Do SSRI:s increase the level of BDNF in the brain?
John123
If I recall correctly I've heard that SSRI:s are supposed to indirectly
increase the Brain Derived Nerve growth Factor (BDNF) in the brain, which in
turn is responsible for the well being of neurons. This is apparently the
new theoretical explanation of why Anti Depressants (AD:s) work. Now my
question is if current AD:s already increase BDNF, is there any reason to
develop new drugs targetting BDNF directly. What will be the benefit of
that? Why should these new drugs be any more efficient than the current
AD:s?
Ken W.
"John123" <a@b.c> wrote:
> If I recall correctly I've heard that SSRI:s are supposed to indirectly
> increase the Brain Derived Nerve growth Factor (BDNF) in the brain, which in
> turn is responsible for the well being of neurons. This is apparently the
> new theoretical explanation of why Anti Depressants (AD:s) work.
It is a theory with some support. For instance, it takes about eight weeks for
a new neuron to mature to functionality and that coincides with the time most
antidepressants take to work. Maybe the drugs rewire the brain (that's my hope)
> Now my
> question is if current AD:s already increase BDNF, is there any reason to
> develop new drugs targetting BDNF directly. What will be the benefit of
> that? Why should these new drugs be any more efficient than the current
> AD:s?
The goal would be that targetting BDNF would have fewer side effects, but
it is just a theory at this time. Celexa and other antidepressants may
indirectly
cause this effect. By the way, Celexa is well tested and was used in Sweden
for years before the FDA approved it.
John123
> > increase the Brain Derived Nerve growth Factor (BDNF) in the brain,
which in
> > turn is responsible for the well being of neurons. This is apparently
the
> > new theoretical explanation of why Anti Depressants (AD:s) work.
>
> It is a theory with some support. For instance, it takes about eight
weeks for
> a new neuron to mature to functionality and that coincides with the time
most
> antidepressants take to work. Maybe the drugs rewire the brain (that's my
hope)
If it takes 8 weeks for a neuron to mature to functionality, maybe we should
give an SSRI medication more than 2 months before we decide it isn't
working? I mean, if the theory holds, after 2 months the new neurons will
just have *started* to appear. Maybe it takes another 2 months or more
before enough new neurons are created to have an effect?
> > Now my
> > question is if current AD:s already increase BDNF, is there any reason
to
> > develop new drugs targetting BDNF directly. What will be the benefit of
> > that? Why should these new drugs be any more efficient than the current
> > AD:s?
>
> The goal would be that targetting BDNF would have fewer side effects, but
> it is just a theory at this time. Celexa and other antidepressants may
> indirectly
> cause this effect. By the way, Celexa is well tested and was used in
Sweden
> for years before the FDA approved it.
>
Still I keep hearing some people claiming SSRI:s can cause permanent brain
damage? Is this true? In that case, what are those damages more
specifically?
.
> Still I keep hearing some people claiming SSRI:s can cause permanent brain
> damage? Is this true? In that case, what are those damages more
> specifically?
People claim that SSRIs have caused some "subtle" brain damage. I've
seen no real evidence of such damage. Perhaps emotional damage, but
definitely not cognitive damage.
--
Regards,
.
.
> every day there is more evidence of SSRI's causing severe movement disorders.
Reference?
--
Regards,
.
John123
Could you be a bit more precises as to what you mean by "emotional damage"?
Do you mean that some people become permanent emotional zombies, that lose
the ability to experience any desire or feelings whatsoever? I'd call that
more than *subtle* brain damage!
Joe D.
underpinnings of depression. There is no doubt that current
antidepressants work fairly well for about 70% of patients, however
the neurotransmitter-oriented theory about their method of
action is probably wrong. There are several factors supporting this:
- the neurotransmitter changes (e.g. increased serotonin) take place
almost immediately, yet it takes at least 4 weeks for depression to lift.
- modulating any individual neurotransmitter (serotonin, norepinephrine,
dopamine) can help depression, sometimes in the same
individual. This kind of depression is obviously not caused by a
deficit of (for example) serotonin, since modulating the others lessen
symptoms as well.
- The antidepressant Stablon (tianeptine), made in France, *decreases*
serotonin level, yet is as effective as Paxil.
Since current ADs work fairly well (although causing side effects),
they probably trigger a biochemical cascade, the final result of
which is some biological change that reduces depression. Hence in theory
it should be possible to design new drugs that skip the neurotransmitter
stage entirely (along with the associated side affects) and target
the final biological pathway common to all successful antidepressant
techniques.
There is increasing evidence that BDNF may be the "final common path"
that underlies how not only traditional antidepressants work, but also
how ECT and physical exercise can lessen depression (which also
increase BDNF).
Although the BDNF theory is very logical, has increasing support,
and explains lots of things that earlier theories don't, it's not the
only new theory.
Here is some more info. The first article below is especially good.
http://www.findarticles.com/cf_dls/m1175/2_32/53985475/p1/article.jhtml
http://news.bbc.co.uk/hi/english/health/newsid_1072000/1072301.stm
Here's more evidence of the biological basis for depression. Very
recently the DEP1 gene underlying certain types of depression has
been isolated. I don't know the relationship of this to BDNF. However
BDNF is related to gene transcription of cyclic AMP, so it's possible
they're related:
Depression gene DEP1:
http://biz.yahoo.com/prnews/030204/latu026_1.html
Promising as the BDNF theory looks, there are also other new
theories:
- Neurokinin hypothesis: concentrates on a totally new class of "peptide"
neurotransmitters known as "neurokinins (also sometimes called tachykinins).
This includes the often hyped Substance P neuropeptide. There are
substance P-based ADs being researched right now.
- The cortisol theory of depression (CRF). One of the more advanced
theories for the biological basis of depression. This theory basically
states that some genetically susceptible individuals who
are severely, chronically stressed, produce excess levels of stress hormones
such as the corticosteroid cortisol. Corticosteroids are well implicated in the
development of mood disorders. Over time, excess cortisol levels "burns out"
certain regions of the brain resulting in major depression. There are drugs in
development called "CRF-Antagonists" which will directly combat this particular
problem, hopefully resulting in new ways to fight depression.
The good news is great progress is being made in finding the
biological basis for depression. New biological pathways are being
isolated, and rational drug design can target these. It's very likely
that in time new ADs will exist that avoid many of the side affects
of current drugs.
The bad news is this will likely take a while. Drug approval
moves very slowly. Prozac was developed in 1972 yet wasn't
FDA approved until 1988. Hopefully the new ADs will take
less time.
Ironically might be possible to "tweak" current ADs to fix
side affects. The biological cause of most side affects is well known:
stimulating certain neuronal receptors unrelated to the antidepressant
efficacy. For example Mirtazepine (Remeron) has very few SSRI-like
side affects because it blocks the 5HT2A serotonin receptor that
causes these. Unfortunately Remeron causes weight gain and
sedation, however the cause of this is also known -- it activates
the H1 (histamine) receptor. In theory an enhanced version of
Remeron that avoided H1 stimulation would be very good. It's
possible this development path might result in better ADs before
the newer, more exotic drugs are ready.
The above notwithstanding, many types of depression may
actually be caused by other physical problems. For example
hormonal disorders (hypothyroidism, hypogonadism,
growth hormone deficiency, etc.) can cause depression-like
symptoms. Before taking any AD, I'd suggest any patient
have a complete hormone test panel. Drs often don't understand
how common this relationship is, so you might need to insist.
And although the above focuses on biological causes of depression,
it's important to accept and use any psychiatric "talk therapy"
or lifestyle modification that helps you. Although many
types of depression have clear and provable biological causes,
the psychological patterns thus engendered often require
psychiatric help to heal, even after the biological basis is
corrected.
-- Joe D.
Joe D.
>
> Still I keep hearing some people claiming SSRI:s can cause permanent brain
> damage? Is this true? In that case, what are those damages more
> specifically?
>
scientists don't know exactly how antidepressants work, it seems
unlikely anybody could rationally explain the specific alleged
biological damage.
In general the side affects from newer antidepressants seem to
stop whenever the drug is discontinued. There may be anecdotal
cases where this doesn't happen, but I haven't seen any
controlled studies.
There's a problem with assessing "subtle" emotional side affects
after discontinuing SSRIs. You don't take SSRIs unless you have
a problem. That problem usually fluctuates and exhibits varying
symptoms over time. Hence it's obviously possible a person who
feels emotionally abnormal after discontinuing an SSRI is just
experiencing yet another phase of his previously existing
problem.
To properly evaluate this, you'd need to give SSRIs to perfectly
healthy people, note the side affects, then track them after
discontinuing the med. You'd also need a placebo control
group.
That said, the vast majority of people experiencing side affects
on SSRIs see this entirely abate after discontinuing the
medication. However to properly evaluate this would require
a controlled study.
Although not classified as antidepressants, it's certain that prolonged use
esp at higher dosages of some anti-psychotics (Haldol, etc) can
cause apparently permanent side affects such as Tardive
Dyskenesia (twitching). Newer anti-psychotic drugs such as
Zyprexa seem to cause this less often.
-- Joe D.
jim
"Joe D." <j...@nospam.invalid> wrote in message
news:sFUqa.264$K6.2...@news.uswest.net...
Thanks for this summary. It was informative and is very much appreciated.
Jim
John123
That was a really excellt post that very well summed up some of the most
interesting current research. You have a talent for describing things in a
way that's easy to understand. As for the point you made regarding hormones
being an underdiagnosed cause of depression, I can certainly agree. If you
for example take a look in the "alt.support.impotence" newsgroup, you'll
find alot of guys with hormonal imbalances such as low Testosterone, high
Estradiol, high Prolactin and so on. Amazingly the symptoms they descibe
very closely resembles those of depressed people. Typically they experience
a low energy level, cognative impairment, low mood, low libido, erectile
dysfunction and general apathy.
What's also interesting is that when they start treating their hormonal
imbalance, they experience a relief from their symptoms that is much more on
the target than what anti-depressants usually accomplish for people with
"normal" depression. Typical comments are "finally I feel just the way I did
before I started having these problems" or "now I feel perfectly normal
again, all my symptoms are gone". In contrast, typical comments from
depressed people being treated with AD:s are "now I'm starting to feel
better again" or "atleast I don't experience the deepest lows anymore". I
know there are some people who have much better success with AD:s too, but
very rarely do you hear people on AD:s descring that they feel "completely
normal". I guess this is just a sign of that current AD:s aren't hitting
right on the target. They appear to be a much more blunt tool generating a
cascade of events, some of which are bad and some good, but not exactly on
the spot. In contrast, if your depression is due to a lack a certain
hormone, and start treating this by supplying that hormone externally, you
hit right on the target and hence you can feel truely normal again.
Now the question is whether new drugs acting on BDNF, CRF, Subastance P and
so on may be more precise tools. Even if BDNF may be the final common
pathway for depression as some theories say it is, there may be a multitude
of reasons causing the low BDNF in the brain. As I see it, the only way to
restore things to a perfect non-disease state is to treat the excact root of
the problem. If there are a vast number of existing roots, you'd have to
taylor make AD:s that each will suit only a small number of people. This is
ofcourse not doable. Do you think this reasoning is correct, or do you think
low BDNF itself *is* to root of the problem?
Finally, do you know if there are any ongoing FDA trials for drugs
targetting BDNF, CRF, Substance P and so on? If so, what has been the
outcome of these trials so far?
Once again, thanks for your excellent reply.
Best regards,
John
.
> Could you be a bit more precises as to what you mean by "emotional damage"?
>
>
I'm still on meds, but it's definitely still present. It beats being
depressed hands down though.
--
Regards,
.
Joe D.
>
> Now the question is whether new drugs acting on BDNF, CRF, Subastance P and
> so on may be more precise tools. Even if BDNF may be the final common
> pathway for depression as some theories say it is, there may be a multitude
> of reasons causing the low BDNF in the brain. As I see it, the only way to
> restore things to a perfect non-disease state is to treat the excact root of
> the problem. If there are a vast number of existing roots, you'd have to
> taylor make AD:s that each will suit only a small number of people. This is
> ofcourse not doable. Do you think this reasoning is correct, or do you think
> low BDNF itself *is* to root of the problem?
I don't think scientists yet know whether BDNF is the root cause
of depression. It may be depression is actually a syndrome, with
many discrete biological causes. We already know hormonal problems
can cause depression, and sometimes these patients are not helped
by ADs yet they are helped by correcting the hormonal imbalance.
Likewise even if BDNF is the underlying biological cause of (say)
50% of depressions, the other 50% might have different causes.
Of course the hope is BDNF is the cause of a high %, and fixing
that will fix most depressions. There's some evidence that
all ADs, including electro-convulsive therapy, and exercise,
all increase BDNF.
Re why BDNF might be low, there are likely several possible reasons.
However it's not necessary to understand the underlying cause
to treat the imbalance and gain relief. Asperin's method of action
wasn't understood until recently, yet for a hundred years it provided relief
for millions of people. Hopefully in due time the underlying biological cause
of depression will also be known, but as new effective ADs become
available they can immediately help people.
>
> Finally, do you know if there are any ongoing FDA trials for drugs
> targetting BDNF, CRF, Substance P and so on? If so, what has been the
> outcome of these trials so far?
>
Merck has tested a substance P-based AD called MK-869:
http://www.psychiatrictimes.com/p981101b.html
Unfortunately one trial indicated it wasn't significantly
more effective than a placebo. However that same trial
also indicated an SSRI was no better than placebo. Since
hundreds of controlled studies have indicated otherwise, it's possible
the trial was flawed in some way. I think they're now re-running more
trials.
There are early CRF receptor antagonist drugs that look
promising in animal studies.
BDNF is more complex since it's the final product of a several-stage
biochemical chain. In theory you could intervene at any point
and modulate BDNF. Some animal studies indicate directly
infusing BDNF-increasing drugs into the brain can lessen
depressive behavior.
I'm not familiar with the status of human trials for drugs
targeting BDNF, but in general it's being actively researched.
-- Joe D.
NecroVizier
The *smartest* scientists couldn't locate their freakin' bunghole and a dick
without a handbook.
Our *smartest* scientists suck.
"Joe D." <j...@nospam.invalid> wrote in message
news:a8Vqa.265$K6.2...@news.uswest.net...
Joe D.
> The *smartest* scientists can't even land a freakin' dinky on Mars properly.
> The *smartest* scientists couldn't locate their freakin' bunghole and a dick
> without a handbook.
> Our *smartest* scientists suck.
Those scientists are why you can post this from your personal
computer to the internet.
jake
wrote:
really?
I thought it was paying for your connection?
they are for hire ..
Drugs inquiry thrown into doubt over members' links with manufacturers
http://www.guardian.co.uk/uk_news/story/0,3604,915715,00.html
Drugs inquiry links to makers
Sarah Boseley, health editor
Monday March 17, 2003
The Guardian
The credibility of a government inquiry intended to settle the
controversy surrounding widely prescribed anti-depressant drugs was
thrown into question yesterday by revelations that most of the members
have shareholdings or other links to the manufacturers.
The "intensive review" of the side effects of Seroxat, Prozac and
other antidepressants of the SSRI (selective serotonin reuptake
inhibitor) class was announced in the House of Commons by health
minister Hazel Blears in December last year. It was a response to
mounting concern from large numbers of patients who say they have been
unable to come off Seroxat because of severe withdrawal symptoms.
It is also looking at allegations that the SSRIs have caused a small
number of people who were previously not in a severely depressed state
to kill themselves. Last week a coroner in Wales called for Seroxat to
be withdrawn pending an investigation after returning an open verdict
on a retired headteacher who killed himself shortly after starting the
drug.
But campaigners and patients say they are deeply unhappy with the
membership of the review team, drawn from the committee on the safety
of medicines, which is part of the Department of Health's medicines
control agency, and with one of the expert witnesses.
Two of the four CSM scientists, Michael Donaghy, a reader in clinical
neurology from Oxford University, and David Nutt, professor of
psychopharmacology at Bristol University, hold shares in
GlaxoSmithKline, manufacturers of Seroxat. They have to leave the room
when Seroxat is discussed, although they stay for debate on the SSRI
drugs as a class.
Prof Nutt and the invited expert, David Baldwin, senior lecturer in
psychiatry at Southampton University, jointly fronted the promotional
press launch of Seroxat after it won a licence to be prescribed for
social anxiety disorder and was popularly dubbed the "shyness pill".
Charles Medawar, of the watchdog organisation Social Audit, is seeking
a reference to the ombudsman over the composition of the review.
He is also unhappy with the choice of chairman. Angus Mackay, director
of mental health services in Lomond and Argyle, Scotland, was one of
the signatories to an influential paper produced by the CSM in 1996
which concluded that withdrawal symptoms from SSRIs are rare,
"relatively mild and do not have features of a physical drug
dependency syndrome".
Mr Medawar said the review must be impartial and seen to be impartial.
The Seroxat users group, which has 4,000 members who have experienced
problems with the drug personally or through relatives, is equally
concerned. "We're not at all happy," said Sarah Venn of the group.
Their Cardiff-based lawyer, Mark Harvey, said he was concerned that
two of the review members had shareholdings in GSK. "The review could
go two ways," he said. "If it says the drug is beneficial, the share
price goes up and you make a profit. If it says the drug is dreadful,
the price goes down and you make a loss. I do not see any way at all
that you can be expected to give an impartial judgment. This is
absolutely unacceptable."
Mr Harvey was also unhappy that the review has not undertaken to
consider the first-hand evidence of patients on the side effects they
say they have suffered - only the reports from their doctors will be
considered - although it has invited representatives of the Seroxat
users group to a meeting.
The medicines control agency and the committee on the safety of
medicines have always maintained that it is sufficient for members to
declare their interests in drug companies before meetings and to leave
the room if they have personal interests such as shareholdings.
At the meeting of the review group on November 21, Prof Nutt and Dr
Donaghy declared personal interests in GSK and left the room for two
items on the agenda that dealt with Seroxat, although they remained
for discussions on the SSRIs as a class of drug.
Dr Baldwin declared a personal interest in Lundbeck, manufacturers of
the drug Citalopram. According to the minutes, however, he did not
declare his connections with five other companies, including Seroxat
manufacturers SmithKline Beecham, which is now GlaxoSmithKline.
Questioned by the Guardian, he said that although it was hard to
remember the detail, he did declare participating in advisory boards
for SmithKline Beecham, Bristol-Myers Squibb, Eli Lilly, Organon, and
Pharmacia. His department had also been funded for studies by the same
five companies and he had been paid by them for speaking at symposia
to other doctors about the drugs. "I mentioned all this at the
meeting," he said.
A spokesman for the MCA said the minutes would not have omitted
anything. "The minutes containing the declared interests would contain
everything, including studies declared," he said.
The MCA insists, however, that the system for preventing conflicts of
interests works well. "All members of committees and associated
working groups are professionals of the highest standing in their
fields and there has never been any evidence that members have acted
other than with the highest integrity," it said.
--
Regimes planted by bayonets do not take root
Ronald Reagan
NecroVizier
Takin' em a long time to use gravity.
Useless.
"Joe D." <j...@nospam.invalid> wrote in message
news:HHIra.109$gD3.1...@news.uswest.net...
NecroVizier
I'd rather choose teleportation rather than usenet anyday.
"Joe D." <j...@nospam.invalid> wrote in message
news:HHIra.109$gD3.1...@news.uswest.net...
Joe D.
> The entire Serotonin thing can
> end up being just one more of the world's hoaxes and if so, could
> take a decade or two to get rid of.
The fact ADs have helped millions of people (about 70% of those
who try them) will never be found a hoax. There have been
literally hundreds of placebo-controlled, double-blind tests
that corroborate this. However there's no question they cause
unpleasant side affects for many, which for a few can be
extremely bad. In a few cases (like Serzone) side affects are
found that in a very few people are severe. But it's no hoax that ADs
work for lots of people.
>
> There is something like that right now.
>
> And it is not called drugs or pills or chemical inbalance or
> anything else that infers that a drug must be used to fix.
> whatever it is.
>
> That something else is called therapy. Often the CBT type of
> therapy. Which is to get rid of negative thoughts, replace with
> positive thoughts.
There's no question talk therapies have helped many, and CBT
is effective. However it's not the "evil" medical industry
"forcing" drugs on people and denying them psychotherapy.
Rather the insurance industry (in the US) in many cases does not cover
psychotherapy, but they do cover antidepressant drugs more
frequently. This isn't your family doctor's fault -- it's the insurance
industry's and by extension the political system's fault -- put the
blame there. You can hardly blame individuals for accepting generic Prozac
for free or a reduced cost, when their option is paying $150 per hour out of
their own pocket to see a psychotherapist.
> However the article here by emphasizing this as a"biological
> pathway", tends to elevate the status of drugs to make it appear
> that the solution will be a drug. When the solution could be a
> drug, or it could be a non drug such as therapy. Especially if
> the old connection , or pathway etc might have become less than
> desired because of "thoughts" in the first place..
The Psychology Today article of course focused on biological
pathways -- that was the article theme. Plenty (in fact most)
articles in that magazine focus on non-biological mental health issues.
Just because they write *one* article an in attempt to bring people
up to date on current research doesn't mean the emphasis is
misplaced or inappropriate.
>
> Kick it, shake it up, rattle it etc until or if something useful
> happens (some of the time); That is also a " common path" with
> the druggings.
A better analogy is the skilled TV repair technician who could
very frequently fix things by shaking the TV. Nobody knew how
he did it (in fact he himself didn't understand), but he fixed it
70% of the time this way -- he had the golden touch.
Likewise new research is showing that ADs don't really work
on the neurotransmitter level, but they perturb, or disrupt a
multi-stage sequence of neural pathways that ultimately
results in symptom relief.
Of course a more subtle approach would be preferred, and
that's what researchers are working on.
>
> All sounds just too high and mighty. In the simplest terms
> there are a number of ways to keep the stress under control which
> have nothing to do with drugs. And the more the doctors try to
> pretend that drugs are essential even for something like stress,
> the more chance people will end up getting drugged when they
> shouldn't be.
If you want high and mighty, simply look at those who for
decades told men with sexual dysfunction it was "all in their
head". Oops -- turns out 90% of problems are biological.
Or those who for decades told mothers their autistic children
were made so by "poor mothering". Psychiatrists said it wasn't a
biological problem, it was a psychiatric behavioral problem
imposed by the mother. Oops -- turns out it's a clear biological
problem that now shows up on MRI scans.
Or those who for decades told mothers their schizophrenic
children were made so by (yet again) "poor mothering".
Psychiatrists even coined a special term for this alleged
misdeed -- schizophrenogenic mothers. Oops -- turns out
it's largely a biological problem. The sad thing is decades ago
simple inheritance and identical twin studies showed this. But people
were so fixated on blaming behavior, or mothering, or
"character", they were misled from accepting the evidence.
The damage from such preconceived biases has been incalculable.
If you've ever seen a mother who years ago was so accused,
the blame, tears, and falsely-imposed guilt was tremendously
damaging, and often leaves scars even today.
These are just a few examples of the damage that has occurred
by being biased away from biology. The lesson is simply accept
what the facts show -- try not to have a preconceived bias
for either biology or behavior. The fact is we (and our problems)
are a mixture of both.
That said, the recent momentum has been on the biology
side. This isn't a conspiracy -- it's largely a product of bona fide
technical advances in understanding biological neuroscience. Two decades ago
they didn't have MRI scanners, nor was the human genome decoded.
It's only logical that some of these advances will result in a better
understanding of what biological basis (if any) underlies each
individual mental health disorder.
>
> As if the emphasis is somehow or other on the word biological
> rather than on true causes of cures etc. Everything has to be
> "biological basis" or it gets pooh poohed.
That's not exactly correct -- it is very well understood that stress
is often the catalyst for mental health disorders. Drs frequently
emphasize this, plus the mental health (and other) benefits of
regular exercise. I heard one bioscience researcher so convinced
of this and so frustrated at his patients not exercising, he was
tempted to give them sugar pills with a label saying "must exercise
30 min after each pill".
>
> But anything better that what there is now could be something to
> welcome. Provided the improvements,should there be some,do not
> lead to drugging even more people than might be warranted. That
> is one of the problems with the current SSRIs. Supposed to be so
> much better than the old ones, that doctors just end up giving it
> to almost anyone that might have almost anything.
>
It's true that ADs are in some cases given too freely. Yet the
big picture is mental health disorders are significantly undertreated,
not overtreated. While some people take ADs who don't need them,
vastly more people need either psychotherapy or ADs and aren't
getting either one. Whether it's psychotherapy, meditation,
nutrition or antidepressants, they need one or all of these, whatever
is most effective for them.
Joe D.
> On Fri, 2 May 2003 21:08:08 -0700, "Joe D." <j...@nospam.invalid>
> wrote:
>
>
> You have made lots of good points. Will need to cogitate on some
> of them.
>
> It is not too hard to believe that things are biological, or at
> least partly biological. Whatever theory gets answers to the
> problems of emotional disorders, and beyond, can be of value.
>
I forgot to mention the hormone angle. People often
overlook this when investigating depression, yet there's
overwhelming evidence that certain depression and anxiety
"disorders" are actually biological hormone imbalances.
Thyroid, testosterone, estradiol, prolactin, cortisol -- any
of these can cause depression and anxiety if out of balance,
esp in certain individuals that sensitive to it.
If you have depression induced by a hormone problem,
you can do talk therapy until doomsday, and you'll never get
well.
This is *definitely* an area where Drs frequently push antidepressants
too soon, without proper testing. It's ironic since there are
simple, quick, relatively inexpensive blood tests for hormone
problems. Unfortunately you often have to fight Drs to get this done.
In addition to hormone tests, the patient should have a complete
evaluation of his/her nutrition, exercise, life stress, and sleep hygiene.
I agree too often ADs are prescribed as a band-aid to fix problems
that are induced by these areas. For some people, poor nutrition
combined with too much caffeine, alcohol, and stress,
and too little sleep and exercise will produce anxiety or clinical
depression. It doesn't happen to everybody, so there's probably
a genetic propensity to depression when under these stressors.
But regardless of this, it doesn't make sense to immediately prescribe
an antidepressant without at least evaluating these items first.
Unfortunately this is another area the current medical system often doesn't
prioritize properly.
-- Joe D.