Suicide risk in schizophrenia: learning from the past to change the future

Suicide is a major cause of death among patients with schizophrenia. Research indicates that at least 5–13% of schizophrenic patients die by suicide, and it is likely that the higher end of range is the most accurate estimate. There is almost total agreement that the schizophrenic patient who is more likely to commit suicide is young, male, white and never married, with good premorbid function, post-psychotic depression and a history of substance abuse and suicide attempts. Hopelessness, social isolation, hospitalization, deteriorating health after a high level of premorbid functioning, recent loss or rejection, limited external support, and family stress or instability are risk factors for suicide in patients with schizophrenia. Suicidal schizophrenics usually fear further mental deterioration, and they experience either excessive treatment dependence or loss of faith in treatment. Awareness of illness has been reported as a major issue among suicidal schizophrenic patients, yet some researchers argue that insight into the illness does not increase suicide risk. Protective factors play also an important role in assessing suicide risk and should also be carefully evaluated. The neurobiological perspective offers a new approach for understanding self-destructive behavior among patients with schizophrenia and may improve the accuracy of screening schizophrenics for suicide. Although, there is general consensus on the risk factors, accurate knowledge as well as early recognition of patients at risk is still lacking in everyday clinical practice. Better knowledge may help clinicians and caretakers to implement preventive measures. This review paper is the results of a joint effort between researchers in the field of suicide in schizophrenia. Each expert provided a brief essay on one specific aspect of the problem. This is the first attempt to present a consensus report as well as the development of a set of guidelines for reducing suicide risk among schizophenia patients

Affective lability and difficulties with regulation are differentially associated with amygdala and prefrontal response in women with Borderline Personality Disorder

The present neuroimaging study investigated two aspects of difficulties with emotion associated with Borderline Personality Disorder (BPD()): affective lability and difficulty regulating emotion. While these two characteristics have been previously linked to BPD symptomology, it remains unknown whether individual differences in affective lability and emotion regulation difficulties are subserved by distinct neural substrates within a BPD sample. To address this issue, sixty women diagnosed with BPD were scanned while completing a task that assessed baseline emotional reactivity as well as top-down emotion regulation. More affective instability, as measured by the Affective Lability Scale (ALS()), positively correlated with greater amygdala responses on trials assessing emotional reactivity. Greater difficulties with regulating emotion, as measured by the Difficulties with Emotion Regulation Scale (DERS()), was negatively correlated with left inferior frontal gyrus (IFG()) recruitment on trials assessing regulatory ability. These findings suggest that, within a sample of individuals with BPD, greater bottom-up amygdala activity is associated with heightened affective lability. By contrast, difficulties with emotion regulation are related to reduced IFG recruitment during emotion regulation. These results point to distinct neural mechanisms for different aspects of BPD symptomology

Comparison of familial and non-familial suicidal behaviors among people with major depressive disorder: Testing the discriminative predicting role of high-yield clinical variables

Background Suicidal behavior in first-degree relatives of people diagnosed with major depressive disorder (MDD) increases the risk of suicidal behavior. Such an effect may be the result of genetic risk factors or environmental ones, including imitation, or both. Surprisingly few studies have examined this question and thus, there still is little known about the effect of first-degree family history of suicidal behavior on the type of suicidal behavior and profile of risk factors related to the diathesis for suicidal behavior. Even less is known about intra-familial risk transmission. Methods Patients with MDD (n = 252) experiencing a current major depressive episode and who had a previous suicide attempt were studied. Those with and without a family history of first-degree relatives who had made a suicide attempt or died by suicide were compared across clinical and suicide-related characteristics. Results Suicide attempters with (FDR+, n = 59) and without a first-degree relative with suicide attempt or suicide (FDR−, n = 193) were similar in terms of type or frequency of suicide attempts, level of lifetime aggression and impulsivity, age of onset of depression and age at first suicide attempt. Limitations Cross-Sectional study. Lack of additional external validators. Conclusions Contrary to our hypothesis and the concept of “genetic anticipation”, a first-degree family history of suicide attempt or suicide in currently depressed attempters with MDD was not associated with a range of clinical and suicide-related characteristics. Longitudinal studies incorporating external validators and potential biological markers may advance this area of research

Low plasma eicosapentaenoic acid levels are associated with elevated trait aggression and impulsivity in major depressive disorder with a history of comorbid substance use disorder

Major depressive disorder (MDD) is associated with low levels of omega-3 polyunsaturated fatty acids (PUFAs), holding promise for new perspectives on disease etiology and treatment targets. As aggressive and impulsive behaviors are associated with low omega-3 PUFA levels in some clinical contexts, we investigated plasma PUFA relationships with trait aggression and impulsivity in patients with MDD. Medication-free MDD patients (n=48) and healthy volunteers (HV, n=35) were assessed with the Brown-Goodwin Aggression Inventory. A subset (MDD, n=39; HV, n=33) completed the Barratt Impulsiveness Scale. Plasma PUFAs eicosapentaenoic acid (EPA, 20:5n-3), docosahexaenoic acid (DHA, 22:6n-3), and arachidonic acid (AA, 20:4n-6) were quantified and ln-transformed to mitigate distributional skew. Ln-transformed PUFA (lnPUFA) levels were predictors in regression models, with aggression or impulsivity scores as outcomes, and cofactors of sex and diagnostic status (MDD with or without a history of substance use disorder [SUD], or HV). Interactions were tested between relevant PUFAs and diagnostic status. Additional analyses explored possible confounds of depression severity, self-reported childhood abuse history, and, in MDD patients, suicide attempt history. Among PUFA, lnEPA but not lnDHA predicted aggression (F(1,76)=12.493, p=0.001), and impulsivity (F(1,65)=5.598, p=0.021), with interactions between lnEPA and history of SUD for both aggression (F(1,76)=7.941, p=0.001) and impulsivity (F(1,65)=3.485, p=0.037). Results remained significant when adjusted for childhood abuse, depression severity, or history of suicide attempt. In conclusion, low EPA levels were associated with aggression and impulsivity only in patients with MDD and comorbid SUD, even though in most cases SUD was in full sustained remission