|
Black box warning labels DECREASE suicide
No Significant increase since HUGE REDUCTION in
SSRI Use!
SSRI's Increase
Suicide Risk
Recently people have been reporting that SINCE
the anti-depressant medications have obtained a
Black Box Warning Label, indicating they can
CAUSE people to feel suicidal, there has been a
significant reduction in the use of these drugs,
there has been a 16-18% increase in suicides…due
to not taking the medications. THIS IS SIMPLY
FALSE AND MISLEADING.
While one obvious rebuttal for this
antidepressant/suicide story is that correlation
does not equal causation -- and researcher Dr.
David Antonuccio, PhD makes a good point about
neglecting to consider the increase in anti-psychotics for
kids as the contributing factor for any increase
observed (i.e. as well as many other potential
variables). There is however, an even MORE GLARING
REASON that Newsweek and other media should be
ashamed of itself for suggesting this idea.
Read Below.
Only wishful thinking on the part of
antidepressant manufacturers leads to a
conclusion that the drop in SSRI prescriptions
for 5-18 year old in 2004 has resulted in
increased suicide for that age group. The
researcher who told Newsweek that reduced
antidepressant prescribing has led to more
suicides in kids is on the advisory board of Eli
Lilly (manufacturers of Prozac). If
one examines suicide rates for the entire period
from 1999 to 2003, when antidepressant use for
this age group was high, one sees that 2004
suicide rates are unremarkable.
According to official CDC statistics, the rate
of suicide for CDC's 5-14 age group in 2004 is
exactly the same rate as in both 2001 and 2000.
Similarly, the suicide rate for CDC's 15-24 age
group in 2004 is actually slightly lower than
the 2000 rate. Should there actually ever be a
substantive increase in suicide rates, history
tells us the likely source will not be a lack of
psychiatric treatment but rather social or
economic upheavals.
Sources: If you would like
to check out the actual CDC suicide statistics,
I have the CDC links and tables demonstrating that suicide rates have not increased
after the decrease in antidepressant prescriptions for
5-18 year-olds.
http://www.cdc.gov/nchs/data/nvsr/nvsr54/nvsr54_13.pdf
CDC's National Vital Statistics Report Deaths:
Final Data 2003 (which includes data from
1999-2003)
http://www.cdc.gov/nchs/data/nvsr/nvsr54/nvsr54_19.pdf
CDC's National Vital Statistics Report: Deaths
Preliminary Data 2004
Deaths per 100,000
Intentional self-harm
(suicide) 5-14 years
2004 0.7
2003 0.6
2002 0.6
2001 0.7
2000 0.7
1999 0.6
Intentional self-harm
(suicide) 15-24 years
2004 10.1
2003 9.7
2002 9.9
2001 9.9
2000 10.2
1999 10.1
Intentional self-harm
(suicide) All Ages
2004 10.8
2003 10.8
2002 11.0
2001 10.8
2000 10.4
1999 10.5
"Pharmacoepidemiological studies
examining the relationship between trends in
sales or prescription fills of SSRIs have
consistently shown a relationship between
increases in SSRI prescription rates and
declines in adolescent suicide rates (9, 35–37).
On the basis of those studies, one might expect
that the adolescent suicide rate would begin
increasing in the wake of the FDA advisory after
a decade of steady decline. {p. 890}"
The Newsweek article stated
prescriptions for pediatric depression (ages 5 -
18) dropped more than 50% between 2003 and 2005
-- a 2-year period. This is also not what the
article in Am J. Psychiatry stated. Rather,
it
stated prescription rates for pediatric
depression had been steadily rising since 1998,
and that after the October 2003 black box
warning prescription rates in October 2005
were 58% lower than they would have been had
they continued to rise between October 2003 and
October 2005 at the same average rate at
which they had risen between October 1998 and
October 2003. Using their figures, the
actual decline in prescription rates for SSRIs
for pediatric depression between October 2003
and October 2005 was 45.5%.
Then the article states that "in a parallel
development, the number of teen suicides jumped
a record 18% between 2003 and 2004." It
mentioned no source. It did mention that the CDC
will release suicide figures for 2005 in
December of 2008. This leads me to believe
that the Newsweek article used CDC above.
If they used the CDC data for the ages 5 -
14, using only one significant figure (we could
use more than one) the increase between 2003 and
2004 is 0.7 / 0.6 = 16.67%.
In the 15 - 24
"teenager" age group the increase between 2003
and 2004 is
10.1 / 9.7 = 4.1%.
I would expect to find more
teenagers in this group than in the former, and
would certainly expect a higher suicide rate in
the latter group.When
the two age groups are aggregated into one (5 -
24), there was no change, the rate remained 10.8
per 100000.
In this case a reversal from increases in
suicide rates over time to no significant rate
change over time. It isn't really a paradox. It
is just the result of combining groups of
different sizes and comparing aggregates with
the separate groups. It looks as someone picked
the group that best fit what they wanted and
ignored the aggregate data. When discussing teen
suicides I think that the 5 - 14 group is the
least significant of the three.
Now this "18 % increase in teen suicides from
2003 to 2004" is being broadcasted all over the
place as if it is an actual fact.
Tony Dokoupil’s Trouble in a ‘Black Box’ (July
16 article) importantly addresses the risks and
benefits of prescribing antidepressants to
children. However, the referenced study is far
from “compelling” evidence for removing the FDA
Black Box warning and such an interpretation of
its findings is misleading.
An inspection of this Eli
Lily funded study reveals that the precipitous
drop in SSRI prescriptions did not occur, as
reported, from 2003 to 2005, but rather from
February to October of 2005 (over 85% of the
drop in the last 6 months of the reported time).
The so-called “parallel development” of
increased suicides occurred between 2003 and
2004—and therefore had no relationship to the
drop in prescription rates reported in this
study. Given that the decrease in
prescription rates and increase in suicides
occurred in different time periods, it begs the
question of how such unsubstantiated statements
could be made by the experts cited in the a
rticle.
Only 3 of 15
clinical trials have shown antidepressants to be
superior to a sugar pill on primary measures.
Children and parents in those 15 studies
reported no advantage of antidepressants over a
sugar pill.
Data from the
FDA and its British counterpart demonstrate that
children and adolescents taking antidepressants
are twice as likely to experience
suicide-related events. Given the
meager results and increased risk for
suicide-related events (as well as other serious
adverse events), antidepressants are not a good
choice for youth struggling with depression—a
conclusion reached after an extensive
risk/benefit analysis conducted by the American
Psychological Association’s Work Group on
Psychotropic Medication (e.g first choice).
Given that depression tends to remit over time,
and so suicidality, do these studies really
prove anything other than that any possible
increase in suicidality caused by the
medications is insufficient to overwhelm the
natural average decrease in suicidality expected
to be seen in any depressed population over
time?
To make the conclusions they are trying to make,
that the medications did not increase
suicidality or even decreased it, they would
have to have a comparison group identified as
equally depressed, not given medication, then
remeasured later. They apparently don't have
this group so they can't make that conclusion.
Barbui, C., at el, 2008, Paroxetine (Paxil)
not superior to placebo (sugar pills)
amount adults with major depression, In Canadian
Medical Association Journal, Jan. 29. Among
adults, paroxetine was not superior to placebo
(sugar pill) in terms of overall effectiveness.
Researchers undertook a systematic review of
published and unpublished clinical trial data to
determine the effectiveness and acceptability of
Paxil. The researchers searched the Cochrane
Collaboration Depression, Anxiety and Neurosis
Controlled Trials Register, the Cochrane Central
Register of Controlled Trials, the
Glaxo-SmithKline Clinical Trial Register,
MEDLINE and EMBASE up to December 2006.
Published and unpublished randomized trials
comparing paroxetine with placebo in adults with
major depression were eligible for inclusion.
The research team included 29 published and 11
unpublished clinical trials in their review,
with a total of 3,704 patients who received
paroxetine and 2,687 who received with placebo.
Significantly more patients in the paroxetine
group than in the placebo group left their
respective studies because of side effects
(random effect RR 1.77, 95% CI 1.44-2.18)
or experienced suicidal tendencies (odds ratio
2.55, 95% CI 1.17-5.54).
Thus, if your depressed and an adult, taking
Paxil instead of just a sugar pill increases
your odds of becoming suicidal by 2.5 times.
CMAJ 2008;178(3):296-305.
Fava, G.,Journal of
Clinical Psychiatry 64:2, February 2003 page
123-133. This was forwarded to me by Dr.
Gary Kohls, MD. Thank you Gary.
Long-term use of antidepressant drugs may
increase biochemical vulnerability to depression
and worsen the long-term outcome and
symptomatic expression of the illness,
decreasing both the likelihood of subsequent
response to pharmacologic treatment and the
duration of symptom-free periods.The findings
of this article call for a more cautious
attitude among clinicians in prescribing
antidepressant drugs, because these drugs may
worsen the course of depression. A
statistical trend suggested that the longer the
drug treatment, the higher the likelihood of
relapse. Systematic treatment with tricyclic
antidepressants has proved to be associated with
an increase in the total number of recurrences.
In a
recently randomized, double-blind crossover
study comparing the effects of Remeron and
Zoloft in 20 healthy volunteers, 2 subjects
reported becoming depressed and 2 others
reported becoming suicidal, a dramatic incidence
of 20% serious depression, obviously caused by
the drugs. Another trial for
panic disorder comparing an antidepressant, (imipramine)
cognitive-behavioral therapy (CBT) or a
combination of the two modalities
resulted in
much higher 6 month response rates with the CBT
plus placebo (41%) than CBT plus drug (26%).
The occurrence of mania in depressed patients
upon treatment with antidepressant drugs is a
relatively old clinical observation, even with
the use of “mood stabilizers.” Antidepressants
may double the incidence of a switch into mania
(50% in some cases) compared with placebo (25%
of cases). Antidepressant-induced mania is not
simply a temporary and reversible phenomenon,
but a complex biochemical mechanism of illness
deterioration.
The return of depressive symptoms during
maintenance antidepressant treatment was found
to occur in 9% to 57% of patients in published
trials. Possibilities include pharmacologic
tolerance, loss of placebo effect, increase in
disease severity, change in disease
pathogenesis, accumulation of a detrimental
metabolite, unrecognized drug-induced mania and
prophylactic inefficacy.
Discontinuation of antidepressant drugs may
trigger hypomania or mania despite adequate
concomitant mood-stabilizing treatment. Mood
elevation may also occur by decreasing the
antidepressant dose.
Processes that change the number or
properties of drug-sensitive receptor
populations, have very limited explanatory power
in terms of the clinical phenomena previously
described. A therapeutic action of
antidepressant drugs (e.g., down-regulation of
postsynaptic 5-HT2 receptors) may, under certain
conditions, trigger changes in post-receptor
signal transduction, in intraneuronal signaling
pathways, or in neuronal architecture that are
likely to affect the balance of serotonin
receptors.
Impairment in neurogenesis may be the key
pathophysiologic event in depression.
Antidepressant drugs may yield changes in
connections or sensitivity to neurotransmitters
indirectly related to the specific actions.
Both sensitization to stressors and episode
sensitization may occur in mood disorders and
become encoded at the level of gene expression.
Stressors and the biochemical concomitants of
the episode can themselves induce the
proto-oncogene c-fos and related
transcription factors, which then affect the
expression of neurotransmitters, receptors, and
neuropeptides that alter responsiveness in a
long-lasting way.
The use of antidepressant drugs is so
prevalent that it is difficult to recruit
clinical populations who have never been exposed
to them! CBT appears to reduce the risk
of depressive relapse and may have a more
durable effect than pharmacotherapy alone.
Researchers thus should demonstrate that the
combination of psychotherapy and pharmacotherapy
is inferior in terms of relapse prevention to
psychotherapy alone. Patients with past
antidepressant treatment had more episodes of
depression and a longer duration of illness.
We strongly suspect that many patients who are
simply unhappy receive these drugs, with
predictable consequences in terms of morbidity
from side effects, mortality from overdose,
economic waste, and irrational, unproductive
clinical management. A treatment that
is helpful on average may be harmful for some
patients, as shown by a re-analysis of the
Beta-Blocker Heart Attack Trial.
Certainly, researchers working along these lines
are likely to encounter tremendous difficulties
in disclosing their results in journals and
symposia or in getting their studies started and
funded, in view of the current ideological and
pharmaceutically driven climate. We
should be aware that we are stretching the
original indications (major depressive episodes)
of drugs of modest efficacy to include
prevention of relapse, anxiety disorders and
demoralization. Antidepressant drugs may
speed improvement and change the boundary
between “responders” and “non-responders.”
However, when we prolong treatment to more than
6 to 9 months, we may recruit different
phenomena, such as tolerance, episode
acceleration, and paradoxical effects.
Excerpting, some paraphrasing
and underlining by Gary G. Kohls, MD, Duluth,
MN.
Maurizio
Fava et al have published a very important
paper in J Clin Psych 2006;67:1754-1759.
They found that >30% of patients on long-term
antidepressants were found to have cognitive
symptoms (apathy, inattentiveness,
forgetfulness, word-finding
difficulty,
and mental slowness) and 40% have physical
symptoms of fatigue and sleepiness and sedation.
The authors thought it was
likely that
the symptoms were both residual symptoms of
depression and side effects of medication.
Thus, if you take an anti-depressant, 30+%
will have symptoms of ADHD as a result of the
drug. Therefore, be careful you are not
given a second diagnosis and another medication
to get rid of the side effect from the first
medication.
Wheeler, B. from the University of Bristol, in
the United Kingdom, was published online
February 14, 2008 in British Medical Journal.
Reduced
prescribing of selective serotonin reuptake
inhibitor (SSRI) antidepressants for young
people in the United Kingdom following
regulatory action in 2003 did not lead to an
increase in suicidal behavior, according to an
ecological time series study.
They analyzed 3 sets of data from 1993 to 2006:
antidepressant prescriptions for 12- to
19-year-olds in the United Kingdom, annual
deaths from suicide in 12- to 17-year-olds in
England and Wales, and hospital admissions for
self-harm in 12- to 17-year-olds in England.
They found that
among young people, antidepressant prescribing
doubled from 1999 to 2003 and then dropped back
to the 1999 level by 2005. Deaths from suicides,
however, declined annually from 1993 to 2005,
and the rate of hospital admission for self-harm
remained relatively stable. "These data
for England do not indicate that reductions in
antidepressant use have led to an increase in
suicidal behavior," the group writes. The
findings differ from those of Gibbons and
colleagues, who reported that mortality rates
for suicides in 5- to 19-year-olds in the United
States increased in 2004, the year following
regulatory action (Gibbons RD et al. Am J
Psychiatry 2007;164:1356-1363), said Dr.
Wheeler. More recent critiques of that study,
however, suggest that the US situation may not
actually differ that much from the United
Kingdom's, he noted (Letters to the editor.
Am J Psychiatry 2007;164:1907-1910).
|