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BACKGROUND: Mental health conditions impose a major burden worldwide, especially in low- and middle-income countries (LMICs), where health specialists are scarce. A challenge to closing LMICs’ mental health treatment gap is determining the most cost-effective task-shifting pathway for delivering mental health services using evidence-based interventions (EBIs). This article discusses the protocol for the first study implementing comprehensive mental health services in LMICs. METHODS: In partnership with the Mozambican Ministry of Health, this cluster-randomized, hybrid implementation effectiveness type-2 trial will evaluate implementation, patient, and service outcomes of three task-shifting delivery pathways in 20 Mozambican districts (population 4.7 million). In pathway 1 (usual care), community health workers (CHWs) and primary care providers (PCPs) refer patients to district-level mental health clinics. In pathway 2 (screen, refer, and treat), CHWs screen and refer patients to PCPs for behavioral and pharmacological EBIs in community clinics. In pathway 3 (community mental health stepped care), CHWs screen patients and deliver behavioral EBIs in the community and refer medication management cases to PCPs in clinics. Mixed-methods process evaluation will be used to examine factors affecting pathway implementation, adoption, and sustainability. Clinical activities will occur without research team support. Ministry of Health personnel will coordinate training and supervision. RESULTS: The most cost-effective pathway will be scaled up in all districts for 12 months. NEXT STEPS: This novel study integrating comprehensive mental health services into primary care will inform a toolkit to help the Mozambican Ministry of Health scale up the most cost-effective pathway for mental health services and can be a template for other LMICs.

Despite increased access to mental health care for the previously uninsured and expanding evidence-based treatments for mood, anxiety, psychotic, and substance use disorders, suicide is on the rise in the United States. Since 1999, the age-adjusted suicide rate in the United States has increased 33%, from 10.5 per 100,000 standard population to 14.0. As of yet, there are no clinically available biomarkers, laboratory tests, or imaging to assist in diagnosis or the identification of the suicidal individual. Suicide risk assessment remains a high-stakes component of the psychiatric evaluation and can lead to overly restrictive management in the name of prevention or to inadequate intervention because of poor appreciation of the severity of risk. This article focuses primarily on suicide risk assessment and management as a critical first step to prevention, given the fact that more research is needed to identify precision treatments and effective suicide prevention strategies. Suicide risk assessment provides the clinical psychiatrist with an opportunity for therapeutic engagement with the ultimate goals of relieving suffering and preventing suicide.

Objective:Bipolar disorder is associated with high risk for suicidal behavior that often develops in adolescence and young adulthood. Elucidation of involved neural systems is critical for prevention. This study of adolescents and young adults with bipolar disorder with and without a history of suicide attempts combines structural, diffusion tensor, and functional MR imaging methods to investigate implicated abnormalities in the morphology and structural and functional connectivity within frontolimbic systems.Method:The study had 26 participants with bipolar disorder who had a prior suicide attempt (the attempter group) and 42 participants with bipolar disorder without a suicide attempt (the nonattempter group). Regional gray matter volume, white matter integrity, and functional connectivity during processing of emotional stimuli were compared between groups, and differences were explored for relationships between imaging modalities and associations with suicide-related symptoms and behaviors.Results:Comp...

Sexual abuse during childhood is surprisingly common, with estimates in the general population ranging from 15% to 38% (1). It is associated with significant psychiatric sequelae, including the development of major depression and posttraumatic stress disorder (PTSD). These common consequences of exposure to trauma can emerge in the aftermath of natural disasters as well as those in which humans have a hand (2). Some responses, such as suicidal behavior, are not only life-threatening but have multigenerational repercussions, as individuals who report childhood sexual abuse are at risk not only for suicidal behavior themselves but also for transmitting suicidal behavior and mood disorders to their offspring (3). The timing (4) and severity of childhood sexual abuse are also relevant to its consequences (5). Earlier age at onset of childhood sexual abuse is associated with more intent during suicide attempts (6) as well as greater severity of PTSD (7) and depressive symptoms (8). Similarly, the severity of sexual abuse during development is reportedly related to earlier-onset suicidal behavior (6), greater depression severity (9), and more pronounced symptoms among patients with borderline personality disorder (5). Interestingly, other forms of early life stress, such as childhood emotional abuse and neglect, have been found to be stronger predictors of subsequent depression in adulthood than childhood sexual or physical abuse (10). Following the excitement generated by the gene-environment interaction literature, researchers are now exploring the biological substrates that may mediate effects of early traumatic experiences on later psychopathology. Elegant studies in animal models have identified epigenetic mechanisms through which the early environment may induce enduring effects on gene expression and, with it, behavioral phenotypes (11). Reports of environmental effects on biological alterations more proximal to clinical phenotypes are also emerging, including effects on neurocognitive, neuroendocrine, and neuroimmune function. Structural and functional neuroimaging provide powerful tools to explore long-term effects of life experience on neurodevelopment. Most, but not all, structural MRI studies examining neuroanatomical correlates of childhood sexual abuse thus far describe volume reductions in a variety of structures. Decreased volume of the corpus callosum, the left hippocampus, the anterior cingulate, the caudate nucleus, the amygdala, and the visual cortex, as well as more general decreased cerebral volume, have all been reported in survivors of childhood sexual abuse (for reviews, see references 12 and 13). In this issue of the Journal, Heim et al. (14) make use of the burgeoning structural MRI technique of measuring cortical brain thickness to understand neuroplastic responses to childhood trauma. The authors studied 51 medically healthy women, of whom 55% (N=28) reported moderate-to-severe maltreatment, 18% (N=9) had PTSD, and 24% (N=12) had major depression. Cortical thinning was found to be present in the brain areas involved in the perception or processing of behaviors that are specific to the type of abuse experienced. For example, childhood sexual abuse was associated with cortical thinning in the genital representation field of the primary somatosensory cortex, whereas emotional abuse was associated with cortical thinning in regions linked to self-awareness and self-evaluation (15). The authors conclude that cortical adaptation to traumatic events may lead to decreases in the density of dendritic spines, leading to cortical thinning. They suggest that such changes relate to the child’s sensory processing of the abusive experience, which alters cortical representation fields in a regionally specific fashion, based on the nature of the abuse itself. This finding comports with another recent work in which young adults, compared with an unexposed group, who witnessed domestic violence as children had decreased visual cortex gray matter (15), in terms of both volume and cortical thickness, regardless of whether or not they developed psychopathology. In addition, Heim et al. noted that age at onset, although not severity of childhood sexual abuse, was related to cortical thinning in the left temporal pole, the left parietal lobe, the left frontal pole, and the right frontal pole, areas associated with autobiographical memory among other functions. This, they postulate, may serve as the neuroanatomical basis for the observation that victims of childhood sexual abuse often have poor, if any, recollection of the experience and report overgeneralized memories. A question that arises from this finding is whether individuals who experience trauma at a later age, outside the window of peak vulnerability for cortical thinning, develop psychopathology through a mechanism that is distinct from the one responsible for consequences in those who experience trauma during an earlier, critical period. What is the relevance of these neuroanatomical findings to the broader picture? If replicated, these data provide compelling evidence about the enduring structural effects on the brain as a function of early life experience that are not defined on the basis of a specific psychiatric diagnostic context. Given the nature of the environmental stressor and the difficulties in identifying victims at the time sexual abuse is occurring, it is unlikely that we will be able to develop longitudinal studies to more completely test the hypothesis. Nonetheless, this research may pave the way for the characterization of endophenotypes associated with trauma-related effects on the brain. The possible mechanisms the authors invoke to explain the neuroplasticity observed in this study may not be dependent on epigenetic effects and may suggest alternative molecular pathways underlying early life experience effects on neurodevelopment and psychopathology. Moreover, if life experience can have a role in brain restructuring during development, then appropriately timed experiential or behavioral interventions may have utility in mitigating the effects of negative environmental input or genetic deficits. Indeed, at the behavioral level, perceived social support protects against the development of adult depression among victims of childhood abuse (10). Consistent with this finding, murine studies suggest that enriched environments can mitigate the deleterious effects of low maternal licking and grooming behavior early in development (16). Of note, the question of whether the “active ingredient” of such enrichment is simply aerobic exercise (17), which is linked to hippocampal neurogenesis, has been recently raised. Finally, if sensory input in general has the potential to precipitate neuroarchitectural restructuring, then observed dose effects of the environmental insults may be related to multimodal sensory input from the traumatic experience. Although it stands to reason that more severe experiences would have more profound effects on an individual, elucidation of the exact mechanism for this observation may uncover the neurophysiological basis of such a relationship. Studies such as the one by Heim et al. bring us closer to delineating the mechanisms that lead to changes in brain morphology and function, which are so critical to developing effective behavioral and pharmacological interventions. We need to understand the role of several key elements leading to these neurobiological changes—the relative contributions of the severity, timing, and nature of a stressor in the context of genetic endowment. Equally important for future research is to study the role of resilience and its neurobiological underpinning, a sorely neglected area. The more clearly we can delineate a biological pathway from environment to psychopathology, the more likely we are to develop interventions to mitigate, cure, or even prevent what ails our patients.

Three articles in this issue detail the process and results of reliability tests for proposed DSM-5 diagnoses and cross-diagnosis symptom domains. The editorial highlights the good reliability of borderline personality disorder and relates the questionable reliability of major depressive disorder to its heterogeneity. The editorial is also available in Spanish, Traditional Chinese, and Simplified Chinese.

Bipolar disorder is associated with high risk for suicidal acts. Observational studies suggest a protective effect of lithium against suicidal behavior. However, testing this effect in randomized clinical trials is logistically and ethically challenging. The authors tested the hypothesis that lithium offers bipolar patients with a history of suicide attempt greater protection against suicidal behavior compared to valproate.Patients with bipolar disorder and past suicide attempts (N=98) were randomly assigned to treatment with lithium or valproate, plus adjunctive medications as indicated, in a double-blind 2.5-year trial. An intent-to-treat analysis was performed using the log-rank test for survival data. Two models were fitted: time to suicide attempt and time to suicide event (attempt or hospitalization or change in medication in response to suicide plans).There were 45 suicide events in 35 participants, including 18 suicide attempts made by 14 participants, six from the lithium group and eight from the valproate group. There were no suicides. Intent-to-treat analysis using the log-rank test showed no differences between treatment groups in time to suicide attempt or to suicide event. Post hoc power calculations revealed that the modest sample size, reflective of challenges in recruitment, only permits detection of a relative risk of 5 or greater.Despite the high frequency of suicide events during the study, this randomized controlled trial detected no difference between lithium and valproate in time to suicide attempt or suicide event in a sample of suicide attempters with bipolar disorder. However, smaller clinically significant differences between the two drugs were not ruled out.

The lower expressing allele of the serotonin transporter gene 5' promoter region (5-HTTLPR) polymorphism is reported to be associated with susceptibility to depression and suicidality in response to stressful life events. The authors examined the relationship of a triallelic 5-HTTLPR polymorphism to stressful life events, severity of major depression, and suicidality.Mood disorder subjects (N=191) and healthy volunteers (N=125), all Caucasian subjects of European origin, were genotyped for the triallelic 5-HTTLPR polymorphism (higher expressing allele: L(A); lower expressing alleles: L(G), S). All subjects underwent structured clinical interviews to determine DSM-IV diagnoses, ratings of psychopathology, stressful life events, developmental history, and suicidal behavior. CSF 5-HIAA was assayed in a subgroup of subjects.Lower expressing alleles independently predicted greater depression severity and predicted greater severity of major depression with moderate to severe life events compared with the higher expressing L(A) allele. No associations with suicidal behavior and CSF 5-HIAA were found.Lower expressing transporter alleles, directly and by increasing the impact of stressful life events on severity, explain 31% of the variance in major depression severity. The biological phenotype responsible for these effects remains to be elucidated.

OBJECTIVE: CSF analysis, neuroendocrine challenges, serotonin depletion studies, and treatment studies implicate the serotonergic system in the pathophysiology of major depressive disorder. On the basis of postmortem and imaging studies, the authors hypothesized that subjects with major depressive disorder in a major depressive episode have fewer serotonin transporter sites, compared with healthy subjects. METHOD: Serotonin transporter binding potential (f1Bmax/Kd) was determined using positron emission tomography with [11C]McN 5652 in six brain regions in 25 medication-free subjects with DSM-IV major depressive disorder during a major depressive episode and in 43 healthy volunteer comparison subjects. All subjects had arterial lines placed to determine metabolite-corrected arterial input functions. RESULTS: Serotonin transporter binding potential differed significantly by brain region and group. Post hoc analysis revealed lower binding potential in subjects with major depressive disorder, relative to the...

Ethnic and racial diversity in the United States increases daily through immigration and population shifts, and multiculturalism in the mental health field has had a difficult time keeping pace. Delivery of adequate mental health care to Hispanics, now the largest and fastest-growing ethnic minority, has been plagued by low utilization rates and inadequate or delayed mental health services. Among the issues compounding the problem are the diversity that exists within the Hispanic population, the varied ways that symptoms are experienced and expressed, and the unique sets of risk factors and barriers facing U.S. Hispanic groups. This review provides an epidemiologic overview of the mental health status of the three largest U.S. Hispanic subgroups, with particular attention to diagnosis and treatment of major depressive disorder. Also discussed is the gap between the need for and the delivery of services, which is characterized in terms of problems with access to care, utilization of mental health services,...

The authors examined effects of a triallelic functional polymorphism of the human serotonin-transporter-linked promoter region (5-HTTLPR) on in vivo expression of serotonin transporter in the brain in healthy volunteers and subjects with major depressive disorder.Twenty-five medication-free subjects with DSM-IV major depressive disorder during a major depressive episode and 42 healthy volunteers were clinically evaluated and genotyped. Serotonin transporter binding potential (f(1)B(max)/K(d)) was determined by using positron emission tomography with the radiotracer [(11)C]McN 5652 and metabolite-corrected arterial input functions.There was no difference in serotonin transporter binding potential by genotype in healthy volunteers or in subjects with major depressive disorder. Allelic frequencies did not differ between subjects with major depressive disorder and healthy volunteers.Associations of the 5-HTTLPR polymorphism to clinical phenotypes appear to be due to developmental effects of 5-HTTLPR on expression and not due to its direct effect on serotonin transporter binding in adulthood.

First-degree relatives of persons with mood disorder who attempt suicide are at greater risk for mood disorders and attempted or completed suicide. This study examined the shared and distinctive factors associated with familial mood disorders and familial suicidal behavior.First-degree relatives' history of DSM-IV-defined mood disorder and suicidal behavior was recorded for 457 mood disorder probands, of whom 81% were inpatients and 62% were female. Probands' lifetime severity of aggression and impulsivity were rated, and probands' reports of childhood physical or sexual abuse, suicide attempts, and age at onset of mood disorder were recorded. Univariate and multivariate analyses were carried out to identify predictors of suicidal acts in first-degree relatives.A total of 23.2% of the probands with mood disorder who had attempted suicide had a first-degree relative with a history of suicidal behavior, compared with 13.2% of the probands with mood disorder who had not attempted suicide (odds ratio=1.99, 95% CI=1.21-3.26). Thirty percent (30.8%) of the first-degree relatives with a diagnosis of mood disorder also manifested suicidal behavior, compared with 6.6% of the first-degree relatives with no mood disorder diagnosis (odds ratio=6.25, 95% CI=3.44-11.35). Probands with and without a history of suicide attempts did not differ in the incidence of mood disorder in first-degree relatives (50.6% versus 48.1%). Rates of reported childhood abuse and severity of lifetime aggression were higher in probands with a family history of suicidal behavior. Earlier age at onset of mood disorder in probands was associated with greater lifetime severity of aggression and higher rates of reported childhood abuse, mood disorder in first-degree relatives, and suicidal behavior in first-degree relatives.Risk for suicidal behavior in families of probands with mood disorders appears related to early onset of mood disorders, aggressive/impulsive traits, and reported childhood abuse in probands. Studies of such clinical features in at-risk relatives are under way to determine the relative transmission of these clinical features.

The authors investigated the predictive potential of a stress-diathesis model for suicidal behavior based on correlates of past suicidal acts. In this model, suicidal acts are precipitated by stressors such as life events or a major depressive episode in the setting of a propensity for acting on suicidal urges. This diathesis is expressed as the tendency to develop more pessimism in response to a stressor and/or the presence of aggressive/impulsive traits. The predictive potential of the diathesis was tested by determining whether clinical correlates of past suicidal behavior predict suicidal acts during a 2-year follow-up of patients with a major depressive episode.Patients with DSM-III-R major depressive disorder or bipolar disorder (N=308) were assessed at presentation for treatment of a major depressive episode. Potential predictors of suicidal acts in the 2 years after study enrollment were identified on the basis of an association with previous suicidal behavior and were tested by using Cox proportional hazards regression analysis. In addition, pessimism and aggression/impulsivity factors were generated, and their predictive ability was tested by using Cox proportional hazards regression analysis.The three most powerful predictors of future suicidal acts were a history of suicide attempt, subjective rating of the severity of depression, and cigarette smoking, each of which had an additive effect on future risk. The pessimism and aggression/impulsivity factors both predicted suicidal acts, and each factor showed an additive effect.In addition to obtaining a history of suicidal behavior, clinicians may find it useful to assess patients' current level of pessimism, aggressive/impulsive traits, and comorbidity with substance use disorders, including nicotine-related disorders, to help identify patients at risk for suicidal behavior after major depression. Interventions such as aggressive pharmacotherapeutic prophylaxis to prevent relapse or recurrence of depressive symptoms may protect such at-risk individuals from future suicidal behavior.

The authors sought to determine 1) whether the risk for familial transmission of suicidal behavior is greater with increased family loading for suicide attempts, and 2) whether the transmission of suicidal behavior is mediated by impulsive aggression.A reanalysis of a high-risk study compared the offspring of three mood disorder proband groups: suicide attempters with a sibling who also attempted suicide (N=19), suicide attempters whose siblings never made a suicide attempt (N=73), and nonsuicidal probands whose siblings also never engaged in suicidal behavior (N=73). Probands and offspring were assessed with respect to psychopathology, suicide attempt history, impulsive aggression, and exposure to familial adversity.Offspring of suicide attempters with siblings concordant for suicidal behavior showed a higher risk of suicide attempt than did offspring of nonsuicidal probands and had an earlier age at onset of suicidal behavior than offspring of suicide attempters with siblings discordant for suicidal behavior. Probands from sibling pairs concordant for suicidal behavior and their offspring reported greater lifetime impulsive aggression compared with each of the other two proband/offspring groups. In the offspring, impulsive aggression was the most powerful predictor of early age at first suicide attempt.Familial loading for suicide attempts may affect rates of transmission as well as age at onset of suicidal behavior, and its effect may be mediated by the familial transmission of impulsive aggression.

In subjects with mood disorders, positron emission tomography (PET) with [(18)F]fluorodeoxyglucose has shown prefrontal cortical metabolism deficits, including in a subgenual region in subjects with familial illness. The authors applied a dl-fenfluramine challenge method to study metabolic response in this region to serotonergic challenge in familial major depression.The study group consisted of 19 depressed subjects with major depressive disorder or bipolar disorder, all of whom had at least one first-degree relative with history of major depression, and 10 healthy volunteers with similar age and gender distributions. PET images were acquired under placebo and challenge conditions, and volumetric MRI scans were also obtained. Group comparisons of metabolic and volumetric data were performed. Ratings of acute mood change during serotonergic challenge were compared with the imaging data.Within Brodmann's area 32, a glucose metabolism deficit in the depressed subjects on placebo day was observed by voxel-level analysis, but no volumetric deficit was found in the subgenual regions examined. Under challenge, both groups suppressed metabolism similarly. Within the patient group, the correlation between acute mood improvement during challenge and greater metabolic suppression approached significance.In familial mood disorders, a ventromedial prefrontal cortical deficit in baseline metabolism is not due to altered structural volume, and the response to serotonergic challenge appears predictive of acute mood response. The potential to predict treatment response can be tested by a combined challenge and treatment study.

Objective: Suicide rates differ between ethnic groups in the United States. Since suicide is commonly associated with a mood disorder, the authors compared suicide rates relative to depression rates in five ethnic groups in the United States. Method: Rates of major depression were generated from the Epidemiologic Catchment Area study and the Hispanic Health and Nutrition Epidemiologic Survey. Sociodemographic effects were determined by examining depression rates for respondents who were separated or divorced, earning low incomes, or not working for pay. The survey data were analyzed with age and sex standardization to generate 1-year prevalence rates of major depression. The depression rates of the different ethnic groups were compared and were examined in relation to suicide rates. Results: The 1-year prevalence rates of major depression were 3.6% for whites, 3.5% for blacks, 2.8% for Mexican Americans, 2.5% for Cuban Americans, and 6.9% for Puerto Ricans. Compared to the rate for whites, the rate of depression was significantly higher in Puerto Ricans and significantly lower in Mexican Americans. Relative to the depression rates, the annual suicide rates were higher for males than for females. Mexican American and Puerto Rican males had lower relative suicide rates than white males. Conclusions: Identifying reasons for differences in suicide rates relative to depression among ethnic groups and between males and females may suggest interventions to reduce suicide rates. Some possibilities are that depression differs in form or severity or that unidentified factors protect against suicide in different subgroups.

Delusions have been considered a risk factor for suicidal behavior. To determine whether specific delusion types are related to suicidal behaviors, the authors compared the clinical characteristics of patients with mood disorders and schizophrenia who did and did not have a history of suicide attempts.After admission for inpatient or outpatient psychiatric treatment, 429 patients (ages 14-72 years; 47.1% male; and 73.0% Caucasian) were assessed with a structured clinical interview that generated axis I and II diagnoses. In addition, their psychiatric symptoms, history of suicide attempts, and overall functioning were rated.Data for three diagnostic subgroups (223 patients with major depression, 150 with schizophrenia, and 56 with bipolar disorder) were analyzed separately. Multivariate analyses did not find evidence of a relationship between delusions and history of suicidal ideation or suicide attempts in any of the diagnostic groups.This study did not find evidence that the presence of delusions distinguished persons with or without a history of suicide attempt.

The authors' goal was to determine whether suicide attempters with major depression received more intensive antidepressant treatment than depressed patients who had not attempted suicide.One hundred eighty inpatients who met DSM-III-R criteria for a major depressive episode according to the Structured Clinical Interview for DSM-III-R were enrolled in the study. All patients were assessed for lifetime history of suicide attempts. Depressive symptoms at the index hospitalization were assessed with the Hamilton Depression Rating Scale and the Beck Depression Inventory. Strength of antidepressant treatment over the 90 days preceding the hospitalization was scored by using the Antidepressant Treatment History Form.A large majority of the depressed patients with a history of suicide attempts, who were at higher risk for future suicide and suicide attempts, received inadequate treatment. Similarly, most of the depressed patients at lower risk for suicide attempts also received inadequate treatment.Major depression is undertreated pharmacologically, regardless of history of suicide attempt. Some suicide attempts may be preventable if the problem of underdiagnosis and undertreatment of depression can be overcome by psychoeducation for health professionals and the public.

Low levels of docosahexaenoic acid, a polyunsaturated fatty acid, and elevated ratios of omega-6/omega-3 fatty acids are associated with major depression and, possibly, suicidal behavior. Predicting risk of future suicidal behaviors by essential fatty acid status merits examination.Plasma polyunsaturated fatty acid levels in phospholipids were measured in 33 medication-free depressed subjects monitored for suicide attempt over a 2-year period. Survival analysis examined the association of plasma polyunsaturated fatty acid status and pathological outcome.Seven subjects attempted suicide on follow-up. A lower docosahexaenoic acid percentage of total plasma polyunsaturated fatty acids and a higher omega-6/omega-3 ratio predicted suicide attempt.A low docosahexaenoic acid percentage and low omega-3 proportions of lipid profile predicted risk of suicidal behavior among depressed patients over the 2-year period. If confirmed, this finding would have implications for the neurobiology of suicide and reduction of suicide risk.

Use of a patient's second language in psychiatric evaluation and treatment has a variety of effects. Patients frequently undergo psychiatric evaluation in their second language, yet competence in a second language varies depending on the phase of illness. Evaluation of bilingual patients should ideally be done in both their languages, preferably by a bilingual clinician or by a monolingual clinician with the help of an interpreter trained in mental health issues. Cultural nuances may be encoded in language in ways that are not readily conveyed in translation, even when the patient uses equivalent words in the second language. The monolingual clinician may clarify these nuances through consultation with a clinician who shares the patient's first language and culture or with an interpreter. In psychotherapy, patients may use a second language as a form of resistance, to avoid intense affect. Therapists may use language switching to overcome this resistance and to decrease emotional intensity, if necessary. Psychotherapy can also be affected by the attitudes toward speaking that are part of the patient's culture. Discussions with bilingual and bicultural consultants can elucidate these effects for the therapist who is unfamiliar with the patient's culture.

Suicidal behavior (death and attempts) is usually a complication of psychiatric conditions, most commonly mood disorders (1). However, it also occurs in schizophrenia, substance use disorders (particularly with alcohol), and personality and anxiety disorders, among others (1). About 10% of those who commit or attempt suicide have no identifiable psychiatric illness. However, our current nomenclature considers suicidal behavior a symptom of major depressive episode or borderline personality disorder. During assessment, clinicians evaluate the principal diagnosis responsible for the chief complaint and use overview questions to identify comorbid conditions. If no evidence is found for major depressive episode or borderline personality disorder, questions about past suicidal behavior may not be pursued. Since the mental status examination targets the present condition, patients who deny suicidality may not be asked about past suicidal acts, potentially leading to an underestimate of suicide risk. Yet a history of suicidal behavior is the most reliably replicated risk factor for future suicide attempt or completion, whereas expressions of suicidality wax and wane and may be absent during an interview (2). Thus, current diagnostic algorithms may lead clinicians to overlook suicidal ideation or behavior in patients with posttraumatic stress disorder, where patients may contemplate suicide as an escape from their flashbacks, or in those with alcoholism, where disinhibition during intoxication may render patients less able to resist suicidal thoughts. Suicidality in these high-risk groups can easily go unidentified. Even when a clinician identifies suicidal ideation or behavior, the patient receives a diagnosis that does not highlight suicide risk as a focus of concern. We recommend that suicidal behavior be considered a separate diagnostic category documented on a sixth axis. Suicidal behavior meets the criteria for diagnostic validity set forth by Robins and Guze (3), and it does so as well as most conditions we treat. It is clinically well described (4), research has identified postmortem and in vivo laboratory markers (1), it can be subjected to a strict differential diagnosis (4), follow-up studies confirm its presence at higher rates in those with a past diagnosis (2), and it is familial (5). With suicidal behavior in a sixth axis, it would be identified through review-of-systems questions, in addition to inquiry during the mental status examination. This proposed solution would address both conceptual and practical issues. Suicidal behavior might be conceptualized as an impulse-control disorder not elsewhere classified, but it is not always impulsive. Classification among “other conditions that may be a focus of clinical attention” diminishes its hierarchical position among diagnoses. Practically, an axis for suicidal acts would compel clinical and administrative structures to determine the suicide risk status of individuals assessed in psychiatric settings. In this manner, suicide risk can be documented as part of a multiaxial diagnosis, giving it the prominence that it deserves in written reports and treatment planning for vulnerable patients.