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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 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) |
Maris and colleagues 5,6
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 Roy 19
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 survey 20
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's 21
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
|
| Figure 1: General model of
suicidal behaviours
Reproduced from reference 6 by permission of Guilford Press. Not all
interactions are depicted. |
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 others 23
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.
| 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 Pokorny 24
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. Beck 26
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.
| 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.
In the early 1970s
Äsberg 30 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 5HT 1A and serotonin 5HT 2A receptors,
smaller serotonin neurons, and more numerous, less functional neurons
than have controls. Such individuals also had raised concentrations of
norepinephrine, tyrosine hydroxylase, and 2-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.
|
| 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
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.
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 i coefficient predicts the optimum degree of
self-preservation. i should be negatively correlated with suicide
rates. For example, a polygynous man of 25 years would have a i of five versus a i of zero for a single man of 32 with no kin
contact who was unsuccessful with women.
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
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 Fawcett 43
showed that depressed people who later committed suicide had very high
concentrations of urinary 17-hydroxycorticosterone (  9 mg/24 h for women and  14 mg for men). Plasma cortisol is a precursor of 17
hydroxycorticosterone. Kreiger 43
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
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.
J John Mann assisted
with the biology section of the manuscript. There
was no funding for this article.
1 O'Carroll PW, Berman
AL, Maris RW, et al. Beyond the tower of Babel:
a nomenclature for Suicidology. Suicide Life Threat Behav 1996; 26: 237-52. [ PubMed]
2 Comtosi K. Research and usual care prevention effort across
psychiatric diagnoses. In: Goldstein, ed. Risk factors for suicide.
Washington, DC: National Academy Press, 2001: 13. 3 World Health
Organization. The ICD-10 classification of mental and behavioral
disorder. Geneva: WHO, 1992.
4 American Psychiatric Association. DSM-IV-TR. Washington, DC: APA,
2000.
5 Maris RW, Berman AL, Silverman MM. Comprehensive textbook of
suicidology. New York: Guilford, 2000: 71-73.
6 Maris RW, Berman AL, Maltsberger JT, et al, eds. Assessment and
prediction of suicide. New York: Guilford, 1992: 65-87.
7 Maris RW. Suicide. In: Dulbecco R, ed. Encyclopedia of human biology,
vol 8, 2nd edn. New York: Academic Press, 1997: 255-68.
8 Kreitman N, ed. Parasuicide. New York: Wiley, 1977.
9 Berman AL, Farberow NL. In: Maris RW, Berman AL, Silverman MM,
eds. Comprehensive textbook of suicidology. New York: Guilford, 2000:
427-55.
10 Mancinelli WR. Mass suicide: historical and psychodynamic
considerations. Suicide Life Threat Behav 2002; 32: 91-100. [ PubMed]
11 Moscicki E. Epidemiology of suicide. In: Goldsmith S, ed.
Risk factors for suicide. Washington, DC: National Academy Press, 2001:
1-4.
12 Beck AT. Cognitive approaches to suicide. In: Goldsmith S,
ed. Suicide prevention and intervention. Washington, DC: National
Academy Press, 2001: 10-12.
13 Schmidtke A. Perspectives: suicides in Europe. In: Maris RW,
Takahashi Y, eds. Suicide: individual, cultural, international
perspectives. New York: Guilford Press, 1997.
14 Maris, RW. Racial, ethnic, and cultural aspects of suicide.
In: Maris RW, Berman AL, Silverman MM. Comprehensive textbook of
suicidology. New York: Guilford, 2000: 170-92.
15 Yip SFY. An epidemological profile of suicides in Beijing, China.
Suicide Life Threat Behav 2001; 31: 62-70. [ PubMed]
16 Fernquist RM. Attitudes toward the unification of Western
Europe and cross-national suicide rates: eight European countries,
1973-1990. Suicide Life Threat Behav 2001; 31: 333-41. [ PubMed]
17 McIntosh, JL. USA suicide 1999, official final data. Washington, DC:
American Association of Sucidology, 2001.
18 Tanney BL. Psychiatric diagnoses and suicide. In: Maris RW,
Berman AL, Silverman MM, eds. Comprehensive textbook of suicidology.
New York: Guilford, 2000: 311-41.
19 Roy A, Linnoila M. Alcoholism and suicide. In: Maris RW. Biology of
suicide. New York: Guilford, 1986: 244-73.
20 Maris RW. Pathways to suicide. Baltimore: Johns Hopkins University
Press, 1981.
21 Bregin, PD. Listening to prozac. New York: Viking, 1993.
22 Maris RW, Berman AL, Silverman, MM. Treatment and prevention
of suicide. Comprehensive textbook of suicidology. New York: Guilford,
2000: 509-35.
23 Isaacson G, Risch CL. Depression, antidepressants, and
suicide: pharmacological evidence for suicide prevention. In: Maris RW,
Silverman MM, Canetto SS, eds. Review of suicidology, 1997. New York:
Guilford, 1977.
24 Pokorny AD. Prediction of suicide in psychiatric patients. Arch
Gen Psychiatry 1983; 40: 249-57. [ PubMed]
25 Rothberg JM, Geer-Williams C. A comparison and review of
suicide prediction scales. In: Maris RW, Berman AL, Maltsberger JT, et
al, eds. Assessment and prediction of suicide. New York: Guilford,
1992: 202-17.
26 Kovacs M, Beck AT, Weisman A. Hopelessness: an indicator of suicide
risk. Suicide 5: 98-103.
27 Goldston D. Issues in measurement of suicide risk factors in
youth. In: Goldsmith S, ed. Risk factors for suicide. Washington, DC:
National Academy Press, 2001: 5-8.
28 Brown G. Issues in measurement of suicide risk factors in
adults. In Goldsmith S, ed. Risk factors for suicide. Washington, DC:
National Academy Press, 2001: 5-8.
29 Addy CL. Statistical concepts of prediction. In: Maris RW,
Berman AL, Maltsberger JT, et al, eds. Assessment and prediction of
suicide. New York: Guilford, 1992: 218-34.
30 Äsberg M, Träskman L, Thoren P. 5-HIAA in the
cerebrospinal fluid: a biochemical suicide predictor? Arch Gen
Psychiatry 136: 559-62.
31 Arango V, Underwood M, Mann JJ. Biological alterations in the
brainstem of suicides. In: Mann JJ, ed. Psychiatric clinics of North
America: Suicide. Philadelphia: Saunders, 1997.
32 Plutchik R. Aggression, violence, and suicide. In: Maris RW,
Berman AL, Silverman MM, eds. Comprehensive textbook of suicidology.
New York: Guilford, 2000: 407-26.
33 Menninger K. Man against himself. New York: Harcourt Brace &
World, 1938.
34 Brown GL, Markku I, Linnoila MD, et al. Impulsivity,
aggression and associated affects: relationship to self-destructive
behavior and suicide. In: Maris RW, Berman AL, Maltsberger JT, et al,
eds. Assessment and prediction of suicide. New York: Guilford, 1992:
589-606.
35 Murphy GE, Wetzel R. Family history of suicidal behavior among
suicide attempters. J Nerv Ment Dis 170: 86-90.
36 Egeland J, Sussex J. Suicide and family loading for affective
disorders. JAMA 254: 915-18.
37 Roy A, Segal NL, Centerwall BS, et al. Suicide in twins. Arch
Gen Psychiatry 48: 29-32.
38 Kety SS. In: Maris RW, Berman AL, Silverman MM, eds. Comprehensive
textbook of suicidology. New York: Guilford, 2000: 381.
39 Byerly W. Strategies to identify genes for complex processes.
In: Goldsmith S, ed. Risk factors for suicide. Washington, DC: National
Academy Press, 2001: 11-13.
40 De Catanzaro, D. Prediction of self-preservation failures on
the basis of quantitative evolutionary biology. In: Maris RW, Berman
AL, Maltsberger JT, et al, eds. Assessment and prediction of suicide.
New York: Guilford, 1992: 607-24.
41 Murphy GE. Suicide in alcoholism. New York: Oxford, 1992.
42 Lester D. Alcoholism, substance abuse, and suicide. In: Maris
RW, Berman AL, Silverman MM, eds. Comprehensive textbook of
suicidology. New York: Guilford, 2000: 357-75.
43 Maris RW, ed. Biology of suicide. New York: Guilford, 1986.
44 Silverman MM, Goldblatt MJ. Physical illness and suicide. In:
Maris RW, Berman AL, Silverman MM, eds. Comprehensive textbook of
suicidology. New York: Guilford, 2000: 342-56.
45 Hughes D, Kleepies P. Suicide in the medically ill. Suicide Life
Threat Behav 2001; suppl: 48-60.
46 Maris RW. Pathways to suicide. Baltimore: Johns Hopkins University
Press, 1981.
47 Maris, RW, Berman AL, Silverman MM. Comprehensive textbook of
suicidology. New York: Guilford, 2000: 599.
48 Hammond WR. Suicide prevention: broadening the field toward a public
health approach. Suicide Life Threat Behav 2001; suppl: 1-2.
49 Brent DA. Firearms and suicide. In: Hendin H, Mann JJ. The
clinical science of suicide prevention. New York: New York Academy of
Science, 2001: 225-40.
50 Maris, RW, Berman AL, Maltsberger JT, et al, eds. New York:
Guilford, 1992: 80.
51 Maris RW, Silverman, MM. Suicide prevention: toward the year 2000.
New York: Guilford, 1995.
52 Maris RW, Berman AL, Silverman MM. Comprehensive textbook of
suicidology. New York: Guilford, 2000: 376-406.
53 Maltsberger JT. The psychodynamic formulation: an aid in
assessing suicide risk. In: Maris RW, Berman AL, Maltsberger JT, et al,
eds. Assessment and prediction of suicide. New York: Guilford, 1992:
25-49.
54 Fawcett JA. Suicide risk factors in depressive disorders and in
panic disorders. J Clin Psychiatry 53: 217-20.
55 Yufit RI, Bongar B. Suicide, stress, and coping with
life-cycle events. In: Maris RW, Berman AL, Maltsberger JT, et al, eds.
Assessement and prediction of suicide. New York: Guilford, 1992: 553-73.
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