![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 25 of 29. This is the beginning of the thread.
Posted by reb on November 13, 2002, at 23:30:56
hello all,
i recently heard (from a pharmacist of all people!) that researchers have found that the long-term effects of prozac use was DENDRITE SHRINKAGE... and that it was only intended for short-term use. (scary, huh?)
so, i was wondering if anyone else has heard this or if there is any truth to this. if so, i also wanted to know if the same could be true with effexor- which is what i take- (or other SSRI's)--???
kind of hard to justify taking something for depression- that could cause permanent brain damage in the future, leading to more depression... hhhmmmmm......i'm trying to be optimisitc & trusting of the pharmaceutical industry, but it's kinda hard when the public has been made into guinea pigs and LIED TO so many times before....
i just want the TRUTH so i can make an informed decision.
any info is appreciated. THANKS!
Posted by bluedog on November 14, 2002, at 5:46:30
In reply to prozac/effexor=dendrite shrinkage?, posted by reb on November 13, 2002, at 23:30:56
First of all DO NOT become overly focused on the medication side of your treatment and beat yourself up with the possible long term effects of the medications. This is a VERY easy trap to fall into!!!!
I doubt that there is not a person on this board who has not had concerns about the possible long term side effects of the medications that they are taking.
I am currently taking generic Prozac but.... not so long ago I made a decision when I was in a particularly depressed state of mind to stop taking my medications (If you do decide to decrease or stop your medications DO NOT do this without medical supervision as you will need to taper down gradually) . At the time I wrote the following to a close friend of mine
"I am now frightened of the anti-depressants because they seem to f*#k with your body and your mind to such a degree. I keep finding information on the net that lists certain side effects of ssri's such as permanent negative changes in brain chemistry, and other permanent side effects like cell death at various sites of the body especially in the brain, liver and kidneys and severe negative interference with the body and brain's natural chemical processes(they say that all of the foregoing points are the reason that ssri's have side effects). A lot of these internet sites have there own agenda's (or sales pitches) just like the drug companies. It gets to the point that you don't really know what to believe and you have ongoing propaganda battles between the drug companies and third parties both citing this or that (seriosly flawed) study to support their arguments. It seems impossible to get accurate and unbiased information on the true long term side effects of the ssri's. My personal opinion is that nobody really knows the true side effects of the ssri's that perhaps it is better to be safe than sorry and to stop taking them. (in other words.... "where there is smoke there is fire") What do you think of the above situation and do you have any information or sites on the net where I can get truly unbiased information? I don't want to find out in several years that taking ssri's interfered with some natural antioxidant process in my body or brain allowing cancer cells to get a foothold or leading to accelerated mental decline etc etc etc (I'm sure you get the picture!"
My friend who has worked as a psychiatric nurse and who has also recovered from depression in her life gave me the best advice I could ever have received. She very simply wrote back back and advised me that I was over-focused on the medication side of my treatment. I would personally advise the following:1. Yes, the ssri's have not been around so long and the long term side effects are not not really known and there is little or no long information available about the long term side effects, HOWEVER
2. At this very time in your life you have to question whether your life is better with or without the medication. If you function better with the medication to allow you to work better on all aspects of your recovery so that you can eventually cease the drugs then I would not worry about some imagined catastrophe about the possible side effects of the drugs. Worrying about the medication is not going to help you.
3. The side effects of depression are far more immediate and devastating to your life than the possible long term side effects of medications with loss of self esteem, possible loss of job, problems of self medication by drug and alcohol abuse, and possible loss of life through suicide. I found out very quickly that at the stage of my illness I was at that I was not ready to stop my medication and I am still not ready but I keep making some slow progress.
4. Be aware that neither the drug companies nor the third parties who are vehemently anti-medication or anti-psychiatry are ever truly unbiased and often have their own sales pitches and agendas. For example the following website http://www.prozactruth.com/index.html appears very factual and scientific as an anti ssri site until you realise that the entire web site is actually set up as one big sales pitch for their product "immunocal". I found it difficult to find any references in the entire site to any published and peer reviewed studies to support their views. Again any studies they do cite are not really on point and possibly taken out of the context of the original purpose of the study.
In other words the studies they cite are twisted around to fit their sales pitch.5. Whether you take the medications or not is a very personal decision but take the decision with a balanced consideration of the alternatives.
Good luck
Posted by djmmm on November 14, 2002, at 7:38:39
In reply to prozac/effexor=dendrite shrinkage?, posted by reb on November 13, 2002, at 23:30:56
I believe this is probably the study your pharmacist was referring to.
Brain Res 2000 Mar 6;858(1):92-105
Comparative study of fluoxetine, sibutramine, sertraline and dexfenfluramine on the morphology of serotonergic nerve terminals using serotonin immunohistochemistry.Kalia M, O'Callaghan JP, Miller DB, Kramer M.
Department of Biochemistry, Molecular Pharmacology and Anesthesiology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19107, USA. mkalia@msn.com
We compared the effects of treatment with high doses of fluoxetine, sibutramine, sertraline, and dexfenfluramine for 4 days on brain serotonergic nerve terminals in rats. Methylenedioxymethamphetamine (MDMA) and 5,7-dihydroxytryptamine (5,7-DHT) were used as positive controls because both compounds deplete brain serotonin. Food intake and body weight changes were also monitored and yoked, pair-fed animals were used to control for possible changes in morphology due to nutritional deficits. Fluoxetine, sibutramine, sertraline and dexfenfluramine all produced a significant reduction in body weight. Fluoxetine, sibutramine and sertraline treatment resulted in no depletion of brain serotonin but produced morphological abnormalities in the serotonergic immunoreactive nerve network. In contrast, dexfenfluramine and MDMA depleted brain serotonin and produced morphological changes in the serotonin nerve network. These results indicate that even though fluoxetine, sibutramine and sertraline do not deplete brain serotonin, they do produce morphological changes in several brain regions (as identified by serotonin immunohistochemistry). Dexfenfluramine and MDMA, on the other hand, markedly deplete brain serotonin and also produce morphological changes. Collectively, these results lend support to the concept that all compounds acting on brain serotonin systems, whether capable of producing serotonin depletion or not, could produce similar effects on the morphology of cerebral serotonin systems.
Studies that negate the results of the Kalia M, O'Callaghan JP, Miller DB, Kramer M study:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10963746&dopt=Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10357514&dopt=Abstract
Posted by oracle on November 14, 2002, at 11:48:17
In reply to Re: prozac/effexor=dendrite shrinkage?, posted by djmmm on November 14, 2002, at 7:38:39
> We compared the effects of treatment with high doses of fluoxetine, sibutramine, sertraline, and dexfenfluramine for 4 days on brain serotonergic nerve terminals in rats.
All this study says is the for RATS, HIGH doses
can cause CHANGES. No one has shown what the effect of the changes are, so all are reaching
if they use this study to prove damage. No one
has shown there is a one to one relationship between rats, humans, and doses.
Posted by djmmm on November 15, 2002, at 7:51:24
In reply to Re: prozac/effexor=dendrite shrinkage?, posted by oracle on November 14, 2002, at 11:48:17
well, it actually states..."Fluoxetine, sibutramine and sertraline treatment resulted in no depletion of brain serotonin BUT produced morphological abnormalities in the serotonergic immunoreactive nerve network. In contrast, dexfenfluramine and MDMA depleted brain serotonin and produced morphological changes in the serotonin nerve network. These results indicate that even though fluoxetine, sibutramine and sertraline do not deplete brain serotonin, they do produce morphological changes in several brain regions (as identified by serotonin immunohistochemistry)."
FWIW, almost 95% of the aminals used for medical study are rodents. We use rodents because their physiology and genetic make-up is similar to humans. It is believed that the genome of a rodent contains essentially the same complement of genes found in the human genome... If you choose to deny, or brush off results of a scientifc study, based on the fact that rodents are used, thats your choice. I think you will find that the original testing of the majority of medication you take, began on rodents.
Posted by Ritch on November 15, 2002, at 9:31:43
In reply to Re: prozac/effexor=dendrite shrinkage?, posted by djmmm on November 15, 2002, at 7:51:24
> well, it actually states..."Fluoxetine, sibutramine and sertraline treatment resulted in no depletion of brain serotonin BUT produced morphological abnormalities in the serotonergic immunoreactive nerve network. In contrast, dexfenfluramine and MDMA depleted brain serotonin and produced morphological changes in the serotonin nerve network. These results indicate that even though fluoxetine, sibutramine and sertraline do not deplete brain serotonin, they do produce morphological changes in several brain regions (as identified by serotonin immunohistochemistry)."
>
> FWIW, almost 95% of the aminals used for medical study are rodents. We use rodents because their physiology and genetic make-up is similar to humans. It is believed that the genome of a rodent contains essentially the same complement of genes found in the human genome... If you choose to deny, or brush off results of a scientifc study, based on the fact that rodents are used, thats your choice. I think you will find that the original testing of the majority of medication you take, began on rodents.
>
>
Hi, is this the smae thing as "dendritic 'pruning'"? I remember reading about this a couple of years ago. The speculation was that depressed and suicidal people have excessive serotonin receptors and an "overgrowth" of dendrites as a result. THe author's conclusion was that SSRI's raise the level of extracellular serotonin which reduces the density of serotonin receptors (down-regulation), and "prunes" the overgrown dendrites. Perhaps there is some overpruning going on? Would that be dose related?
Posted by reb on November 15, 2002, at 9:35:15
In reply to Re: prozac/effexor=dendrite shrinkage?, posted by djmmm on November 15, 2002, at 7:51:24
OK... so taking into account what everyone has said:
well, i can appreciate the idea of "would you rather suffer now or worry about the consequences later?" -because suffering now for many people certainly does include loss of work, social life, possibility of suicide, etc... but to deny the very real possibility that in the FUTURE, there may be some PERMANENT physical consequences that may affect you, bring the depression BACK, etc.... is also unwise.
i.e., what is the point of trying to find a way to cope with/cure/tolerate a severe depression now, if it causes it to get worse in the future, with or without the meds??? that just doesn't make sense to me, that the very thing you're doing to try to help yourself is only going to make it worse in the long run. and as for me, i have enough to worry about in the future (very little social security coming my way, where am i going to live & how am i going to survive??, etc...) without having to worry about the burden of depression being even greater & interfering with my life even more than it does now. ESPECIALLY if i am doing something TO MYSELF to cause damage, to the very thing i am trying to fix!! how ironic is that?!
so yes, even though we must deal with the present & find a way to get through each day-- the concern about the future is very real for many of us.
what i need to do is ask my pharmacist if he knows exactly where that study can be found. if it does exist, you can bet your last dollar every effort has been made to supress it from the public.
the study cited here seems vague to me, so perhaps he was talking about a different one. and as for the rodents, well... i guess researchers use them for a reason. if they are finding some new info about long-term damage using rodents, i definitely think the public needs to know.
so my next question is, if there IS damage cause by long-term use of prozac &/or other SSRI's, is it reversable? i.e., will the neurons eventually heal themselves, and if so, how?
this brings up the idea that sometimes the "cure", when used to long, will cause the afflicted area to atrophy, instead of being strong again. think of a cast left on too long, or staying in bed too long after an injury without recieving physical therapy. why should the brain be any different?
Posted by oracle on November 15, 2002, at 11:55:09
In reply to Re: prozac/effexor=dendrite shrinkage?, posted by djmmm on November 15, 2002, at 7:51:24
If you choose to deny, or brush off results of a scientifc study, based on the fact that rodents are used, thats your choice. I think you will find that the original testing of the majority of medication you take, began on rodents.
Most resonable people realize the where neurology
is conscrned, there is a BIG difference between humans and rats. Othe issues are comparable but
neurology is FAR FAR advanced in humans.
Posted by reb on November 15, 2002, at 12:00:21
In reply to Re: prozac/effexor=dendrite shrinkage?, posted by oracle on November 15, 2002, at 11:55:09
OK, but rats or no rats-- i think one can still be reasonable and wonder if there IS some truth to this issue.
Posted by IsoM on November 15, 2002, at 14:22:27
In reply to Re: prozac/effexor=dendrite shrinkage?, posted by reb on November 15, 2002, at 12:00:21
Reb, I'm not dismissing your concerns but would like to tell you a bit about my experiences that may put some of your fears to rest.
I've been taking anti-depressants for 17 years now. I first started with tricyclics like imipramine, went on to SSRIs when they came out as the side-effects from TCAs were bothersome. At three separate times, I decided to stop all ADs but the black void opened each time again so I'm now resigned to taking them for the rest of my life.
For these last 17 years, my immune system has never changed - I still don't get colds or infections. My arthritis (from injured joints) hasn't changed for the worse or better. My weight has remained roughly the same - no gain or loss. My physical health & fitness has remained excellent except for problems I've had for many years previously (migraines & joint pains).
As for my mental capacities, I'd say it's much better now. By treating my depression, it's enabled me to pursue interests that I may not have otherwise. When I went back to university, I still was able to receive top marks. My mind is sharp (I have difficulties with my everyday short-term memory but I always have - I'm very much the absent-minded sort - more an ADD attribute) & my zest & interest in life is still great.
You wrote: "this brings up the idea that sometimes the "cure", when used to long, will cause the afflicted area to atrophy, instead of being strong again. Think of a cast left on too long, or staying in bed too long after an injury without receiving physical therapy. Why should the brain be any different?"
That's a good thing to be aware of but there's way to counter that. Your brain can be "exercised" just like a muscle. Use it or lose it also applies to our mind.
Need ideas?
Brain Exercises: http://me.essortment.com/brainexercises_rcas.htm
Mental Agility Games: http://www.mentalagility.com/games.htm
There are books that are full of tips & exercises, but they're really not necessary. Anything that makes you use your mind is an exercise for your brain. Even odd things we wouldn't think about use our minds.1. Hold a good-sized mirror horizontal (parallel to the floor) & walk about your house using the mirror as your guide. It'll give you a new perspective on how you see your place.
2. Drive a different route to work or the store, or whatever. It doesn't need to be out of the way, just not your regular route. Yes, it uses your brain in a somewhat diff way, forging new links between neurons.
3. If you're not in a hurry, eat your meal with your non-dominant hand.
4. Sing, sing, sing - uses new areas of your brain, combining the language area with a part that's also used for math. Yes, many mathematicians have strong musical skills.
5. If you don't draw, spend a bit of time drawing every week. Nothing fancy, it makes your mind work at transferring a 3-D image into a 2_d form.
6. When you shower, if you normally start on your head & work down, do the opposite.All these small, supposedly silly tasks keep areas of your mind sharp & help improve other cognitive functioning too.
Posted by oracle on November 15, 2002, at 14:59:25
In reply to Re: prozac/effexor=dendrite shrinkage?, posted by reb on November 15, 2002, at 12:00:21
> OK, but rats or no rats-- i think one can still be reasonable and wonder if there IS some truth to this issue.
Well, we do know that depression, left untreated, is neurotoxic in humans. Not threating depression causes neurology to die.
I have been on AD's for 20 years and do not find
the meds cause long trem problems.
Posted by djmmm on November 15, 2002, at 16:04:51
In reply to Re: prozac/effexor=dendrite shrinkage?, posted by oracle on November 15, 2002, at 11:55:09
will all due respect, It is obvious with regards to neurology that humans are more advanced, but the use of rodents (and some primates) is THE only way we have to do such research. Most rodents used for neurological/psychological research are genetically produced to mimic various neurologic conditions (knock-out rodents)...
I understand you dont agree with the results of the study, I don't either, I just post the info...but if you dissagree because of the test subjects, then you have no scientific "leg" to stand on, because this is how it's done, and even if you were to find 50 refuting OR supporting studies, they would all be done on rodents or at best primates.
Posted by oracle on November 15, 2002, at 17:22:43
In reply to Re: prozac/effexor=dendrite shrinkage?, posted by djmmm on November 15, 2002, at 16:04:51
Come one here, please ! The neurology of humans
is orders of magnitudes greater than rats. Even primates are not as advanced.This is an issue that is well discussed amoung the experts in this field. Seek out the writings
of Dr Shungrin
Posted by Larry Hoover on November 15, 2002, at 18:19:17
In reply to Re: prozac/effexor=dendrite shrinkage?, posted by reb on November 15, 2002, at 9:35:15
> so my next question is, if there IS damage cause by long-term use of prozac &/or other SSRI's, is it reversable? i.e., will the neurons eventually heal themselves, and if so, how?
> this brings up the idea that sometimes the "cure", when used to long, will cause the afflicted area to atrophy, instead of being strong again. think of a cast left on too long, or staying in bed too long after an injury without recieving physical therapy. why should the brain be any different?There is evidence that fluoxetine and other SSRIs helps to restore the size and connectivity of the hippocampi. There's a lot of stuff we don't know about how brain cells create connections, or how they're disconnected. Maybe healing from depression means pruning away certain connections?
Up until about a decade ago, it was common knowledge that you were born with a certain number of brain cells, and it was downhill from there. We now know that new brain cells grow when the brain is stimulated, and that connections between brain cells are not fixed and permanent. There is a new concept called neuronal plasticity which accounts for the adaptability of the brain.
In my perhaps not always humble opinion, untreated depression is a bigger danger to the brain than attempting to alleviate the depression.
Posted by oracle on November 15, 2002, at 18:55:38
In reply to Re: prozac/effexor=dendrite shrinkage?rebb, posted by Larry Hoover on November 15, 2002, at 18:19:17
> In my perhaps not always humble opinion, untreated depression is a bigger danger to the brain than attempting to alleviate the depression.
That is the argument I have always made. Many are also quick to call changes "damage". Till we can describe the life cycle of a neuron, and understand all the changes that can happen and
what they mean (how they effect behavior)
it is a guess. Let alone what changes in non human neurons have to de with human neurons.
Posted by linkadge on November 16, 2002, at 10:05:48
In reply to Re: prozac/effexor=dendrite shrinkage?rebb, posted by oracle on November 15, 2002, at 18:55:38
If I remember correctly this study was
done with Fluxotine at doses 100 x the
standard human dose. When Lilly was questioned
they responded that this study concluded
nothing as the doses were far above the
average dose.Lets put things into perspective. Some people
are depressed and refuse to take antidepressants
because they believe they are evil or mind
controlling or something. The truth is
that untreated depression does FAR more dammage
to the brain than any of the current antidepressants do. Elevated cortisol from
stress destroys neural connections in the
seritogenic and dopamanergic areas of the brain,
not to mention the reduced hippocampal volume.Studies have shown many things such as. How
antidepresants improve the quality of people's
lives, how they reduce physical illness from
elevated stress, and how they can even extend
ones life. This study is far from conclusive
about anythingLinkadge
Posted by djmmm on November 16, 2002, at 14:13:44
In reply to Re: prozac/effexor=dendrite shrinkage?, posted by oracle on November 15, 2002, at 17:22:43
> Come one here, please ! The neurology of humans
> is orders of magnitudes greater than rats. Even primates are not as advanced.
>
> This is an issue that is well discussed amoung the experts in this field. Seek out the writings
> of Dr Shungrinhuh?...I'm not disputing that, obviously. I'm confused, you seem to be arguing a point, here, that I agree with...I realize that there are neurological differences between humans/rodents/non-human primates. My point was that you dismissed the results of a study on the sole fact that rodents were used as test subjects... if this is your position, then you are also ignoring the results of many years of positive research on just about every medication that exists. The reason why we use rodents is because they have proven countless times to be accurate test subjects.
Posted by Larry Hoover on November 16, 2002, at 14:40:26
In reply to Re: prozac/effexor=dendrite shrinkage? » djmmm, posted by Ritch on November 15, 2002, at 9:31:43
> Hi, is this the smae thing as "dendritic 'pruning'"? I remember reading about this a couple of years ago. The speculation was that depressed and suicidal people have excessive serotonin receptors and an "overgrowth" of dendrites as a result. THe author's conclusion was that SSRI's raise the level of extracellular serotonin which reduces the density of serotonin receptors (down-regulation), and "prunes" the overgrown dendrites. Perhaps there is some overpruning going on? Would that be dose related?
>Here's an article showing protective and healing effects of fluoxetine on hippocampal dendrites. The full-text has compelling micrographs.
Acta Pharmacol Sin 2001 Oct;22(10):865-70
Fluoxetine inhibits dendrite atrophy of hippocampal neurons by decreasing nitric oxide synthase expression in rat depression model.Luo L, Tan RX.
State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing 210093, China. rxtan@netra.nju.edu.cn
AIM: To study the effect of fluoxetine on dendrite atrophy of hippocampal neurons in rat depression model. METHODS: CMS (chronic mild stress), mimicking human depression, was used as the animal depression model. The neurons shape and numbers of nitric oxide synthase positive cells in the hippocampal subfields were measured by Nissl staining and histochemical staining of NADPH (nicotinamide adenine dinucleotide phosphate)-diaphorase respectively. RESULTS: CMS deforms neurons in the hippocampal formation, and fluoxetine can renormalize the deformed neurons by inhibiting the nitric oxide synthase catalyzing the over-production of NO, which lead subsequently to the morphological abnormality in the circumscribed area of brain. CONCLUSION: Fluoxetine, an antidepressant, renormalizes dendrite atrophy of hippocampal neurons by inhibiting nitric oxide synthase overexpression in rat chronic mild stress model.
Full-text at:
http://www.chinaphar.com/1671-4083/22/865.pdf
Posted by Ritch on November 16, 2002, at 17:23:45
In reply to Re: prozac/effexor=dendrite shrinkage?, posted by Larry Hoover on November 16, 2002, at 14:40:26
Posted by leslieg on November 16, 2002, at 19:41:44
In reply to The truth to this study, posted by linkadge on November 16, 2002, at 10:05:48
I feel much the way reb does; very worried about trading the future for the present. I didn't worry like this 10 years ago when I first took Zoloft, but after a bad half-year on Effexor and the withdrawal from it, I can't help but wonder if the Effexor did any permanent damage (I think it did). I am at a point that I *must* take ADs, whether I want to or not. My present is more important than my future because I've got an 18-month old child.
Maybe the "problem" is that in order to not notice any damage, one must stay on ADs. (Does that mean I'll never enjoy sex the way I used to? That isn't something I want to give up for the rest of my life!)
I'm sure my stress hormones were doing damage; but I tend to believe the body has ways of repairing damage done by itself -- the human race has lived with high-stress situations for a long time ... But I'm not so sure my body can fix problems introduced by ADs.
This leads to a major concern of mine (and why I had to get off the Effexor in the first place). What does the presence of these drugs do to an embryo? How can it be that the developing brain doesn't develop differently when constantly subjected to a chemical enviornment different from normal? How many children born to moms who were on ADs have gone through the brain changes of puberty? How can we *know* there isn't damage that shows up as the brain matures? It amazes me that I could have been arrested for taking ritalin when pregnant, yet plenty of pdocs (including mine) don't see a problem with keeping a moderatly depressed woman on ADs during pregnancy.
I think there are too many people who see SSRIs as harmless; this type of study took saccharine off the market for years and made people think twice about artificial sweeteners. More people do need to think twice about taking SSRIs.
> If I remember correctly this study was
> done with Fluxotine at doses 100 x the
> standard human dose. When Lilly was questioned
> they responded that this study concluded
> nothing as the doses were far above the
> average dose.
>
> Lets put things into perspective. Some people
> are depressed and refuse to take antidepressants
> because they believe they are evil or mind
> controlling or something. The truth is
> that untreated depression does FAR more dammage
> to the brain than any of the current antidepressants do. Elevated cortisol from
> stress destroys neural connections in the
> seritogenic and dopamanergic areas of the brain,
> not to mention the reduced hippocampal volume.
>
> Studies have shown many things such as. How
> antidepresants improve the quality of people's
> lives, how they reduce physical illness from
> elevated stress, and how they can even extend
> ones life. This study is far from conclusive
> about anything
>
> Linkadge
>
>
Posted by Larry Hoover on November 16, 2002, at 20:18:46
In reply to Re: The truth to this study, posted by leslieg on November 16, 2002, at 19:41:44
> This leads to a major concern of mine (and why I had to get off the Effexor in the first place). What does the presence of these drugs do to an embryo? How can it be that the developing brain doesn't develop differently when constantly subjected to a chemical enviornment different from normal?
These are very important questions you're asking, and you can be sure that others share your concern. There is a recent report that you might find interesting (published this month).
Am J Psychiatry 2002 Nov;159(11):1889-95
Child development following exposure to tricyclic antidepressants or fluoxetine throughout fetal life: a prospective, controlled study.Nulman I, Rovet J, Stewart DE, Wolpin J, Pace-Asciak P, Shuhaiber S, Koren G.
OBJECTIVE: Previous work suggested that first-trimester exposure to tricyclic antidepressants or fluoxetine does not affect adversely child IQ and language development. However, many women need antidepressants throughout pregnancy to avoid morbidity and suicide attempts. Little is known about the fetal safety of tricyclic antidepressants and fluoxetine when taken throughout pregnancy. The goal of this study was to assess the effects of tricyclic antidepressants and fluoxetine used throughout gestation on child IQ, language, and behavior. METHOD: In a prospective study, mother-child pairs exposed throughout gestation to tricyclic antidepressants (N=46) or fluoxetine (N=40) and an unexposed, not depressed comparison group (N=36) were blindly assessed. The three groups were compared in terms of the children's IQ, language, behavior, and temperament between ages 15 and 71 months. The authors adjusted for independent variables such as duration and severity of maternal depression, duration of pharmacological treatment, number of depression episodes after delivery, maternal IQ, socioeconomic status, cigarette smoking, and alcohol use. RESULTS: Neither tricyclic antidepressants nor fluoxetine adversely affected the child's global IQ, language development, or behavior. IQ was significantly and negatively associated with duration of depression, whereas language was negatively associated with number of depression episodes after delivery. CONCLUSIONS: Exposure to tricyclic antidepressants or fluoxetine throughout gestation does not appear to adversely affect cognition, language development, or the temperament of preschool and early-school children. In contrast, mothers' depression is associated with less cognitive and language achievement by their children. When needed, adequate antidepressant therapy should be instituted and maintained during pregnancy and postpartum.
>How many children born to moms who were on ADs have gone through the brain changes of puberty?We haven't gotten that far yet.
>How can we *know* there isn't damage that shows up as the brain matures? It amazes me that I could have been arrested for taking ritalin when pregnant, yet plenty of pdocs (including mine) don't see a problem with keeping a moderatly depressed woman on ADs during pregnancy.
They're paying attention to the outcome. The decision should be made on a case-by-case basis, according to the known risk arising from untreated depression during pregnancy.
Am J Psychiatry 2001 Oct;158(10):1728-30
Pregnancy outcome following gestational exposure to venlafaxine: a multicenter prospective controlled study.Einarson A, Fatoye B, Sarkar M, Lavigne SV, Brochu J, Chambers C, Mastroiacovo P, Addis A, Matsui D, Schuler L, Einarson TR, Koren G.
The Motherisk Program, The Hospital for Sick Children, University of Toronto, Ontario, Canada. einarson@sickkids.on.ca
OBJECTIVE: Because there are no studies available on the safety of venlafaxine during pregnancy, the authors' goal in this study was to determine whether venlafaxine increases the risk for major malformations. METHOD: Data on 150 women exposed to venlafaxine during pregnancy in seven pregnancy counseling centers were compared with data from studies of pregnant women who 1) received selective serotonin reuptake inhibitor antidepressants (SSRIs) (N=150) and 2) who received nonteratogenic drugs (N=150). RESULTS: Among the 150 women who were exposed to venlafaxine during pregnancy, 125 had live births, 18 had spontaneous abortions, and seven had therapeutic abortions; two of the babies had major malformations. There were no significant differences between these women and the two comparison groups on any of the measures analyzed. CONCLUSIONS: These results suggest that the use of venlafaxine during pregnancy does not increase the rates of major malformations above the baseline rate of 1%-3%.
> I think there are too many people who see SSRIs as harmless; this type of study took saccharine off the market for years and made people think twice about artificial sweeteners. More people do need to think twice about taking SSRIs.Serious medication should be reserved for serious medical problems.
Posted by Larry Hoover on November 16, 2002, at 20:38:15
In reply to Re: The truth to this study, posted by leslieg on November 16, 2002, at 19:41:44
Here's one more that might be important, if further monitoring of these infants occurs.
Pediatr Res 2002 Apr;51(4):443-53
Prolonged prenatal psychotropic medication exposure alters neonatal acute pain response.Oberlander TF, Eckstein Grunau R, Fitzgerald C, Ellwood AL, Misri S, Rurak D, Riggs KW.
Department of Pediatrics, University of British Columbia, Vancouver, BC, Canada. toberlander@cw.bc.ca
Selective serotonin reuptake inhibitors (SSRIs) and benzodiazepines are frequently used to treat maternal depression during pregnancy, however the effect of increased serotonin (5HT) and gamma-amino-butyric acid (GABA) agonists in the fetal human brain remains unknown. 5HT and GABA are active during fetal neurologic growth and play early roles in pain modulation, therefore, if prolonged prenatal exposure alters neurodevelopment this may become evident in altered neonatal pain responses. To examine biologic and behavioral effects of prenatal exposure, neonatal responses to acute pain (phenylketonuria heel lance) in infants with prolonged prenatal exposure were examined. Facial action (Neonatal Facial Coding System) and cardiac autonomic reactivity derived from the relationship between respiratory activity and short term variations of heart rate (HRV) were compared between 22 infants with SSRI exposure (SE) [fluoxetine (n = 7), paroxetine (n = 11), sertraline (n = 4)]; 16 infants exposed to SSRIs and clonazepam (SE+) [paroxetine (n = 14), fluoxetine (n = 2)]; and 23 nonexposed infants during baseline, lance, and recovery periods of a heel lance. Length of maternal SSRI use did not vary significantly between exposure groups-[mean (range)] SE:SE+ 183 (31-281):141 (54-282) d (p > 0.05). Infants exposed to SE and SE+ displayed significantly less facial activity to heel lance than control infants. Mean HR increased with lance, but was significantly lower in SE infants during recovery. Using measures of HRV and the transfer relationship between heart rate and respiration, SSRI infants had a greater return of parasympathetic cardiac modulation in the recovery period, whereas a sustained sympathetic response continued in the control group. Prolonged prenatal SSRI exposure appears to be associated with reduced behavioral pain responses and increased parasympathetic cardiac modulation in recovery following an acute neonatal noxious event. Possible 5HT-mediated pain inhibition, pharmacologic factors and the developmental course remain to be studied.
Posted by linkadge on November 17, 2002, at 7:36:29
In reply to Re: The truth to this study, posted by Larry Hoover on November 16, 2002, at 20:38:15
I know of many people that have sucessfuly used
antidepressant medication for 5 or so years
and then have discontinued without any problems.
As a general rule if you've used AD medication
for 5 years it may take another 5 to discontinue.I am a sucessful case. I have been using AD medication for over two years. I have discontinued, and am still on this site to
offer support. Has it dammaged my brain ?
Well if it has I shure don't know anything about
it. I've been on Sinequan, Effexor, Remeron, Celexa, Lorazepam, Kava, and St. John's wort.If you feel that it has dammaged your brain
I honestly believe that you probably havn't
fully recovered from your depression.I started taking Omega 3 over a year ago, and
a funny shift started taking place. I started
to feel better at the end of my AD's halflife
(right before I took another dose) I mean
really calm, and happy. I started to slowly taper
and the symptoms havn't returned. Withdrawl was
minimial.Will I go back on them if I need them. Yes.
Am I a better person now than before the whole ordeal- I do believe so.
Linkadge
Posted by Dinah on November 17, 2002, at 10:11:34
In reply to Re: The truth to this study, posted by leslieg on November 16, 2002, at 19:41:44
Is it at all possible that the changes you feel in yourself are do to the hormonal scrambling that comes with giving birth? I do think my brain is different now than it used to be. So does everyone around me. :) But I'm not sure if it was childbirth itself, or the first hypomanic episode on Wellbutrin. It's too long ago now for me to sort it out, but do you remember changes before you started the Effexor?
Posted by leslieg on November 17, 2002, at 11:01:36
In reply to Re: The truth to this study » leslieg, posted by Dinah on November 17, 2002, at 10:11:34
I got off the Effexor at least 5 months before getting pregnant (it was a planned pregnancy). I'd been "unwell" for a few years -- finally diagnosed as narcoleptic just after getting pregnant (and searching for a diagnosis for 2 years). But the quality of my "unwellness" changed from before and after the Effexor. After, I noticed many more neurological-type symptoms when I was very tired. I slurred words, drug my foot when walking, had the urge to let my muscles spasm (ignoring the urge makes it worse, giving in often was followed by crying). The slurring and foot-dragging was not physically oriented. If I thought about it I could talk or walk normally. These symptoms continue. A few months ago I got a copmlete neurological workup, including a full-brain MRI and the doc could find no reason for these symptoms. Oddly enough, the symtoms have significantly lessened since I've started taking Provigil. (I've seen other posts in Psycho Babble indicating similar decrease in post-SSRI s/e's with the use of Provigil. Very interesting.)
Childbirth hormones stay around for a while, especially if you are breastfeeding. I don't blame anyone for wondering if I've confused the two! But in my case I was clearly different before getting pregnant.
> Is it at all possible that the changes you feel in yourself are do to the hormonal scrambling that comes with giving birth? I do think my brain is different now than it used to be. So does everyone around me. :) But I'm not sure if it was childbirth itself, or the first hypomanic episode on Wellbutrin. It's too long ago now for me to sort it out, but do you remember changes before you started the Effexor?
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