the disorder-specific features.Conclusions We discuss the possibility that adult internalizing symptoms and trait neuroticism together may signal the presence of temporally stable vulnerabilities that amplify the impact of childhood adversity on midlife immune alterations. The study highlights the importance of identifying emotional distress in individuals who have experienced childhood adversity to address long-term immune outcomes and enhance overall health.

To compare the effectiveness of the Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5), Section II personality disorder (PD) model, and of the Alternative Model for Personality Disorders (AMPD) model in characterizing vulnerable (VN) and grandiose (GN) narcissism, a sample of clinical psychotherapy participants (N = 369) was administered the Schedule for Nonadaptive and Adaptive Personality-2, the Levels of Personality Functioning Scale-Self Report (LPFS-SR), the Personality Inventory for DSM-5, the Five-Factor Narcissism Inventory-Short Form (FFNI-SF), and the Pathological Narcissism Inventory (PNI). In multiple regression models, the LPFS-SR scales and the Personality Inventory for DSM-5 (PID-5) domain scales explained 34.6% and 23.7% more variance than the self-reports of the 10 Section II PD symptom counts in the FFNI-SF and PNI GN scores, respectively. Similarly, AMPD measures outperformed self-reported symptom counts of the 10 Section II PDs, accounting for 28.8% and 22.6% more variance in the FFNI-SF and PNI VN scale scores, respectively.

For decades, advancements in understanding and treating mental illness have been hindered by a categorical psychiatric nosology that fails to describe and explain how symptoms emerge and relate to one another. In response, two separate initiatives have contributed to a renewed sense of optimism for scientific and translational discovery. First, quantitative models of psychopathology improve clinical description by relying on empirical data to provide a more accurate representation of the structure of mental illness. Chief among these approaches is the Hierarchical Taxonomy of Psychopathology (HiTOP), which organizes psychopathology based on patterns of symptom covariation observed across numerous studies. In parallel, computational psychiatry seeks to identify neurocognitive processes that give rise to psychopathology and leverage them to forecast important clinical and functional outcomes. Here, we highlight points of convergence and complementarity between HiTOP and computational psychiatry and propose further integration. HiTOP provides an empirically based approach to understanding the structure of psychopathology, but lacks strong explanations of how symptom dimensions are connected to underlying neurocognitive processes. Conversely, computational psychiatry’s emphasis on cognitive processes and multivariate prediction make it well-suited to linking lower level dynamics with symptom variability. Yet, many contemporary computational psychiatry findings lack specificity and validity as a result of a continued reliance on categorical diagnoses. We conclude by highlighting potential barriers that will need to be addressed to maximize the productivity of future collaborative efforts between these initiatives.

INTRODUCTION:Nonsuicidal self-injury (NSSI) represents a relevant public health concern, with lifetime prevalence being high in community samples. The present study aimed to examine the latent associations between the Hierarchical Taxonomy of Psychopathology (HiTOP) superspectra and NSSI frequency and motivation. METHODS:A sample of 547 community-dwelling adult participants was administered measures of NSSI, NSSI functions, and psychopathology. RESULTS:The multiple indicators multiple causes model evidenced a significant and nontrivial contribution of the Functional Assessment of Self-Mutilation automatic function latent dimension in predicting the frequency of NSSI. Structural equation modeling analyses showed that the overall frequency of NSSI episodes was uniquely, significantly and positively predicted by the HiTOP Externalizing latent dimension scores. Notably, all FASM motivation factors yielded significant and nontrivial relationships with HiTOP Externalizing, Psychosis, and Emotion Dysfunction latent variables in SEM analyses. CONCLUSIONS:These findings may prove useful in extending our knowledge of transdiagnostic psychopathology dimensions and their implications for NSSI.

Measurement of aging is critical to understanding its causes and developing interventions, but little consensus exists on what components such measurements should include or how they perform in predicting mortality. The aim of this study was to identify factors of aging among a comprehensive set of indicators, and to evaluate their relative performance in predicting mortality. Measurements on 34 clinical, survey, and neuroimaging variables, along with epigenetic age markers, were obtained from two waves (2004-2021) of the Midlife in the United States (MIDUS) study. Mortality data was also available on 11875 participants, including 1908 twins. Factor analyses were used to identify aging factors, and these were used to predict mortality as of 2022. Twin data were used to model predictors of mortality within families. Factor analyses identified 9 major dimensions of aging: frailty, cognition, adiposity, glucose, blood pressure, inflammation, lipids, adaptive functioning, and neurological functioning. The strongest predictors of survival among the aging dimensions were cognition, adaptive functioning, and inflammation, and among the epigenetic markers, the decline-predictive markers (GrimAge and DunedinPACE). When entered in joint prediction models, cognition remained a significant predictor of mortality, but the epigenetic markers did not. Cognition, adaptive functioning, and inflammation remained significant predictors of mortality within twin pairs as well. Aging is a multidimensional construct, with cognition, adaptive functioning, and inflammation being the strongest predictors of survival among the aging dimensions examined. Their association with mortality is observed within families, suggesting that early developmental factors cannot entirely account for their association with survival. Interventions and assessments should prioritize cognition in measures of aging quality, along with adaptive functioning and inflammation.