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Volume 360, Number 9329     27 July 2002
Suicide

Ronald W Maris

Lancet 2002; 360: 319-26
Center for the Study of Suicide, University of South Carolina, Columbia, SC, USA (Prof R W Maris PhD)
Correspondence to: Dr Ronald W Maris, Center for the Study of Suicide, 305 Sloan Building, 911 Pickens Street, University of South Carolina, Columbia, SC 29208, USA. (e-mail:Maris@sc.edu) Epidemiology
Diagnosis, assessment, and measurement
Neurochemistry, biology, and basic science
Treatment and prevention
References
Suicide is a multidimensional concomitant of psychiatric diagnoses, especially mood disorders, and is complex in both its causation and in the treatment of those at risk. It has known risk and protective factors that tend to be fairly consistent worldwide, with some cultural variation. Even with standardised assessment and prediction scales (such as the Hamilton or Beck depression inventories), suicide prediction results in about 30% false positives. The most common biological marker of suicide is reduced concentrations of the serotonin metabolite 5-hydroxyindoleacetic acid in the CSF of suicide cases versus controls. Although suicide prevention is ideally primary, in fact most treatment is secondary or tertiary. Dependent on the individual characteristics present, suicide prevention usually includes a pharmacological cocktail (especially one of the selective serotonin reuptake inhibitors, to raise serotonin concentrations, perhaps combined with an anxiolytic, mood stabilising, or antipsychotic agent), supportive psychotherapy (often cognitive or behavioural therapy), and sometimes electroconvulsive therapy. Perceived danger to self can necessitate treatment in hospital.   One of the biggest difficulties in the reliable diagnosis, assessment, treatment, and prevention of suicides worldwide is the lack of a consistent, common nomenclature and classification procedure for suicidal acts, with operational definitions and reliable, valid measurements of key terms.1,2 Neither WHO's international classification of diseases model ICD-10,3 nor the diagnostic and statistical manual of mental disorders (DSM-IV, American Psychiatric Association)4 have any entries for suicidal acts; although ICD-10 mentions suicidal acts in its E codes and the DSM includes them as symptoms or signs of major depressive episode and borderline personality. In the USA, statistics for suicide are generated by coroners and medical examiners marking suicide in the NASH (natural, accident, suicide, homicide) categories on an individual's death certificate.5 Nevertheless, suicide is a complex biopsychosocial outcome. There are many different types of suicide, each with its own unique causes.6 By suicide we understand that: first, there was a death; second, the death was achieved by the individual who died; third, the death was intentional; and fourth, there was an active or passive agent (eg, it was commission or omission of an act that resulted in the death).7 Suicides are often divided into subtypes--escape, revenge, altruistic, risk-taking, or mixed. People who commit suicide are usually contrasted with non-fatal suicide attempters or suicide ideators, who all have their own subtypes (including instrumental self-destructive behaviour to achieve an end or goal). In Europe, the term parasuicide is sometimes used to mean deliberate self-harm with or without a clear intent to die, especially in overdoses.8 Parasuicide is generally defined as any acute, intentional self-injurious behaviour that creates the risk of death. The continuum of suicide ranges from ideas to gestures, to risky lifestyles, suicide plans, suicide attempts, and, finally, suicide completions. Secondary characteristics of suicidal acts usually include: lethality (the medical certainty or probability that death will result from the act), intent to die (rated low, medium, or high), motive (the presumed reason for the act), certainty (as assessed by the person rating the suicidal act), mitigating circumstances (eg, intoxication, confusion, psychosis), and basic socioepidemiological traits (age, sex, race, method chosen, marital status, occupation, and so on). Suicidal acts also can encompass indirect self-destructive behaviours, such as pathological gambling, risky sports, chronic alcohol or substance abuse, dangerous driving, playing Russian roulette, repeated unprotected sex, obesity, and self-mutilation.9 However, we should be careful not to interpret all partly or indirectly self-destructive behaviour as suicidal. A final point in classification is that although the term suicide is usually reserved for individual self-destruction (or specific types of murder followed by individual suicide, such as those committed by suicide bombers), occasionally there are mass suicides, such as those at Masada in Roman occupied Israel and more recently in Jonestown, Guyana, and mass suicides involving the Order of the Solar Temple, Heavens Gate, and the Uganda Movement for the Restoration of the Ten Commandments.10  

Epidemiology

Epidemiology is the study of distribution and determinants of diseases and injuries in human populations.11 In 2001, two very noteworthy suicide assessment and prevention workshops were convened in the USA under the auspices of the Institute of Medicine of the National Academy of Sciences.2,12 Many of the statistics and findings I report are taken from the National Academy of Sciences workshop reports, and hence refer to suicidal behaviour in the USA. Comparable data for Europe have been published elsewhere.13 We should also be aware of cross-cultural, ethnic, and racial variations in suicidal behaviours.14-16 In 1999 deaths by suicide made up 1·2 % of all deaths in the USA (table 1).17 Table 2 shows that suicide rates in the USA fell steadily from 1990 to 1999 (14% reduction in rate).11 Over that time, suicide had dropped from the eighth to the 11th leading cause of death. For completed suicide attempts the ratio of men to women was 4 to 1 (6·3 to 1 for African-Americans). 90% of suicides in America were by white people; 72 % were by white men. Very few African-American women commit suicide, especially in midlife. 57% of all suicides were by use of firearms (62% of all suicides in men). Suicide rates were increased four to ten times in adolescents if there was a gun in their household. The second leading method of suicide in the USA is hanging for men (the most common method in Europe) and poisoning for women. Suicide rates are more than four times higher in divorced people than in those who are married. There are no official data for non-fatal suicide attempts in the USA.10 However, estimates are that there are ten to 25 non-fatal suicide attempts for every suicide completion, and these numbers rise to 100-200 for adolescents. By contrast with people who successfully commit suicide, three times more women than men attempt suicide.

Rate
Deaths
Diseases of the heart 265·9 725192
Malignant neoplasms 201·6 549838
Cerebrovascular diseases 61·4 167366
Chronic lower respiratory diseases 45·5 124181
Accidents 35·9 97399
Diabetes mellitus 25·1 68399
Influenza and pneumonia 23·4 63730
Alzheimer's disease 16·3 44536
Nephritis and nephrosis 13·0 35525
Septicaemia 11·3 30680
Suicide 10·7 29199
Chronic liver disease and cirrhosis 9·6 26259
Essential hypertension and renal disease 6·2 16968
Homicide 6·2 16889
Aortic aneurysm and dissection 5·8 15807
All other causes 139·0 378970
Total 877·0 2391399
*Deaths per 100 000 population
Table 1: Leading causes of death in the USA, 1999



1990 1991 1992 1993 1994 1995 1996 1997 1998 1999
Age (years)
5-14 0·8 0·7 0·9 0·9 0·9 0·9 0·8 0·8 0·8 0·9
15-24 13·2 13·1 13·0 13·5 13·8 13·3 12·0 11·4 11·1 10·3
25-34 15·2 15·2 14·5 15·1 15·4 15·4 14·5 14·3 13·8 13·5
35-44 15·3 14·7 15·1 15·1 15·3 15·2 15·5 15·3 15·4 14·4
45-54 14·8 15·5 14·7 14·5 14·4 14·6 14·9 14·7 14·8 14·2
55-64 16·0 15·4 14·8 14·6 13·4 13·3 13·7 13·5 13·1 12·4
64-74 17·9 16·9 16·5 16·3 15·3 15·8 15·0 14·4 14·1 13·6
75-84 24·9 23·5 22·8 22·3 21·3 20·7 20·0 19·3 19·7 18·3
85+ 22·2 24·0 21·9 22·8 23·0 21·6 20·2 20·8 21·0 19·2
65+ 20·5 19·7 19·1 19·0 18·1 18·1 17·3 16·8 16·9 15·9
Total 12·4 12·2 12·0 12·1 12·0 11·9 11·6 11·4 11·3 10·7
Men 20·4 20·1 19·6 19·9 19·8 19·8 19·3 18·7 18·6 17·6
Women 4·8 4·7 4·6 4·6 4·5 4·4 4·4 4·4 4·4 4·1
White 13·5 13·3 13·0 13·1 12·9 12·9 12·7 12·4 12·4 11·7
Not white 7·0 6·8 6·8 7·1 7·2 6·9 6·7 6·5 6·2 6·0
African-American 6·9 6·7 6·8 7·0 7·0 6·7 6·5 6·2 5·7 5·6
Table 2: USA suicide rates, 1990-99 (per 100 000 population)

Risk factors

Maris and colleagues5,6 listed fifteen common traits for people who commit suicide. Risk factors can be either distal/chronic/trait or proximal/acute/state. The key difficulty with risk factors for suicides is that they lead to many false-positive predictions. In the USA, older white men have higher suicide rates. Up to 90% of adults who commit suicides have at least one of the DSM-IV psychiatric diagnoses.11 The diagnoses most indicative of suicide are: major depressive episode (15% of depressives who are admitted hospital eventually commit suicide, and sleep disorder, especially terminal insomnia, is an important trait of people who take their own lives);17 bipolar disorder (especially bipolar affective disorder, type I); schizophrenia (with an increased suicide risk in postpsychotic period); borderline personality disorder; and sociopathic personality disorder in adolescent and young adult men.18 Alcohol or substance abuse is also predictive of suicide--there is ten times more research on alcohol than on any other substance with relation to suicide. Up to 50% of all people who commit suicide are intoxicated at the time of death.11 Roy19 estimates that 18% of alcoholics will die by suicide (mean age 47 years; mean duration of alcoholism 25 years). Comorbidity of depressive-mood disorder and substance abuse greatly raises risk of suicide--70-80% of people who commit suicide have comorbid diagnoses.11 Such individuals also tend to have less social involvement than those who do not kill themselves. For example, findings of one study showed that 50% of people who died by suicide in Chicago had no close friends.20 Being alone is very different from having only one other person who is important in one's life; thus, in suicide prevention the presence of a therapist, spouse, or other person can be crucial. Beck and colleagues'12 work clearly showed that patients who ultimately commit suicide are among those who have the least hope (assessed with the Beck hopelessness scale). Indeed, state hopelessness is more predictive of suicide than is depression, whereas trait hoplessness is associated with depressive disorder. A corollary of suicidal hopelessness is cognitive inflexibility, which includes difficulty in believing that there are non-suicidal alternatives to life problems. A family history of suicide or mental disorder, or both, is also predictive of suicide. Results of one large survey20 showed that 11% of completed suicides had another first-degree relative who had committed suicide, whereas none of the non-suicidal controls had such a family history. Most people likely to commit suicide require an aggressive catalyst to do so. Such individuals are typically more angry, willing to be aggressive, irritable, or impulsive than non-suicidal controls. Low serotonin is associated with deregulation of impulses. Early stages of treatment with some selective serotonin reuptake inhibitors (SSRIs, such as fluoxetine) can increase agitation or even produce akathisia. Thus, suicidal patients often need to take a minor tranquilliser or beta-blocker as well as an antidepressant drug. In the life of a suicidal person risk factors tend to interact, and compound and potentiate each other (compare Bregin's21 kindling model of depression). The general model of suicide depicted in figure 1 suggests that everyone has a pain threshold beyond which they cannot function. Just before a suicidal act the individual's adaptive threshold is breached and they may resolve their pain by committing suicide.5
01art/12404(1)
Figure 1: General model of suicidal behaviours Reproduced from reference 6 by permission of Guilford Press. Not all interactions are depicted.

Protective factors

Protective factors against suicide are generally the opposite of risk factors (figure 1, column 3). Non-suicidal people tend to be young, female, and non-white, and to have healthy and extensive social contacts, no guns in their homes, access to effective treatments (especially antidepressants), no psychiatric disorder, proper sleep, exercise, diet, and so on. Additionally, in most organised religions, suicide is not an accepted choice for resolution of life problems. Primary prevention (that is, reduction of number of new cases) of suicide is the ideal method of protection, and requires modification of broad social, economic, and biological conditions, to prevent members of a population from becoming suicidal.22 Such protective factors might include reduction of poverty, divorce rates, illiteracy, and violence (especially in families), and promotion of physical health, proper exercise, diet, sleep, and so on. When members of a population become suicidal, the main protective factors are probably accurate, early diagnosis and effective treatment of psychiatric disorders. Rich and others23 showed that diagnosis and treatment of depressive disorder is of paramount importance; they noted that the larger the dosage of any antidepressant, the lower the suicide rate was in the population. Family doctors need to take an active role in diagnosis and treatment of depressive disorders.
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Diagnosis, assessment, and measurement

Strictly speaking, one does not diagnose suicide, since suicide itself is not an illness, or a disease, but rather is associated with diverse illnesses (especially with major depression/mood disorders). To further complicate matters, the behaviour or outcome that is being predicted or assessed takes various forms.6 As we have seen, suicidal behaviour ranges from ideas, to non-fatal attempts, to completions, all of which have their own different levels of seriousness or lethality and subtypes. Are we trying to assess an individual's or a population's suicide risk, and over what time frame (this weekend, in several weeks, this year, over a lifetime)? The issues of whether a patient is suicidal or not and how suicidal they are is a fundamental distinction in diagnosis. As with cancer or heart disease, specific types of suicidal ideas, attempts, and even completions vary immensely in life expectancy and life quality. When a physician, psychologist, or mental-health worker pronounces a patient to be suicidal, much more precise information is required to make decisions about hospital treatment, precautions against suicide, restraints, inpatient versus outpatient treatment, and so on. How to assess suicide is also important. Often a case begins with self-reports of suicidality. A common phrase in hospital progress notes is: patient denies SI/HI (suicide ideation/homicide ideation). But such information is highly unreliable, especially when a patient wants to avoid hospital restrictions that might prevent their suicide. Mostly, diagnosis, assessment, and prediction relate to the suicide potential of an individual over a fairly short time frame, as established by a psychiatrist using clinical judgment (that is, without use of formal measurements or scales) with some vague reference to the DSM or ICD. When a clinician predicts an individual suicide, there are four possible outcomes: true positive (roughly, sensitivity); true negative (roughly, specificity); false positive; false negative. True positive and false negative outcomes make up all suicides, whereas false positive or true negative outcomes constitute the non-suicides. When the psychiatrist Pokorny24 predicted the suicide outcomes of 4800 psychiatric inpatients (by use of common risk factors such as those described above) and then followed his sample up 5 years later, he recorded, disturbingly, that 30% of patients had false-positive outcomes (44% were false negative). These data are vexing but actually quite routine when attempting to predict any low base-rate outcome. Pokorny's predictive validity was only 2·8%, which is hardly encouraging. Can predictive tools--ie, standard scales or measures--help the clinician to assess suicide? Panel 1 shows some of the scales that both clinicians and suicide researchers have found useful--ie, they have some reliability with respect to construct, concurrent, discriminant, and, especially, predictive validity versus non-suicidal controls.25
Panel 1: Some standardised scales useful in assessment and prediction of suicide
Scale Author Number of items (range of scores)
Hopelessness Beck 20 true/false (0-20)
Beck's depression index Beck 21 (0-63)
Hamilton rating scale Hamilton 17, 21, 24 (0-50 or 62)
for depression
Suicide probability Cull and Gill 36 (0-100)
Suicide ideation Beck 19 (0-38)
Reasons for living Linehan 48 true/false
Usually, one uses either the Hamilton or Beck depression inventory or scale, since suicide outcomes correlate highly with depressive disorders. One caveat is that, strictly speaking, these two methods are measures of the severity of depression, not of suicide risk. Beck26 recommends his hopelessness scale, because it correlates more closely with current suicide intent (r=0·68) and, negatively, with wish-to-live (-0·76), than does depression. Hopelessness also has trait characteristics that persist after depressive symptoms remit. For suicides in young people, only three scales have predictive validity: Beck's hopelessness scale, Linehan's reasons for living scale, and Cull and Gill's suicide probability scale (which measures suicide potential directly).27 In another study,28 patients who scored greater than three on Beck's scale for suicide ideation were 6·5 times more likely to commit suicide than those who scored three or less. It should be noted that no one psychological test, including the widely used Minnesota multiphase personality inventory-2, is highly predictive of suicidal acts. To measure suicide outcome appropriately one needs an adequate sample and, preferably, a longitudinal, not cross-sectional retrospective research design. Note that seriously suicidal probands are usually excluded from clinical trials, so we know little about these patients; and death certificate records have errors of omission. We also need controls (and random assignment to the control and study groups), who should all be given the same instruments under controlled conditions, and we should use multivariate models (rather than single variable models), case-control designs, power equations, and logistic regression or relative-risk log odds ratio statistical procedures.29 Ordinarily, assessment of suicide in patient populations focuses on major depression, bipolar disorder, and schizophrenia, since affective disorders carry a 10-15% lifetime suicide risk. Borderline personality disorder is also often studied, but most of the Axis II disorders (personality disorders and mental retardation) are associated with non-lethal suicide attempts rather than completions. This approach to suicide assessment has many flaws, not the least of which is the imperfect correlation of suicide with depressive disorder.
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Neurochemistry, biology, and basic science

The biology of suicide encompasses a vast panorama of subjects, ranging from neurotransmitter studies to research on aggression, genetic and family history factors, sociobiology, alcoholism and substance abuse, neuroendocrine studies, plasma cortisol concentrations, biological markers, imaging and radiological techniques, and physical illnesses--with the use of CSF, blood, and urine samples, and postmortem brain tissue.

Neurotransmitter studies

In the early 1970s Äsberg30 in Sweden started research into neurotransmitters, and such work continues today.31 The primary biological finding is that suicides (especially violent and less premeditated suicides) tend to have lower concentrations (below 92·5 nmol/L) of the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) in their CSF than do non-suicidal controls. Serotonin is the most studied neurotransmitter in relation to suicide, but dopamine and norepinephrine are also being investigated. Figure 2 compares serotonin receptors in postmortem brainstems of suicides with those of controls (other brain areas studied in people who commit suicide include dorsal raphe nucleus, prefrontal cortex, frontal cortex, temporal lobes, locus coeruleus, hypothalamus, and hippocampus).31 Suicidal behaviour is associated with a deficit in transmission of serotonin (5-hydroxytryprophan or 5HT). The extent of metabolite reduction correlates with the lethality of the suicide attempt. People who commit suicide have fewer serotonin transporter sites, more postsynaptic 5HT1A and serotonin 5HT2A receptors, smaller serotonin neurons, and more numerous, less functional neurons than have controls. Such individuals also had raised concentrations of norepinephrine, tyrosine hydroxylase, and alpha2-adrenergic receptors, and reduced numbers of postsynaptic ß-receptors, locus coeruleus neurons, and norepinephrine transporters. This pattern is similar to that of an excessive stress response that leads to norepinephrine depletion, perhaps because fewer neurons could mean reduced functional reserve.
01art/12404(2)
Figure 2: Models of serotonergic and noradrenergic pathological changes in the brainstems of people who commit suicide Reproduced from Arango V, Underwood MD, Mann JJ. Biologic alterations in the brainstem of suicides. In: Mann JJ, ed. The Psychiatric Clinics of North America: Suicide, vol 20, no 3. Philadelphia: WB Saunders, 1997: 581-94. By permission of WB Saunders.

Aggression, violence, and suicide

I define aggression as an inner state and violence as an overt act, as did Plutchik.32 Suicide is usually aggressive and violent. Menninger33 claimed that suicide includes both a wish-to-die and a wish-to-kill. Types of aggressive behaviour include predatory (which includes sexual aggression), between men, fear-induced, territorial, maternal, irritability related, and instrumental (to achieve some end other than to be aggressive). Usually suicide and aggression correlate positively (about r=0·5). Generally depression is predictive of suicide, but not of aggression. A challenge test (eg, prolactin response to fenfluramine) measures serotonin function indirectly. Patients with the highest aggression scores typically have the lowest prolactin responses, suggesting that aggression and serotonergic activity are negatively associated. Brown and colleagues34 describe a serotonergic trait which includes sleep difficulties, impulsivity, disinhibition, headaches, proneness to pain, glucosteroid abnormalities, mood volatility, disorder of conduct, poor peer relationships, and suicidal behaviours. Neuropeptides (active in neurotransmission) correlate positively and significantly with irritability in patients. Some SSRIs (such as fluoxetine) might cause an initial decrease in serotonin function, but this is debatable (for example, J Mann disagrees; personal communication). Reduced concentrations of cholesterol are also related to increased risk of suicide.11 Last, there are large numbers (60-70) of amplifiers (risk) and a smaller number (15-20) of attenuators (protective) of aggressive behaviour in people at risk of suicide.32

Genetic studies

Suicide tends to run in families. Maris20 reported that in 11% of suicides in Chicago, USA, the person had a first-degree relative who had committed suicide. Murphy and Wetzel35 claimed that 6-8% of suicide attempters had a family history of suicide. Egeland and Sussex36 reported a heavy loading of affective disorder and suicide in specific families in the Amish of Lancaster County, PA, USA. If suicide were inherited genetically, then concordance for suicide should be greater in identical twins than in fraternal twins. Although the relationship is small (10-18% of the sample) it is significant, and almost all of suicidal twins were monozygotic. In another study Roy and co-workers37 reported that monozygotic twin suicides showed greater concordance (p=0·001) than did dizygotic twins. This finding was true for twins who attempted as well as those who completed suicide. Adoptive studies tease out nature versus nurture when suicides had been raised by non-biological parents. Kety38 showed that 4-5% of adoptive parents of people who commit suicide took their own lives, whereas only 0·7% of controls (parents of non-suicides; p=0·01) did so. Genome-wide association studies are now possible, but would be very expensive. For example, the cost of assessing 1000 cases and controls might be about US$300 000 per case.39 One affordable approach to the genetic study of suicide would be to do direct DNA sequencing of all serotonin genes from about 50 patients severely affected with suicidal traits.

Sociobiology

The sociobiology of suicide suggests that individuals are especially vulnerable when they have serious difficulties in relationships with the opposite sex, in health, and in socially successful behaviour.40 These factors lead to a diminished capacity to reproduce, to support their kin, or both. Notably, in the USA suicide rates in women tend to peak at the menopause, whereas male suicide rates peak only in the very old.40 Male reproductive capacity in old age greatly exceeds that of women, and as men become less biologically fit and less able to reproduce, their suicide rate increases. In sociobiology, the psii coefficient predicts the optimum degree of self-preservation. psii should be negatively correlated with suicide rates. For example, a polygynous man of 25 years would have a psii of five versus a psii of zero for a single man of 32 with no kin contact who was unsuccessful with women.

Alcoholism

Alcoholism seems an important risk factor for suicide. Roy and colleagues19 reported that, on average, 18% of alcoholics (almost one in five) eventually committed suicide. However, Murphy41 claimed that in alcoholics the lifetime risk of suicide was only 2-4%. Almost 90% of alcoholic suicides are by men. Alcohol increases brain serotonin in the short term, and suicidal alcoholics might try to alleviate symptoms by use of alcohol. However, ethanol is a depressant, and depletes serotonin in the long term. Consumption of alcohol also reduces impulse control, and over time tends to lead to interpersonal loss and diminished social support--which might predispose the individual to suicide. Beck and Steer42 showed that alcoholism was the strongest single predictor of completed suicide in people who initially made non-fatal suicide attempts. We know very little about non-alcoholic substances and suicide. Before 1999 about 352 studies of suicide and alcohol were published; the next most-studied substances in suicides were cocaine (23 studies) and heroin (13 studies).42

Other biological aspects

Research into the chief metabolites of the neurotransmitter dopamine has shown that homovanillic acid and MHPG (3-methoxy-4-hydroyphenylglycol) are much higher in violent than in non-violent suicides. Results of some studies suggest that the stress system associated with the hypothalamic-pituitary-adrenal cortex axis is overactive in individuals at risk of suicide. Bunney and Fawcett43 showed that depressed people who later committed suicide had very high concentrations of urinary 17-hydroxycorticosterone (ge9 mg/24 h for women and ge14 mg for men). Plasma cortisol is a precursor of 17 hydroxycorticosterone. Kreiger43 found that suicidal patients had high serum cortisol concentrations versus nonsuicidal controls. Increased release of dexamethasone in the brain can be predictive of suicide. Prefrontal binding of corticotropin-releasing factor is reduced in suicide victims, indicating raised concentrations of this factor. There have been many studies of brains of depressives and schizophrenics with CT scans, positron emission tomography, nuclear magnetic resonance, and single photon emission-CT imaging techniques. Most of this research is not specific for brains of people who have died from suicide. Physical illness has a complex relation with suicide, but it is a relevant risk factor. People with diseases affecting the brain have higher suicide rates than those with other types of illnesses, including malignant disease. Some of the relative risks or increased odds ratios for suicide are: in chronic renal failure with dialysis 14·5, malignant neoplasms of the head and neck 11·4, HIV or AIDS 6·6, lupus 4·3, spinal cord injuries 3·8, kidney transplantation 3·8, Huntington's disease 2·9, multiple sclerosis 2·4, and peptic ulcer 2·1.44, 45
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Treatment and prevention

Since suicide is complex, treatment will tend to be complex and multifactorial. People who commit suicide usually die one at a time, and have some individual, idiosyncratic traits or states that require specifically designed interventions. Primary suicide prevention is directed to broad social interventions early in suicidal pathways,46 ideally before suicidal disorders develop.47 This approach forces interventions at the level of the environment and means of self-destruction, rather than focusing on the individual at risk.48 Thus, early suicide interventions might be designed to increase coping skills in children, to restrict access to suicidal means such as firearms,49 and to increase community and parent education about the importance of safe storage of guns. Primary prevention of suicide could also attempt to reduce known population risk factors, such as depression, alcoholism, availability of firearms, social isolation, poverty.50 Models of primary prevention identify different target groups for suicide interventions--for example, broad-based or universal interventions might improve access to health care for all, whereas selective interventions might focus on children of parents who are depressed or substance abusers, or both. Unfortunately primary prevention of suicide does not really exist. Often we settle for secondary prevention--ie, early detection and treatment of suicidal individuals aimed at reduction of cases of suicide--or tertiary prevention, such as treatment of symptoms of serious suicidal disease or disability, or both.51 Usually, management of suicidal individuals includes recognition, accurate diagnosis, and effective treatment of mood disorders, often with comorbid alcohol or substance abuse, or both. In standard treatment (up to 90% of all cases) the physician usually assumes that the suicidal individual has one or more psychiatric diagnoses that could respond to psychopharmacological interventions. Unfortunately, many mood disorders are not recognised, or are ineffectively treated, or both. For example, only 15% of a sample of individuals who killed themselves in Sweden had received any antidepressant drug in the 3 months before their suicide.23 Likewise in New York City, USA, 84% of a sample of people who committed suicide had not taken any antidepressants or neuroleptics.52 All treatment for suicidal patients begins with a thorough individual history. A record of previous suicide attempts and ideations, hospital admissions, treatments, etc, should be obtained both for the patient and for their first-degree relatives. Suicide risk and protective factors should then be assessed, perhaps by use of Minnesota multiphase personality inventory-2, the Hamilton or Beck depression inventories, the Cull and Gill suicide probability scale, a mental status test, and so on. A complete physical examination should also be done; Axis III physical disorders (general medical conditions) need to be discovered or ruled out, recorded, and treated; problems that should be noted might include thyroid abnormalities, brain tumours, alcohol disorders, diabetes, epilepsy, gastrointestinal abnormalities, musculoskeletal disorders, AIDS/HIV, neoplasms (especially of the head or neck), renal failure requiring dialysis, and lupus. Most suicidal patients will then be given a psychotropic cocktail,52 which might include antidepressants (especially one or more of the SSRIs; panel 2), anxiolytics antipsychotics (eg, alprazolam, lorazepam, buspirone, clorazepate, clonazepam, hydroxyzine), hypnotics (zolpidem, temazepam), antipsychotics or major tranquillisers (eg, haloperidol, clozapine, risperidone, quetiapine, olanzapine), mood stabilisers (eg, lithium, which is often the treatment of choice, valproic acid, carbamazepine, neurotine), anti-parkinsonian drugs (eg, trihexyphenidyl, benzatropine, diphenhydramine); with or without a barbiturate or stimulant.
Panel 2: Common antidepressants used to treat suicidal patients
Drug Usual dose (mg)
Tricyclics
Amitriptyline 75-300
Clomipramine 75-300
Desipramine 75-300
Doxepin 75-300
Imipramine 25-100
Nortriptyline 10-100
Tetracyclics
Amoxapine 150-300
Maprotiline 75-300
Mirtazapine 15-30
Selective serotonin reuptake inhibitors
Fluvoxamine 100-300
Fluoxetine 20-80
Paroxetine 20-50
Sertraline 50
Citalopram 20-40
Monoamine oxidase inhibitors
Phenelzine 30-90
Tranylcypromine 20-60
Atypical antidepressants
Bupropion 200-300
Nefazodone 200-600
Trazodone 200-600
Venlafaxine 25-375
Although most suicidal patients with mood disorders will be given an SSRI to begin with, electroconvulsive therapy (ECT) has proved to be more efficacious than standard treatment with antidepressant drugs.52 Depressive disorders usually respond rapidly to ECT, whereas antidepressants can take up to 4-6 weeks for a therapeutic response, if there is one at all (about 30% of patients who take fluoxetine have no antidepressant response). Thus, ECT can be the treatment of choice for acutely suicidal individuals with affective disorders. If a patient is very agitated or psychotic, out of control, dangerous to self or others, or without adequate social support or home care, then treatment in hospital should be considered.There, the patient can be watched closely (eg, 24 hours a day, 7 days a week, within arm's reach, or 15 minute logged observations, occasionally secluded, or restrained) and their drugs and behaviour can be monitored. Often a patient is asked to sign a no-suicide contract, although this precaution will not prevent many such acts. Suicide is the leading cause of death in psychiatric hospitals. Psychiatric hospitals are not safe environments and are difficult to modify to help to prevent suicides without violating the patient's rights (although dangerous articles and architecture should be considered). Written policies and procedures for suicidal crises should be in place in the hospital and the staff should have periodic training and certification in responding to and prevention of asphyxiation, including cardiopulmonary resuscitation.22 One should not assume that the treatment of suicidal patients is solely biological.12,53 Usually, conjoint cognitive psychotherapy, dialectical behavioural therapy, or behavioural modification techniques are useful. People can become suicidal in part because of their faulty or irrational reasoning, inadequate problem solving skills, dichotomous or overly rigid thinking, and generally dysfunctional cognitions, which they acquire over formative years through poor parenting. Psychotherapy can range from brief crisis interventions to long-term psychotherapy or psychoanalysis. The therapist should be sensitive to problems of transference and counter-transference, to reduce iatrogenically-induced suicidal acting-out. The importance of the need for the therapist to try to take the edge off the patient's acute anxiety, panic, desperation, or psychic pain cannot be overemphasised; through the wise use of both anxiolytics and the therapeutic alliance.54 Stress reduction and management is an integral part of this process of tension reduction.55 The suicidal patient needs to be able to tolerate and survive their recovery period.
Search strategy
Sources of information included: original epidemiological research by the authors; classifications and data from WHO, the American and British Psychiatric Associations, US Department of Vital Statistics, and the US National Academy of Sciences; refereed psychiatric journals, especially Suicide and Life-threatening Behaviors and the Archives of General Psychiatry; and research monographs and textbooks about suicide. We used materials published between 1981 and 2001 in the English, German, and French languages. Search topics included: suicide; diagnosis, treatment, and prevention of suicide; biology and pharmacology of suicide; epidemiology of suicide; assessment, measurement, and prediction of suicide; classification of suicide; aggression and violence; and sociobiology of suicide.

Conflict of interest statement

None declared.

Acknowledgments

J John Mann assisted with the biology section of the manuscript. There was no funding for this article.
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References

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