Primary prevention in psychiatry—adult populations
St. John’s Episcopal Hospital, Far Rockaway, NY, USA
SUNY Downstate Medical Center, Brooklyn, NY, USA
St. John’s Episcopal Hospital, Far Rockaway, NY, USA
SUNY Downstate Medical Center, Brooklyn, NY, USA
SUNY Downstate Medical Center, Brooklyn, NY, USAPrakash Chandra, MD
SUNY Downstate Medical Center, Brooklyn, NY, USA
BACKGROUND: The concept of prevention in psychiatry is unique. It includes promotion of mental health, identification of risk factors across the life cycle, and appropriate early interventions. Recent emphasis on intervention early in the development of mental illness has resulted in several preventive programs with varying degrees of success.
METHODS: We reviewed the literature on primary prevention in mental health, categorizing reports as evidence of universal, selective, or indicated prevention.
RESULTS: Indicated prevention through early intervention is the best-researched area of prevention in the spectrum of psychotic disorders, especially schizophrenia. Pharmacotherapy for ultra high-risk individuals combined with cognitive-behavioral therapy (CBT) has shown promising results in several studies. Strategies that teach younger individuals to cope with stress and provide psychosocial support have been effective in preventing mood and anxiety disorders.
CONCLUSIONS: There is evidence that primary prevention may delay the onset of mental illness. Future research on the etiologies of mental illnesses is required to facilitate development of additional primary prevention strategies. These efforts may contribute to reallocation of resources and enactment of public policies that curb the staggering effects of mental illness on society.
KEYWORDS: primary prevention, adult, psychiatry
ANNALS OF CLINICAL PSYCHIATRY 2010;22(4):239–248
Most mental illnesses are debilitating, disabling, and damaging. Permanent cure is still an exception rather than the rule. Consequently, psychiatric disorders are generally chronic, burdening individuals with social, psychological, and economic troubles. Rapidly evolving research has renewed interest in preventing mental illness. Prevention can be primary, secondary, and tertiary.1 Primary prevention deals with reducing disease incidence; secondary prevention is concerned with early identification and treatment; and tertiary prevention aims to reduce disability and prevent relapse. This review assesses the available literature regarding primary prevention of adult psychiatric disorders. Organized by mental disorders, this review considers the varying degrees of evidence for universal, selective, and indicated primary prevention and suggests future directions.
Issues in primary prevention of psychiatric disorders
Debate exists over the appropriate focus of prevention efforts: should these efforts target individuals at high risk of developing mental illness? Or should interventions aim to reduce risk in the whole population? In 1994, a landmark Institute of Medicine Report introduced the concepts of universal, selective, and indicated prevention as part of primary prevention in mental disorders.2 Universal prevention refers to interventions in the general population, irrespective of risk factors. Selective prevention targets populations whose risk of developing a mental disorder is considerably higher than average by virtue of biologic, social, or psychological factors. Indicated prevention targets individuals who manifest detectable signs or symptoms of a mental disorder but who do not yet meet diagnostic criteria for the disorder.
These preventive interventions operate at different levels within the social order.3 Macro-level interventions aim to change society and culture. Micro-level interventions are aimed at individuals, small groups, or social networks. The prevention of major psychiatric illnesses requires greater understanding of their genetic mechanisms, gene-environment interactions, the predictive power of risk factors, effect size of intervention measures, cost effectiveness, and social and ethical acceptance. This review describes the evidence-based risk factors in which primary prevention may be possible. Primary prevention of mental disorders is limited by nonspecific and overlapping risk factors and early symptoms of various mental disorders. The potential for “false positives” undermines preventive efforts from an ethical and economic perspective.
Mental disorders affect individuals worldwide, with deleterious implications for economies and societies. Mental disorders account for 13% of total “disability adjusted life” years, according to the World Health Organization (WHO) report of 20044,5 and billions of dollars are spent annually on mental disorders. Prevention of mental disorders is a public health necessity as well as a priority, requiring the concerted efforts of policy makers and health care personnel.
Schizophrenia and other psychotic disorders
The prevalence of schizophrenia is approximately 1.1% among individuals age >18.6 Men are more likely to develop schizophrenia than women (1.4:1.0). Individuals with schizophrenia have a 2-to 3-fold higher risk of mortality than the general population.
Biologic risk factors. On the basis of epidemiologic and neurobiologic evidence, schizophrenia has been conceptualized as a neurodevelopmental disorder. Evidence is strong for putative susceptibility genes such as neuregulin 1, dysbindin, disrupted in schizophrenia 1, catechol-O-methyltransferase, D-amino acid oxidase activator, regulator of G-protein signaling 4, and glutamate receptor, metabotropic 3; moderate evidence implicates several others. However, no candidate schizophrenia gene has been discovered. Currently, susceptibility to schizophrenia is thought to be related to the interaction of gene polymorphisms and environmental factors. Based on twin and family studies, it has been estimated that the heritability of schizophrenia liability is strong (0.6 to 0.7).7 Population attributable risk for family history is estimated to be 5.5%. One analysis revealed that the risk of schizophrenia increased with the advancing age of the father (age ≥55), suggesting that gene mutations due to advancing paternal age may play a role.8
Environmental risk factors. Cohort studies suggest an association between viral infections and schizophrenia.9,10 Among children with congenital rubella followed in a cohort study, 21% developed schizophrenia spectrum disorders in adulthood.10 Meta-analysis showed a close association between obstetric complications and subsequent development of schizophrenia (odds ratio 2; 95% confidence interval [CI], 1.6 to 2.4).11 A significant association also was found between age of schizophrenia onset and obstetric complications: the earlier the age at onset, the more likely the history of obstetric complications (10 times more likely to have had a complicated caesarean birth).12 Population attributable risk for season of birth and subsequent development of schizophrenia (more among births during the winter/spring) was found to be 10%.13 Population attributable risk for place of birth is estimated to be 34.6-fold higher in urban births.13 Naturalistic studies of the Dutch famine showed that malnutrition or micronutrient deficiency was associated with a higher risk of developing schizophrenia.14-16
In one analysis, the mean relative risk (RR) for developing schizophrenia among first-generation migrants was 2.7 (95% CI, 2.3 to 3.2). Among second-generation migrants, the RR was 4.5 (95% CI, 1.55 to 13.1). For both first-and second-generation migrants, the RR was 2.9 (95% CI, 2.5 to 3.4).17 Thus personal and family history of migration is an important risk factor for schizophrenia.
A prenatal stress study showed an increased risk of schizophrenia among children of mothers with a history of mental illness during pregnancy.18 In a study of the association between head injury and subsequent risk of developing schizophrenia, investigators have shown a 2-fold higher prevalence of premorbid head injury among patients with schizophrenia compared with their unaffected siblings.19,20 Four observational studies—a Swedish conscript cohort, the population-based Netherlands Mental Health Survey and Incidence Study, and 2 cohort studies from New Zealand (Christchurch and Dunedin)—reported that use of cannabis increased the risk of developing psychosis and an earlier age of onset of schizophrenia.21-23 On an individual level, cannabis use confers an 2-fold increase in the RR of developing schizophrenia.21-23
A British cohort study reported that solitary play preference, neurologic soft signs, and cognitive slowness were found to be higher among children age 4 and 6 who later developed schizophrenia than other age-matched children.24
Universal strategies. Better understanding of the genetic underpinnings of schizophrenia and the environmental interactions that contribute to developing this disorder are prerequisites for intervening on modifiable environmental risk factors. The development of primary preventive measures will depend in part on knowledge of schizophrenia genes, the neural basis of psychosis, and the ways that biologic vulnerabilities moderate the effects of environmental experiences.25
Interventions at the genetic level, such as counseling, lack sufficient evidence as a primary preventive measure. However, measures to reduce exposure to environmental factors that are associated with schizophrenia may be beneficial. For example, mandating measles, mumps, and rubella vaccination of all children can reduce the risk of viral infections during pregnancy later in life. Promoting use of prenatal vitamins, particularly folic acid, among women who are pregnant or may become pregnant can improve pregnancy outcomes; in particular facilitating adequate intake of folic acid through fortification will reduce the risk of neural tube defects. Increasing access to essential obstetric care through improved resource allocation may reduce obstetric complications.
Better integration of immigrants and ethnic minorities in a new community may reduce stress. Measures to reduce the stressors of urban life, such as overcrowding and competition for limited resources in an inner city area, could reduce the risk of developing schizophrenia.26
Eliminating cannabis use may reduce the incidence of schizophrenia by approximately 8%, considering a causal association between cannabis and psychotic disorders. The Adolescent Alcohol Prevention Trial27 was a population-based intervention to prevent drug use in teens. Students who received the educational intervention that promoted norms against drug use were 3-fold less likely to initiate marijuana use than students who did not receive the intervention.
The link between head injury and schizophrenia provides another reason to support effective injury prevention programs. The Harlem Hospital Injury Prevention Program showed a 45% reduction in the incidence of childhood injury through measures such as building safe playgrounds and distributing helmets.28
Selective strategies. The Scandinavian Early Treatment and Intervention in Psychosis Study showed that a major public health information campaign and use of early detection teams could reduce delays in receiving mental health treatment by 90%, reducing the rate of subsequent psychosis.29 Following high-risk individuals with a family history that suggests biologic vulnerability to psychotic disorders has low predictive value and produces many false positives. However, “multiple gates screening” and “close in” follow-up of high-risk individuals minimize false positive results.
Indicated strategies. Early interventions occur during prepsychosis or prodromal and early psychosis. The prodromal phase (average length of 2 to 5 years) involves a change from premorbid functioning and extends until the onset of frank psychosis.30 Early prodromal symptoms are nonspecific and include anxiety, irritability, sleep disturbance, poor concentration, fatigue, new and unusual thoughts, preoccupation, and social withdrawal.31 Identifying high-risk individuals during the prodromal phase is a challenge. Instruments such as the Structured Interview for Prodromal Syndromes and the Comprehensive Assessment of At-Risk Mental States have been found to have better predictive validity.32-34 Neuropsychological and neurophysiological testing, genetic analysis, and neuroimaging to evaluate attenuation in gray matter may enhance identification of prodromal cases.
The risk of falsely identifying someone who may never develop schizophrenia remains.35 Nevertheless, the prospective conversion rate to psychosis is substantial. In Australia, the Personal Assessment and Crisis Evaluation intervention reduced rates of conversion to psychosis at 6 months when prodromal patients were given low-dose risperidone (mean dose, 1.3 mg/d), cognitive-behavioral therapy (CBT), and supportive case management compared with individuals who received case management only.36 The Prevention through Risk Identification Management and Education study conducted in North America revealed significant symptomatic improvements in prodromal patients treated with olanzapine for 8 weeks compared with patients who received placebo.37,38 At 1 year, the conversion rate to psychosis was 50% in the untreated group, but it was not statistically significant.39 The studies suggest that early preventive treatment can delay the onset of psychosis and decrease the severity of prodromal symptoms in a high-risk population.36,38
Prolonged duration of untreated psychosis (DUP) contributes to poor outcomes in schizophrenia. Recent evidence indicates that increased duration of untreated illness (DUI)—which includes the prodrome and DUP—also has a deleterious effect.40 Reducing the DUI through pharmacologic and psychosocial interventions improves a patient’s prognosis. Patients who are found to have prodromal symptoms should be given information about their risk status and monitored closely. Such patients should receive support, stress management, and training in social skills, coping skills, and problem solving, and appropriate referral for substance abuse– related problems.38,41
As discussed previously remediation of cognitive and behavioral deficits in children with head injuries may reduce the risk or delay the onset of schizophrenia.28
Early interventions entail some risk, including medication side effects and the social stigma of being treated for a mental disorder. For individuals who turn out to be “false positives” for developing psychosis, the psychological trauma that results from unnecessary treatment could be significant.
Nearly 1 in 5 people experience a major depressive episode in their lifetime. In developed countries, the estimated 12-month prevalence of depression in the general population is between 3.1% and 10.3%.42 Major depressive disorder (MDD) is approximately twice as common in women as in men. MDD is caused by the cumulative effect of genetics, adverse events in childhood, and ongoing or recent stress.
Biologic risk factors. Scientists have not identified a gene or a series of genes that causes depression, but certain gene variations, called polymorphisms, have been found to increase the risk of depression. The serotonin transporter gene is the most studied in MDD. Given that an acute stressor increases serotonin release, an alteration in the transporter may influence a person’s sensitivity to stress.43 In 2003, results from a prospective birth cohort study suggested that a gene-environment interaction makes carriers of the short allele of the serotonin transporter more vulnerable to stress-related depression.44
Several medical illnesses such as diabetes, heart disease, autoimmune disorders, and pain are often comorbid with depression.45,46 The relation between MDD and disabling, chronic disease appears to be bidirectional because the presence of one may influence the prognosis of the other. Gene-environment interactions seem to predict a person’s risk for MDD better than genes or environment alone.
Environmental risk factors. Stress is a common precipitating factor for depression.47 In one analysis, an excess of independent undesirable life events or chronic difficulties in the previous 6 months was seen in patients with depression compared with the general population.48 Childhood adversity predicts higher levels of depressive symptoms in adulthood. Perceived lack of adequate support at the time of crisis has been shown to increase the risk of depression. Children who lose their mothers before age 11 are at increased risk of depression as adults.49 Childhood exposure to the parental style of “affectionless overcontrol” is associated with increased depression in adulthood. Physical and sexual abuse during childhood is associated with an increased risk of depression in later life. Individuals with lower levels of emotional stability, poor resilience, higher levels of interpersonal dependency, and higher levels of neuroticism were found to have higher risk of developing depression.50 High levels of anxiety symptoms and anxiety disorders precede the onset of depression in many cases. 51
Universal strategies. Evidence-based interventions that include measures to reduce child abuse, child neglect, and bullying have been shown to reduce early onset of depression. Enhancing protective factors during times of increased vulnerability to depression has been found to reduce the rate of depressive disorders. Resourceful adolescent programs were shown to decrease depressive symptoms by 50% among adolescents 1 year after the intervention.52 Educating children and adolescents about coping with conflict and crisis and improving life skills may reduce individual vulnerability to depression as adults.
Interventions to limit anxiety disorders are an indirect approach to reducing the risk of depression. Targeted anxiety prevention programs reduced depressive symptoms among children who displayed high levels of anxiety. Improved parental care can have long-term effects on preventing the occurrence of depression. In particular, teaching parenting skills that enhance a child’s self-esteem may reduce the risk of adulthood depression.
Selective strategies. Alloway and Bebbington showed that adequate social support, for example through the presence of a confidante, can reduce development of depression.53 An intervention to improve the psychosocial well-being of parents whose children had conduct problems showed that providing information and training in child-rearing strategies reduced parental depressive symptoms as much as 30%.53 According to the WHO, adequate economic and social support significantly reduce the incidence of depression among refugees and individuals exposed to war trauma.4,5 Many people with winter depression benefit from the exposure to light therapy as a preventive measure.54 High-risk individuals who received pre-divorce counseling experienced fewer symptoms of depression in a follow-up study.55 Among women undergoing surgery for breast cancer, counseling reduced the duration of subsequent depressive episodes and resulted in better post-operative adjustment compared with practical advice.56
Indicated strategies. Measures that supported mothers who were having difficulty managing their children with behavior problems reduced the children’s behavior problems and mood disorders.57 Another program for children from disadvantaged backgrounds with behavior problems reported improvement in problem-solving skills and incidence of depression with an interpersonal problem-solving intervention.58 For individuals with depressive symptoms but not a depressive disorder, education that promotes positive thinking, discourages negative thinking styles, and improves problem-solving skills has lead to reductions in the development of depressive episodes. One randomized controlled trial (RCT) in adolescents showed a decrease in the onset and recurrence of depression by 40% to 70% in the first year after intervention.59 Supporting and counseling recently bereaved individuals may reduce the risk of an abnormal grief reaction.60
Bipolar disorders are seriously disabling conditions and rank high on the list of leading causes of lifetime disability. Bipolar disorder is recurrent, severe, and common, occurring in 1% to 3% of the US population.61
Biologic risk factors. Biologic risk factors for bipolar disorders are highly heritable. Bipolar disorder, especially the most severe type (type I), has a strong genetic component. Family studies suggest evidence of genetic vulnerability. The proband-wise concordance rate was 0.43 (95% CI, 0.1 to 0.82) for monozygotic twins and 0.06 (95% CI, 0.00 to 0.27) for dizygotic twins,62 with the heritability estimates of 93%. The familial transmission risk of bipolar disorder among first-degree relatives of a patient is 1.5% to 10.2%, and risk of any affective disorder is 15% to 20%.63
Universal strategies. As with other mood disorders, large-scale interventions at schools and colleges that promote problem-solving and coping skills are key to prevention. One study of an early, home-based family counseling program in Finland showed that the intervention reduced internalizing problems 10 to 15 years later during adolescence and early adulthood.64 These effects could contribute to preventing the development of bipolar disorder. There is a paucity of literature for other universal strategies in bipolar disorder prevention.
Selective strategies. Substance use, delinquency, and school dropout increase the susceptibility of adolescents to mood disorders. The interventions that are effective in depression may be helpful in the prevention of bipolar disorders. However, further research is needed to substantiate this approach.
Indicated strategies. There is a dearth of evidence for indicated strategies in bipolar disorder and future research is needed.
Anxiety disorders include panic disorder, obsessive-compulsive disorder, posttraumatic stress disorder (PTSD), generalized anxiety disorder, and phobias. Annually, about 18% of Americans age ≥18 have an anxiety disorder.65 Panic disorder and phobic anxiety disorders are common and often chronic and disabling. Genetic epidemiologic studies have documented that these disorders are familial and moderately heritable.
Risk factors. Having anxious parents, experiencing child abuse, violence, war, or natural disaster, and refugee status are risk factors for developing anxiety disorders.4,5 Lack of control, low self-esteem, deficient coping strategies, and neurobiologic vulnerabilities increase the risk of anxiety disorders because of a defective stress-response system.4,5 More MDDs are found in families of probands with generalized anxiety disorder, suggesting common vulnerability factors for some anxiety and mood disorders.4,5
Universal strategies. Most anxiety disorders find their roots in childhood and adolescence. As a result, children and adolescents are the most important target for universal primary prevention. Evidence has shown that most children do not overcome their anxiety symptoms even during adulthood.66 Cognitive-behavioral programs such as the Australian FRIENDS program teach children coping skills for dealing with issues of self-confidence and emotional strength and to enable problem solving. This program was offered universally in schools and resulted in a significant drop in anxiety symptoms.67 FRIENDS has since been put into practice in Sweden and the United States.
The WHO supports reducing common traumatic events by implementing effective safety measures at home, at work, and for transportation, and better safety legislation and gun control laws. These measures, in combination with effective school-based programs, reduce aggressive and delinquent behaviors and contribute to a reduction in anxiety disorders.4,5
Internationally, preventive measures to avoid war and human rights violations have contributed significantly to reducing the incidence of trauma-induced anxiety disorders, especially PTSD. An important determinant of developing anxiety disorders is the duration of exposure to trauma. Emergency evacuation from disaster sites and early detection of violence and abuse contribute to the reduction of trauma-induced anxiety disorders.
CBT may be useful in preventing PTSD, whereas counseling and debriefing are not. Critical incident stress debriefing (CISD) involves coming to terms with, processing, recollecting, and reworking a stressful event within 24 to 72 hours of the trauma. Early attempts to prevent and mitigate the adverse sequelae of PTSD by counseling and debriefing were not found to be effective.68 Additionally, some studies reported that debriefing the victims of road traffic accidents may actually exacerbate long-term sequelae.69 CISD is most useful in the process of recovery from, rather than prevention of, PTSD.70 Conversely, strong evidence from controlled studies indicates that CBT delivered in 5 weekly sessions of 1.5 hours may lower the 6-month incidence of PTSD from 67% to 15%.71
Selective strategies. Therapy provided in a short-term cognitive workshop decreased the incidence of panic disorder from 14% to 2% among individuals who experienced their first panic attacks.72 Rapid resumption of activities is one way to prevent phobia development.
Indicated strategies. In the spectrum of anxiety disorders, selective and indicated strategies often overlap. In the absence of substantial evidence for this category of strategies, individuals with a generally anxious demeanor and children with behavioral problems may benefit from early intervention. There is a paucity of data regarding indicated strategies in the prevention of anxiety disorders. Additional research is needed in this context.
In the United States, anorexia nervosa occurs in 0.5% to 1% of female adolescents, making it the third most common chronic condition in this population. Bulimia nervosa occurs in 0.9% to 4.1% of adolescent females, with 5% to 15% of affected girls using laxatives, diuretics, and self-induced vomiting as methods of choice.73
Risk factors. Risk factors for an eating disorder seem to be largely social, attitudinal, and behavioral. Consequently, professions such as modeling, ballet dancing, and athletics show a higher incidence of eating disorders. Additional risk factors include physical and sexual abuse, low self-esteem, and difficulties in dealing with stressful situations. Individuals with substance abuse, depression, and anxiety disorders often exhibit comorbid eating disorders.4,5
Universal strategies. Large-scale programs offering information about the perils of unhealthy dieting and eating disorders usually target elementary, middle, and high school students as part of universal interventions.74 O’Dea et al initiated an interactive program to address not only eating attitude and behavior, but also issues of self-esteem in young adolescents. This study showed that 1 year after the program, the adolescents’ perception of body image and social acceptance had improved and the drive to stay thin had decreased.75
Media attention that focuses on weight and body shape and the glamorizing of thinness has long been debated as a cause of eating disorders. Increasing media literacy is an important method for reducing eating disorders. A recent Cochrane review indicated that media literacy and advocacy programs may reduce the extent to which individuals accept and internalize social ideals of thinness.74
Selective strategies. Counseling the staff and pupils of ballet and modeling schools where there is pressure to be slim (a high-risk group) will help to prevent eating disorders. In this group, 2 studies proved that Internet-based interventions were successful in changing perceptions of body shape, dieting, and the drive for thinness among at-risk young women.76 Some European countries have developed guidelines regarding the minimum weight for models.
Indicated strategies. Eating disorders frequently develop during adolescence, although they are not uncommon in adulthood. As highlighted in selective strategies, high-risk groups should be counseled as part of preventive strategies. However, health care providers may find it helpful to evaluate the eating patterns of young patients, paving the way for changing harmful eating habits. Specific data from early interventions in eating disorders are needed to help implement these measures.
Substance use disorders
In the 2007 National Survey on Drug Use and Health, the rate of current illicit drug use among persons age ≥12 was found to be 8%. This survey showed that 23.3% of individuals participated in binge drinking and 6.9% in heavy drinking.77 Staggering evidence of the devastating consequences of these behaviors is reason enough to actively invest in universal, selective, and indicated preventive measures.
Risk factors. Drug use flourishes in deprived neighborhoods with poor schools, high unemployment, high levels of marital breakdown, and juvenile and adult delinquencies.4,5
Universal strategies. Strict regulation at all levels—from the local jurisdictions to international laws—and strategies such as taxation, restrictions on availability, and comprehensive advertising bans have helped prevent substance use disorders. International efforts to reduce the supply of heroin, cocaine, and cannabis by destroying crops, providing farmers with financial incentives for growing other crops, establishing stable governments in drug-producing regions, and strengthening measures that reduce drug smuggling are examples of universal primary prevention. Domestic efforts include government policies that restrict prescription of drugs such as methadone, temazepam, barbiturates, amphetamine, and morphine. Establishing a minimum legal age for alcohol use, a strict licensing process for the sale of alcohol, and limits on the place and time alcohol can be sold are other primary preventive measures. Government policies that outlaw and severely penalize the sale and use of drugs will reduce their demand. High duties levied on alcohol reduce demand and per capita consumption. Conviction for public drunkenness and drunk driving are effective measures to curb alcohol consumption. Educational campaigns in schools and colleges increase awareness of the adverse consequences and legal ramifications of alcohol and drug use. Access to detoxification and rehabilitation services for alcohol and drug dependence would reduce long-term complications in high-risk groups.
For every 10% increase in media campaigns to educate the public about the ill effects of tobacco on mental and physical health, there is a 0.5% decrease in cigarette sales.78 Conversely, similar mass media interventions have had only limited impact on alcohol use and alcohol-related problems.79 The Saving Lives project that includes telephone hotlines, peer-led education in colleges, and drunk driving awareness programs showed a 25% reduction in fatal motor vehicle accidents.80 The NORTHLAND (MIDWESTERN) prevention project includes interventions at the individual and community levels and has shown much success.81 These interventions may prove to have long-term effectiveness if combined with other preventive measures.
Selective strategies. A common selective intervention is brief smoking cessation advice from a primary care physician to all smokers. It has been shown that this intervention motivates 40% of patients to attempt to stop, among whom about 5% quit smoking for at least 6 months.82 A 15-minute behavioral intervention that encourages pregnant women to abstain from substance use showed a 6% increase in smoking cessation. The babies of mothers who quit smoking were also 2 pounds heavier at birth.83 Data about selective strategies for preventing alcohol and illicit substance use are limited.
Indicated strategies. Interventions with parents in the home, supportive psychotherapy to address the causes of substance abuse, and efforts that engage personnel at schools and colleges could contribute significantly to the prevention of substance abuse; however, specific data are lacking in this regard.
According to the Centers for Disease Control and Prevention, 32,439 people (approximately 11 per 100,000) died by suicide in the United States in 2004. More than 90% of persons who commit suicide have diagnosable mental disorders. Four times as many men as women die by suicide; however women attempt suicide 2 to 3 times as often as men.84
Risk factors. The most evidence-based risk factors for suicide are psychiatric disorders. Recent social stress, history of suicide in the family and friends, and access to means for committing suicide are other risk factors. However, there are strict ethical barriers to conducting either control studies or RCTs to study these risk factors. The National Confidential Inquiry into Suicide and Homicide found that 24% of persons who committed suicide in England and Wales were in contact with mental health services in the year before death.85 This indicates that suicide rate can be reduced by mental health services alone.
Universal strategies. Reducing access to means of committing suicide has been shown to be an effective suicide prevention measure.86 This includes controlling the availability of sedatives and painkillers, strict security and safety on bridges and high buildings, and detoxification of domestic car and gas exhausts. Restricting access to more toxic psychotropics (eg, tricyclic antidepressants), using safer medications (eg, selective serotonin reuptake inhibitors) and prescribing fewer pills at one time could reduce the frequency of suicide by overdose. Government policies that restrict access to guns and family or police interventions that remove guns from persons with mental illness are barriers to the most lethal means of suicide, particularly among men. Removing structures that can be used in suicide by hanging (eg, noncollapsible curtains, door handles, or coat hooks) in hospitals reduced the inpatient suicide rate by two-thirds.85 These dramatic results prompted the WHO to propose reduction of access to suicidal means as its “human ecological model” in 1998.4,5 Developing sensitivity to representations and portrayals of suicide in the popular media (print, electronic, movies) is a part of comprehensive primary preventative measures. Wider societal change through alterations in family structure and functioning, such as reducing intra-familial conflict and improving parental and family support, is a target area for primary prevention.
Selective strategies. Health care providers can build their capacity to intervene with patients at risk for suicide by training staff to recognize and assess indicators of risk and high-risk periods, managing treatment noncompliance and loss of contact with a patient, and improving communication. Treating all patients with severe mental illness adequately with medication as well as psychological and family interventions would also affect the suicide rate. Managing comorbid alcohol and drug use in high-risk individuals could also reduce the suicide rate.
Increasing accessibility to timely help (eg, via help lines, phone numbers, Web sites, primary care, psychiatric care) would be a good selective, primary preventive measure. Limited evidence is available about the impact of telephone hotline and crisis centers on suicide rates. The information, support, and prompt intervention in medical and psychological emergencies by trained staff at a Tele-Help/Tele-Check service in Padua, Italy significantly reduced suicide rates.87 The “Gatekeepers Program” of Spokane, WA addresses the need to contact non-self referrals by training business personnel (eg, apartment managers, pharmacists) to recognize and refer elderly, distressed individuals to health professionals; this has reduced suicide rates in the elderly.87
The suicide prevention and school crisis management program implemented in Florida showed a 63% annual reduction in the number of suicides among students.87
Indicated strategies. Training primary care physicians to recognize and treat depression early reduced the number of inpatient days and suicides in a Swedish study.88 A number of RCTs have shown a very significant drop in suicide rates with antidepressant treatment in persons diagnosed with depressive disorders. The drugs included paroxetine (82% reduction)89 and lithium (72% reduction).90
There is evidence that suicides cluster in the immediate post-discharge period; the highest risk is during the first week after discharge. Interventions such as immediate follow up with all high-risk patients and better integration of inpatient and outpatient services would be effective at this critical transition phase.
The various aspects of universal, selective, and indicated primary prevention in mental illness are largely influenced by biologic, social, and psychological factors. Therefore, preventive measures would have to encompass a biopsychosocial approach to prove its effectiveness.
Studies of antipsychotics, such as risperidone and olanzapine, used in combination with CBT have shown positive results in improving prodromal symptoms of schizophrenia; however, the ethical conflict in treating individuals who may—or may not—be prodromal is a valid topic of debate.
In addition to medications are help and supportive family psychotherapy for ultra–high-risk individuals. The effects of comorbid substance use on mental illness are of profound importance; thus, obtaining a substance abuse history in psychiatric interviews is of paramount importance. Most adults afflicted by mental illness find the disease origins in childhood and adolescence. Various school-and college-based interventions have shown evidence of preventing or delaying the onset of mood and anxiety disorders and can be viewed as effective universal and selective prevention strategies. Additionally, prevention of child abuse is a way of decreasing the risk of many negative mental health outcomes. Strict legislation governing the accessibility of weapons, recognition of mental illness, and early initiation of antidepressant treatment show strong evidence of decreasing suicide and homicide rates—the most dreaded and fatal fallout of mental illnesses. Early accessibility to psychological intervention for all trauma victims, including survivors of war, refugees, individuals who are victims of life stressors (eg, financial instability, job loss, housing problems), and parents of children with behavioral problems, has long been credited as an effective indicated and selective strategy. Additional research into the etiology of mental illness is needed to further the cause of prevention in psychiatry.
DISCLOSURES: The study was not funded by any agencies. Dr. Brenner has received grant support for drug trials from AstraZeneca, Eli Lilly and Company, Janssen, LP, Pfizer, Inc., and Wyeth and is a member of the speakers’ bureau for Eli Lilly and Company and Janssen, LP. Drs. Madhusoodanan, Puttichanda, and Chandra report no financial relation ships with any company whose products are mentioned in this article or with manufacturers of competing products.
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CORRESPONDENCE: Subramoniam Madhusoodanan, MD, St. John’s Episcopal Hospital, Department of Psychiatry, 327 Beach 19th Street, Far Rockaway, NY 11691 USA, E-MAIL firstname.lastname@example.org
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