>On Fri, 12 May 2000 12:16:56 EDT, Spudboy100@aol.com wrote:
>In a message dated 5/11/00 11:25:53 PM Pacific Daylight Time,
><< As I understand it these take a couple of weeks to take effect. And often
>have disturbing side effects. Not much use in fits of sudden despair. >>
>It does take up to 3 weeks to kick in. Disturbing side-effects, maybe.
>Somebody killing themselves in a fit of despair, as you
>describe it, unusual. Sometimes that would be the tragic death of a loved
>one, other then that, suicidal depression is a spiral
>down, not a fit.
IAN: Note that evidence suggests that SSRIs can
increase the chance of suicide. A leading theory
as to why is that while an antidepressant effect
can take up to 3 weeks to kick in, CNS stimulating
adverse reactions can occur even on the first dose,
which is why a sedative may be given with an SSRI.
These ADRs, such as agitation and hyperactivity,
typically fit into the diagnostic profile of the
condition akathisia. The result is a state of
agitated depression wherein the likelihood that
one would act on suicidal impulses is increased.
Here's a Boston Globe article on the cover-up
of the suicidal risks of Prozac by Eli Lilly:
The following are several journal reports
accessed via the National Library of Medicine:
J Psychopharmacol (Oxf) 1999;13(1):94-9
Suicide in the course of the treatment of depression.
Healy D, Langmaak C, Savage M
North Wales Department of Psychological Medicine, Bangor, UK.
Five different mechanisms have been proposed whereby
antidepressant treatment might lead to suicide: first
by simply ameliorating depressions more rapidly; second
by an action intrinsic to the specific antidepressant
effects; third by toxicity in overdose; fourth by side-
effects of specific antidepressants; and finally by
virtue of treatment inefficacy. Evidence from randomized
control trials (RCT), controlled case studies and
epidemiological studies on this question is reviewed
and it is concluded that antidepressants can be
implicated in some cases of suicide during treatment.
Modifications of clinical trial methods and
pharmacogenetic studies would yield a richer data
set to explore this issue further.
Journal of Clinical Psychiatry, 1999;60 Suppl 2:94-9; discussion 111-6
Antidepressants and suicidal risk.
Muller-Oerlinghausen B, Berghofer A
Department of Psychiatry, Freie Universitat Berlin, Germany.
Only 5% of suicidal patients on the average use their
prescribed antidepressant to commit suicide. Underprescription
of antidepressants and failure of antidepressant therapy appear
to be of greater practical importance than the toxicity of
individual compounds. Prescribing less toxic agents, therefore,
will not be of great advantage, especially if they are less
efficacious. Several antidepressants including the selective
serotonin reuptake inhibitors (SSRIs) may increase suicidal
behavior by energizing depressed patients to act along
preexisting suicidal thoughts or by inducing akathisia with
associated self-destructive impulses. For acutely suicidal
patients, the use of more sedating antidepressants is
recommended. Clinical trials could not confirm a superiority
of SSRIs over tricyclics in reducing the number of suicide
attempts. There is evidence from large international data
sources and a large multicenter controlled trial that lithium
prophylaxis decreases the suicide risk and overall mortality
in affective disorders. A suicide-preventing effect has not
been demonstrated conclusively for antidepressants or
non-lithium mood stabilizers.
Encephale 1997 May-Jun;23(3):218-23
[Fluoxetine, akathisia and suicide]. [Article in French]
Lancon C, Bernard D, Bougerol T
Service hospitalo-universitaire de Psychiatrie,
CHU Sainte-Marguerite, Marseille.
Several cases of suicidal thinking or suicidal behavior during
fluoxetine treatment are described in the literature. Akathisia
or dysphoric extrapyramidal reactions may explain the emergence
of suicidal ideation during fluoxetine treatment. Retrospective
and controlled studies found no relationship between fluoxetine
and the emergence of suicidal ideation. Some cases reports of
akathisia or suicidal ideation with other selective serotonin
reuptake inhibitors (SSRIs) suggest that same mechanisms
(pharmacokinetic or pharmacodynamic interactions) are involved
in extrapyramidal effects during treatment with SSRIs. The
clinical use of SRIs is discussed.
Drug Safety, 1993 Mar;8(3):186-212
Antidepressant drugs and the emergence of suicidal tendencies.
Teicher MH, Glod CA, Cole JO
Department of Psychiatry, Harvard Medical School, McLean
Hospital, Belmont, Massachusetts.
Although antidepressant medications represent the cornerstone
of treatment for patients with moderate to severe clinical
depression, they also carry serious risks. There is evidence
which suggests that antidepressants can, in rare instances,
induce or exacerbate suicidal tendencies. Nine clinical
mechanisms have been proposed through which this may occur.
These are: (a) energizing depressed patients to act on pre-
existing suicidal ideation; (b) paradoxically worsening
depression; (c) inducing akathisia with associated self-
destructive or aggressive impulses; (d) inducing panic
attacks; (e) switching patients into manic or mixed states;
(f) producing severe insomnia or interfering with sleep
architecture; (g) inducing an organic obsessional state;
(h) producing an organic personality disorder with borderline
features; and (i) exacerbating or inducing electroencephalogram
(EEG) or other neurological disturbances. Epidemiological and
controlled studies also provide data on the association between
antidepressant drugs and suicidal ideation, attempts and
fatalities. These include studies which: (a) suggest that
electroconvulsive therapy may be more effective than
antidepressant drugs in reducing the frequency of suicide
attempts; (b) indicate that antidepressants may differ in
their capacity to reduce the frequency of suicide attempts;
(c) find that more overdose attempts were made by patients
receiving maprotiline than placebo; and (d) suggest that
fluoxetine may be associated with a greater risk of inducing
de novo suicidal ideation. Evidence suggests that antidepressants
may vary by at least 15-fold in the number of fatal overdoses
per million prescriptions. Estimated overdose proclivity rates
were derived after adjusting the fatal toxicity data by the
therapeutic index of the drug. These rates were very consistent
between agents with the same pharmacological properties, and
correlated well with known overdose risk rates for amitriptyline,
mianserin and maprotiline. Estimated overdose proclivity rates
suggest that the highly selective noradrenaline (norepinephrine)
uptake inhibitors (desipramine, nortriptyline, maprotiline) may
be associated with a greater risk for overdose than more mixed
uptake inhibitors and monoamine oxidase inhibitors (MAOIs).
Antidepressants are not uniformly neutral in regard to suicidal
ideation and attempts. Data clearly demonstrate that antidepressants
ameliorate suicidal ideation more effectively than placebo in
patients with depression. Although antidepressants diminish
suicidal ideation in many recipients, about as many patients
experience worsening suicidal ideation on active medication as
they do on placebo. Furthermore, at least as many patients
attempted suicide on fluoxetine and tricyclic antidepressants
as on placebo, and more patients attempted to overdose on
maprotiline than placebo. These observations suggest that
antidepressants may redistribute suicide risk, attenuating
risk in some patients who respond well, while possible enhancing
risk in others who respond more poorly.
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