The 2013–2016 West Africa Ebola virus disease pandemic was the largest, longest, deadliest, and most geographically expansive outbreak in the 40-year interval since Ebola was first identified. Fear-related behaviors played an important role in shaping the outbreak. Fear-related behaviors are defined as “individual or collective behaviors and actions initiated in response to fear reactions that are triggered by a perceived threat or actual exposure to a potentially traumatizing event. FRBs modify the future risk of harm.” This review examines how fear-related behaviors were implicated in (1) accelerating the spread of Ebola, (2) impeding the utilization of life-saving Ebola treatment, (3) curtailing the availability of medical services for treatable conditions, (4) increasing the risks for new-onset psychological distress and psychiatric disorders, and (5) amplifying the downstream cascades of social problems. Fear-related behaviors are identified for each of these outcomes. Particularly notable are behaviors such as treating Ebola patients in home or private clinic settings, the “laying of hands” on Ebola-infected individuals to perform faith-based healing, observing hands-on funeral and burial customs, foregoing available life-saving treatment, and stigmatizing Ebola survivors and health professionals. Future directions include modeling the onset, operation, and perpetuation of fear-related behaviors and devising strategies to redirect behavioral responses to mass threats in a manner that reduces risks and promotes resilience.

SUICIDE ATTEMPTERS have decreased serotonergic function compared with psychiatric control subjects as measured by prolactin response to fenfluramine hydrochloride^1,2 and lower cerebrospinal fluid levels of 5-hydroxyindoleacetic acid.^3,4 Higher-lethality suicide attempts in depressed subjects are associated with even lower cerebrospinal fluid 5-hydroxyindoleacetic acid levels⁵ and a more blunted prolactin response to fenfluramine.¹ Postmortem serotonin receptor binding mapping studies indicate that cortical serotonergic abnormalities associated with suicide are localized to the ventral prefrontal cortex (PFC).⁶ Neuroendocrine challenges and cerebrospinal fluid measures do not provide information about the anatomic location of abnormality. We did not find any studies of glucose metabolism in response to fenfluramine and suicidal behavior with the use of positron emission tomography (PET). However, changes in glucose metabolism in the PFC have been reported in impulsive murderers compared with nonimpulsive murderers,⁷ impulsive aggressive subjects compared with normal controls,⁸ and subjects with borderline personality disorder compared with healthy volunteers. Typically in these studies either there is a large proportion of suicide attempters⁹ or the attempter status of the subjects is not described.^7,8 Therefore, we studied regional brain serotonergic function in depressed patients with a history of a high-lethality suicide attempt compared with that of depressed patients with a history of low-lethality suicide attempt by PET of relative regional cerebral uptake of fludeoxyglucose F 18 (¹⁸F) (rCMRglu) in response to serotonin elevation after a fenfluramine challenge relative to a placebo challenge.

Bipolar disorder is associated with a high rate of suicide attempt, and alcohol use disorders have also been associated with elevated risk for suicidal behavior. Whether risk for suicidal behavior is elevated when these conditions are comorbid has not been addressed in epidemiologic studies. 1,643 individuals with a DSM-IV lifetime diagnosis of bipolar disorder were identified from 43,093 general-population respondents who were interviewed in the 2001-2002 National Epidemiologic Survey on Alcohol and Related Conditions. Assessments were made using the National Institute on Alcohol Abuse and Alcoholism Alcohol Use Disorder and Associated Disabilities Interview Schedule-DSM-IV Version (AUDADIS-IV). Lifetime prevalence of reported history of suicide attempt and suicidal thoughts among bipolar disorder respondents with and without DSM-IV lifetime alcohol use disorders (abuse or dependence) was assessed using chi-squared and adjusted odds ratios with confidence intervals. Logistic regression was used to test the relevance of other comorbid clinical conditions to suicide risk in bipolar respondents with and without comorbid alcohol use disorders. More than half of the respondents (54%) who met criteria for bipolar disorder also reported alcohol use disorder. Bipolar individuals with comorbid alcohol use disorder were at greater risk for suicide attempt than those individuals without alcohol use disorder (adjusted odds ratio=2.25; 95% CI, 1.61-3.14) and were more likely to have comorbid nicotine dependence and drug use disorders. Nicotine dependence and drug use disorders did not increase risk for suicidal behavior among those with bipolar disorder, nor did they confer additional risk among bipolar respondents who also reported alcohol use disorder. Despite greater psychopathological burden, individuals with comorbid bipolar disorder and alcohol use disorder did not receive more treatment or more intensive treatment. Suicidal behavior is more likely to occur in bipolar respondents who also suffer from alcohol use disorder. Interventions to reduce suicide risk in bipolar disorder need to address the common and high-risk comorbidity with alcohol use disorders.