![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 20 of 20. This is the beginning of the thread.
Posted by Ame Sans Vie on January 9, 2004, at 10:05:23
First I want to make it very clear that unless I find out that SSRIs invariably cause cancer, stroke, or brain aneurysm, I'm sticking with my Prozac, lol. With that said, there's something that's been bugging me a little bit since early this morning. Obviously there is a reason for the reabsorbtion of neurotransmitters into their originating neurotransmitter after attempting to cross the synapse. I have to wonder then, is it possible that drugs which inhibit the reuptake of serotonin (or dopamine, norepinephrine, whatever) are creating undue stress on our brains which are trying to protect themselves from overload through this reabsorbtion process? I mean, are we forcing more of a certain neurochemical to cross our synapses than our brains can (healthily) handle? This question particularly applies to those who are helped significantly by reuptake inhibiting drugs, of course, as their response to these classes of medications are possibly indicative of a deeper problem than they directly address... i.e. their neurons aren't equipped to handle "normal" (perhaps "adequate" would be a better word) neurotransmission, and so it seems logical that a defense mechanism in the brain would set off, resulting in an increased amount of 5-HT/DA/NE to be "returned to sender" and reabsorbed. If this is in fact the case, I really have to wonder if forcing these chemicals across the synapse is really such a bright idea.
Of course, this is all just conjecture. And I understand that, were any pharmaceutical company to develop a different style of antidepressant, MAOIs excepted, that Paxil, Anafranil, Strattera, Wellbutrin, etc would all be just bad memories for many of us. In other words, I realize that these types of drugs are used for depression today simply because there isn't much else to turn to, and at some point during my lifetime I expect to see the mental illness riddle finally solved completely. But since many of us have to take these drugs in the meantime, I can't help but wonder... are we creating undue stress in our nervous systems?
Posted by crazychickuk on January 9, 2004, at 10:49:56
In reply to A question/concern about 5-HT reuptake inhibition, posted by Ame Sans Vie on January 9, 2004, at 10:05:23
Good point, i must agree, i also think the exact same thing as you, i have never been of a med for longer than 4 mnths, so i havent given my brain time to adjust itself bk to the way it was before my drug abuse, I am going to come remeron and see if i can do it for atleast 6mnths with no meds... would you do that by anychance?
Posted by stjames on January 9, 2004, at 11:03:30
In reply to A question/concern about 5-HT reuptake inhibition, posted by Ame Sans Vie on January 9, 2004, at 10:05:23
I have to wonder then, is it possible that drugs which inhibit the reuptake of serotonin (or dopamine, norepinephrine, whatever) are creating undue stress on our brains which are trying to protect themselves from overload through this reabsorbtion process?
This causes down regulation of other systems, and may account for some of the anti depressant effect.
Posted by PoohBear on January 9, 2004, at 13:13:40
In reply to A question/concern about 5-HT reuptake inhibition, posted by Ame Sans Vie on January 9, 2004, at 10:05:23
I choose to look at it another way: That my depression and ADHD are hereditary, and that my brain is "wired" differently than *normal*.
The Effexor and Wellbutrin I'm taking help my synapses and neurons to work in the way they were 'intended', by being able to bridge the gap normally. I don't believe that my brain has been working to anything near it's potential. At least I feel more like I'm firing on all cylinders, if you get my drift...
At least that's my opinion, which being free, may not be worth much, but it's working for me. I'll probably need to be on some sort of combo for the rest of my life and view the potential complications as a better trade-off than damaged relationships and potential suicide.
TR
Posted by linkadge on January 9, 2004, at 15:45:10
In reply to Re: A question/concern about 5-HT reuptake inhibition, posted by PoohBear on January 9, 2004, at 13:13:40
The reputake is essentially what is broken. One study stuggest a link between a certain unipolar genes and the reputake capacity.
What I mean is that the reputake varies from person to person, some people have a slower reputake and others have a faster reputake.
Some people have low Monoamaine oxidas and others have high monoamine oxidase. So by slowing the reputake process you are essnetially making your brain work more like other peoples.For instance, sleep deprivation (which can acutely improve the mood) slows the reputake process in the brain, which is purportedly why it works.
As long as you feel fairly normal (not unnaturally euphoric) - then your brain is probably working well
Linkadge
Posted by SLS on January 9, 2004, at 16:00:52
In reply to here's the deal, posted by linkadge on January 9, 2004, at 15:45:10
Hi Linkadge.
> For instance, sleep deprivation (which can acutely improve the mood) slows the reputake process in the brain, which is purportedly why it works.Is there any place on the Net where I can find this info?
- Scott
Posted by mattdds on January 9, 2004, at 16:16:58
In reply to A question/concern about 5-HT reuptake inhibition, posted by Ame Sans Vie on January 9, 2004, at 10:05:23
ASV,
Or should I say Mike? Michael?
You bring up some interesting issues that I have thought about as well.
First, though, what exactly do you mean by "undue stress"? Define "stress" in this context. And what potential problems might arise from it? I'm not asking sarcastically, but it would help if you clarified what you meant by that.
First off, let me start by saying that I think we really have *no* idea how antidepressants are working, but that they seem to certainly work in some people.
As I'm sure you're well aware, the brain is amazingly plastic. When there is too much serotonin, for example, in the synapses, compensatory mechanisms like receptor down regulation or desensitization will kick in to ensure that the serotonergic (or DA-ergic, or NE-ergic, etc.) "tone" is not too high.
So you have all this excess serotonin floating around in the synapse, and initially, this creates strain on the system, but after downregulation of postsynaptic receptors, the net serotonergic transmission should be similar to what it was originally.
This is what has always perplexed me. If the net serotonergic transmission returns to equilibrium after a sufficient amount of exposure to say, fluoxetine, how is it even working? Why doesn't it just poop out for everybody? It doesn't, though.
This is not to say it *isn't* working, it's just always puzzled me, and up to this point I haven't seen a convincing explanation.
Same goes with benzodiazepines. Excess stimulation of the GABA-ergic system --> downregulation or desensitization of benzodiazepine receptors (not sure which one it is) --> GABA-ergic transmission similar to baseline after sustained treatment. But what perplexes me (again!), is that the benzos continue to work for me - long after the "stress" has been relieved.
So perhaps, they are somehow normalizing the equilibrium by placing this initial stress, with the subsequent compensatory efforts.
This is just my idea of how it might work, but it seems logical / possible.
So, by "stress", what exactly do you mean, and what potential problems worry you (e.g. Nerve damage? Neoplasia?).
I ask these questions not cynically, but just to perhaps probe a bit more into what exactly you're concerned about.
But I wouldn't worry about "sress" as long as you are feeling better, because we really don't have a clue what these drugs are doing (well, ok, we have *some* clue). That's why I am a big advocate of focusing on *symptoms*, and real life day-to-day functioning...things that we can measure (at least at this point).
Sorry for the rambly, blabbering form this post took. Haha.
Best,
Matt
Posted by Francesco on January 10, 2004, at 4:14:11
In reply to Re: A question/concern about 5-HT reuptake inhibition » Ame Sans Vie, posted by mattdds on January 9, 2004, at 16:16:58
I appreciate very much your post Mattds, it sounds logical and helpful. I just want to add something about 'stress'. I'm much more stressed when I *don't* take meds (don't know about my brain though). If stress isn't *cured* you will be more likely to have organic problems, I think. I'm not referring to the normal and positive stress people experience in everyday life, but rather the unuseful and meaningless stress we experience when we're not properly medicated. I'm not 'pro-meds' anyhow but I was just reflecting about the fact that since I quit my meds a couple of years ago I had problems with many psychosomatic disturbs ... being not functional is stressing, or at least, for me it is. I can't stop thinking when I'm not medicated about the fact that I'm wasting my time, that I'm not doing anything and so on. I don't think this helps my immune system ;-) Sorry for rambling
Posted by linkadge on January 10, 2004, at 6:55:42
In reply to Re: here's the deal, posted by SLS on January 9, 2004, at 16:00:52
Is there any place on the Net where I can find this info?
Not sure, I forget where I read it, perhaps somewhere in the archives of www.biospychiatry.com/refs.htm. Other than that a search for the physiological effects of sleep deprivation might come up with this info.
Linkadge
Posted by Ame Sans Vie on January 12, 2004, at 9:29:34
In reply to Re: A question/concern about 5-HT reuptake inhibition, posted by crazychickuk on January 9, 2004, at 10:49:56
> Good point, i must agree, i also think the exact same thing as you, i have never been of a med for longer than 4 mnths, so i havent given my brain time to adjust itself bk to the way it was before my drug abuse, I am going to come remeron and see if i can do it for atleast 6mnths with no meds... would you do that by anychance?
No way! You're much braver than I! lol :-)
Posted by Ame Sans Vie on January 12, 2004, at 9:30:47
In reply to Re: A question/concern about 5-HT reuptake inhibition, posted by stjames on January 9, 2004, at 11:03:30
> I have to wonder then, is it possible that drugs which inhibit the reuptake of serotonin (or dopamine, norepinephrine, whatever) are creating undue stress on our brains which are trying to protect themselves from overload through this reabsorbtion process?
>
> This causes down regulation of other systems, and may account for some of the anti depressant effect.Interesting point... I hadn't thought of that.
Posted by Ame Sans Vie on January 12, 2004, at 9:48:28
In reply to Re: A question/concern about 5-HT reuptake inhibition, posted by PoohBear on January 9, 2004, at 13:13:40
> I choose to look at it another way: That my depression and ADHD are hereditary, and that my brain is "wired" differently than *normal*.
Oh, I absolutely agree -- there isn't a single member of my family that I know of (I've never met my father) who doesn't have some sort of disorder... anorexia nervosa, bulimia, OCD, panic disorder, social anxiety, generalized anxiety, depression, and self-medication with alcohol and/or drugs are rampant amongst my immediate and extended family.
> The Effexor and Wellbutrin I'm taking help my synapses and neurons to work in the way they were 'intended', by being able to bridge the gap normally. I don't believe that my brain has been working to anything near it's potential. At least I feel more like I'm firing on all cylinders, if you get my drift...
I should have made myself more clear -- I also believe that our brains are "wired" differently. But I worry that there is a reason our reuptake processes are all screwy, that being that there is some defect in our nervous systems which only allows less than adequate amounts of neurotransmitters to cross the synapse completely. And I worry that this may be because the receiving neurons may already be absorbing as much as they can handle, due to this "defect". It concerns me that reuptake inhibition may be forcing neurochemicals across these synapses when our very problem may be that our brains can't handle that much at once... the only analogy that immediately comes to mind would be blowing up a balloon -- the balloon itself represents the receiving neuron, and the air filling it represents *INSERT NEUROTRANSMITTER NAME HERE*. The balloon can only handle so much air -- blow it up too much and it pops. So I ask if our neurons are already taking in as much as they can handle, and if forcing extra into them could cause them to "pop"? Not explode, of course, but to overload and, well, fry.
> At least that's my opinion, which being free, may not be worth much, but it's working for me. I'll probably need to be on some sort of combo for the rest of my life and view the potential complications as a better trade-off than damaged relationships and potential suicide.I absolutely concur -- I was just wondering if anyone had any info on this. Thanks for the input! :-)
Michael
Posted by Ame Sans Vie on January 12, 2004, at 10:08:23
In reply to Re: A question/concern about 5-HT reuptake inhibition » Ame Sans Vie, posted by mattdds on January 9, 2004, at 16:16:58
Hiya Matt,
> ASV,
>
> Or should I say Mike? Michael?Mike's fine. :-)
> You bring up some interesting issues that I have thought about as well.
>
> First, though, what exactly do you mean by "undue stress"? Define "stress" in this context. And what potential problems might arise from it? I'm not asking sarcastically, but it would help if you clarified what you meant by that.Well, I don't mean emotional stress. I'm talking about stress on our nervous systems from overworking. There's a better explanation in my post to PoohBear.
> First off, let me start by saying that I think we really have *no* idea how antidepressants are working, but that they seem to certainly work in some people.
>
> As I'm sure you're well aware, the brain is amazingly plastic. When there is too much serotonin, for example, in the synapses, compensatory mechanisms like receptor down regulation or desensitization will kick in to ensure that the serotonergic (or DA-ergic, or NE-ergic, etc.) "tone" is not too high.
>
> So you have all this excess serotonin floating around in the synapse, and initially, this creates strain on the system, but after downregulation of postsynaptic receptors, the net serotonergic transmission should be similar to what it was originally.
>
> This is what has always perplexed me. If the net serotonergic transmission returns to equilibrium after a sufficient amount of exposure to say, fluoxetine, how is it even working? Why doesn't it just poop out for everybody? It doesn't, though.Food for thought... Odd that I've never thought of that.
> This is not to say it *isn't* working, it's just always puzzled me, and up to this point I haven't seen a convincing explanation.
>
> Same goes with benzodiazepines. Excess stimulation of the GABA-ergic system --> downregulation or desensitization of benzodiazepine receptors (not sure which one it is) --> GABA-ergic transmission similar to baseline after sustained treatment. But what perplexes me (again!), is that the benzos continue to work for me - long after the "stress" has been relieved.
>
> So perhaps, they are somehow normalizing the equilibrium by placing this initial stress, with the subsequent compensatory efforts.
>
> This is just my idea of how it might work, but it seems logical / possible.Very good point! It seems very plausible.
> So, by "stress", what exactly do you mean, and what potential problems worry you (e.g. Nerve damage? Neoplasia?).
Well, as for the stress thing, see above... and I'm not worried about any problems really. I certainly don't have any specific concerns in mind (considering how little we know about these drugs, it would be quite hard to do so!). This whole thing was just a notion that popped into my head and kept nagging at me, so I had to ask! lol
> I ask these questions not cynically, but just to perhaps probe a bit more into what exactly you're concerned about.
>
> But I wouldn't worry about "sress" as long as you are feeling better, because we really don't have a clue what these drugs are doing (well, ok, we have *some* clue). That's why I am a big advocate of focusing on *symptoms*, and real life day-to-day functioning...things that we can measure (at least at this point).Very much agreed. Thanks so much for the insight! :-)
> Sorry for the rambly, blabbering form this post took. Haha.
Don't worry -- I am King of Unnecessary Verbiage, lol.
Michael
Posted by temoigneur on January 19, 2004, at 1:03:34
In reply to Re: A question/concern about 5-HT reuptake inhibition » mattdds, posted by Ame Sans Vie on January 12, 2004, at 10:08:23
> Hiya Matt,
>
> > ASV,
> >
> > Or should I say Mike? Michael?
>
> Mike's fine. :-)
>
> > You bring up some interesting issues that I have thought about as well.
> >
> > First, though, what exactly do you mean by "undue stress"? Define "stress" in this context. And what potential problems might arise from it? I'm not asking sarcastically, but it would help if you clarified what you meant by that.
>
> Well, I don't mean emotional stress. I'm talking about stress on our nervous systems from overworking. There's a better explanation in my post to PoohBear.
>
> > First off, let me start by saying that I think we really have *no* idea how antidepressants are working, but that they seem to certainly work in some people.
> >
> > As I'm sure you're well aware, the brain is amazingly plastic. When there is too much serotonin, for example, in the synapses, compensatory mechanisms like receptor down regulation or desensitization will kick in to ensure that the serotonergic (or DA-ergic, or NE-ergic, etc.) "tone" is not too high.
> >
> > So you have all this excess serotonin floating around in the synapse, and initially, this creates strain on the system, but after downregulation of postsynaptic receptors, the net serotonergic transmission should be similar to what it was originally.
> >
> > This is what has always perplexed me. If the net serotonergic transmission returns to equilibrium after a sufficient amount of exposure to say, fluoxetine, how is it even working? Why doesn't it just poop out for everybody? It doesn't, though.
>
> Food for thought... Odd that I've never thought of that.
>
> > This is not to say it *isn't* working, it's just always puzzled me, and up to this point I haven't seen a convincing explanation.
> >
> > Same goes with benzodiazepines. Excess stimulation of the GABA-ergic system --> downregulation or desensitization of benzodiazepine receptors (not sure which one it is) --> GABA-ergic transmission similar to baseline after sustained treatment. But what perplexes me (again!), is that the benzos continue to work for me - long after the "stress" has been relieved.
> >
> > So perhaps, they are somehow normalizing the equilibrium by placing this initial stress, with the subsequent compensatory efforts.
> >
> > This is just my idea of how it might work, but it seems logical / possible.
>
> Very good point! It seems very plausible.
>
> > So, by "stress", what exactly do you mean, and what potential problems worry you (e.g. Nerve damage? Neoplasia?).
>
> Well, as for the stress thing, see above... and I'm not worried about any problems really. I certainly don't have any specific concerns in mind (considering how little we know about these drugs, it would be quite hard to do so!). This whole thing was just a notion that popped into my head and kept nagging at me, so I had to ask! lol
>
> > I ask these questions not cynically, but just to perhaps probe a bit more into what exactly you're concerned about.
> >
> > But I wouldn't worry about "sress" as long as you are feeling better, because we really don't have a clue what these drugs are doing (well, ok, we have *some* clue). That's why I am a big advocate of focusing on *symptoms*, and real life day-to-day functioning...things that we can measure (at least at this point).
>
> Very much agreed. Thanks so much for the insight! :-)
>
> > Sorry for the rambly, blabbering form this post took. Haha.
>
> Don't worry -- I am King of Unnecessary Verbiage, lol.
>
> MichaelHi Michael, How are you, good to see you again. I don't think we've talked since we've I started nardil. What's happening is last time I was on Nardil and tried to come off zyprexa, my OCD came back with a vengeance. Do I remember correctly you saying that tramadol could work brilliantly for OCD/anxiety as long as you took a substance like DMX to ward off tolerance.
I was wondering if you knew of any opiate drug that wouldn't be contraindicated, or has at least a reasonably safe track record in combination with MAOI's. I have OCD, SP, GAD, and PD. I'm getting a new pdoc who doesn't have a problem with perscribing trazodone with MAOI's, as I have insomnia on it. Convincing him to let me try a narcotic will be a feat
Is your current combination working for you? Do you mind me asking what your diagnosis is again.
I'm writing you today because my OCD is bound to come back tomorrow or the next day, as I've cut back on the zyprexa. It can be difficult to write and look for help with my OCD as it is always telling me that I must go through emotionally draining rituals before I am worthy of asking for help and if I don't I risk having a panic attack so I thought I'd write you today when I'm cognizant enough that I can get something across, but my zyprexa has not worn off to the point where it becomes hard.
thanks so much
if you would rather email me, my email address is Bentley79@hotmail.com
Ben
Posted by Questionmark on January 19, 2004, at 11:04:11
In reply to A question/concern about 5-HT reuptake inhibition, posted by Ame Sans Vie on January 9, 2004, at 10:05:23
> First I want to make it very clear that unless I find out that SSRIs invariably cause cancer, stroke, or brain aneurysm, I'm sticking with my Prozac, lol. With that said, there's something that's been bugging me a little bit since early this morning. Obviously there is a reason for the reabsorbtion of neurotransmitters into their originating neurotransmitter after attempting to cross the synapse. I have to wonder then, is it possible that drugs which inhibit the reuptake of serotonin (or dopamine, norepinephrine, whatever) are creating undue stress on our brains which are trying to protect themselves from overload through this reabsorbtion process? I mean, are we forcing more of a certain neurochemical to cross our synapses than our brains can (healthily) handle? This question particularly applies to those who are helped significantly by reuptake inhibiting drugs, of course, as their response to these classes of medications are possibly indicative of a deeper problem than they directly address... i.e. their neurons aren't equipped to handle "normal" (perhaps "adequate" would be a better word) neurotransmission, and so it seems logical that a defense mechanism in the brain would set off, resulting in an increased amount of 5-HT/DA/NE to be "returned to sender" and reabsorbed. If this is in fact the case, I really have to wonder if forcing these chemicals across the synapse is really such a bright idea.
>
> Of course, this is all just conjecture. And I understand that, were any pharmaceutical company to develop a different style of antidepressant, MAOIs excepted, that Paxil, Anafranil, Strattera, Wellbutrin, etc would all be just bad memories for many of us. In other words, I realize that these types of drugs are used for depression today simply because there isn't much else to turn to, and at some point during my lifetime I expect to see the mental illness riddle finally solved completely. But since many of us have to take these drugs in the meantime, I can't help but wonder... are we creating undue stress in our nervous systems?Ame (/Mike[?]), you brought up a really good question. It's one i wonder about a great deal at different at different points-- esp. when i got off Paxil and felt like absolute s**t for months on end.
i have a partial answer to your question, i believe (if you hadn't thought of this before at least). In regard to why we have any reuptake process at all (which is not exactly what you asked, but a sort of indirect variation maybe), i'm sure it's as a safeguard. I.e., if we did not, and then we had a high release of a certain neurotransmitter-- whether from some emotional response or an exogenous substance or what have you-- then the continued presence of that neurotransmitter in the synapse could produce toxic reactions in the postsynaptic neuron. Plus there would then be insufficient amounts of that transmitter in the PREsynaptic terminal, which would then eventually result in an under-supply of that neurochemical in the synapse.
(i hope that at least somewhat helped in answering your question, and wasn't just obvious information. Sorry if the latter).
As far as whether or not antidepressants (and other psychoactive meds) are somehow detrimental or something-- since they disrupt the naturally occurring processes of the brain-- i don't know. But i really wonder. However, i think the fact that no one fully knows the answer to this question shows that the psychiatric industry is far more naive and liberal in prescribing potent psychotropic drugs that it should be. i know so many people on some SSRI it's not even funny. There are so many people drugged up these days-- many of whom don't even have any specific psychiatric diagnosis, or if they do, just some mild case of Seasonal Affective Disorder or PMDD or irritability or dissatisfaction with life or what have you. i'm not saying these meds aren't needed or worthwhile sometimes-- oftentimes even, maybe-- but i do think they are overprescribed and we need to be much more careful and judicious with them. And don't even get me started on the outrageous number of children who are (forced, no less, to be) on potent psychostimulants, and pretty d*mn high doses no less, in this country.
ANYway!... (sorry, the caffeine is 'causing' me to ramble this morning). i think maybe the sustained overstimulation of certain receptors that antidepressants create does cause excessive [chemical] stress to certain neurons/brain areas. The fact that we feel "good" or better as a result of these drugs does not negate this possibility any more than the use of a euphoriant drug temporarily results in feeling "good" or better as well-- even if this drug could cause some amount of brain damage and/or causes physiological dependence (e.g., cocaine, morphine, alcohol, barbiturates, MDMA, amphetamines, benzodiazepines, etc.). The main difference, as far as i can tell, is that with the last example (of using euphoriant drugs occasionally and w/ temporary duration) one is just getting "messed up" occasionally or, say, with the shorter acting drugs, even once a day. So during the time that s/he is not using the respective drug, s/he can notice how s/he feels without it in his/her system-- and can feel the withdrawal or come-down or what have you. However, with the typically prescribed psychiatric medication schedule-- esp. with SSRIs or benzos (since they usually have effects that last all day)-- one is getting the effects every day and oftentimes *all* day. So any come-down ("rebound") effect is more effectively bypassed and dependence (via noticing withdrawal) is goes unnoticed indefinitely until the person tries to finally go off the drug.
Also, maybe there is a good reason for why, in certain people, neurotransmitter reuptake and/or enzyme metabolization at the "normal" (drug-free) activity/levels for that particular person occurs when s/he has a "psychiatric disorder" or whatever-- and needs to have reuptake inhibition, enzyme inhibition, or neurotransmitter agonism or sometimes antagonism in order for him/her to feel well. (Sorry for the run-on!) Maybe it is because through genetics and, to some degree, the habituated behavior and responses to various environmental stimuli, a person's brain (or certain neural pathways) gets adjusted to acting in a specific manner, and then its "normal" activity (neurochemically) gets refined to being ABnormal (psychologically/behaviorally). Thus, without some extensive, sufficient behavioral and cognitive therapy (and/or changes and/or exercises), or without some adequate pharmacological intervention, this person will likely stay "disordered" or "abnormal" indefinitely. For (a simplified) example, say a child-- say even one who is neurogenetically healthy-- is raised in a home in which one or both the parents are extremely concerned and strict with being clean and germ-free. This child's brain could then quite easily develop in a manner that would eventually result in OCD-type thoughts and behavior being his/her normal state. (This kind of change in neurobiological normalcy would not, i would assume, have to take place in childhood either. It's just more extreme, fast, and easy in childhood.)
Anyhow, those are my two many cents. Sorry for the length and the unneeded conjecture. Can't help it. But let me know what yous think.Oh, also, in response to Mattd:
he/you said, "This is what has always perplexed me. If the net serotonergic transmission returns to equilibrium after a sufficient amount of exposure to say, fluoxetine, how is it even working? Why doesn't it just poop out for everybody? It doesn't, though.
This is not to say it *isn't* working, it's just always puzzled me, and up to this point I haven't seen a convincing explanation."
Thats a really good question too. i'm convinced, though, that the net neurotransmitter (whichever is directly involved) transmission does not completely return to equilibrium. Be it the receptors or intracellular processes, i believe something must still be occurring different than normal. Or, maybe as someone else said, there have simply been changes in other neurotransmitter systems.
OK thats all!!
Posted by Ame Sans Vie on January 21, 2004, at 2:12:52
In reply to Ame Sans Vie, Nardil + Tramadol? suggestion » Ame Sans Vie, posted by temoigneur on January 19, 2004, at 1:03:34
> Hi Michael, How are you, good to see you again.
Hi there, it's been a while! I just returned to the boards after a bit of a break.
>I don't think we've talked since we've I started nardil. What's happening is last time I was on Nardil and tried to come off zyprexa, my OCD came back with a vengeance. Do I remember correctly you saying that tramadol could work brilliantly for OCD/anxiety as long as you took a substance like DMX to ward off tolerance.
Tramadol can definitely be one of those elusive miracle drugs for OCD, but combining it with an MAOI would certainly be tricky business... though I do believe it could be done (see my post to Ace further down on the board re: tramadol + MAOIs). And just to avoid confusion, the cough suppressant that helps prevent tolerance to various drugs is DXM (dextromethorphan), not DMX. :-)
> I was wondering if you knew of any opiate drug that wouldn't be contraindicated, or has at least a reasonably safe track record in combination with MAOI's. I have OCD, SP, GAD, and PD. I'm getting a new pdoc who doesn't have a problem with perscribing trazodone with MAOI's, as I have insomnia on it. Convincing him to let me try a narcotic will be a featA feat? lol What a master of understatement that you are. ;-) Really though, it just takes having an open-minded doctor and bringing in information to prepare him/her for the possible addition of an opioid drug. Easier said than done, I know. lol
Many opioids have safely been taken with MAOIs. Morphine, codeine, hydrocodone, hydromorphone, methadone, butorphanol, pentazocine, buprenorphine, levomethorphan, oxycodone, oxymorphone, and fentanyl are among those which have safely been used with MAOIs in the past. The primary ones to avoid are Demerol (meperidine/pethidine), obviously, and the opioid anaesthetics (i.e. alfentanil, sufentanil, remifentanil).
If your doctor is willing to experiment, I'd suggest keeping buprenorphine (Subutex/Suboxone) in mind, as it seems to help plenty of people with depression without significant development of tolerance. And it seems that all opioids can be useful for OCD, so surely bupe could help.
> Is your current combination working for you? Do you mind me asking what your diagnosis is again.
It's working great, thanks for asking! My primary diagnoses are social anxiety disorder, avoidant personality disorder, panic disorder, depression, and agoraphobia, and I also have mild-moderate symptoms of both OCD and ADD. I'm taking 8mg/day Klonopin, 60mg/day Adderall XR, and 20mg/day Prozac; then there's also the one gram Somnote and 200mg Tuinal that I switch back and forth between for sleep when needed, though I haven't needed them much lately.
> I'm writing you today because my OCD is bound to come back tomorrow or the next day, as I've cut back on the zyprexa. It can be difficult to write and look for help with my OCD as it is always telling me that I must go through emotionally draining rituals before I am worthy of asking for help and if I don't I risk having a panic attack so I thought I'd write you today when I'm cognizant enough that I can get something across, but my zyprexa has not worn off to the point where it becomes hard.
I'm sorry it took me a few days to respond -- my computer was acting up on me. I hope this can help, and if you'd like to e-mail me, the address is amesansvie@yahoo.com.
Michael
Posted by Ame Sans Vie on January 21, 2004, at 2:13:03
In reply to Ame Sans Vie, Nardil + Tramadol? suggestion » Ame Sans Vie, posted by temoigneur on January 19, 2004, at 1:03:34
> Hi Michael, How are you, good to see you again.
Hi there, it's been a while! I just returned to the boards after a bit of a break.
>I don't think we've talked since we've I started nardil. What's happening is last time I was on Nardil and tried to come off zyprexa, my OCD came back with a vengeance. Do I remember correctly you saying that tramadol could work brilliantly for OCD/anxiety as long as you took a substance like DMX to ward off tolerance.
Tramadol can definitely be one of those elusive miracle drugs for OCD, but combining it with an MAOI would certainly be tricky business... though I do believe it could be done (see my post to Ace further down on the board re: tramadol + MAOIs). And just to avoid confusion, the cough suppressant that helps prevent tolerance to various drugs is DXM (dextromethorphan), not DMX. :-)
> I was wondering if you knew of any opiate drug that wouldn't be contraindicated, or has at least a reasonably safe track record in combination with MAOI's. I have OCD, SP, GAD, and PD. I'm getting a new pdoc who doesn't have a problem with perscribing trazodone with MAOI's, as I have insomnia on it. Convincing him to let me try a narcotic will be a featA feat? lol What a master of understatement that you are. ;-) Really though, it just takes having an open-minded doctor and bringing in information to prepare him/her for the possible addition of an opioid drug. Easier said than done, I know. lol
Many opioids have safely been taken with MAOIs. Morphine, codeine, hydrocodone, hydromorphone, methadone, butorphanol, pentazocine, buprenorphine, levomethorphan, oxycodone, oxymorphone, and fentanyl are among those which have safely been used with MAOIs in the past. The primary ones to avoid are Demerol (meperidine/pethidine), obviously, and the opioid anaesthetics (i.e. alfentanil, sufentanil, remifentanil).
If your doctor is willing to experiment, I'd suggest keeping buprenorphine (Subutex/Suboxone) in mind, as it seems to help plenty of people with depression without significant development of tolerance. And it seems that all opioids can be useful for OCD, so surely bupe could help.
> Is your current combination working for you? Do you mind me asking what your diagnosis is again.
It's working great, thanks for asking! My primary diagnoses are social anxiety disorder, avoidant personality disorder, panic disorder, depression, and agoraphobia, and I also have mild-moderate symptoms of both OCD and ADD. I'm taking 8mg/day Klonopin, 60mg/day Adderall XR, and 20mg/day Prozac; then there's also the one gram Somnote and 200mg Tuinal that I switch back and forth between for sleep when needed, though I haven't needed them much lately.
> I'm writing you today because my OCD is bound to come back tomorrow or the next day, as I've cut back on the zyprexa. It can be difficult to write and look for help with my OCD as it is always telling me that I must go through emotionally draining rituals before I am worthy of asking for help and if I don't I risk having a panic attack so I thought I'd write you today when I'm cognizant enough that I can get something across, but my zyprexa has not worn off to the point where it becomes hard.
I'm sorry it took me a few days to respond -- my computer was acting up on me. I hope this can help, and if you'd like to e-mail me, the address is amesansvie@yahoo.com.
Michael
Posted by Ame Sans Vie on January 21, 2004, at 2:16:18
In reply to Re: A question/concern about 5-HT reuptake inhibition, posted by Questionmark on January 19, 2004, at 11:04:11
Thanks a lot for the in-depth response! Your interpretation/explanation of the issue was exactly what I was trying to say -- I was just having trouble finding the words... a little preoccupied lately, lol. A lot of interesting and valid points there... looks like I should do some more reading!
Michael
Posted by temoigneur on January 21, 2004, at 19:38:40
In reply to Re: Ame Sans Vie, Nardil + Tramadol? suggestion » temoigneur, posted by Ame Sans Vie on January 21, 2004, at 2:13:03
Hi Michael it's so nice to have you back on board. Many thanks for your helpful response -
Ben
Posted by Questionmark on January 23, 2004, at 0:37:03
In reply to Re: A question/concern about 5-HT reuptake inhibition » Questionmark, posted by Ame Sans Vie on January 21, 2004, at 2:16:18
This is the end of the thread.
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