The Common Factors of Grit, Hope, and Optimism Differentially Influence Suicide Resilience.

No study to date has simultaneously examined the commonalities and unique aspects of positive psychological factors and whether these factors uniquely account for a reduction in suicide risk. Using a factor analytic approach, the current study examined the relationships between grit, hope, optimism, and their unique and overlapping relationships in predicting suicide ideation. Results of principle axis factor analysis demonstrated close relationships between these variables at both the construct and item level. Item-level analyses supported a five-factor solution (Stick-to-Itiveness, Poor Future, Consistency of Interest, Positive Future, and Poor Pathways). Four of the five factors (excluding Stick-to-Itiveness) were associated with suicide ideation. Additionally, results of a multiple regression analysis indicated that two of the five factors (Consistency of Interest and Positive Future) negatively predicted suicide ideation while Poor Future positively predicted suicide ideation. Implications regarding the interrelationships between grit, hope, and optimism with suicide ideation are discussed.

The indirect effect of perceived burdensomeness on the relationship between indices of social support and suicide ideation in college students.

OBJECTIVE: Research has demonstrated that a lack of social support is related to suicide risk. This study examines perceived burdensomeness and thwarted belongingness, of the Interpersonal Theory of Suicide, as mechanisms of the social support-suicide relationship in college students. METHOD: The study consisted of 207 students from a Midwestern university. Data were collected from 2007 to 2008. Two multiple mediation analyses were conducted to examine whether perceived burdensomeness and thwarted belongingness mediated the relationship between indices of social support and suicide ideation. RESULTS: Perceived burdensomeness mediated the relationships between perceived social support and suicide ideation (95% confidence interval [CI] -.02 to -.00, effect size = -.01) and social connectedness and suicide ideation (95% CI -.03 to -.00, effect size = -.03). Thwarted belongingness did not mediate either relationship. CONCLUSIONS: Results suggest that a lack of social support could lead to perceptions of being a burden on others, which could lead to suicide ideation.

How Veterans Health Administration Suicide Prevention Coordinators Assess Suicide Risk.

This cross-sectional study was designed to examine the suicide risk assessment practices of Suicide Prevention Coordinators (SPCs) within the Veterans Health Administration. Specifically, this study sought to (1) identify factors SPCs consider most important in assessing risk and patient priority; (2) measure the level of consistency and agreement between SPCs in assessing suicide risk and prioritizing cases; and (3) measure individual SPC consistency between cases. SPCs (n = 63) responded to online survey questions about imminent and prolonged risk for suicide in response to 30 fictional vignettes. Combinations of 12 acute and chronic suicide risk factors were systematically distributed throughout the 30 vignettes using the Fedorov () procedure. The SPCs were also asked to identify the level of priority for further assessment both disregarding and assuming current caseloads. Data were analysed using clinical judgement analysis. Suicidal plan, ß = 1.64; 95% CI (1.45, 1.82), and preparatory behaviour, ß = 1.40; 95% CI (1.23, 1.57), were considered the most important acute or imminent risk factors by the SPCs. There was less variability across clinicians in the assessment of risk when alcohol use (p = 0.02) and hopelessness (p = 0.03) were present. When considering acute or imminent risk factors, there was considerable variability between clinicians on a vignette-by-vignette basis, median SD = 0.86 (range = 0.47, 1.13), and within individual clinicians across vignettes, median R2 = 0.80 (0.49, 0.95). These findings provide insight into how this group of providers think about acute and chronic risk factors contributing to imminent suicide risk in Veterans. Copyright © 2016 John Wiley & Sons, Ltd. KEY PRACTITIONER MESSAGE: Identifies factors that practitioners consider most important in suicide risk assessment Discusses how to distinguish between chronic and acute risk for suicide Identifies factors that lead to more consistent clinical judgments.

Ecological Momentary Assessment is a Neglected Methodology in Suicidology.

Ecological momentary assessment (EMA) is a group of research methods that collect data frequently, in many contexts, and in real-world settings. EMA has been fairly neglected in suicidology. The current article provides an overview of EMA for suicidologists including definitions, data collection considerations, and different sampling strategies. Next, the benefits of EMA in suicidology (i.e., reduced recall bias, accurate tracking of fluctuating variables, testing assumptions of theories, use in interventions), participant safety considerations, and examples of published research that investigate self-directed violence variables using EMA are discussed. The article concludes with a summary and suggested directions for EMA research in suicidology with the particular aim to spur the increased use of this methodology among suicidologists.

Physical Activity, Suicide Risk Factors, and Suicidal Ideation in a Veteran Sample.

The association between current level of suicidal ideation and physical activity was tested in a broad sample of veterans seeking care from the Veterans Health Administration. It was hypothesized that the two variables would be significantly inversely related. It was further hypothesized that the relationship would be mediated by depressive symptoms, disturbed sleep, and a measure of heart rate variability based on existing research regarding physical activity and sleep. Due to the first hypothesis not being supported, the second could not be tested. Post hoc correlation analyses did find associations between physical activity and depressive symptoms, in expected directions, and are discussed. Possible explanations for the negative findings along with recommendations for future research to continue exploring links between suicide risk and physical activity are presented. We conclude by suggesting that physical activity may have promise as a risk reduction intervention and that prospective data are more likely to yield significant results than the cross-sectional methodology employed in the current study.

Risk Factors, Warning Signs, and Drivers of Suicide: What Are They, How Do They Differ, and Why Does It Matter?

Research investigating suicide attempts and deaths by suicide has yielded many specific risk factors and warning signs for future suicidal behaviors. Yet, even though these variables are each valuable for suicide prevention efforts, they may be limited in their applicability to clinical practice. The differences among risk factors, warning signs, and "drivers," which are person-specific variables that lead individuals to desire death by suicide, are highlighted. The scarce evidence on drivers is described and specific recommendations for conducting future drivers-focused research and targeting them in clinical practice are suggested.

Interpersonal suicide risk for American Indians: investigating thwarted belongingness and perceived burdensomeness.

American Indians (AIs) experience increased suicide rates compared with other groups in the United States. However, no past studies have examined AI suicide by way of a recent empirically supported theoretical model of suicide. The current study investigated whether AI suicidal ideation can be predicted by two components: thwarted belongingness and perceived burdensomeness, from the Interpersonal-Psychological Theory of Suicide (T. E. Joiner, 2005, Why people die by suicide. Cambridge, MA: Harvard University Press). One hundred seventy-one AIs representing 27 different tribes participated in an online survey. Hierarchical regression analyses showed that perceived burdensomeness significantly predicted suicidal ideation above and beyond demographic variables and depressive symptoms; however, thwarted belongingness did not. Additionally, the two-way interaction between thwarted belongingness and perceived burdensomeness significantly predicted suicidal ideation. These results provide initial support for continued research on the components of the Interpersonal-Psychological Theory of Suicide, an empirically supported theoretical model of suicide, to predict suicidal ideation among AI populations.

The impact of exercise on suicide risk: examining pathways through depression, PTSD, and sleep in an inpatient sample of veterans.

Suicide has a large public health impact. Although effective interventions exist, the many people at risk for suicide cannot access these interventions. Exercise interventions hold promise in terms of reducing suicide because of their ease of implementation. While exercise reduces depression, and reductions in depressive symptoms are linked to reduced suicidal ideation, no studies have directly linked exercise and suicide risk. The current study examined this association, including potential mediators (i.e., sleep disturbance, posttraumatic stress symptoms, and depression), in a sample of Veterans. SEM analyses revealed that exercise was directly and indirectly associated with suicide risk. Additionally, exercise was associated with fewer depressive symptoms and better sleep patterns, each of which was, in turn, related to lower suicide risk.

Symptoms of attention-deficit/hyperactivity disorder (ADHD) moderate suicidal behaviors in college students with depressed mood.

OBJECTIVE: College students with attention-deficit/hyperactivity disorder-related hyperactive/impulsive (HI) and/or inattentive (IA) symptoms may be at greater risk for suicidal behavior due to core and secondary symptoms that increase their potential to engage in behaviors that put them at risk for suicidal behavior. Consequently, the current study examined the moderating effect of combined HI/IA symptoms, in addition to independent HI and IA symptoms on the relationship between depressed mood and suicidal thoughts and behavior. METHOD: A sample of 1,056 undergraduate students (61.5% female, 96.4% aged 18-24 years) provided self-report ratings of mood, suicidal behavior (thoughts, self-harm, attempts, and need for medical attention), and current HI/IA symptoms. RESULTS: Significant moderation effects were detected, such that greater HI/IA symptoms were associated with a stronger relationship between depressed mood and suicidal ideation and attempts, but not self-harm. Current HI and IA symptoms significantly moderated the relationship between depressed mood and suicidal thoughts and suicide attempts, but did not moderate the relationship between depressed mood and self-harm and need for medical attention. CONCLUSIONS: The current findings suggest that the presence of combined HI/IA symptoms conveys increased suicide risk for depressed college students. Additionally, results suggest a complex relationship between independent HI and IA symptoms and severe suicidal outcomes.

Can perceived burdensomeness explain the relationship between suicide and perfectionism?

The perception of being a burden to others has been associated with suicidal ideation and behavior. Maladaptive aspects of perfectionism have also been associated with suicidal thinking and behavior. The purpose of the current study was to investigate whether perceived burdensomeness would act as a mediator between maladaptive perfectionism and suicidal ideation. Results indicated that perceived burdensomeness mediated the relationship between maladaptive perfectionism and suicidal ideation, which suggest that the perception of burdensomeness may be one aspect of the mechanism by which perfectionism can lead to such psychological distress that it becomes a predictor of suicidal ideation. Clinical implications of this relationship are discussed.

The Great Black Hope: Hope and its relation to suicide risk among African Americans.

Positive psychology has garnered considerable scholarly interest recently and has been suggested to hold promise in the application to suicide research and prevention; however, empirical research has lagged behind these suggestions. This is the first study to examine the relationship between hope and a specific theory of suicide in African Americans. It was hypothesized that (1) hope would negatively predict the interpersonal suicide risk factors of burdensomeness and thwarted belongingness; and positively predict acquired capability to enact suicide; (2) hope would negatively predict suicidal ideation; and (3) the interpersonal suicide risk factors would predict suicidal ideation. Results were primarily as predicted. Implications for hope theory and Joiner's theory of suicidal behavior are discussed, as well as implications for clinical practice.

Hope as a predictor of interpersonal suicide risk.

The current study hypothesized that (1) hope would negatively predict burdensomeness, thwarted belongingness, and acquired capability to enact lethal injury; (2) hope would negatively predict suicidal ideation; and (3) the interpersonal suicide risk factors would predict suicidal ideation. Results indicated that hope negatively predicted burdensomeness and thwarted belongingness, but positively predicted acquired capability to enact suicide. Contrary to our second hypothesis, hope did not predict suicidal ideation, but interpersonal risk factors for suicide predicted suicidal ideation. Results are discussed in terms of implications for hope theory and Joiner's (2005) interpersonal risk factors for suicide, and for clinical practice.

Impaired fear response in mice lacking GIT1.

G protein-coupled receptor kinase interacting protein 1 (GIT1) belongs to the family of Arf GAP proteins and has been implicated in the regulation of G protein-coupled receptor (GPCR) sequestration, cell migration, synapse formation and dendritic spine morphogenesis in neurons. To extend these cellular studies on GIT1 to an in vivo system, we generated mice with globally inactivated Git1 gene by breeding mice carrying a conditional Git1(flox) allele with mice expressing the CMV-Cre transgene. Although many GIT1 knockout (GIT1-KO) animals died shortly after birth, homozygous mutants that survived the early post-partum period developed normally into adulthood and were fertile. Behavioral analyses of adult GIT1-KO mice revealed normal exploratory, anxiety- and depressive-like behaviors. However, GIT1-KO mice show impaired responses to fear conditioning and fear-potentiated startle. Overall, these findings suggest that GIT1 is involved in the regulation of amygdala-mediated experience-based emotional behaviors.

Anxiety-like behaviors in mice lacking GIT2.

G protein-coupled receptor kinase-interactor 2 (GIT2) is a signaling scaffold protein that also functions as GTPase-activating protein (GAPs) for ADP-ribosylation factor (Arf) small GTP-binding proteins. GIT2 has been implicated in the regulation of G protein-coupled receptor trafficking and cell adhesion and migration. To evaluate possible neurobehavioral functions of GIT2 in vivo, we evaluated GIT2-knockout (KO) mice for abnormalities in emotionality and mood. Male and female GIT2-KO mice presented with anxiety-like behaviors in the zero-maze and light-dark emergence tests. Immobility times in tail suspension were reduced in GIT2-KO males, but were normal in GIT2-KO females. Hence, GIT2-KO mice display anxiety-like behavior in an absence of depressive-like responses.

Differential expression of the ARF GAP genes GIT1 and GIT2 in mouse tissues.

GIT1 and GIT2 belong to the family of ADP-ribosylation factor GTPase-activating proteins (ARF-GAP) and have been implicated in the regulation of G protein-coupled receptor sequestration, cell migration, T-cell activation, neuronal spine formation, and aggregate formation in Huntington's disease. Examination of endogenous GIT protein expression in tissues, however, has been hampered by the lack of GIT2-specific antibodies. To visualize GIT1 and GIT2 gene expression in mouse tissues, we created mice with beta-galactosidase (beta-Gal) reporters inserted into the two GIT genes. beta-Gal staining confirmed the broad tissue distribution of GIT1 and GIT2 in the mouse but also revealed striking differences. GIT2 is expressed in most cells of the body, whereas GIT1 is restricted to only a subset of cells. For example, GIT2 is uniformly expressed throughout lung and liver, whereas GIT1 is restricted to cells lining blood vessels, bronchi, and bile ducts. Expression of GIT1 and GIT2 is mutually exclusive in the testes, where a developmental expression shift occurs, with GIT2 present in spermatogonia but GIT1 in mature spermatids. In conclusion, analysis of endogenous GIT expression revealed a nearly ubiquitous distribution of GIT2, whereas GIT1 is restricted to specific cell types even in tissues with apparently high GIT1 expression and is entirely absent from some tissues.

GIT1 utilizes a focal adhesion targeting-homology domain to bind paxillin.

The GIT proteins, GIT1 and GIT2, are GTPase-activating proteins for the ADP-ribosylation factor family of small GTP-binding proteins, but also serve as adaptors to link signaling proteins to distinct cellular locations. One role for GIT proteins is to link the PIX family of Rho guanine nucleotide exchange factors and their binding partners, the p21-activated protein kinases, to remodeling focal adhesions by interacting with the focal adhesion adaptor protein paxillin. We here identified the C-terminal domain of GIT1 responsible for paxillin binding. Combining structural and mutational analyses, we show that this region folds into an anti-parallel four-helix domain highly reminiscent to the focal adhesion targeting (FAT) domain of focal adhesion kinase (FAK). Our results suggest that the GIT1 FAT-homology (FAH) domain and FAT bind the paxillin LD4 motif quite similarly. Since only a small fraction of GIT1 is bound to paxillin under normal conditions, regulation of paxillin binding was explored. Although paxillin binding to the FAT domain of FAK is regulated by tyrosine phosphorylation within this domain, we find that tyrosine phosphorylation of the FAH domain GIT1 is not involved in regulating binding to paxillin. Instead, we find that mutations within the FAH domain may alter binding to paxillin that has been phosphorylated within the LD4 motif. Thus, despite apparent structural similarity in their FAT domains, GIT1 and FAK binding to paxillin is differentially regulated.

The protein stannin binds 14-3-3zeta and modulates mitogen-activated protein kinase signaling.

The molecular mechanisms underlying the selective toxicity of trimethyltin (TMT) remain unclear. Stannin (Snn), a protein preferentially expressed in TMT-sensitive cells, provides a direct link to the molecular basis for TMT toxicity. Recent evidence demonstrated that Snn peptides bind and de-alkylate TMT to dimethyltin (DMT); Snn may mediate both TMT and DMT toxicity. In this study, we demonstrate that Snn co-immunoprecipitates with a scaffolding protein 14-3-3, specifically with 14-3-3zeta isotype. Consistent with this, a detailed amino acid sequence analysis shows that Snn contains a putative 14-3-3 protein-binding site located within its hydrophilic loop. In addition, we present the evidence that Snn overexpression results in reduced extracellular regulated kinase activation and increased p38 activation. In contrast, the activity of c-Jun N-terminal kinase did not change following Snn overexpression. This is the first evidence that demonstrates a direct interaction between Snn and MAPK signaling molecules. Together, these findings indicate a role of Snn in modulation of MAPK signaling pathways through its interactions with 14-3-3zeta.

Protein kinase C epsilon regulates tumor necrosis factor-alpha-induced stannin gene expression.

Stannin (Snn) is a highly conserved vertebrate protein that has been closely linked to trimethyltin (TMT) toxicity. We have previously demonstrated that Snn is required for TMT-induced cell death. Others have shown that TMT exposure results in tumor necrosis factor-alpha (TNFalpha) production and that TNFalpha treatment induces Snn gene expression in human umbilical vein endothelial cells (HUVECs). In this study, we investigated a signaling mechanism by which Snn gene expression is regulated by TMT and demonstrated that TNFalpha stimulates Snn gene expression in a protein kinase C epsilon-dependent manner in HUVECs in response to TMT exposure. Supporting this, we show that TMT-induced toxicity is significantly blocked by pretreatment with an anti-TNFalpha antibody in HUVECs. Using a quantitative real-time polymerase chain reaction assay, we also show that the level of Snn gene expression is significantly increased in HUVECs in response to either TMT or TNFalpha treatment. This TNFalpha-induced Snn gene expression is blocked when HUVECs were pretreated with bisindolylmaleimide I, an inhibitor of protein kinase C (PKC). In contrast, when HUVECs were treated with phorbol 12-myristate 13-acetate, a PKC activator, we observed a significant increase in Snn gene expression. Using isotype-specific siRNA against PKC, we further show that knockdown of PKC epsilon, but not PKC delta or PKC zeta, significantly blocked TNFalpha-induced Snn gene expression. Together, these results indicate that TNFalpha-induced, PKC epsilon-dependent Snn expression may be a critical factor in TMT-induced cytotoxicity.

Role of gustatory thalamus in anticipation and comparison of rewards over time in rats.

Rats reduce intake of a palatable saccharin solution when it is followed by access to a preferred sucrose solution. This phenomenon, referred to as an anticipatory contrast effect (ACE), is thought to occur because the value of the saccharin conditioned stimulus pales in comparison to the highly rewarding sucrose unconditioned stimulus expected in the near future. Although relatively little is known about the underlying neural substrates, lesions of the gustatory thalamus fully disrupt the phenomenon (Reilly S, Bornovalova M, and Trifunovic R. Behav Neurosci 118: 365-376, 2004; Reilly S and Pritchard TC. Behav Neurosci 110: 746-759, 1996). The present set of experiments revisited this issue to determine the nature of this deficit. Rats with bilateral ibotenic acid lesions of the gustatory thalamus were given 3-min access to 0.15% saccharin and, after a 0-s or 5-min interval, were given 3-min access to either the same saccharin solution or a highly preferred 1.0 M sucrose solution. In experiment 1, ACE testing began with the 5-min interstimulus interval (ISI) and then switched to the 0-s ISI. For experiment 2, the order of ISI testing was reversed. The results show that axon-sparing, neurotoxic lesions of the gustatory thalamus prevent ACEs with a 0-s ISI and lead to a reversal (i.e., a reinforcement effect) with a 5-min ISI. Together, the results suggest that the lesion leads to a specific reward comparison deficit, whereby the rats fail to compare the value of an available reward with the memory of a preferred reward that is anticipated in the near future.

Stannin, a protein that localizes to the mitochondria and sensitizes NIH-3T3 cells to trimethyltin and dimethyltin toxicity.

Stannin (Snn) is a highly conserved, 88-amino acid protein that may mediate the selective toxicity of organotins. Snn is localized in tissues with known sensitivity to trimethyltin (TMT), including the central nervous system, immune system, spleen, kidney and lung. Cells in culture that do not express Snn show considerable resistance to TMT toxicity. In vitro, Snn peptide can bind TMT in a 1:1 ratio and can de-alkylate TMT to dimethyltin (DMT). We now show that transfection with Snn sensitized TMT-resistant NIH-3T3 mouse fibroblasts to both TMT and DMT cytotoxicity. Triple label confocal microscopy of Snn-transfected cells and Percoll gradient purification of mitochondria showed Snn localized to the mitochondria and other membrane structures. The mitochondrial localization of Snn, coupled with its ability to bind and dealkylate organotin compounds, indicates a possible mechanism by which selective alkyltin toxicity might be mediated.