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The increased use of antidepressants has contributed to the worldwide reduction in suicide rates

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Abstract

Numerous ecological studies have shown an inverse association between antidepressant use and suicide rates and a smaller number of individual-based studies have shown an association between current antidepressant use and reduced suicide risk. Such evidence is often cited in support of the notion that antidepressants prevent suicide. However, more recently, the premises underlying this proposition, namely that suicide is caused by depression and that antidepressants relieve depression, have been challenged and the potential harm caused by antidepressants has been highlighted. In this article, Goran Isacsson and Charles Rich debate with Jon Jureidini and Melissa Raven the motion that the increased use of antidepressants has contributed to the worldwide reduction in suicide rates.
For
Suicide rarely occurs in the absence of depression.
1,2
Therefore,
the hypothesis that suicide might be prevented by the treatment
of depression is not far-fetched.
The total use of antidepressants in Sweden in 1990 was
sufficient to treat less than 1% of the population, whereas the
prevalence of depression was around 5%. Toxicological
investigations of suicides in 1990–91 estimated that this amount
of treatment prevented around 100 suicides annually in Sweden.
It was suggested that the use of antidepressants had to increase
fivefold if suicide rates were to be lowered by 25%.
3,4
By 1996, suicide had decreased in Sweden by 19% concurrent
with a 3.4-fold increased use of antidepressants. Similar inverse
associations were also seen in Norway, Denmark, Finland,
Hungary and the USA. Consequently, this was described as a
‘medical breakthrough’ in the prevention of suicide.
5,6
Since then,
21 ecological studies with different designs replicated this inverse
correlation.
7–9
These studies presented data from Australia,
Sweden, Denmark, Finland, Great Britain, Hungary, Israel, Italy,
Japan, New Zealand, Norway, Slovenia and the USA, as well as
from across 27 other countries. Only one study from Iceland
(population 285 000) failed to demonstrate a decrease in suicide
parallel to an increase in the use of antidepressants. Also worth
noting is the increase in child suicide in the USA coinciding with
a decrease in the prescribing of antidepressants to children
following the Food and Drug Administration (FDA) warnings.
10
The possibility that this association is spurious cannot be
ruled out by ecological study.
However, no good alternative explanation for the decreases in
suicide has been claimed or supported by data. To prove causality,
the individual exposure to antidepressants has to be ascertained. It
is meaningless to demand randomised clinical trials, since such
studies are impossible for statistical and ethical reasons.
Observational study with scientific standards is therefore
necessary to provide empirical data which either increase or
decrease the plausibility that the hypothesis is true.
There is also an increasing number of individual-based studies
providing evidence that the decrease in suicide has indeed
occurred among individuals who were exposed to antidepressants.
Utilising a national prescription database in Denmark, So
¨nderga
˚rd
et al found that the more antidepressants dispensed to an
individual, the lower the individual’s risk of suicide.
11
Jick et al
demonstrated in a controlled study of the UK General Practice
Research Database that the relative risk for suicide was 38 times
higher in those prescribed an antidepressant 1–9 days before
suicidal behaviour compared with those who were prescribed an
antidepressant 90 days or more before.
12
Angst et al found that
in a 40- to 44-year Swiss follow-up study the standardised
mortality ratio for suicide was 13.8 for individuals treated with
antidepressants v. 33.3 for untreated individuals.
13
In Finland,
Tiihonen et al found that, among those who attempted suicide
who had ever used an antidepressant, the current use of
medication was associated with a markedly decreased risk of
suicide.
14
Our group recently published a controlled individual-
based study of forensic toxicological screenings of 16 937 suicides
in Sweden between 1995 and 2005.
15
We found that the trend in
the detection of antidepressants over the 11 years was what would
be expected if the decrease in suicide had occurred among
individuals treated with antidepressants.
There is undoubtedly a unique chain of various causal factors
behind each individual suicide.
Most people who die by suicide have one factor in common
however – depression.
Consequently, a large amount of evidence has accumulated
over the years supporting the hypothesis that treatment with anti-
depressants prevents suicide. Go
¨ran Isacsson & Charles L. Rich
Against
Like most who claim that increased use of antidepressants has
contributed to reductions in suicide rates, Isacsson & Rich’s
interpretation of evidence is shaped by the following deductive
reasoning:
.suicide is caused by depression (premise 1)
.depression is relieved by antidepressants (premise 2)
.therefore antidepressants prevent suicide.
However, both premises are flawed. Premise 1 privileges
depression over many other potential contributors to suicide, both
429
The increased use of antidepressants
has contributed to the worldwide reduction
in suicide rates
Go
¨ran Isacsson & Charles L. Rich / Jon Jureidini & Melissa Raven
Summary
Numerous ecological studies have shown an inverse
association between antidepressant use and suicide rates
and a smaller number of individual-based studies have
shown an association between current antidepressant use
and reduced suicide risk. Such evidence is often cited in
support of the notion that antidepressants prevent suicide.
However, more recently, the premises underlying this
proposition, namely that suicide is caused by depression
and that antidepressants relieve depression, have
been challenged and the potential harm caused by
antidepressants has been highlighted. In this article, Goran
Isacsson and Charles Rich debate with Jon Jureidini and
Melissa Raven the motion that the increased use of
antidepressants has contributed to the worldwide reduction
in suicide rates.
Declaration of interest
G.I. has received fees from several companies selling
antidepressants; C.L.R.: none / J.J. & M.R. are members of
Healthy Skepticism.
The British Journal of Psychiatry (2010)
196, 429–433. doi: 10.1192/bjp.bp.109.076166
In debate
proximal (e.g. alcohol intoxication, acute interpersonal conflict,
access to lethal methods) and distal (e.g. poverty, unemployment).
The strongest support for Isacsson & Rich’s statement that
‘suicide rarely occurs in the absence of depression’ comes from
psychological autopsy studies. However, their methodology is
problematic.
16
Relatives often seek relatively socially acceptable
explanations, and may be unaware of or unwilling to disclose
certain problems, particularly those that generate shame.
17
Additionally, a psychiatric history would increase the likelihood
of an ambiguous death being classified as suicide. Even so, one
of Isacsson & Rich’s own studies found that only 36% of
individuals had depression,
2
as did Zonda, who argued that
depression is overemphasised to the neglect of more commonly
found psychosocial factors and severe somatic disease.
18
Premise 2 is undermined by the fact that antidepressants are
not very effective at treating depression. The evidence is weak
that antidepressants improve scores on depression rating scales
to a clinically significant degree, let alone improving substantive
long-term outcomes.
19
Nevertheless, we agree that ‘the hypothesis that suicide might
be prevented by the treatment of depression is not far-fetched’.
However, Isacsson & Rich have failed to produce robust evidence
for their much stronger claim that ‘treatment with antidepressants
prevents suicide’.
Most evidence used to argue that antidepressants reduce
suicide comes from ecological studies. Unfortunately, many
commentators conflate correlation with causation, and ignore
the heterogeneity of diagnoses for which antidepressants are
prescribed. In addition, many ecological studies focus on short
time periods, ignoring decreases in suicide rates preceding the
introduction of selective serotonin reuptake inhibitors (SSRIs)
20
and fluctuations in suicide rates over time in response to socio-
economic, cultural and religious factors.
21
Most studies fail to
consider that increased antidepressant consumption may reflect
chronic use rather than more users.
22
Few ecological studies move
beyond crude correlations. Of those that do, one found no
association between antidepressant prescribing and suicide after
adjusting for gender, age, year, and proportion of prescriptions
for SSRIs.
23
Another, controlling for gender, age, county-level
variations, unemployment and alcohol consumption, found a
positive relationship between antidepressant use and suicide in
young people.
24
Isacsson & Rich’s claim that only one ecological study has not
found decreased suicide rates paralleling increased antidepressant
use ignores these and several other contrary studies.
20,25,26
Their
claim that increases in child suicide coincided with decreased
antidepressant prescribing has been refuted.
27
However, we agree
with their conclusion that ecological studies cannot settle this
debate.
Isacsson & Rich cited five individual-based studies that
provide stronger evidence than ecological studies. However, there
are problems with these studies and Isacsson & Rich’s inter-
pretation of them. First, they claim that Sønderga
˚rd et al ‘found
that the more antidepressants dispensed to an individual, the
lower the individual’s risk of suicide’.
11
In fact, 1995–1999 suicide
rates in Denmark decreased for both antidepressant users and
non-users. Unlike many studies, this one acknowledged the
possible contribution of non-pharmacological factors (e.g.
restriction of the availability of paracetamol) to the decrease in
suicide. Second, Jick et al’s
12
finding that the relative risk for
suicide was 38 times higher in those treated with an antidepressant
for 1–9 days v. 90+ days does not unequivocally support a
protective effect. Instead, as they acknowledged, it could be
because of natural fluctuations in depression severity or because
antidepressants worsen depression in the short term. Third, Angst
et al’s participants were seriously ill hospitalised patients, 61% of
whom had psychosis. As they noted, it is inappropriate to
generalise from such patients to people with depression in
general.
13
Tiihonen et al also focused on patients admitted to
hospital because of suicide attempts.
14
The more antidepressants
used prior to hospitalisation, the higher the risks of suicide,
suicide attempts, and mortality during follow-up, a finding not
necessarily attributable to confounding by severity. Also, patients
using antidepressants during follow-up had significantly higher
rates of suicide than people who never used them.
Finally, as in most suicide toxicology studies, Isacsson et al
15
did not consider the possibility of suicide being triggered by anti-
depressant withdrawal, which is not detectable by toxicological
screening. Furthermore, the study fails to take account of the
correlation between decreased official suicide rates and decreased
autopsy rates and increased ill-defined death rates in Nordic
countries.
22
In summary, Isacsson & Rich’s premises are flawed and they
have overstated their case with selective citation and biased
interpretation of evidence. Jon Jureidini & Melissa Raven
For: Rebuttal
Jureidini & Raven are sceptical of two premises: (1) suicide is
caused by depression; and (2) depression is relieved by anti-
depressant medication. Both of these premises are supported by
large bodies of evidence. Neither is a necessary condition,
however, for our proposition that treatment with antidepressants
prevents suicides. However, we believe that they offer the most
plausible mechanism to explain how antidepressants would
prevent suicides. Thus they form the logic behind our conclusion.
It is also perfectly possible to postulate that antidepressants have
direct antisuicidal effects. It is equally reasonable to posit indirect
antisuicidal effects by improving the ability of a person with
depression to maintain social relationships, employment and
sobriety. None of these effects would be mutually exclusive.
As we stated in our opening argument, the criticisms Jureidini &
Raven present to the evidence we cited in support of our
conclusion are perfectly legitimate. There will never be
indisputable evidence that any intervention prevented a suicide
since a non-suicide is a non-event. Even rigidly controlled
experimental studies may be disputed as demonstrated by
Jureidini & Raven. Of course, naturalistic studies are more subject
to dispute. Regardless, we wish to do something to prevent
suicides in the absence of definitive proof, and we believe the
weight of evidence points at the treatment of depression with anti-
depressants as an important strategy. We do not know how
Jureidini & Raven define the term ‘robust evidence’ so we cannot
respond to their call for it.
We previously concluded, ‘There is undoubtedly a unique
chain of various causal factors behind each individual suicide.’
Clinical science is, however, more about finding generalities that
identify practical targets for intervention in a population. Jureidini
& Raven imply that reducing alcoholism, somatic disease, inter-
personal conflicts, access to lethal methods, poverty and
unemployment would prevent suicides. This might very well
be true. It is, however, a daunting task to come up with suitable
interventions along these lines. Then there remains the challenge
of finding evidence, ‘robust’ or otherwise, for the effectiveness
of proposed interventions.
Jureidini & Raven suggest that we have ignored three
ecological studies that had not found inverse correlations between
antidepressant use and suicide rates. Two of the three studies are
from Italy. The first studied trends from 1988 to 1996 during
430
Isaccson & Rich / Jureidini & Raven
Suicide and antidepressants
which time the sales of antidepressants increased by 53%, and
suicide rates increased by 4% in men and decreased by 18% in
women.
25
The second studied trends during 1983–2000 when sales
increased by 236%, paralleled by decreases of suicide rates by 22%
in men and by 35% in women.
26
We did not include these two
studies because of low-quality exposure data. In a newer study
from Italy
28
with individual-based data for the period 1997–
2006, the number of individual users increased by 376% and the
suicides rates decreased by 34%. We think it is fair to say that
the inverse correlation has been demonstrated also in Italy. The
third study provides no data on the use of antidepressants and
therefore adds nothing to this issue.
20
Besides low-quality (or absent) exposure data, a failure to
demonstrate a correlation may also result from limited statistical
power. With this in mind, we cannot agree with Jureidini & Raven
when they claim that the study by Gibbons et al
29
that found 248
more suicides (+14%) among 5- to 19-year-olds in the USA in
2004 compared with 2003 is ‘refuted’ by Wheeler et al who found
four more suicides among 12-to 17-year-olds in the UK in 2004
compared with 2003, and 10 fewer in 2005.
27
Those numbers
are too small for any conclusions.
Jureidini & Raven also criticise the use of ‘crude rates’ in
ecological studies and favour ‘adjusted rates’. That may sound
intriguing, but each variable that is introduced as a covariate
includes an assumption that the variable influences suicide rates
(causality). Introduction of irrelevant covariates might obscure
true ‘crude’ rates. One example of such irrelevant variables is
‘decreased autopsy rates’ as demanded by Jureidini & Raven.
Clinical autopsy has indeed decreased but, at least in Sweden,
suicide is investigated by means of forensic autopsy, which has
not decreased. Neither is the decrease in suicide offset by an
increase in ‘ill-defined’ death. Contrary to Jureidini & Raven’s
claims, the latter has decreased even more than suicide. In
summary, we believe our basic premises are backed by solid
science, our selected citations are comprehensive, and our
interpretation is fair.
Go
¨ran Isacsson & Charles L. Rich
Against: Rebuttal
Without adding significant evidence, Isacsson & Rich reassert that
antidepressants prevent suicide. We agree that it is difficult to
intervene with the important contributors to suicide (notwith-
standing a range of successful public health interventions).
32
We
disagree that this justifies promoting antidepressants, unless they
are proven helpful – doing nothing is better than doing something
useless or harmful. Given the weak evidence for clinically mean-
ingful effectiveness of antidepressants, we cannot ignore suggestive
evidence of serious harm. Randomised controlled trials are not
designed and powered to detect suicidal behaviour and routinely
exclude people considered suicidal; therefore, when such
behaviour is unexpectedly found, it should not be dismissed.
There is unequivocal evidence that antidepressants can increase
suicidal behaviour in younger patients,
33
and trigger suicidal
behaviours in healthy volunteers
34
and hostility in both patients
and healthy volunteers.
35
Furthermore, those arguing for wider
use of antidepressants generally fail to take account of other risks
such as sexual dysfunction, pregnancy complications, and falls
among older people, and the opportunity costs of unnecessary/
ineffective prescribing.
With regard to other claims made by Isacsson & Rich:
.Barbui et al
25
and Guaiana et al
26
did find inverse correlations
between antidepressant use and suicide rates. However,
Isacsson & Rich ignore the fact that these authors explicitly
rejected a causal interpretation (a point we should have
made), noting that decreases in suicide preceded the introduc-
tion of SSRIs, an issue previously mentioned by us, but
ignored by Isacsson & Rich.
.Isacsson & Rich seem to have confused Wheeler et al’s 2009
international study
27
with a 2008 paper, which focused on
the UK.
30
Our claim that the study refuted a relationship
between increased child suicide and decreased prescribing
was based on the finding of a ratio of 0.999 between actual
suicides and suicides predicted from the linear trends in
10- to 14-year-olds and 15- to 19-year-olds internationally.
27
With regard to the newly cited Gibbons et al,
29
the authors
of that study seriously misrepresented the data in their
conclusions.
31
.We agree that introduction of irrelevant covariates in
ecological studies might obscure true correlations, but no
one advocates using covariates without evidence of relevance,
nor did we suggest use of autopsy rates as a covariate.
However, it is crucial to control for potential confounding
factors such as alcohol consumption; none of Isacsson &
Rich’s cited studies did.
.Isacsson & Rich have misinterpreted our point about autopsy
rates. Clinical autopsies sometimes detect previously
unsuspected suicides, so doing fewer autopsies would likely
reduce official suicide rates. Their claim that ill-defined
deaths in Sweden have decreased even more than suicides
contrasts with Reseland et al’s Fig. 1B (p. 80),
22
which shows
a substantial increase since 1997 with minor yearly
fluctuations. Perhaps Isacsson & Rich have exploited these
fluctuations to suit their argument.
Finally, Isacsson & Rich’s selected citations are not comprehensive.
In fact, they demonstrate the distorted and selective citation prac-
tices that muddy the antidepressant/suicide debate and the antide-
pressant literature more generally. Examples include the following:
.Failing to cite unfavourable studies: Isacsson & Rich’s claim
that only one study failed to demonstrate a decrease in
suicide paralleling increased antidepressant use ignores two
other negative studies.
36,37
.Ignoring unfavourable aspects of a study: Isacsson & Rich did
not report Barbui et al’s conclusion that SSRIs may increase
suicidality in adolescents.
9
In summary, Isacsson & Rich selectively ignore evidence of harms,
unfavourable results and interpretations, and crucial method-
ological issues.
Jon Jureidini & Melissa Raven
For: Conclusions
Jureidini & Raven demonstrate impressive scepticism regarding
evidence for antidepressants preventing suicide. They dismiss
numerous randomised clinical trials plus 50 years of clinical
experience demonstrating that antidepressants are effective for
treating depression. They dismiss many investigations
demonstrating that suicide is mostly a concomitant of depression,
and the score of ecological studies demonstrating decreases in
suicide paralleling increases in antidepressant use. They produce
arguments against individual-based studies showing the same
result. Ironically, Jureidini & Raven suspend their sceptic skills
regarding possible harms of antidepressants. They find
‘unequivocal evidence’ that antidepressants can increase ‘suicidal
behaviour’ without acknowledging that this debate is about
431
Isaccson & Rich / Jureidini & Raven
suicide, not the more common occurrences of non-fatal suicidal
ideation and behaviour. They cite other side-effects of anti-
depressants which are well known but do not prevent many people
with depression from choosing to take them. Nonetheless,
Jureidini & Raven recommend doctors would be better ‘doing
nothing’ rather than prescribing antidepressants for depressed
and potentially suicidal patients. This position demonstrates a
somewhat surprising naivety regarding a classic concept in
medical practice, i.e. the risk/benefit ratio.
Jureidini & Raven do not seem concerned that the
‘unequivocal evidence’ consists of by-products from the
randomised controlled trials they have judged inferior with regard
to the primary outcome. Nor do they find it problematic that
these leftovers consist of unsystematic observations from studies
in which most individuals of interest were systematically excluded.
If these individuals, judged to be at risk of suicide, had not been
excluded, it might have been possible to demonstrate the benefits
of antidepressants with regard to suicidal behaviour. Personally,
we find this information interesting but not compelling and
certainly equivocal at best.
Although Oravecz et al found no significant correlation
between suicide rates and the use of antidepressants between
1985 and 1997 in Slovenia (about 600 suicides annually), their
later analysis of 1971–2002 demonstrated that suicide had
decreased in Slovenia after a peak during the 1987–1994 period.
38
These data have greater statistical power.
The consumption of alcohol was considered in the previously
cited studies from Sweden, Hungary and Northern Ireland, and
could not explain the decrease in suicide. We are not aware of
any significant decrease in alcohol consumption elsewhere that
might explain decreases in suicide.
Suicide decreased in Sweden by 8% between 1980 and 1989
before SSRIs were introduced. However, use of pre-SSRI anti-
depressants in Sweden increased by 46% during the 1980s. Several
public health projects aimed at improving the treatment of
depression were also going on in the 1980s (e.g. Gotland Project,
Defeat Depression, DART). The fact that suicide in many
countries started to decrease before SSRIs supports our
hypothesis.
We have not exploited minor fluctuations in autopsy rates. In
a letter to the Editor,
39
we described what we believe are fallacies
in the earlier Reseland et al
22
paper on this topic. A diagram of
true Swedish rates of suicides and uncertain deaths is provided
in that letter.
We think the most important consideration is to acknowledge
what is in front of us. If antidepressants increase the risk of
suicide, the more than fivefold increase in their use since 1990
should have led to a suicide catastrophe (cf. thalidomide).
However, no such catastrophe has occurred. Instead, we have
witnessed a substantial worldwide decrease in suicide. This is
the reality that any theory of the effects of antidepressants must
address. As we stated in our initial argument, it is not possible
to definitively establish that these decreases have been caused by
antidepressants. Real-world observations have shown, however,
that decreases in suicide in different countries have been
proportional to respective increases in the use of anti-
depressants.
40
Likewise, individual-based studies have shown that
the decrease in suicide has occurred in the part of the population
that was treated with antidepressants.
15
We have not heard any
convincing alternative explanation of these facts. We find the
weight of the evidence makes a strong case for doctors offering
their patients with depression treatment with antidepressant
medication and saving many of them from suicide instead of
‘doing nothing’.
Go
¨ran Isacsson & Charles L. Rich
Against: Conclusions
Lacking good evidence that depression causes suicide or that anti-
depressants make a clinically important difference to depression out-
comes, Isacsson & Rich have claimed that increasing antidepressant
prescribing decreases suicide. This claim is based primarily on
correlations in ecological studies and on individual-based studies
with unrepresentative inclusion/ exclusion criteria and equivocal
findings. They have also cited a post-mortem toxicology study
that ignores withdrawal, which has been linked to suicidality,
41
assumes that only people with detectable antidepressant levels
have been exposed, and uses an unrepresentative control group.
Ioannidis has demonstrated how the myth of antidepressant
effectiveness is supported by small, biased randomised trials with
clinically irrelevant outcomes and selective and distorted reporting
and interpretation.
42
We have endeavoured to show how Isacsson
& Rich are key proponents of a similar myth that antidepressants
reduce suicide rates. Greenberg has outlined how distorting
citations can generate ‘information cascades’ (bandwagons) that
give ‘unfounded authority’ to claims.
43
We have highlighted
multiple examples of Isacsson & Rich’s use of citation bias and
‘citation diversion’ (misrepresentation of findings) to give
unfounded authority to their claims. Far from dismissing’ studies,
we have critically analysed whether their methodology and
findings support Isacsson & Rich’s interpretations. Mostly they
do not, but Isacsson & Rich have ignored many of our specific
criticisms and misunderstood others.
Isacsson & Rich continue to confuse autopsy rates and ill-
defined death rates; we mentioned fluctuations in the latter, not
the former. They argue that a diagram plotting suicides and
‘uncertain cases’ (an undefined term from an unstated data
source) supports their claim that ill-defined deaths have decreased
more than suicides in Sweden; it actually shows the opposite.
There are other factual inaccuracies: the Defeat Depression
Campaign ran in the 1990s,
44
not the 1980s, and alcohol was
not considered in the previously cited Hungarian study.
5
Isacsson & Rich seem unaware of normal assessment of
candidate covariates in multivariate analyses. Furthermore, they
imply that if alcohol consumption was a confounder, it should
explain suicide trends. Having settled on depression as a single
dominant cause of suicide and antidepressants as a single
dominant solution, they argue that critics should similarly suggest
a single alternative cause and solution.
Isacsson & Rich, who accuse us of naivety, seem unaware that
the opposite of benefit is harm, and that risk/benefit ratios are
inherently flawed.
45
Becoming suicidal while taking anti-
depressants is a serious harm, whether or not there is increased
risk of completed suicide. They suggest that including individuals
who are suicidal in trials might reveal benefits of antidepressants,
but ignore the possibility that it might expose harms. We do share
their concern that evidence of suicidal behaviour comes from
unsystematic observations; evidence would be stronger if trials
were not biased against detection of harms.
45
Isacsson & Rich close by distorting our comment that ‘doing
nothing is better than doing something useless or harmful’,
accusing us of advocating ‘doing nothing’ for people with
depression. They ‘wish to do something to prevent suicide’. So do
we. Were it the topic of this debate, we could elaborate on public
health interventions. Regardless of alternatives, the injunction to
‘first do no harm’ requires that we not prescribe potentially harmful
antidepressants based on wishful thinking. The idea that there is a
single cause and a simple solution to the tragic reality of suicide is
enormously appealing, and misinformed.
Jon Jureidini & Melissa Raven
432
Suicide and antidepressants
For: Go
¨ran Isacsson, MD, PhD, Karolinska University Hospital in Huddinge, M59,
Stockholm S-141 86, Sweden. Email: goran.isacsson@sll.se; Charles L. Rich, MD,
Mobile, Alabama, USA
Against: Jon Jureidini, PhD, MBBS, FRANZCP, Discipline of Psychiatry, University of
Adelaide, South Australia 5005, Australia. Email: jon.jureidini@health.sa.gov.au;
Melissa Raven, MPsych(Clin), MMedSci(ClinEpid), Department of Public Health,
Flinders University, Adelaide, Australia
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433
10.1192/bjp.bp.109.076166Access the most recent version at DOI:
2010, 196:429-433.BJP
Göran Isacsson, Charles L. Rich, Jon Jureidini and Melissa Raven
worldwide reduction in suicide rates
The increased use of antidepressants has contributed to the
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... T here is ongoing debate about the impact of antidepressant use on the risk of suicide, at both the individual level and the population level. 1,2 Meta-analyses of clinical trials have found either no definite association between antidepressant use and risk of (attempted) suicide or significantly increased risk. [3][4][5][6][7] Observational studies likewise produced inconsistent results. ...
... 9 Nevertheless, based on the findings from ecological studies, various authors have concluded that the increased prescription of SSRIs and other new-generation antidepressants has likely contributed to lower suicide rates in the population. 2,10,11 Such strong claims are not firmly supported by the evidence though, as the results of ecological studies are inconsistent. Some studies have found negative correlations between antidepressant prescriptions and suicide rates, some no association, and yet others even positive correlations. ...
... They can neither prove nor disconfirm that antidepressants alter the suicide risk, a serious limitation that was not sufficiently acknowledged by various authors. 2,22,36 This study has several limitations. First, due to its ecological design, the data capture only suicides at the population level and are restricted to Italy, Austria and Switzerland. ...
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Article
Background: Ecological studies have explored associations between suicide rates and antidepressant prescriptions in the population, but most of them are limited as they analyzed short-term correlations that may be spurious. The aim of this long-term study was to examine whether trends in suicide rates changed in three European countries when the first antidepressants were introduced in 1960 and when prescription rates increased steeply after 1990 with the introduction of the serotonin reuptake inhibitors (SSRIs). Methods: Data were extracted from the WHO Mortality Database. Suicide rates were calculated for people aged 10–89 years from 1951–2015 for Italy, 1955–2016 for Austria and 1951–2013 for Switzerland. Trends in suicide rates stratified by gender were analyzed using joinpoint regression models. Results: There was a general pattern of long-term trends that was broadly consistent across all three countries. Suicide rates were stable or decreasing during the 1950s and 1960s, they rose during the 1970s, peaked in the early 1980s and thereafter they declined. There were a few notable exceptions to these general trends. In Italian men, suicide rates increased until 1997, then fell sharply until 2006 and increased again from 2006 to 2015. In women from all three countries, there was an extended period during the 2000s when suicide rates were stable. No trend changes occurred around 1960 or 1990. Conclusions: The introduction of antidepressants around 1960 and the sharp increase in prescriptions after 1990 with the introduction of the SSRIs did not coincide with trend changes in suicide rates in Italy, Austria or Switzerland.
... Studies have shown that with the increased rate of the prescription of antidepressants; while being effective in controlling depression as one of the most important risk factors of suicide, they are causing an increased incidence of poisoning through suicide or drug overdose. However, in some countries increased prescription of the antidepressants was beneficial (35,36). Findings showed that benzodiazepines were the second agent responsible for the poisoning in Iran. ...
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Article
Objective: Acute poisoning is a major health problem and one of the most common causes of emergency visits worldwide. Since most poisoning subjects present with a decreased level of consciousness and due to unreliable disease history, recognizing the etiological cause of the poisoning represents a critical part in arranging the treatment strategy. This study aimed at examining the prevalence of etiological causes of poisoning in Iran in a systematic review and meta-analysis. Method: This systematic review and meta-analysis investigated the cross-sectional studies published from 1990 to 2020, reporting specific poisoning agents among acute poisoning cases in Iran. Persian and English articles on this subject were collected by searching the Scientific Information Database (SID), ScienceDirect, PubMed, Medlib, IranMedex, Scopus, Magiran, and Google Scholar databases. The heterogeneity of the studies was investigated using the I2 index and the probability of bias in the publication was assessed by the Begg and Mazumdar test with a significance level of 0.1. Data analysis was performed by Comprehensive Meta-analysis software version 3 (Biostat, Englewood, NJ, USA). Results: In our review, 19 studies appraising 143,251 cases of poisoning were included. The ranking of the OR of each agent was done; Opium poisoning was the most prevalent poisoning case followed by benzodiazepine, acetaminophen, antipsychotic medications, organophosphates, aluminum phosphide, amphetamine, pesticide, tricyclic antidepressant (TCA), alcohol, chemicals, carbon monoxide (CO), nonsteroidal anti-inflammatory drugs (NSAIDs), and selective serotonin reuptake inhibitors (SSRIs). Conclusion: While proper judgment on the cause of poisoning and selection of suitable treatment manners could be followed by a very good prognosis in patients with acute poisoning; this demands an epidemiological perception of the prevalence of the etiological poisoning agents. Our study ranked the most likely agents leading to the poisoning, to be at the top of the list of differential diagnoses of physicians.
... Meta-analyses of randomized clinical trials conducted by Brent et al., 2009 suggested the use of SSRI in depressed young adults is found to be associated with suicidal ideation (Brent et al., 2009). Postmortem studies have shown that suicide in depressed patients is more common than in those who do not take antidepressants (Isacsson et al., 2010). Elevated levels of serotonin in the synapse can cause suicidal traits (Graeff, 2004). ...
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The purpose of the work was to evaluate the effect of buspirone (BUS) on social isolation induced anger, aggression and suicidal tendencies in rats. The male Wistar rats were randomized in 6 groups (n = 6) and caged individually for 14 days to elicit anger and aggression. They were then divided into the following groups vehicle control (no isolation), Stress control (SC), fluoxetine (Flx; 30 mg/kg, p.o), BUS (10 mg/kg, p.o), BUS (20 mg/kg, p.o), BUS (40 mg/kg, p.o). All treatments were administered from day 14 through day 28. On the last day of treatment, assessment of anger, aggression and suicide-related traits were performed. Serum cortisol, blood pressure were measured and magnetic resonance imaging (MRI) of the rat's brain and of BDNF expression were performed. SC group showed significant increase in anger (wheel rolling activity), aggression (increased number of attack bites, wrestling, chasing behavior), irritability score, learned helplessness (number of attempts of escape success and failure, escape latency), increased level of serum cortisol as compared to normal confirming induction of anger, aggression and suicidal ideation. BUS significantly reduced all behavioral traits associated with anger, aggression and suicidal ideation, reduced cortisol levels and significantly increased BDNF compared to stress control. Blood pressure increased substantially in stress control was significantly reduced by BUS, but not by Flx. Neuroimaging studies in stress control brains showed a reduction in amygdala size compared to normal, while animals under BUS treatment mitigated this reduction. Buspirone has been found to be effective in preventing anger, aggression and suicidal tendencies.
... Moreover, the presence of suicidality can attenuate the clinical response to antidepressant treatment, independently of clinical confounders or the type of antidepressant [38]. A systematic review of several randomized clinical trials raised concerns regarding the increase in suicidality in young psychiatric patients receiving SSRIs [39], whereas several pharmacoepidemiological studies have demonstrated the protective effects of antidepressants with respect to suicidal behaviour in depressive patients [40]. This controversial context demands clinical trials to be designed specifically for depressed patients at significant risk for suicide. ...
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Article
Background Antidepressant response is a complex trait influenced by clinical, demographic and genetic factors. Objectives To explore the influences of baseline depression severity, gender and type of depressive episode on efficacy and safety of escitalopram (10–20 mg/day) in South Indian patients with major depressive disorder (MDD). Methods The study was conducted on 18–65-year-old patients ( n = 151) suffering from a first or recurrent episode of MDD with a 17-item Hamilton Depression Rating Scale (HDRS-17) score of ≥ 18 at baseline. Efficacy assessments were done using HDRS-17, Montgomery-Asberg Depression Rating Scale (MADRS), and Clinical Global Impression (CGI) at baseline and weeks 4, 8 and 12. Patients were monitored for adverse drug reactions (ADRs). Clinical outcomes were compared among various groups based on gender, type of depressive episode (first or recurrent episode) and baseline HDRS-17 scores (moderate depression—score between 17 and 23; severe depression—score ≥ 24). Results Among the 148 subjects who completed the 12-week study, 43.9% and 42.6% achieved response and remission, respectively. The decline in HDRS-17 and MADRS scores from baseline was significant ( p value < 0.05) at all follow-up visits and a similar pattern was seen with CGI. Efficacy outcomes were better in the moderate baseline depression group compared with severe depression. There were no associations of efficacy with gender and type of depressive episode. A total of 247 adverse drug reactions (ADR) were reported and 119 (80.41%) subjects experienced at least one ADR during the study period. No serious ADR was reported. Male patients experienced more ADRs compared with females. The safety profile of escitalopram was similar across various groups based on baseline depression severity and type of depressive episode. Conclusion The study revealed that escitalopram is efficacious in south Indian MDD patients with a favourable safety profile. The efficacy was influenced by baseline depression severity whereas more ADRs were reported by male patients.
... -Mayores riesgos asociados a su uso, especialmente desde que hace más de 10 años se alertase sobre la posibilidad de un incremento en el riesgo de acontecimientos relacionados con el suicidio (conductas e ideación suicida) en niños y adolescentes, extendido posteriormente a adultos jóvenes, que ha suscitado un intenso debate y controversia en la literatura con datos contradictorios y argumentos encontrados (197)(198)(199)(200)(201)(202). ...
... In the Australian debate following the FDA warning, there were isolated voices, including the three authors of this paper, two as researchers (62) and one as a parliamentarian (63), concerned about the effect of increasing antidepressant use on youth suicide rates. Yet these voices had little impact and, Australia-wide, there appears to have been a culture of uncritical group-think about the relationship between treatment and youth suicide. ...
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Article
In 2004, the US Food and Drug Administration (FDA) controversially issued a black box warning that antidepressants were associated with an increased risk of suicidal thoughts and behaviours in people aged under 18 years. In 2007, the warning was expanded to include young adults aged under 25 years. In 2005, the Australian Therapeutic Goods Administration responded to the FDA warning by requiring Product and Consumer Information leaflets to be updated to reflect the risk. However, there was considerable debate, and at times emotive backlash, in academic journals and the international media. Prominent US and Australian mental health organisations and psychiatrists challenged the FDA warning. They argued that, on balance, antidepressant use was likely to reduce the risk of suicide. Several ecological studies were cited misleadingly as evidence that decreasing antidepressant use increases suicide risk. From 2008 to 2018, Australian per-capita child, adolescent and young adult antidepressant dispensing (0–27 years of age) and suicide (0–24 years) rates have increased approximately 66% and 49%, respectively. In addition, there was a 98% increase in intentional poisonings among 5 to 19 year-olds in New South Wales and Victoria between 2006 and 2016, with substantial overlap between the most commonly dispensed psychotropics and the drugs most commonly used in self-poisoning. These results do not support claims that increased antidepressant use reduces youth suicide risk. They are more consistent with the FDA warning and the hypothesis that antidepressant use increases the risk of suicide and self-harm by young people. Causal relationships cannot be established with certainty until there is a vast improvement in post-marketing surveillance. However, there is clear evidence that more young Australians are taking antidepressants, and more young Australians are killing themselves and self-harming, often by intentionally overdosing on the very substances that are supposed to help them.
Article
Purpose The purpose of this study was to investigate the relationship between physical activity and depression according to the presence of disease. Methods A survey and basic assessment were conducted for 2,754 (Male=1,025 and Female=1,729) aged 40 and over who participated in the rural-based cohort study. The survey included physical activity, depression scale and disease preservation. The basic assessment measured height, weight, and body fat percentage. The measured data were analyzed by using logistic regression to examine the relationship between physical activity and depression prevalence. Results First, physical activity reduced the prevalence of depression by 33% and 51%, respectively, in the general population and in patients with the disease. Second, physical activity once or twice per week reduced the prevalence of depression in patients with disease by 51%, and at least three physical activities reduced the prevalence of depression by 37% in the general population and 33% of patients with disease. Third, physical activity less than 150 minutes per week reduced the prevalence of depression in patients with disease by 43%, and physical activity of more than 150 minutes and less than 300 minutes per week reduced the prevalence of 43% of the general population and 52% of patients with disease. Physical activity over 300 minutes per week had a 38% reduction in the prevalence of depression in the general population. Conclusions This study suggests that the level of physical activity suggested by the ACSM guidelines is appropriate to reduce the prevalence of depression. In addition, the patients with the disease was found to be effective with less frequency and amount of physical activity than the general person.
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Despite growing evidence of the relationship between residential environment and depressive symptoms, little is known about this longitudinal relationship for elderly. Based on the follow-up survey (2011, 2013, and 2015) of the China Health and Retirement Longitudinal Study (CHARLS), this study investigated the association between residential environment and depressive symptoms among Chinese middle- and old-aged adults using repeated measures mixed models and Cox proportional hazards regression models. We found that external building characteristics, indoor space layout, household facilities, and indoor environment have significant effects on depressive symptoms in the elderly. Therefore, residential environment interventions such as external built environments promotion, reasonable indoor space layout, and indoor household facilities and environment improvement can be effective ways to reduce risk of depressive symptoms among Chinese middle- and old-aged adults as well as decrease related public health burden.
Article
The substantive delay (often 4–6 weeks) between the commencement of an antidepressant and any discernible improvement in depressive symptoms is an ongoing concern in the management of depressive disorders. This delay incurs the risk of cessation of medication, self-harm/suicide and ongoing ‘damage’ to the brain caused by the illness. Both historically and now, off-label polypharmacy has been used in clinical practice in an attempt to facilitate both immediate- and long-term relief from symptoms. While somewhat effective, this strategy was unregulated and associated with severe adverse side effects for patients. In this article we proffer an alternative paradigm to achieve a more rapid antidepressant response by conceptualising the gap in terms of windows of response. The Windows of Antidepressant Response Paradigm (WARP) frames treatment response as windows of time in which a clinical response can be expected following initiation of an antidepressant. The paradigm defines three distinct windows—the immediate-response window (1–2 days), fast-response window (up to 1 week) and slow-response window (from 1 week onwards). Newer agents such as rapid-acting antidepressants are considered to act within the immediate-response window, whereas atypical antipsychotic augmentation strategies are captured within the fast-response window. The slow-response window represents the delay experienced with conventional antidepressant monotherapy. Novel agents such as esketamine and brexpiprazole are discussed as examples to better understand the clinical utility of WARP. This framework can be used to guide research in this field and aide the development of newer, more effective antidepressant agents as well as providing a strategy to guide the prescription of multiple agents in clinical practice.
Article
Background: As part of the Taiwan Aboriginal Study Project, a case-control study of suicide among two aboriginal groups and the Han Chinese was carried out in East Taiwan.Methods: Biographical reconstructive interviews were conducted for consecutive suicides from each of the three ethnic groups (a total of 116 suicides), 113 of whom were matched with two controls for age, sex, and area of residence.Results: In all three groups, a high proportion of suicides suffered from mental illness before committing suicide (97% to 100%). The two most prevalent psychiatric disorders were depression and alcoholism, and the most common comorbid pattern was depression with substance use disorders. The risk for suicide was significantly associated with all of these psychiatric conditions, previous suicide attempts, and a family history of suicide and depression. Fifty-one percent of all suicides had consulted medical professionals in the previous month.Conclusion: Despite the widely different rates of depressive illness and alcoholism in different cultures previously reported, the psychiatric antecedents of suicide are the same in the West and the East.
Article
Major descriptors of Slovenian suicide statistics are presented for the 13-year period ending in 1997. The purpose of the present study was to discover whether the introduction of antidepressant therapy influenced the Slovenian suicide dynamic. Collected national data on the rate of suicide and seasonal dispersion of suicide were compared with the prescription rates of antidepressives for the same period. No significant correlation between increased antidepressant prescriptions and decreased suicide rate were found. A possible decrease in the springtime suicide rate was observed. The Slovenian data, presented in a recent article, suggested some precaution toward descriptions of strong correlation between suicide and antidepressant therapy.
Article
In the course of a randomised double-blind crossover study comparing the effects of reboxetine and sertraline in a group of healthy volunteers, two volunteers became suicidal on sertraline. This paper describes the characteristics of the reactions experienced by both subjects. These problems were associated with a combination of akathisia and disinhibition. Dysphoric or akathisic responses on their own to either drug did not lead to suicidality in this group of subjects. Primary Care Psychiatry 2000: 6:23-28, Copyright (C) 2000 by LibraPharm Limited.
Article
PurposeConcerns that selective serotonin reuptake inhibitors (SSRIs) may increase the risk of suicidal behaviour amongst young people led to regulatory action in 2003/4 in many countries. Antidepressant prescribing to young people in various countries declined, but subsequent analyses have demonstrated mixed effects on population suicide rates.Methods Annual, national suicide mortality rates from 1990 to 2006 for 10–19 year-olds in World Health Organisation (WHO) Mortality Stratum A countries were studied using the WHO mortality database. Departures from country-specific trends in 2004–2006 relative to overall trends 1990–2006 were calculated to estimate the impact of regulatory actions in 2003/4.ResultsThere was no consistent change in rate after 2003, with some countries experiencing more and some fewer suicides than expected. Amongst 15–19 year olds the rate ratio was 0.999 (95%CI: 0.971–1.028), and in 10–14 year olds was 0.999 (95%CI: 0.929–1.074). There was some evidence of differential results for males and females. In 15–19 year olds there were 1.8% fewer (95%CI: −5.0 to +1.5%) suicides than expected amongst males and 8.1% more (95%CI: +1.9 to +14.6%) suicides than expected amongst females during 2004–2006. Rate ratios for 10–14 year-olds demonstrated a similar pattern, but with much greater uncertainty.Conclusions There was no evidence of an overall effect on suicides of regulatory action to restrict prescribing of SSRIs to young people, although there was weak evidence of an increase in suicide amongst young women internationally. Copyright © 2009 John Wiley & Sons, Ltd.
Article
Suicide takes the lives of around a million people each year, most of whom suffer from depression. In recent years there has been growing controversy about whether one of the best-selling anti-depressants – selective serotonin reuptake inhibitors (SSRIs) – increases or decreases the risk of completed suicide. Randomized clinical trials are not informative in this application because of small samples and other problems. We present what we believe are the most scientifically credible estimates to date on how SSRI sales affect suicide mortality using data from 26 countries for up to 25 years. We exploit just the variation in SSRI sales that can be explained by institutional differences in how drugs are regulated, priced, and distributed, as reflected by the sales growth of new drugs more generally. We find an increase in SSRI sales of 1 pill per capita (12% of 2000 sales levels) reduces suicide by 5%.