![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 21 of 21. This is the beginning of the thread.
Posted by doxogenic boy on October 22, 2013, at 12:46:02
Hi.
In this thread I would like to hear from those of you who have experienced that long-term use of antidepressants has worsened your depression and/or made you treatment-resistant. Did you feel better before you started with antidepressants?
I am satisfied with my meds, but it seems that there are a lot who dont get better.
There is some research that indicates that antidepressants worsen depression for some antidepressant users.
http://www.ncbi.nlm.nih.gov/pubmed/20728491
Excerpt from abstract above:Prog Neuropsychopharmacol Biol Psychiatry. 2011 Aug 15;35(7):1593-602.
Epub 2010 Aug 20.
The mechanisms of tolerance in antidepressant action.
Fava GA, Offidani E.
There is increasing awareness that, in some cases, long-term use of antidepressant drugs (AD) may enhance the biochemical vulnerability to depression and worsen its long-term outcome and symptomatic expression, decreasing both the likelihood of subsequent response to pharmacological treatment and the duration of symptom-free periods.
Quote end.Do you feel antidepressants have had this effect on you? How did they change your condition, and how long had you used antidepressants when your depression worsened?
- doxogenic
Posted by doxogenic boy on October 22, 2013, at 12:55:10
In reply to Do antidepressants worsen your depression?, posted by doxogenic boy on October 22, 2013, at 12:46:02
> There is some research that indicates that antidepressants worsen depression for some antidepressant users.
Today, more people than ever before get antidepressants for depression, and still there are a lot more patients with treatment-resistant depression. Could it be that the antidepressants make patients treatment-resistant, and do they get better if they stop taking their antidepressants?Below are two more articles which show that long-term use of antidepressants may worsen depression. (I have mentioned them is this message before:
http://www.dr-bob.org/babble/20130930/msgs/1052513.html ).
http://www.madnessradio.net/files/tardivedysphoriadarticle.pdfI have quoted parts of this study below. When I leave out something is use this: "[...]".
Tardive dysphoria: The role of long term antidepressant use in-inducing
chronic depressionRif S. El-Mallakh, Yonglin Gao, R. Jeannie Roberts
Mood Disorders Research Program, The University of Louisville Depression Center, Department of Psychiatry and Behavioral Sciences,
University of Louisville School of Medicine, Louisville, KY, USAArticle history:
Received 30 May 2010
Accepted 12 January 2011Abstract
BACKGROUND:
Treatment-resistant and chronic depression appear to be increasing. The recent identification of antidepressant tachyphylaxis, the loss of antidepressant efficacy over time, is only a partial explanation. This is an emerging evidence that, in some individuals, persistent use of antidepressants may be prodepressant.
METHODS:
A literature search of PubMed utilizing the terms: antidepressant tachyphylaxis, treatment-resistant depression, chronic depression, and antidepressant tolerance was performed, and relevant articles were used.
RESULTS:
Depressed patients who ultimately become treatment resistant frequently have had a positive initial response to antidepressants and invariably have received these agents for prolonged time periods at high doses. Parallels between this course and tardive dyskinesia are noted. It is proposed that neuroplastic processes related to dendritic arborization may underlie the treatment resistant depression that occurs in the setting of chronic antidepressant use. Since the prodepressant effect is seen after prolonged antidepressant use, the term tardive dysphoria is proposed.
CONCLUSIONS:
Tardive dysphoria, needs to be considered in studies of treatment resistant depression, and should be examined in blinded, randomized antidepressant discontinuation trials.
[...]
For many patients recurrence of depressive symptoms may oc-
cur despite ongoing antidepressant treatment [17]. When optimi-
zation of treatment fails, such patients are noted to have
treatment-resistant depression (TRD). TRD may comprise 3050%
of people with major depressive illness [17,18]. The cause of TRD
is unknown, but its prevalence appears to be increasing. In 2006,
a meta-analysis reported that nearly 40% of depressed patients had
TRD [19]. However, in the early 1990s it was reported that only
1015% of patients had TRD [20].[...]
Alternatively, the loss of efficacy of the antidepressant may be related to clinical issues suchas inadequate dosing of antidepressants [22 or antidepressant tolerance [23]. There are reasons to believe that antidepressant
treatment itself may contribute to a chronic depressive syndrome [24,25].Tachyphylaxis
Tachyphylaxis (also known as antidepressant tolerance, antide-
pressant poop-out, or breakthrough depression) is a condition
in which patients experience a good initial antidepressant re-
sponse which is lost over time with repeated or prolonged antide-
pressant treatment [23,2628]. This phenomenon is distinct from
an initial non-response or a partial response. Up to 80% of patients
diagnosed with major depressive disorder will experience a recur-
rence of depressive episode despite constant maintenance dose of
an antidepressant [12,23,29,30]. Attempts to treat these individu-
als frequently result in poor response and the rise of TRD [30].[...]
More recently, there have been several re-
ports of the loss of antidepressant efficacy. For example, Solomon
et al.[29] found that relapse occurred in 25% of 171 episodes. A
long-term placebo-controlled, blinded maintenance study of fluox-
etine in major depression, found no difference after 62 weeks in
subjects who were still euthymic on fluoxetine (11%) or placebo
(16%) [31]. Fifteen patients who had lost their response to antide-
pressants failed multiple treatment strategies including augmenta-
tion with mood stabilizers and, in some cases, electroconvulsive
therapy (ECT)[32]. When antidepressants were discontinued and
patients were left on mood stabilizers only, they improved even
though most (73%) had unipolar depression [32]. Similarly, in a
small case series of 11 TRD cases, none of the patients had a lasting
response to different classes of antidepressants
[26].Once initial treatment response is lost, subsequent improve-
ment is unlikely. If patients with TRD respond to a subsequent
antidepressant, the extent of improvement is inferior to the initial
response[33]. Patients who lost response to a MAOI not only did
not respond to subsequent treatment, but reported greater extent
of depression after relapse than before the new treatment was ini-
tiated[34,35].Antidepressant-induced depression
The possibility of antidepressant-induced depression was intro-
duced by Fava[36]. He suggested that a neurobiochemical mecha-
nism increasing vulnerability to depression might play a role in
this phenomenon and contribute to the observed worsening long-term outcome of major depression[24]. Other authors have also introduced similar ideas
[25,37].Several studies support these assertions. Van Scheyen
[38] naturalistically followed 84 depressed adults and found that long
term treatment with TCAs increased the likelihood of a depressive
recurrence. Long term treatment with imipramine is associated
with worsening mood in mildly depressed patients [39]. Anxious
patients without a history of a mood disorder may develop depres-
sion after long-term treatment with antidepressants for their anx-
iety disorder[40,41]. In a recent study 27% of patients without any
history of a mood disorder who had received antidepressants for
an average of 29 months for panic disorder, developed a cyclothy-
mic illness that persisted for 1 year after antidepressant discontin-
uation [42]. Normal controls receiving antidepressants in research
studies were reported to experience depression [43].[...]
Tardive dysphoria (TDp)
It is proposed that tardive dysphoria (TDp) is an abnormal dys-
phoric state that develops in some predisposed individuals with
prolonged antidepressant treatment. Patients with this syndrome
may comprise a significant fraction of TRD subjects. TDp is defined
as a chronic, frequently treatment resistant, depressive state with
onset in the setting of ongoing, persistent antidepressant treat-
ment. Antidepressants may be initially administered for any reason
(e.g., anxiety or depression), but afflicted subjects with a history of
a recurrent major depressive disorder would have historically
experienced an initial positive response to antidepressant medica-
tion (generally with their first exposure).The depressive state is
perpetuated (and possibly worsened) by continuing the antide-
pressant. It is believed that SRI antidepressants might be selec-
tively associated with the development of TDp. Discontinuation
of the antidepressant results in a slow and gradual improvement
of the chronic depressive symptoms. However, in some individuals
who have experienced TDp for a very prolonged period of time, dis-
continuation of antidepressant may not result in reversal of the
symptoms. This is superficially similar to TD. Subjects who
ultimately develop TDp will have frequently had an initial positive
response to antidepressants, helping to cement adherence. Depres-
sion recurs in 957%, or perhaps as high as 93% in the effectiveness
trial STAR*D (relapse and dropout of study) [59], of patients
despite ongoing antidepressant treatment [23]. In such patients,
an increase in dose [60,61], change to another antidepressant agent
[62,63] or adding another antidepressant [64,65] may be effective
in 3060% of patients. However, there is evidence that switch may
not be helpful [66], and if patients do respond relapse occurs with-
in 6 months in some 20% [61]. Ultimately, 3050% of such patients
will develop TRD [17,18].In the subset of such patients who have
developed TDp, ongoing attempts to treat the depression with anti-
depressants perpetuate the TRD, and may ultimately make the
chronic depression permanent. TDp is different from conditioned tolerance
[67] in that it is not merely the loss of the drug effect, but viewed as an active process in which adepressive picture is caused by continued administration of the antidepressant. In conditioned tolerance, environmental and behavioral conditional compensatory responses mediate tolerance
by in the presence of cues usually associated with the drug [67].[...]
Summary
A chronic and treatment-resistant depressive state is proposed
to occur in individuals who are exposed to potent antagonists of
serotonin reuptake pumps for prolonged time periods. Due to the
delay in the onset of this chronic depressive state, it is labeled tar-
dive dysphoria (TDp). TDp manifests as a chronic dysphoric state
that is initially transiently relieved by but ultimately becomes
unresponsive to antidepressant medication. Serotoninergic anti-
depressants may be of particular importance in the development of
TDp.The incidence or predisposing risk factors are as yet unknown,
but younger age at onset of antidepressant exposure and genetic
underexpression of the serotonin transporter, such as with the
short form of the serotonin transporter, may increase the risk of
TDp. Investigations attempting to discern the existence of TDp
would comprise blinded, randomized antidepressant discontinua-
tion/continuation trials in TRD patients, over at least 1 year. As
with TD, one would expect that some individuals who discontinue
the antidepressant will remain depressed.Subjects more likely to benefit from antidepressant discontinuation would be those who have had a briefer prior exposure to antidepressants, have more
neuroplastic potential (e.g., younger and without chronic medical
illnesses), and have the long form of the serotonin transporter.
Until such studies are performed the treatment recommendations
must remain unchanged, but clinical trials of antidepressant taper and discontinuation for 612 months in patients who have failed
most other options appear reasonable.Quote end.
-------------------------------------
-------------------------------------I quote parts of the article below.
Can Long-Term Treatment With Antidepressant Drugs Worsen the Course of Depression?
Giovanni A. Fava, M.D.
[...]
Results:
A number of reported clinical find-
ings point to the following possibilities: very un-
favorable long-term outcome of major depression
treated by pharmacologic means, paradoxical
(depression-inducing) effects of antidepressant
drugs in some patients with mood and anxiety
disturbances, antidepressant-induced switching
and cycle acceleration in bipolar disorder, occur-
rence of tolerance to the effects of antidepressants
during long-term treatment, onset of resistance
upon rechallenge with the same antidepressant
drug in a few patients, and withdrawal syndromes
following discontinuation of mood-elevating
drugs. These phenomena in susceptible individu-
als may be explained on the basis of the opposi-
tional model of tolerance. Continued drug treat-
ment may recruit processes that oppose the initial
acute effects of a drug and may result in loss of
clinical effect. When drug treatment ends, these
processes may operate unopposed, at least for
some time, and increase vulnerability to relapse.[...]
(J Clin Psychiatry 2003;64:123133)
Received June 21, 2001; accepted Aug. 8, 2002. From the Department
of Psychiatry, State University of New York at Buffalo, Buffalo; and the
Affective Disorders Program, Department of Psychology, University of
Bologna, Bologna, Italy.[...]
Corresponding author and reprints: Giovanni A. Fava, M.D.,
Dipartimento di Psicologia, Viale Berti Pichat 5, 40127 Bologna, Italy.[...]
The most common conviction among re-
searchers and clinicians has probably been the recognition
of the chronic nature and increasing incidence of depres-
sive illness. 4However, we seem to forget and do not want to entertain another possibility: the likelihood that antide-pressant drugs may be depressogenic, at least in some
cases. 14
[...]Fux et al.36 observed the emergence of depres-
sive symptoms in 7 (9%) of 80 patients during the treat-
ment of panic disorder with fluvoxamine. These patients
had no history of mood disorder, and no symptoms of
depression were present before treatment with fluvox-
amine. The symptoms abated when fluvoxamine was dis-
continued and a tricyclic antidepressant or clonazepam
was prescribed, and they reappeared when fluoxetine
was administered. Fux et al. 36 suggest the possibility of
a vulnerability among some panic disorder patients to a
noradrenergic-serotonergic imbalance caused by selec-
tive serotonin reuptake inhibitors (SSRIs).The question that arises is whether such paradoxical
phenomena may affect only a few individuals or are
manifestations of a subtle, but general effect. The results
of a recent randomized controlled trial comparing
cognitive-behavioral therapy (CBT), imipramine, or their
combination for panic disorder 37 point to the possibility
of a general effect in panic disorder. Six months after
treatment discontinuation, response rates were 41% for
CBT plus placebo, compared with 26% for CBT com-
bined with imipramine. A relationship between use of
antidepressant drugs and increased relapse risk of panic
disorder has been reported by other investigators, 3840
and depression was found to occur during the follow-up of
patients receiving tricyclic antidepressants for panic dis-
order. 41Another intriguing phenomenon involves the con-
cept of a therapeutic window, which was originally ap-
plied to nortriptyline, 42 but was subsequently described
with SSRI therapy. 4347
The possibility of paradoxical or no effects occurring above a certain dosage would be in line with the phenomena described with patients with
affective disorders and healthy controls.[...]
In the early 1980s, Kukopulos et al. 50,51 observed how treat-
ment by antidepressant drugs may contribute to changes
of course from unipolar to bipolar illness and to an in-
creased frequence of cyclicity. Cycle acceleration has
been subsequently confirmed by other investigators. 48Kukopulos et al. 50,51 deserve credit in raising the possi-
bility that antidepressant-induced mania is not simply a
temporary and fully reversible phenomenon, but may trig-
ger complex biochemical mechanisms of illness deterio-
ration. A case of tricyclic-induced mania in a 60-year-old
woman with a long-standing history of unipolar depres-
sion (that was followed by rapid cycling refractory to
lithium) illustrates the hormonal implications of such
mechanisms. 52[...]
Tolerance to Antidepressant Drugs
The return of depressive symptoms during mainte-
nance antidepressant treatment was found to occur in 9%
to 57% of patients in published trials. 54Possible explana-
tions include pharmacologic tolerance, loss of placebo
effect, increase in disease severity, change in disease
pathogenesis, accumulation of a detrimental metabolite,
unrecognized rapid cycling, and prophylactic inefficacy.
54Several clinical observations point to the existence of
tolerance phenomena during antidepressant treatment.
24,55 Some data point to dispositional (pharmacokinetic) toler-
ance, which reduces the concentration of a drug. For in-
stance, patients who relapsed while on fluoxetine treat-
ment (20 mg/day) responded to an increased dosage of the
same drug (40 mg/day).56Other studies, however, suggest the likelihood of pharmacodynamic processes that change sensitivity to the drug. Mann 57 observed loss of antidepres-
sant effect with long-term monoamine oxidase (MAO) inhibitor treatment without loss of MAO inhibition. Lieb and Balter 58 described the development of tolerance to an-
tidepressant effects that was refractory to dosage increase.
[...]Donaldson 69 described 3 patients with major depres-
sion who relapsed while on phenelzine treatment and de-
veloped a severe chronic depression that was refractory
to other treatments. The phenomenon of resistance was
analyzed in a study of 122 patients who, after initially
responding to fluoxetine, were assigned to placebo. About
half of the patients relapsed. After reinitiation of med-
ication, 38% of the patients either did not respond or ini-
tially responded but again relapsed. 70 Similar results were obtained after discontinuation of an SSRI in obsessive-
compulsive disorder. 71The few data available thus indicate that when drug
treatment is reinstituted, the patient may not respond to
the same antidepressant that improved depressive symp-
toms the first time. The prevalence of this resistance that
ensues varies. Patients who respond to reinstitution of the
same antidepressant drug may display a subsequent loss
of therapeutic effect. 70This suggests that resistance and loss of clinical effects may be related and share a common mechanism. Episodes that are simply classified as respon-
ding poorly to antidepressant drugs 72 may underlie the
phenomena described here (previous successful response
to antidepressant drugs). This issue is currently neglected,
but it is worthy of research attention.[...]
We know that discontinuation of antidepressant drugs
may trigger hypomania or mania 81,82 despite adequate con-
comitant mood-stabilizing treatment. 83 Furthermore, mood shifts to euthymia or hypomania are not rare events in patients withdrawn from medication because of a lack of efficacy. 84Mood elevation may also occur with anti-
depressant dose decrease,85
and patients who failed to re-
spond to mood stabilizers in combination with antide-
pressant drugs may improve on discontinuation of the
antidepressant drugs. 86These data suggest a relationship between antidepressant drug discontinuation and cycle acceleration in bipolar disorder. 83
In unipolar depression,withdrawal phenomena may be associated with recur-
rence acceleration.[...]
The opposi-
tional model of tolerance, 87 however, seems to entail sev-
eral important implications. According to this model, con-
tinued drug treatment may recruit processes that oppose
the initial acute effects of a drug or of receptor alterations.This model may explain the onset of tolerance in some
patients. Use of antidepressant drugs may also propel the
illness to a more malignant and treatment-unresponsive
course, as was suggested in bipolar disorder.
When drug treatment ends, oppositional processes may
operate for some time, resulting in appearance of with-
drawal symptoms and increased vulnerability to relapse.As Baldessarini 20 remarks, the assumption that such
physiologic processes will readjust after a withdrawal
phase is not supported by current awareness in the field of
drug dependence. Several months may be necessary (or
the processes may even have an irreversible connotation),
as has been found with, for instance, the sex-specific re-
sidual effects of cannabis on visuospatial memory. 88[...]
Activation of hormonal markers of stress response fol-
lowing discontinuation of SSRI has been described
103 and thus may lead to increased vulnerability to relapse in sus-
ceptible individuals.[...]
Researchers thus should demonstrate that the com-
bination of psychotherapy and pharmacotherapy is infe-
rior in terms of relapse prevention to psychotherapy
alone.
In a controlled trial study, [114] patients with recurrent
depression were allocated to 3 groups: short-term and
maintenance (2 years) treatment with antidepressant
drugs, CBT in the short-term and maintenance phases,
and antidepressant use in the short-term phase and CBT
for maintenance. Cognitive therapy displayed a similar
prophylactic effect to maintenance medication. The long-
term outcome of the group receiving both short-term
and maintenance treatment with cognitive therapy was
slightly better than that of the group who received phar-
macotherapy followed by psychotherapy. 114Furthermore, an additive effect of combination therapy has been shown
only with the more complex depressive disorders.
115 How-ever, all results may be affected by the presence of pa-
tients who were previously treated with antidepressant
drugs.[...]
It is conceivable that, once drug treatment has
been discontinued, despite substantial clinical improve-
ment in anxiety symptoms during active treatment, pa-
tients treated with antidepressant drugs may suffer from
episodes of major depression more than patients treated
with placebo or benzodiazepines.[...]
Antidepressant drugs were developed for and found to
be effective in the treatment of major depressive epi-
sodes.6 In recent years, their use has been extended to
maintenance and prevention. 31 However, treatments that
are effective in the acute phase of illness are not necessar-
ily the most suitable for postacute and residual phases or
maintenance. 3 Different antidepressant drugs may yield a differential rate of tolerance in the long term, with par-ticular reference to the HPA axis.98[...]
Are withdrawal phenomena simply bothersome and
self-limiting reactions, or are they a manifestation of
an increased vulnerability to relapse once drug treatment
has been discontinued? There is evidence that certain
SSRIs are more likely to induce withdrawal reactions than
others. 78,79According to the oppositional tolerance model,
this would mean that they also facilitate (or fail to protect
from) relapse once they are discontinued. This effect
could explain the high rate of relapse on switching from
an SSRI to placebo, which may be different from one drug
to another and be demonstrated by follow-up studies.[...]
Yet, at present, the opposi-
tional tolerance model applied to antidepressant drugs
may provide room for a number of clinical phenomena
that would otherwise lack explanation. We should be
aware that we are stretching the original indications (ma-
jor depressive episodes) of drugs of modest efficacy
135 to include prevention of relapse, anxiety disorders, and de-
moralization. Antidepressant drugs may speed improve-
ment and change the boundary between responders and
nonresponders.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. 136 Commonly shared clinical assump-
tions (the longer the antidepressant drug treatment, the
better; the higher the dosage, the better) are challenged by
research evidence. It is time to switch gears in depression
research and start tackling the basic issues concerned with
long-term treatment of depression.End quote.
Have you experienced tardive dysphoria/worsening of depression because of antidepressants, as described above?
- doxogenic
Posted by SLS on October 22, 2013, at 16:18:04
In reply to Re: Do antidepressants worsen your depression?, posted by doxogenic boy on October 22, 2013, at 12:55:10
Generally speaking, I see no reason to dispute the existence of these adverse effects. My only caveat is that untreated depressive disorders tend to get worse over time naturally. I only skimmed your post, so I didn't see any methodologies that take this into consideration.
More study. More open minds.
Thanks for posting this.
Some antidepressants exacerbate my depression to the point of producing suicidality. Tachyphylaxis is very dramatic with me. I experience a robust antidepressant effect for about 3 days before relapsing.
- Scott
Posted by doxogenic boy on October 22, 2013, at 16:53:13
In reply to Re: Do antidepressants worsen your depression? » doxogenic boy, posted by SLS on October 22, 2013, at 16:18:04
> Generally speaking, I see no reason to dispute the existence of these adverse effects. My only caveat is that untreated depressive disorders tend to get worse over time naturally.
Thank you very much for your reply. I agree with that, so maybe it could be made a study comparing treatment-resistant depression in a developing country (where most people can't afford antidepressants) with western countries to see where TRD is most frequent. I think there should have been much more research into the problem of tardive dysphoria and tachyphylaxis.
> Thanks for posting this.
>
> Some antidepressants exacerbate my depression to the point of producing suicidality.This happened to me on Nardil. I had intense and repeating suicidal thoughts, and I went to a mountain to look for a place to jump from. I went to the edge of a drop, so I could have fallen in death by accident. I don't understand how I dared it, since I have fear of heights.
I also woke up once every hour in the night because I had to urinate.
>Tachyphylaxis is very dramatic with me. I experience a robust antidepressant effect for about 3 days before relapsing.
I experienced something like that the first time i took tianeptine. Then I probably took 25 - 50 mg, and I think it was monotherapy.
- doxogenic
Posted by Phillipa on October 22, 2013, at 18:57:12
In reply to Re: Do antidepressants worsen your depression? » SLS, posted by doxogenic boy on October 22, 2013, at 16:53:13
Given to me for anxiety disorder when thyroid went and felt worse ever since. My brain is now addicted or whatever to luvox. I was fine with just a benzo. Taken for over 43 years now and never raised the dose. I should have said no to the doc back 15 or so years ago. But the SSRI' and SNRI's were the rage so to speak then. More reason to ditch them. Phillipa
Posted by Bob on October 22, 2013, at 21:33:25
In reply to Re: Do antidepressants worsen your depression? » doxogenic boy, posted by SLS on October 22, 2013, at 16:18:04
> Generally speaking, I see no reason to dispute the existence of these adverse effects. My only caveat is that untreated depressive disorders tend to get worse over time naturally. I only skimmed your post, so I didn't see any methodologies that take this into consideration.
>
> More study. More open minds.
>
> Thanks for posting this.
>
> Some antidepressants exacerbate my depression to the point of producing suicidality. Tachyphylaxis is very dramatic with me. I experience a robust antidepressant effect for about 3 days before relapsing.
>
>
> - Scott
I have tried many treatments where there is an antidepressant effect literally for about a day or only hours. This has gotten much more common and more severe in recent years. My response to psychiatric drugs is very different than when I first tried them about 20 years ago.Bob
Posted by Bob on October 22, 2013, at 21:35:41
In reply to Do antidepressants worsen your depression?, posted by doxogenic boy on October 22, 2013, at 12:46:02
> Hi.
>
> In this thread I would like to hear from those of you who have experienced that long-term use of antidepressants has worsened your depression and/or made you treatment-resistant. Did you feel better before you started with antidepressants?
>
> I am satisfied with my meds, but it seems that there are a lot who dont get better.
>
> There is some research that indicates that antidepressants worsen depression for some antidepressant users.
>
> http://www.ncbi.nlm.nih.gov/pubmed/20728491
> Excerpt from abstract above:
>
> Prog Neuropsychopharmacol Biol Psychiatry. 2011 Aug 15;35(7):1593-602.
> Epub 2010 Aug 20.
> The mechanisms of tolerance in antidepressant action.
> Fava GA, Offidani E.
> There is increasing awareness that, in some cases, long-term use of antidepressant drugs (AD) may enhance the biochemical vulnerability to depression and worsen its long-term outcome and symptomatic expression, decreasing both the likelihood of subsequent response to pharmacological treatment and the duration of symptom-free periods.
> Quote end.
>
> Do you feel antidepressants have had this effect on you? How did they change your condition, and how long had you used antidepressants when your depression worsened?
>
> - doxogenic
>
>
Like most theories along these lines of thinking, I don't see a viable alternative for ameliorating the symptoms of someone who is experiencing a severe mental health issue. What are the alternatives to antidepressants?Bob
Posted by doxogenic boy on October 23, 2013, at 5:56:36
In reply to Re: Do antidepressants worsen your depression?, posted by Phillipa on October 22, 2013, at 18:57:12
> Given to me for anxiety disorder when thyroid went and felt worse ever since. My brain is now addicted or whatever to luvox.
Did Luvox worsen your anxiety and make you more depressed? What kind of long-term side effects do you have from it?
>I was fine with just a benzo. Taken for over 43 years now and never raised the dose.
That is impressive. Good for you that it still works.
>I should have said no to the doc back 15 or so years ago. But the SSRI' and SNRI's were the rage so to speak then. More reason to ditch them.
Here is an article from O.B. Fasmer, a professor in psychiatri that I have met as a patient once:
http://tidsskriftet.no/article/2978165/en_GB
Excerpt from article:A discontinuation of antidepressant drugs should be considered in patients who have used such drugs over a long period. The patients should be informed in detail about the development of tolerance and withdrawal reactions. Symptoms that occur after discontinuation are rarely an effect of recidivation. The effect of such drugs after more than six months use are not scientifically documented (27). In patients who have used the drugs over a long period, the dosage should be gradually reduced. There is some documentation showing that mood-stabilising antiepileptic drugs may have an effect on withdrawal reactions, as a monotherapy and in combination with antidepressants during discontinuation (26).
End quote.- doxogenic
Posted by doxogenic boy on October 23, 2013, at 6:22:48
In reply to Re: Do antidepressants worsen your depression? » doxogenic boy, posted by Bob on October 22, 2013, at 21:35:41
> Like most theories along these lines of thinking, I don't see a viable alternative for ameliorating the symptoms of someone who is experiencing a severe mental health issue. What are the alternatives to antidepressants?
I agree with that, but it is important with more research into predicting who becomes better from antidepressants, and who doesn't. Maybe there is a genetic predisposition, that explain the reason why antidepressants worsen the depression in some individuals. When they know this, they may try cognitive behavioral therapy instead.
http://www.madnessradio.net/files/tardivedysphoriadarticle.pdf
Quote from article:It is proposed that tardive dysphoria (TDp) is an abnormal dys-phoric state that develops in some predisposed individuals with prolonged antidepressant treatment. Patients with this syndrome may comprise a significant fraction of TRD subjects.
[...]
The incidence or predisposing risk factors are as yet unknown, but younger age at onset of antidepressant exposure and genetic
underexpression of the serotonin transporter, such as with the short form of the serotonin transporter, may increase the risk of
TDp. End quote.It also is important for the patient to know of both short-term and long-term side effects, to be able to make an informed decision.
- doxogenic
Posted by SLS on October 23, 2013, at 6:47:49
In reply to Re: Do antidepressants worsen your depression? » SLS, posted by Bob on October 22, 2013, at 21:33:25
> > Generally speaking, I see no reason to dispute the existence of these adverse effects. My only caveat is that untreated depressive disorders tend to get worse over time naturally. I only skimmed your post, so I didn't see any methodologies that take this into consideration.
> >
> > More study. More open minds.
> >
> > Thanks for posting this.
> >
> > Some antidepressants exacerbate my depression to the point of producing suicidality. Tachyphylaxis is very dramatic with me. I experience a robust antidepressant effect for about 3 days before relapsing.
> >
> >
> > - Scott> I have tried many treatments where there is an antidepressant effect literally for about a day or only hours.
Me, too! Literally hours! It is a terrible disappointment when relapse occurs. Have you ever seen the movie "Awakenings"?
> This has gotten much more common and more severe in recent years. My response to psychiatric drugs is very different than when I first tried them about 20 years ago.
>
> BobI have no doubt that exposure to antidepressants leaves the brain changed in some way. That "poop-out" occurs at all is evidence of this. Perhaps one change involves the downregulation of serotonin autoreceptors. This could explain the development of a hypersensitivity and intolerance to a SSRI drug after it is discontinued for an extended period of time. If a case history demonstrates extremely chronic or recurrent depression, it is a good idea to consider indefinite treatment to prevent treatment resistance.
- Scott
Posted by poser938 on October 23, 2013, at 21:31:35
In reply to Do antidepressants worsen your depression?, posted by doxogenic boy on October 22, 2013, at 12:46:02
Psychiatric meds have definitely "enhanced my biochemical vulnerability to depression and worsened its long-term outcome and symptomatic expression, decreasing both the likelihood of subsequent response to pharmacological treatment and the duration of symptom-free periods."
It is unofficially referred to as Tardive Dysphoria. Simialr to how an antibiotic will help in the beginning p, but then your bodies defense mdchanisms are weakened, and then you become much more vulnerable to untreatable infections. Luckily drug companies, Psychiatry and their medications can avoid blaming the most severe effects of their mediications on the condition it is meant to treat.
You can explore all over Pubmed and read about the many effects psychiatric meds have that can make the brain less capable of functioning normally. Some peoples brains may recover after they stop filling their brain with chemicals like Prozac. And some dont.
Posted by Phillipa on October 23, 2013, at 23:13:59
In reply to Re: Do antidepressants worsen your depression?, posted by poser938 on October 23, 2013, at 21:31:35
From what you wrote I compare it to now how we have MSRA and flesh eating bacteria which antibiotics used to not only treat but cure. I've heard so many people now in real life with infection such as bronchitis that are not treatment resistant. Pays to not take antibiotics unless absolutely necessary. Phillipa
Posted by Phillipa on October 23, 2013, at 23:17:07
In reply to Re: Do antidepressants worsen your depression? » poser938, posted by Phillipa on October 23, 2013, at 23:13:59
Meant resistant bronchitis to antibiotic, ear infections, etc
Posted by doxogenic boy on October 24, 2013, at 9:48:11
In reply to Re: Do antidepressants worsen your depression? » Bob, posted by SLS on October 23, 2013, at 6:47:49
> I have no doubt that exposure to antidepressants leaves the brain changed in some way. That "poop-out" occurs at all is evidence of this. Perhaps one change involves the downregulation of serotonin autoreceptors.
I have some more quotes from the two articles I mentioned earlier in this thread. (I left some of the contents of the articles out, so it shouldn't be too much to read in one message.) Now I also have quoted the references from part of the articles.Do you have any comments to the quotes below? I will greatly appreciate any response.
lnteractions Between Different Types of Serotonin Receptors
There is increasing awareness of the complex mutual inhibitory effects of different serotonin receptors, particu-larly 5-HT1 and 5-HT2 receptors.89 Berendsen90 has sug-gested that an important function of antidepressants is
to restore a disturbed balance between 5-HT1A, 5-HT1B, and 5-HT2 receptors. It is, therefore, conceivable that a therapeutic action of antidepressant drugs (e.g., down-regulation of postsynaptic 5-HT2 receptors) may, under certain conditions, trigger changes in postreceptor signal transduction, in intraneuronal signaling pathways, or in neuronal architecture that are likely to affect the balance of serotonin receptors. There is preclinical evidence of the
autoregulation of serotonin and its potential effect on neurogenesis. 91,92 Jacobs et al.93 have recently proposed an impairment in neurogenesis as the key pathophysiologic event in depression.Interactions Between Different Neurotransmitters
In the same vein, there is increasing awareness of the complex mutual inhibitory effects of different neurotrans-mitter systems that may be affected in depression. 89 Anti-depressant drugs may yield changes in connections or sensitivity to neurotransmitters indirectly related to the
specific actions.Interactions Between Neurotransmitter Balance and the Hypothalamic-Pituitary-Adrenal Axis
Neurophysiologists have used the term sensitization, as opposed to habituation, to refer to the long-lasting in-crement in response occurring on repeated presentation of a stimulus that reliably elicits a response at its initial pre-sentation. 94 Psychostimulants such as amphetamine and cocaine have been found to induce sensitization. Anti-depressant therapy, however, may also induce time-dependent sensitization.95
There is extensive evidence that the hypothalamic-pituitary-adrenal (HPA) axis, through an action on corticotropin-releasing factor neurons, 96
can modulate both sensitization and tolerance. 97
Of particular interest is the relationship between serotonin receptors and HPA axis. 98 By facilitating 5-HT1 receptormediated neurotransmission, 5-HT2 postsynaptic down-regulation, a pu-tative final common pathway of the actions of different antidepressants, 89 may induce an activation of the HPA axis. This activation, in turn, may unfavorably affect sero-tonin receptor functioning.
99 An example of this interac-tion is provided by the use of specific 5-HT2 receptor an-tagonists (ritanserin and ketanserin) in Cushings disease, which often yields only a temporary decrease in adreno-corticotropic hormone (ACTH) and cortisol secretion, followed by an escape phenomenon. 100An impressive body of evidence 101,102 supports the concept of an antidepressant mechanism of action that exerts its effects beyond the cell membrane receptors of biogenic amines and leads to enhanced glucocorticoid receptor function and expression. Thus, the phenomena observed with long-term use of serotonin receptor antago-nists in Cushings disease have considerable relevance, particularly considering the fact that long-term treatment with inhibitors of steroid production is unlikely to yield the same phenomenon. 98 It has thus been postulated 98 that long-term treatment with antidepressant drugs in nonendocrine depression, after an initial phase of normal-ization of the HPA axis, may recruit its ACTH-dependent activation, which results in loss of clinical effect. The poor prognosis of remitted patients who still display abnormalities of the HPA axis is in line with this hypothesis. 98
Activation of hormonal markers of stress response fol-lowing discontinuation of SSRI has been described 103 and thus may lead to increased vulnerability to relapse in sus-ceptible individuals.
Cross-Sensitization With Behavioral and Cognitive Phenomena
Activation of the HPA axis may be permissive for re-peated psychostimulant sensitization. 96 Indeed, the acute and sensitizing effects of amphetamine are diminished by adrenalectomy. There is considerable evidence of cross-
sensitization between psychoactive drugs and environ-mental stressors,104 and such cross-sensitization may be HPA mediated.Post 105 postulated that both sensitization to stressors and episode sensitization may occur in mood disorders and became encoded at the level of gene expression. In particular, 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 transmitters, receptors, and neuropep-tides that alter responsiveness in a long-lasting way. 105Segal et al. 106 extended these possibilities to negative pat-terns of information processing, and Benazzi 107 extended them to residual symptomatology. In this context, antide- pressant drugs may display a protective effect. We cannot
exclude, however, thatthrough an action mediated by the HPA axisthey may also potentiate both sensitization
of stressors and episode sensitization
89. Leonard BE. Serotonin receptors and their function in sleep, anxiety
disorders, and depression. Psychother Psychosom 1996;65:667590. Berendsen HG. Interactions between 5-hydroxytryptamine receptor
subtypes. Pharmacol Ther 1995;66:173991. Baker MW, Croll RP. Modulation of in vivo neuronal sprouting by
serotonin in the adult CNS of the snail. Cell Mol Neurobiol 1996;16:
56157692. Diefenbach TJ, Sloley BD, Goldberg JI. Neurite branch development of
an identified serotonergic neuron from embryonic Helisomer: evidence
for autoregulation by serotonin. Dev Biology 1995;167:28229393. Jacobs BC, Van Praag H, Gage PH. Adult brain neurogenesis and psy-
chiatry: a novel theory of depression. Mol Psychiatry 2000;5:26226494. Groves PM, Thompson RF. Habituation: a dual-process theory. Psychol
Rev 1970;77:41945095. Antelman SM, Gershon S. Clinical application of time-dependent
sensitization to antidepressant therapy. Prog Neuropsychopharmacol
Biol Psychiatry 1998;22:657896. Koob GF, Cador M. Psychomotor stimulant sensitization: the
corticotropin-releasing factor-steroid connection. Behav Pharmacol
1993;4:35135497. Ritzmann RF, Colbern DL, Zimmermann EG, et al. Neurohypophyseal
hormones in tolerance and physical dependence. Pharmacol Ther
1984;23:28131298. Sonino N, Fava GA. CNS drugs in Cushings disease: pathophysio-
logical and therapeutic implications for mood disorders. Progr
Neuropsychopharmacol Biol Psychiatry 2002;26:1011101899. Van Praag HM. Faulty cortisol/serotonin interplay. Psychiatry Res
1996;65:143157100. Sonino N, Fava GA, Fallo F, et al. Effect of the serotonin antagonists
ritanserin and ketanserin in Cushings disease. Pituitary 2000;3:5559101. Holsboer F, Barden N. Antidepressants and the hypothalamic-pituitary-
adrenocortical regulation. End Rev 1996;17:187205102. Pariante C, Miller AH. Glucocorticoid receptors in major depression.
Biol Psychiatry 2001;49:391404103. Michelson D, Amsterdam J, Apter J, et al. Hormonal markers of stress
response following interruption of selective serotonin reuptake inhibitor
treatment. Psychoneuroendocrinology 2000;25:169177104. Stewart J, Badiani A. Tolerance and sensitization to the behavioral
effects of drugs. Behav Pharmacol 1993;4:289312105. Post RM. Transduction of psychosocial stress into the neurobiology
of recurrent affective disorder. Am J Psychiatry 1992;149:9991010106. Segal ZV, Williams JM, Teasdale JD, et al. A cognitive science
perspective on kindling and episode sensitization in recurrent affective
disorder. Psychol Med 1996;26:371380107. Benazzi F. Prevalence and clinical correlates of residual depressive
symptoms in bipolar II disorder. Psychother Psychosom 2001;70:
232238-----------------------------------------------
http://www.madnessradio.net/files/tardivedysphoriadarticle.pdf
(TDp = tardive dysphoria)Serotonin transporter polymorphism
A genetic polymorphism has been identified in which the pro-moter region of the serotonin transporter gene has a 44 base inser-tion or deletion[68,69]. The deletion variation is generally labeled the short form or s form of the serotonin transporter and is asso-ciated with roughly a 50% reduction in the number of serotonin transporter units in the membrane [70]. Subjects with this variant are at a greater risk of experiencing a major depressive illness inthe setting of adversity[7173]. Additionally, when these individ-uals are treated with an SRI antidepressant, they are either less likely to respond or have delayed response [7477].
It is not known how this increased risk for depression comes
about, but neuroplastic changes may play a role. It is known that
modification of serotonergic neurotransmission alters arborization
of the dendritic tree of serotonergic neurons [78,79]. Mice that lack
the serotonin transporter have fewer serotonergic neurons and re-
duced serotoninergic function and express more behaviors associ-
ated with anxiety and depression [80]. This phenotype can be
mimicked by treatment of normal mice with the SRI fluoxetine in
early life. New born mouse pups given fluoxetine for only 1 week
express anxiety symptoms as adults [81].The reduction in the number of synaptic serotonin transporters
associated with the short form of the serotonin transporter is very
similar to the chronic 6085% blockade of these transporters that
occurs with SRI treatment [82,83]. This suggests that the s allele
might serve as a model for chronic exposure to an SRI antidepres-
sant,particularlywhenadministeredtoyoungindividuals.Inyoung
animals, reducing or eliminating serotonin transporter function
causes changes in serotoninergic architecture and function and
associated increased depressive and anxious behaviors [81,84].Similar experiments have not been performed in adult animals
whose brains are less plastic and have already completed develop-
ment. Nonetheless, it would seem likely that chronic treatment
with an SRI in adults might result in neuroplastic changes in the
serotonin system similar to those seen in the animal experiments.
These changes may underlie the observation that tryptophan
depletion experiments are much more likely to induce depression,
or induce a more severe depression, if the subjects have been tak-
ing serotonin reuptake inhibiting drugs [85]. In this case the con-
traction of the serotoninergic system removes the reserve, so
that depletion is much more likely to cause depression.In humans, chronic exposure to antidepressants might induce
neuroplastic changes in the serotonin system similar to those that
occur in early development of subjects possessing the short form.
This effect might be more pronounced if the antidepressant expo-
sure occurred when the brain was more plastic (e.g., younger age),
or if the individual already has reduced serotonin transporter func-
tion due to a genetic variant such as the short for of the serotonin
transporter. These groups might be considered particularly high
risk for the development of TDp.[68] Heils A, Teufel A, Petri S, et al. Functional promoter and polyadenylation site mapping of the human serotonin (5-HT) transporter gene. J Neural Transm
1995;102:24754.[69] Heils A, Teufel A, Petri S, et al. Allelic variation of human serotonin transporter gene expression. J Neurochem 1996;66:26214.
[70] Lesch KP, Bengel D, Heils A, et al. Association of anxiety-related traits with a polymorphism in the serotonin transporter gene regulatory region. Science
1996;274:152731.[71] Caspi A, Sugden K, Moffitt TE, et al. Influence of life stress on depression: moderation by a polymorphism in the 5-HTT gene. Science 2003;301:3869.
[72] Wilhelm K, Mitchell PB, Niven H, et al. Life events, first depression onset and the serotonin transporter gene. Br J Psychiatry 2006;188:2105.
[73] Jacobs N, Kenis G, Peeters F, Deron C, Vlietinck R, van Os J. Stress-related negative affectivity and genetically altered serotonin transporter function: evidence of synergism in shaping risk of depression. Arch Gen Psychiatry 2006;63:98996.
[74] Murphy GM, Hollander SB, Rodrigues HE, Kremer C, Schatzberg AF. Effects of
the serotonin transporter gene promoter polymorphism on mirtrazapine and
paroxetine efficacy and adverse events in geriatric major depression. Arch Gen
Psychiatry 2004;61:11639.[75] Durham LK, Webb SM, Milos PM, Clary CM, Seymour AB. The serotonin
transporter polymorphism, 5HTTLPR, is associated with a faster response time
to sertraline in an elderly population with major depressive disorder.
Psychopharmacology (Berlin) 2004;174(4):5259.[76] Yu YW, Tsai SJ, Chen TJ, Lin CH, Hong CJ. Association study of the serotonin transporter promoter polymorphism and symptomatology and antidepressant response in major depressive disorders. Mol Psychiatry 2002;7:11159.
[77] Pollock BG, Ferrell RE, Mulsant BH, et al. Allelic variation in the serotonin transporter promoter affects onset of paroxetine treatment response in late-life depression. Neuropsychopharmacology 2000;23:58790.
[78] El-Mallakh RS, Peters C, Waltrip C. Antidepressant treatment and neural
plasticity. J Child Adoles Psychopharmacol 2000;10:28794.[79] Baker MW, Croll RP. Modulation of in vivo neuronal sprouting by serotonin in adult CNS of the snail. Cell Mol Neurobiol 1996;16:56176.
[80] Lira A, Zhou M, Castanon N, et al. Altered depression-related behaviors and
functional changes in the dorsal raphe nucleus of serotonin transporter-
deficient mice. Biol Psychiatry 2003;54(10):96071.[81] Ansorge MS, Zhou M, Lira A, Hen R, Gingrich JA. Early-life blockade of the 5-HT transporter alters emotional behavior in adult mice. Science
2004;306:87981.[82] Voineskos AN, Wilson AA, Boovariwala A, et al. Serotonin transporter
occupancy of high-dose selective serotonin reuptake inhibitors during major
depressive disorder measured with [11C]DASB positron emission tomography.
Psychopharmacology (Berlin) 2007;193(4):53945.[83] Meyer JH, Wilson AA, Sagrati S, et al. Serotonin transporter occupancy of five selective serotonin reuptake inhibitors at different doses: an [11C]DASB
positron emission tomography study. Am J Psychiatry 2004;161(5):82635.[84] Gaspar P, Cases O, Maroteaux L. The developmental role of serotonin: news
from mouse molecular genetics. Nat Rev Neurosci 2003;4(12):100212.[85] Ruhé HG, Mason NS, Schene AH. Mood is indirectly related to serotonin,
norepinephrine and dopamine levels in humans: a meta-analysis of
monoamine depletion studies. Mol Psychiatry 2007;12(4):33159
-------------Does this seem reasonable to you?
- doxogenic
Posted by doxogenic boy on October 24, 2013, at 9:57:43
In reply to Re: Do antidepressants worsen your depression?, posted by poser938 on October 23, 2013, at 21:31:35
> Psychiatric meds have definitely "enhanced my biochemical vulnerability to depression and worsened its long-term outcome and symptomatic expression, decreasing both the likelihood of subsequent response to pharmacological treatment and the duration of symptom-free periods."
Thank you for your response. Have you used antidepressants for a long time? What kind of long-term side effects have they had to you?
- doxogenic
Posted by poser938 on October 24, 2013, at 19:27:09
In reply to Re: Do antidepressants worsen your depression? » poser938, posted by doxogenic boy on October 24, 2013, at 9:57:43
I took Mirapex off-label to help with persisting numbing of my emotions 2 years after I took Effexor. Took the Mirapex daily for about 6 weeks. It was slightly beneficial for the 6 weeks began the last day of taking it, my ability to feel pleasure was drastically reduced. Along with that came extreme apathy and feeling extremely depressed. I stopped taking Mirapex and ordered Tianeptine, which I took occasionally in the past with benefit to my mood with a single dose. But this time taking it, there was no benefit to my mood with a single dose. I took it chronically this time with my mood becoming even worse after 10 days. Then on to Ritalin that my pdoc prescribed. I took one dose and felt a slight benefit but my mood became worse and worse as time sent by with it in my system.
After all this, it was as if each unnatural increase in dopamine stimulation just worked to put my brains own dopamine functioning out of business. Since its natural for your brain to try to keep homeostasis in response to turbocharging the neurotransmitter systems with psychiatric meds. Of course this is described much more technically in articles on Pubmed.
But, I think my brain is sensitive meds because I had Viral Encephalitis when I was 12 in 2001 that resulted in a 5 day coma. After I woke up from it every muscle in my body was extremely weak and I just laid there drooling on myself. But over the weeks I fully recovered. But then, going through my teens I experienced mild depression, but was a fully functional person. Started taking psychiatric meds when I was 17 only to basically have my brain assaulted by them, and my emotions haven't been the same since
My slightly educated hypothesis is that when a med alters my brains neuroplasticity, it sees no reason to go back to normal once I stop the med. I don't know bow common this is in others.
Posted by doxogenic boy on October 25, 2013, at 2:46:04
In reply to Re: Do antidepressants worsen your depression?, posted by poser938 on October 24, 2013, at 19:27:09
> But, I think my brain is sensitive meds because I had Viral Encephalitis when I was 12 in 2001 that resulted in a 5 day coma. After I woke up from it every muscle in my body was extremely weak and I just laid there drooling on myself. But over the weeks I fully recovered. But then, going through my teens I experienced mild depression, but was a fully functional person. Started taking psychiatric meds when I was 17 only to basically have my brain assaulted by them, and my emotions haven't been the same since
---
Thank you for telling your story. Are you medication-free now, and do you have any hope for the future that your brain will heal itself in the absence of drugs?- doxogenic
Posted by SLS on October 25, 2013, at 7:43:15
In reply to Re: Do antidepressants worsen your depression?, posted by poser938 on October 24, 2013, at 19:27:09
> My slightly educated hypothesis is that when a med alters my brains neuroplasticity, it sees no reason to go back to normal once I stop the med. I don't know bow common this is in others.My hypotheses is no more educated than yours. I like what you wrote here. It might not be an exact model of the neurophysiology involved in the evolution of these phenomena, but your proposed concepts make sense.
- Scott
Posted by Bob on October 31, 2013, at 21:12:26
In reply to Re: Do antidepressants worsen your depression? » Bob, posted by SLS on October 23, 2013, at 6:47:49
> > > Generally speaking, I see no reason to dispute the existence of these adverse effects. My only caveat is that untreated depressive disorders tend to get worse over time naturally. I only skimmed your post, so I didn't see any methodologies that take this into consideration.
> > >
> > > More study. More open minds.
> > >
> > > Thanks for posting this.
> > >
> > > Some antidepressants exacerbate my depression to the point of producing suicidality. Tachyphylaxis is very dramatic with me. I experience a robust antidepressant effect for about 3 days before relapsing.
> > >
> > >
> > > - Scott
>
> > I have tried many treatments where there is an antidepressant effect literally for about a day or only hours.
>
> Me, too! Literally hours! It is a terrible disappointment when relapse occurs. Have you ever seen the movie "Awakenings"?
>
> > This has gotten much more common and more severe in recent years. My response to psychiatric drugs is very different than when I first tried them about 20 years ago.
> >
> > Bob
>
> I have no doubt that exposure to antidepressants leaves the brain changed in some way. That "poop-out" occurs at all is evidence of this. Perhaps one change involves the downregulation of serotonin autoreceptors. This could explain the development of a hypersensitivity and intolerance to a SSRI drug after it is discontinued for an extended period of time. If a case history demonstrates extremely chronic or recurrent depression, it is a good idea to consider indefinite treatment to prevent treatment resistance.
>
>
> - Scott
I have heard of the movie Awakenings with Robert DeNiro I believe. I saw it quite a long time ago, but the clinical observations shown in the movie have indeed reminded me of some of the effects I've experienced with my mental illness and the treatments I've tried. I imagine many people struggling with these issues have had the same type of thoughts as you and I have.Bob
Posted by Dr. Bob on November 2, 2013, at 0:09:20
In reply to Re: Do antidepressants worsen your depression? » SLS, posted by Bob on October 31, 2013, at 21:12:26
> I have heard of the movie Awakenings with Robert DeNiro I believe.
I'd just like to plug the double double quotes feature at this site:
http://www.dr-bob.org/babble/faq.html#amazon
The first time anyone refers to a book, a movie, or music without using this option, I post this to try to make sure he or she is at least aware of it.
Bob
Posted by babbler20 on November 2, 2013, at 18:50:34
In reply to Do antidepressants worsen your depression?, posted by doxogenic boy on October 22, 2013, at 12:46:02
This is depressing news
This is the end of the thread.
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