Parity at a Price: The Emerging Professional Liability of Mental Health Providers

This Article considers the issues associated with emerging professional liability claims against mental health care providers. Part II supplies background information regarding this liability, including the elements of these claims. Part III details the decreasing stigma associated with obtaining mental health services and its impact on professional liability, while Part IV summarizes advancements in mental health treatment that have enhanced the functional capacities of potential litigants. The remaining Parts explore changes in the delivery of mental health care where litigation may be focused, including the increasing use of psychotropic medications (Part V), the expanding role of primary care physicians and other health care providers with limited training and experience pertaining to the treatment of mental illness (Part VI), the surge in pediatric psychotropic prescriptions (Part VII), the emergence of the informed consent doctrine and psychiatric advance directives (Part VIII), and the continuing development of Tarasoff-related liability (Part IX)

Assessment of variation in immunosuppressive pathway genes reveals TGFBR2 to be associated with risk of clear cell ovarian cancer.

BACKGROUND: Regulatory T (Treg) cells, a subset of CD4+ T lymphocytes, are mediators of immunosuppression in cancer, and, thus, variants in genes encoding Treg cell immune molecules could be associated with ovarian cancer. METHODS: In a population of 15,596 epithelial ovarian cancer (EOC) cases and 23,236 controls, we measured genetic associations of 1,351 SNPs in Treg cell pathway genes with odds of ovarian cancer and tested pathway and gene-level associations, overall and by histotype, for the 25 genes, using the admixture likelihood (AML) method. The most significant single SNP associations were tested for correlation with expression levels in 44 ovarian cancer patients. RESULTS: The most significant global associations for all genes in the pathway were seen in endometrioid ( p = 0.082) and clear cell ( p = 0.083), with the most significant gene level association seen with TGFBR2 ( p = 0.001) and clear cell EOC. Gene associations with histotypes at p < 0.05 included: IL12 ( p = 0.005 and p = 0.008, serous and high-grade serous, respectively), IL8RA ( p = 0.035, endometrioid and mucinous), LGALS1 ( p = 0.03, mucinous), STAT5B ( p = 0.022, clear cell), TGFBR1 ( p = 0.021 endometrioid) and TGFBR2 ( p = 0.017 and p = 0.025, endometrioid and mucinous, respectively). CONCLUSIONS: Common inherited gene variation in Treg cell pathways shows some evidence of germline genetic contribution to odds of EOC that varies by histologic subtype and may be associated with mRNA expression of immune-complex receptor in EOC patients

International Lung Cancer Consortium: pooled analysis of sequence variants in DNA repair and cell cycle pathways

Abstract Background: The International Lung Cancer Consortium was established in 2004. To clarify the role of DNA repair genes in lung cancer susceptibility, we conducted a pooled analysis of genetic variants in DNA repair pathways, whose associations have been investigated by at least 3 individual studies. Methods: Data from 14 studies were pooled for 18 sequence variants in 12 DNA repair genes, including APEX1, OGG1, XRCC1, XRCC2, XRCC3, ERCC1, XPD, XPF, XPG, XPA, MGMT, and TP53. The total number of subjects included in the analysis for each variant ranged from 2,073 to 13,955 subjects. Results: Four of the variants were found to be weakly associated with lung cancer risk with borderline significance: these were XRCC3 T241M [heterozygote odds ratio (OR), 0.89; 95% confidence interval (95% CI), 0.79-0.99 and homozygote OR, 0.84; 95% CI, 0.71-1.00

Discovery of 95 PTSD loci provides insight into genetic architecture and neurobiology of trauma and stress-related disorders

Posttraumatic stress disorder (PTSD) genetics are characterized by lower discoverability than most other psychiatric disorders. The contribution to biological understanding from previous genetic studies has thus been limited. We performed a multi-ancestry meta-analysis of genome-wide association studies across 1,222,882 individuals of European ancestry (137,136 cases) and 58,051 admixed individuals with African and Native American ancestry (13,624 cases). We identified 95 genome-wide significant loci (80 novel). Convergent multi-omic approaches identified 43 potential causal genes, broadly classified as neurotransmitter and ion channel synaptic modulators (e.g., GRIA1, GRM8, CACNA1E ), developmental, axon guidance, and transcription factors (e.g., FOXP2, EFNA5, DCC ), synaptic structure and function genes (e.g., PCLO, NCAM1, PDE4B ), and endocrine or immune regulators (e.g., ESR1, TRAF3, TANK ). Additional top genes influence stress, immune, fear, and threat-related processes, previously hypothesized to underlie PTSD neurobiology. These findings strengthen our understanding of neurobiological systems relevant to PTSD pathophysiology, while also opening new areas for investigation

Perceptual sensitivity to emotion expressions: Associations with age and psychopathology from childhood through early adulthood

The ability to infer others’ emotions from facial expressions is an important social skill, and weak emotion expression perception skills are associated with psychopathology. Some evidence suggests that emotion expression perception abilities improve with age, especially for lower intensity expressions like those observed in daily life. This study investigates age-related differences in perceptual sensitivity to categorizing prototypical emotion expressions and how this perceptual sensitivity relates to psychopathology. A sample of 184 participants aged 4-25-years viewed posed angry, fearful, sad, and happy faces morphed with neutral faces at 10-90% intensity. Thin plate regression smoothing splines were used to identify nonlinear associations between age and the perceptual threshold needed to label each target emotion expression. Results suggest that sensitivity to perceiving happiness peaked by age 4. Sensitivity to perceiving anger improved from ages 4-8 and then plateaued. In contrast, sensitivity to perceiving fear and sadness demonstrated protracted development, not reaching a plateau until age 16. Reduction in selecting the “Don’t know” response was the primary driver of age-related improvement on the task. Fear required the most perceptual information to be perceived, as lower intensity morphs were frequently confused with sadness, and fear perception demonstrated the most marked improvement from early childhood to adulthood. Further, perceiving fear with less perceptual information was associated with lower levels of internalizing and externalizing symptoms. This study provides evidence on the development of perceptual sensitivity to perceiving emotions in facial expressions and the particular importance of sensitivity to perceiving fear as a marker of vulnerability to psychopathology

Low Emotional Awareness as a Transdiagnostic Mechanism Underlying Psychopathology in Adolescence

The ability to identify and label one’s emotions is a precursor to effective emotion regulation, suggesting that emotional awareness is important for mental health. We evaluated how emotional awareness was related to psychopathology and whether low emotional awareness was a transdiagnostic mechanism explaining the increase in psychopathology during the transition to adolescence and as a function of childhood trauma—specifically violence exposure. In Study 1, children and adolescents (N=120, aged 7-19 years) reported on emotional awareness and psychopathology. Emotional awareness was negatively associated with psychopathology (p-factor) and decreased across age in females but not males. In Study 2 (N=262, aged 8-16 years), we replicated these findings and demonstrated longitudinally that low emotional awareness mediated increases in p-factor as a function of age in females and violence exposure. These findings indicate that low emotional awareness may be a transdiagnostic mechanism linking adolescent development, sex, and trauma with the emergence of psychopathology

Common genetic contributions to high-risk trauma exposure and self-injurious thoughts and behaviors

Background: Prior research has documented shared heritable contributions to non-suicidal self-injury (NSSI) and suicidal ideation (SI) as well as NSSI and suicide attempt (SA). In addition, trauma exposure has been implicated in risk for NSSI and suicide. Genetically informative studies are needed to determine common sources of liability to all three self-injurious thoughts and behaviors, and to clarify the nature of their associations with traumatic experiences. Methods: Multivariate biometric modeling was conducted using data from 9526 twins [59% female, mean age = 31.7 years (range 24–42)] from two cohorts of the Australian Twin Registry, some of whom also participated in the Childhood Trauma Study and the Nicotine Addiction Genetics Project. Results: The prevalences of high-risk trauma exposure (HRT), NSSI, SI, and SA were 24.4, 5.6, 27.1, and 4.6%, respectively. All phenotypes were moderately to highly correlated. Genetic influences on self-injurious thoughts and behaviors and HRT were significant and highly correlated among men [rG = 0.59, 95% confidence interval (CI) (0.37–0.81)] and women [rG = 0.56 (0.49–0.63)]. Unique environmental influences were modestly correlated in women [rE = 0.23 (0.01–0.45)], suggesting that high-risk trauma may confer some direct risk for self-injurious thoughts and behaviors among females. Conclusions: Individuals engaging in NSSI are at increased risk for suicide, and common heritable factors contribute to these associations. Preventing trauma exposure may help to mitigate risk for self-harm and suicide, either directly or indirectly via reductions in liability to psychopathology more broadly. In addition, targeting pre-existing vulnerability factors could significantly reduce risk for life-threatening behaviors among those who have experienced trauma