![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 26 to 50 of 77. Go back in thread:
Posted by SLS on March 23, 2002, at 8:55:19
In reply to Re: ltp in the hippocampus » SLS, posted by JohnX2 on March 23, 2002, at 0:24:09
Hi John.
Glad you interjected...
> I want lithium because of its neuroprotective and neurotrophic potential. It is supposed to promote plasticity. Maybe this would help to restore the size and function of the hippocampus. What do you think? Depression has greatly impaired my memory.
> Sorry to budge in on your thread. I'm interested on your comment about lithium and its effects on plasticity in the hippocampus? Can you direct me to any information on this?
What is "ltp"?
I have been keeping an eye on research involving lithium and its ability to change the neuronal output of nerve growth factors and to increase the volume of certain brain regions. Much of this work has been done by Husseini Manji, MD. From what I remember, valproate has also demonstrated some these properties, but not to as great a degree as lithium.
Here a few summary articles from the NDMDA website. Note the damnable observation that there is indeed a neurodegenerative process involved in mood-disorders, particularly with bipolar disorder and conditions involving a chronic overproduction of cortisol. An optimistic perspective lies in the fact that the brain remains plastic and perhaps capable of a significant arresting and reversal of atrophy along with the sprouting of new neurons and neural connections.
LITHIUM: THE ULTIMATE BRAIN FOOD?
http://www.ndmda.org/McManamy.html
Antidepressants have also been shown to restore the size of the hippocampus. However, I wonder if this phenomenon is actually a consequence of an extended remission rather than being intrinsic to the drug itself.
ANTIDEPRESSANTS AND BRAIN CELL GROWTHhttp://www.ndmda.org/ResearchUpdate2-6.html
In another post, you mentioned something regarding 5-HT2 receptors being somehow linked to NMDA function. Can you elaborate?Thanks.
What's going on with you, by the way? It seems that you have had a few "false starts" recently. What gives?
I'm still playing with nortriptyline. There might be something I can glean from it in the absence of Effexor. It seems that Effexor may have interfered with my responding to both nortriptyline and imipramine. Although tricyclics don't do the job, they seem to be of some help when combined with Lamictal.
- Scott
Posted by btrout on March 23, 2002, at 9:12:24
In reply to Re: treatment resistant depression -Suggestions? » btrout, posted by Ron Hill on March 19, 2002, at 11:55:00
Hi Ron and Everyone,
Thanks for the suggestion, Ron, and the kind words. Actually, I tried SAMe at 1600mg/ day for a month ($$$$!), and I didn't feel anything. Interestingly, I do have somewhat of a response to large doses of folic acid, which is also a part of the methylation process.
I recently tried St. John's Wort, which made me sicker. I think that doing anything to increase serotonin makes my immune system worse. I read that both serotonin and SSRI's raise IL-6. I think my IL-6 is already sky high and any more just kills me.
Right now, I'm giving a trial to the herb feverfew, if you can believe it. It is reported to inhibit the enzyme that causes the release of IL-6 and TNF-alpha. Incidentally, it is also reported to block the 5-HT2a and 5-HT2b receptors. Blocking these receptors prevents serotonin from causing a rise in intracellular calcium. High intracellular calcium leads to high inflammatory cytokine release.
Next week, I am going to try a drug called cycloserine which is a partial agonist at the glycine site of the NMDA receptor. It also inhibits sphingolipid synthesis which in turn inactivates the same enzyme that feverfew inactivates. Cycloserine seems to be neuroprotective and anticonvulsant. It is reported to decrease the T helper cell/ T suppressor cell ratio, which is elevated in depression, and with my insane immune system, I know it is elevated in me. I think this drug could be a very good immune modulator. Exciting.Take care everyone.
Btrout
Posted by SLS on March 23, 2002, at 13:51:45
In reply to Re: treatment resistant depression » SLS, posted by Ron Hill on March 21, 2002, at 16:33:03
Hi Ron.
> I want to help you! You have been in pain too long, and you are too nice of a guy for me to just dismiss.
It means so much to me that someone should take such an interest. I have been bouncing back between hope and despair for a long time.
> For six years I went from one drug trial to the next never finding long term relief for the depressive side of my BPII. Thanks to a pdoc that does more than just listen to what the drug company reps tell him, I now have my solution; 600 mg/day Lithobid and 200 mg/day SAM-e. (B-6, folic acid, and SUBLINGUAL bioactive B-12 must also be taken. I also add some phosphatidylserine and phosphatidylcholine 'cause they feel good in my brain.
Questions:
1. What is your blood level of lithium at 600mg/day?
2. Do you experience any side effects of lithium, i.e. apathy, amotivation, loss of creativity etc.?
3. How does your (hypo)mania manifest? How often does it happen?
4. 200mg of S-AMe sounds wonderful. How frequently do you think that someone should respond to such a low dosage? How did you go about establishing your optimum dosage? Did you initially take more?
5. Is it safe to combine S-AMe with a MAO-inhibitor?
> For you, it might be 300 mg/day Lamictal and 400 mg/day SAM-e (or as high as 1600 mg/day SAM-e if needed). Start by using 100 or 200 mg/day of SAM-e as an add-on to your current cocktail, then play it by ear to see if you can discontinue your AD.> PLEASE read the very well written and technically informative SAM-e article (posted previously by davex) linked below. All I can do is put out the bread; it's up to you to decide whether or not to eat.
Thank you very much. I think I'll move S-AMe near the top of my list. At this point in time, I am planning to:
1. Try to find an optimum dosage of nortriptyline that will maintain a partial response.
2. Add Nardil, titrating to perhaps 90mg.
Perhaps this would be a good point to try adding S-AMe. What do you think?
3. Retry an atypical neuroleptic. Previous trials produced mild transient improvements followed by the emergence of unacceptable cognitive side effects at higher dosages.
- Zyprexa (olanzapine)
- Geodon (ziprasidone)
- Abilitat (aripiprazole)4. Add Mirapex.
5. Finish reading your S-AMe article. :-)
- Scott
Posted by JohnX2 on March 24, 2002, at 2:20:06
In reply to Re: ltp in the hippocampus » JohnX2, posted by SLS on March 23, 2002, at 8:55:19
> Hi John.
>
> Glad you interjected...
>>
> What is "ltp"?
>
ltp = long term potentiation. For learning, etc.
> I have been keeping an eye on research involving lithium and its ability to change the neuronal output of nerve growth factors and to increase the volume of certain brain regions. Much of this work has been done by Husseini Manji, MD. From what I remember, valproate has also demonstrated some these properties, but not to as great a degree as lithium.
>
> Here a few summary articles from the NDMDA website. Note the damnable observation that there is indeed a neurodegenerative process involved in mood-disorders, particularly with bipolar disorder and conditions involving a chronic overproduction of cortisol. An optimistic perspective lies in the fact that the brain remains plastic and perhaps capable of a significant arresting and reversal of atrophy along with the sprouting of new neurons and neural connections.
>
>
>
> LITHIUM: THE ULTIMATE BRAIN FOOD?
>
> http://www.ndmda.org/McManamy.html
>Thats a pretty cool read.
>
> Antidepressants have also been shown to restore the size of the hippocampus. However, I wonder if this phenomenon is actually a consequence of an extended remission rather than being intrinsic to the drug itself.
>
>
> ANTIDEPRESSANTS AND BRAIN CELL GROWTH
>
> http://www.ndmda.org/ResearchUpdate2-6.html
>
>
> In another post, you mentioned something regarding 5-HT2 receptors being somehow linked to NMDA function. Can you elaborate?
>I need to check my notes, my memory is failing. Maybe i need some lithium. ;)
> Thanks.
>
> What's going on with you, by the way? It seems that you have had a few "false starts" recently. What gives?
>Actually I'm not doing too bad. I dropped Zyprexa and added Serzone (which is the ONLY AD for me that works and doesn't poopout). The Serzone induced a chronic mild agitated hypomania. I quit it for a few days and became a bit depressed. I restarted it with some Zyprexa and now I feel good. Rats. The zyprexa may be giving me a dystonia, so I may be adding Li instead.
> I'm still playing with nortriptyline. There might be something I can glean from it in the absence of Effexor. It seems that Effexor may have interfered with my responding to both nortriptyline and imipramine. Although tricyclics don't do the job, they seem to be of some help when combined with Lamictal.
>
>
> - ScottGood luck on your medicines Scott.
I did a little research on the hippocampus thing.
I think you can get an MRI to see if you have actually been nailed, right?Anyways, I found 1 really good paper describing the degenerative process and possible treatments.
It goes into how many different disorders can more or less have the same cascade of neurodegeneration (stress,aging,depression).This is a really good read:
http://www.utdallas.edu/~tres/aging_seminar2001/mcewen.pdf
This paper suggests the old stand-by hypothesis of excess glucocorticoids hyperstimulating neurons to death. The paper suggests treatment with possibly phenytoin, nmda antagonist, or by facilitating serotonin reuptake with something like tianeptine.
I would think Lithium may be useful as it modulates glutamate release. Do you recall the hypothesis set forth by the articles you read on Lithium and neurotrophic factor expression?
The nmda antagonists look interesting too. I found an abstract implying that memantine induces brain-derived neurotrophic factor expression.
Both Li and memantine look like interesting medicines to help with poop out and brain shrinkage and possibly cognition.
What do you think?
Best Regards,
John----------------------------------------------
The neuroprotective agent memantine induces brain-derived neurotrophic factor and trkB receptor expression in rat brain.
Mol Cell Neurosci 2001 Sep;18(3):247-58 (ISSN: 1044-7431)
Marvanova M; Lakso M; Pirhonen J; Nawa H; Wong G; Castren E
A. I. Virtanen Institute, University of Kuopio, Kuopio, 70211, Finland.
Memantine is a medium-affinity uncompetitive N-methyl-d-aspartate receptor antagonist and has been clinically used as a neuroprotective agent to treat Alzheimer's and Parkinson's diseases. We have examined the effect of memantine (ip 5-50 mg/kg; 4 h) on the expression of brain-derived neurotrophic factor (BDNF) and trkB receptor mRNAs in rat brain by in situ hybridization. Memantine at a clinically relevant dose markedly increased BDNF mRNA levels in the limbic cortex, and this effect was more widespread and pronounced at higher doses. Effects of memantine on BDNF mRNA were also reflected in changes in BDNF protein levels. Moreover, memantine induced isoforms of the BDNF receptor trkB. Taken together, these data suggest that the neuroprotective properties of memantine could be mediated by the increased endogenous production of BDNF in the brain. These findings may open up new possibilities of pharmacologically regulating the expression of neurotrophic factors in the brain. [Copyright 2001 Academic Press.].
Posted by JohnX2 on March 24, 2002, at 2:54:41
In reply to Re: ltp in the hippocampus » JohnX2, posted by SLS on March 23, 2002, at 8:55:19
>
> In another post, you mentioned something regarding 5-HT2 receptors being somehow linked to NMDA function. Can you elaborate?
>
> Thanks.I had this thought regarding SSRI poopout, amphetamine poopout, and NMDA antagonists. I don't have the details on hand, but I found a quick abstract confirming the link. If my memory serves me correct, the 5-ht2a receptors serve to depolarize (decrease the voltage threshold required to fire) the NMDA receptors somehow (directly or indirectly). Take this with a grain of salt.
John
Serotonin 5-HT2 receptor activation potentiates N-methyl-D-aspartate receptor-mediated ion currents by a protein kinase C-dependent mechanism.
J Neurosci Res 1996 Jul 15;45(2):153-60 (ISSN: 0360-4012)
Blank T; Zwart R; Nijholt I; Spiess J
Department of Molecular Neuroendocrinology, Max Planck Institute for Experimental Medicine, Gottingen, Germany.
Modulation of N-methyl-D-aspartate (NMDA) receptor-mediated ion currents by serotonin was investigated with a two-electrode voltage clamp technique in Xenopus oocytes injected with rat brain RNA. After a 1-min application of 200 nM serotonin a transient potentiation of the NMDA receptor-mediated ion currents was observed. The serotonin-induced enhancement was mimicked by the protein kinase C activators 1-oleoyl-2-acetyl-sn-glycerol (100 microM) and phorbol 12-myristate 13-acetate (10 nM), whereas the inactive phorbol ester 4-alpha-phorbol 12-myristate 13-acetate (10 nM) had no effect. From these observations it was concluded that protein kinase C was involved in the enhancement of NMDA-induced currents. In agreement with this conclusion, it was found that the serotonin effect was inhibited by the protein kinase C inhibitors sphingosine (1 microM) or staurosporine (1 microM) added 20 min before NMDA application and by oocyte injection of protein kinase C (PKC)-inhibitor peptide (500 ng/oocyte) 1 hr prior to recordings. The serotonin receptor involved was identified as a 5-HT2 receptor subtype by the finding that 200 nM of the selective 5-HT2 receptor agonist alpha-methyl-5-hydroxytryptamine mimicked the potentiation of NMDA-induced ion currents by serotonin. Furthermore, the observed potentiation was significantly reduced by co-application of serotonin with 100 microM of the selective 5-HT2 receptor antagonist ketanserin. These results indicate that 5-HT2 receptors enhance NMDA receptor function via phosphoinositol hydrolysis and subsequent stimulation of PKC.
Posted by JohnX2 on March 24, 2002, at 4:06:43
In reply to Re: ltp in the hippocampus » SLS, posted by JohnX2 on March 24, 2002, at 2:20:06
This always seemed curious to me, how an NMDA antagonist which generally may inhibit long term potentiation (and hence sensitization) may also enhance learning and cognition. This is what memantine is market for in regards to neurodegenerative diseases (alzheimers dementia, etc).Here is one explanation (naturally funded by the pharmaceutical maker):
Uncompetitive NMDA receptor antagonists attenuate NMDA-induced impairment of passive avoidance learning and LTP.
Zajaczkowski W, Frankiewicz T, Parsons CG, Danysz W.
Department of Pharmacology, Merz and Co., Frankfurt/M, Germany. wdanysz@t-online.de
In general, N-methyl-D-aspartate (NMDA) receptor antagonists inhibit learning and long term potentiation (LTP). However, it has been suggested that direct tonic, i.e. non-temporal, activation of NMDA receptors, in contrast to learning, may lead to an increase in synaptic "noise" and, in turn, to a loss of association detection. In the present study, a two-choice passive avoidance task and LTP in vitro (CA1 hippocampal region) were used to address this issue. Dark avoidance learning was impaired by systemic NMDA administration (starting at 25 mg/kg) that was not related to either toxic effects or state-dependent learning. NMDA-induced amnesia was antagonized by ((+)-5-methyl-10,11-dihydro-5H-dibenzocyclohepten-5,10-imine maleate (MK-801) and 1-amino-3,5-dimethyladamantane (memantine), starting at low doses of 0.05 and 2.5 mg/kg, respectively, in a bell-shaped dose-response relationship. A competitive NMDA receptor antagonist CGP-39551 failed to reverse NMDA-induced amnesia. In hippocampal slices, NMDA (10 microM) depressed (S)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolproprionic acid (AMPA) receptor-mediated field potentials in CA1 and also caused a moderate reduction of LTP induction/expression. It was this latter effect that was antagonized by memantine (1 microM). Thus, under conditions of tonic activation of NMDA receptors, uncompetitive NMDA receptor antagonists can paradoxically reverse deficits in learning and synaptic plasticity.
PMID: 9257940 [PubMed - indexed for MEDLINE]
John
> > Hi John.
> >
> > Glad you interjected...
> >
>
> >
> > What is "ltp"?
> >
>
>
> ltp = long term potentiation. For learning, etc.
>
>
> > I have been keeping an eye on research involving lithium and its ability to change the neuronal output of nerve growth factors and to increase the volume of certain brain regions. Much of this work has been done by Husseini Manji, MD. From what I remember, valproate has also demonstrated some these properties, but not to as great a degree as lithium.
> >
> > Here a few summary articles from the NDMDA website. Note the damnable observation that there is indeed a neurodegenerative process involved in mood-disorders, particularly with bipolar disorder and conditions involving a chronic overproduction of cortisol. An optimistic perspective lies in the fact that the brain remains plastic and perhaps capable of a significant arresting and reversal of atrophy along with the sprouting of new neurons and neural connections.
> >
> >
> >
> > LITHIUM: THE ULTIMATE BRAIN FOOD?
> >
> > http://www.ndmda.org/McManamy.html
> >
>
> Thats a pretty cool read.
>
> >
> > Antidepressants have also been shown to restore the size of the hippocampus. However, I wonder if this phenomenon is actually a consequence of an extended remission rather than being intrinsic to the drug itself.
> >
> >
> > ANTIDEPRESSANTS AND BRAIN CELL GROWTH
> >
> > http://www.ndmda.org/ResearchUpdate2-6.html
> >
> >
> > In another post, you mentioned something regarding 5-HT2 receptors being somehow linked to NMDA function. Can you elaborate?
> >
>
> I need to check my notes, my memory is failing. Maybe i need some lithium. ;)
>
> > Thanks.
> >
> > What's going on with you, by the way? It seems that you have had a few "false starts" recently. What gives?
> >
>
> Actually I'm not doing too bad. I dropped Zyprexa and added Serzone (which is the ONLY AD for me that works and doesn't poopout). The Serzone induced a chronic mild agitated hypomania. I quit it for a few days and became a bit depressed. I restarted it with some Zyprexa and now I feel good. Rats. The zyprexa may be giving me a dystonia, so I may be adding Li instead.
>
>
> > I'm still playing with nortriptyline. There might be something I can glean from it in the absence of Effexor. It seems that Effexor may have interfered with my responding to both nortriptyline and imipramine. Although tricyclics don't do the job, they seem to be of some help when combined with Lamictal.
> >
> >
> > - Scott
>
> Good luck on your medicines Scott.
>
> I did a little research on the hippocampus thing.
> I think you can get an MRI to see if you have actually been nailed, right?
>
> Anyways, I found 1 really good paper describing the degenerative process and possible treatments.
> It goes into how many different disorders can more or less have the same cascade of neurodegeneration (stress,aging,depression).
>
> This is a really good read:
>
> http://www.utdallas.edu/~tres/aging_seminar2001/mcewen.pdf
>
> This paper suggests the old stand-by hypothesis of excess glucocorticoids hyperstimulating neurons to death. The paper suggests treatment with possibly phenytoin, nmda antagonist, or by facilitating serotonin reuptake with something like tianeptine.
>
> I would think Lithium may be useful as it modulates glutamate release. Do you recall the hypothesis set forth by the articles you read on Lithium and neurotrophic factor expression?
>
> The nmda antagonists look interesting too. I found an abstract implying that memantine induces brain-derived neurotrophic factor expression.
>
> Both Li and memantine look like interesting medicines to help with poop out and brain shrinkage and possibly cognition.
>
> What do you think?
>
> Best Regards,
> John
>
> ----------------------------------------------
>
> The neuroprotective agent memantine induces brain-derived neurotrophic factor and trkB receptor expression in rat brain.
> Mol Cell Neurosci 2001 Sep;18(3):247-58 (ISSN: 1044-7431)
> Marvanova M; Lakso M; Pirhonen J; Nawa H; Wong G; Castren E
> A. I. Virtanen Institute, University of Kuopio, Kuopio, 70211, Finland.
> Memantine is a medium-affinity uncompetitive N-methyl-d-aspartate receptor antagonist and has been clinically used as a neuroprotective agent to treat Alzheimer's and Parkinson's diseases. We have examined the effect of memantine (ip 5-50 mg/kg; 4 h) on the expression of brain-derived neurotrophic factor (BDNF) and trkB receptor mRNAs in rat brain by in situ hybridization. Memantine at a clinically relevant dose markedly increased BDNF mRNA levels in the limbic cortex, and this effect was more widespread and pronounced at higher doses. Effects of memantine on BDNF mRNA were also reflected in changes in BDNF protein levels. Moreover, memantine induced isoforms of the BDNF receptor trkB. Taken together, these data suggest that the neuroprotective properties of memantine could be mediated by the increased endogenous production of BDNF in the brain. These findings may open up new possibilities of pharmacologically regulating the expression of neurotrophic factors in the brain. [Copyright 2001 Academic Press.].
Posted by JohnX2 on March 24, 2002, at 4:13:28
In reply to Re: ltp in the hippocampus » JohnX2, posted by SLS on March 23, 2002, at 8:55:19
anyone,Ever thought about giving a medicine like Tianeptine a go? May as well go for the back-assword medicines in some cases. ;)
John
Posted by OldSchool on March 24, 2002, at 22:22:34
In reply to Re: ltp in the hippocampus » SLS, posted by JohnX2 on March 23, 2002, at 0:24:09
> I want lithium because of its neuroprotective and neurotrophic potential. It is supposed to promote plasticity. Maybe this would help to restore the size and function of the hippocampus. What do you think? Depression has greatly impaired my memory.
> >
>I tried lithium augmentation of Effexor once. The lithium was a total disaster, it brought me down sooooo much. A total mood dampener it was for me. I stayed on it for about eight weeks. Everybody around me said I was terrible on it. After I went off of it though, I found that the Effexor seemed to work better in subtle ways. Not as bad poop out as before. The lithium definitely did something, I dont know what.
I dont think lithium is the med for me, but after I took it for a few months with an AD my ADs worked a little better.
Old School
Posted by SLS on March 25, 2002, at 6:22:24
In reply to Re: ltp in the hippocampus, posted by OldSchool on March 24, 2002, at 22:22:34
Hi OldSchool.
How much lithium were you taking? Do you recall what your blood levels were?
> I tried lithium augmentation of Effexor once. The lithium was a total disaster, it brought me down sooooo much. A total mood dampener it was for me. I stayed on it for about eight weeks. Everybody around me said I was terrible on it. After I went off of it though, I found that the Effexor seemed to work better in subtle ways. Not as bad poop out as before. The lithium definitely did something, I dont know what.
I don't like the way I feel when I take lithium at dosages of 600mg/day and higher. It definitely flattens-out my affect, leaves me apathetic and unmotivated, and without creativity. Overall, I felt more depressed on it. I think my blood-level at 600mg was 0.45 ng/ml. For bipolar disorder, the therapeutic range is accepted to be somewhere between 0.8 and 1.2.Dr. Manji and others have investigated the neuroprotective and neurotrophic effects of lithium at low, subtherapeutic dosages. Even at these low dosages, lithium exerted marked positive effects. I am hoping that a dosage of 300mg - 450mg will help with these things.
When lithium is employed as an augmentor of antidepressants, dosages of between 300mg - 600mg are often optimal. I don't know what range of blood-levels this represents. I would guess something like 0.4 - 0.6.
- Scott
Posted by OldSchool on March 25, 2002, at 15:28:20
In reply to Re: ltp in the hippocampus » OldSchool, posted by SLS on March 25, 2002, at 6:22:24
> Hi OldSchool.
>
> How much lithium were you taking? Do you recall what your blood levels were?I was taking 600 mg Lithobid with 300 mg Effexor XR. The Lithium totally made me more depressed and honestly, more sappy and cranky feeling. Everyone hated me on it. Then, after I got the lithium level my Pdoc told me the level was a bit low and told me to go up to 900 mg, which I did. When I did that, my vision got kinda blurry but I did start feeling a little better. I didnt like the blurry vision thing at all, nor the metallic taste in my mouth I got from lithium and it didnt have much of an AD effect in me. So after just two or three days on 900 mg, I quit it and went back to plain old Effexor.
>
> > I tried lithium augmentation of Effexor once. The lithium was a total disaster, it brought me down sooooo much. A total mood dampener it was for me. I stayed on it for about eight weeks. Everybody around me said I was terrible on it. After I went off of it though, I found that the Effexor seemed to work better in subtle ways. Not as bad poop out as before. The lithium definitely did something, I dont know what.
>
>
> I don't like the way I feel when I take lithium at dosages of 600mg/day and higher. It definitely flattens-out my affect, leaves me apathetic and unmotivated, and without creativity. Overall, I felt more depressed on it. I think my blood-level at 600mg was 0.45 ng/ml. For bipolar disorder, the therapeutic range is accepted to be somewhere between 0.8 and 1.2.Lithium totally flattened me out like a pancake. Made me feel like a depressed robot. However, Ive wondered maybe what just lithium by itself at a theraputic level would do for me. Maybe just 900 mg lithium and no antidepressant for me? Maybe I will try that right before I have ECT.
>
> Dr. Manji and others have investigated the neuroprotective and neurotrophic effects of lithium at low, subtherapeutic dosages. Even at these low dosages, lithium exerted marked positive effects. I am hoping that a dosage of 300mg - 450mg will help with these things.Lithium at low doses made me depressed as dirt.
>
> When lithium is employed as an augmentor of antidepressants, dosages of between 300mg - 600mg are often optimal. I don't know what range of blood-levels this represents. I would guess something like 0.4 - 0.6.Maybe I should go back and just try plain old lithium, by itself, nothing else. Get rid of antidepessants and go to adequate blood levels. Maybe I should do that right before I have ECT to be sure Im not bipolar.
Old School
>
>
> - Scott
Posted by Chloe on March 25, 2002, at 20:40:40
In reply to Re: Im thinking of trying lithium one more time, posted by OldSchool on March 25, 2002, at 15:28:20
Old School,
Lithobid, the pink enteric coated pills, gave me a nasty, pasty taste in my mouth. So my pdoc switched me to the Eskilith Controlled Release which gives me totally different side effects than the Lithobid. It's still released slowly throughout the day, but it's a different form (hard yellow pill that comes in scored 450 mg pills). And I like it better. You may find you also don't get the blurry vision. Who knows?I found lithobid alot like a "drug". I had dry mouth, constipation (seems impossible on Lithium!). On the Esklith CR, I feel much better. No dry mouth or constipation or anything but a little polyuria, for which lithium is so famous!
So you might want to switching brands of Lithium before you throw the whole drug in the trash heap. The brands really very for my experience.
Just an FYI!
Take care,
Chloe
Posted by JohnX2 on March 26, 2002, at 4:40:54
In reply to Re: Im thinking of trying lithium one more time, posted by OldSchool on March 25, 2002, at 15:28:20
>
> Maybe I should go back and just try plain old lithium, by itself, nothing else. Get rid of antidepessants and go to adequate blood levels. Maybe I should do that right before I have ECT to be sure Im not bipolar.
>
> Old SchoolOS,
I wouldn't rule out a Lamictal trial if you haven't tried it. It is generally benign on the side effects and it has a decent reputation for TRD and bipolar.
Regards,
John
Posted by Ron Hill on March 30, 2002, at 11:50:40
In reply to Re: treatment resistant depression » Ron Hill, posted by SLS on March 23, 2002, at 13:51:45
Scott,
Sorry to take so long to get back to you. I have, however, prayed for you daily since I sent my original post to you.
After six years of dysfunction, my household project to-do list is very long and, therefore, I've been busy. But I'll tell ya what, Scott, I am very thankful to be well!!! I want the same for you. Here are my replies to your one-week old questions:
> Questions:
>
> 1. What is your blood level of lithium at 600mg/day?0.4 mEq/l
> 2. Do you experience any side effects of lithium, i.e. apathy, amotivation, loss of creativity etc.?
No. Small amount of rash. Frequent urination initially, but no longer a side effect.
> 3. How does your (hypo)mania manifest? How often does it happen?
Hypomania is not much of an issue since starting Lithobid almost three years ago, except on the first day of AD trials, and on one occasion when I increased my SAM-e dose from 200 mg/day to 400 mg/day. (I went back down to 200 mg/day and it went away).
For me, hypomania usually consists of racing thoughts, great ideas, jumping from one task to another without finishing any of them, insomnia, and often a low tolerance to frustration. Sometimes I would call it a dysphoric hypomania while at other times it's more of a euphoric hypomania.
> 4. 200mg of S-AMe sounds wonderful. How frequently do you think that someone should respond to such a low dosage? How did you go about establishing your optimum dosage? Did you initially take more?
Several people that post to this board have responded to low dosage of SAM-e, but this is probably the exception and not the rule. It is my observation (not a scientific study) that the patients most likely helped by low dosage SAM-e are those that experience relief (at least initial relief) from depression by taking micro doses of AD's (SSRI's in particular).
I determined my SAM-e dose by trial and error. For years I was stuck. Like you, I'm Bipolar II. Lithobid adequately controls my hypomania but does nothing for my depression. Any of the SSRI's will take away my "I want to die" mood but leave me with side effects (loss of ambition, loss of energy, lack of motivation, blunted emotions, etc). I attribute these symptoms to low dopamine transport. I have tried a ton of other ADs over the years, but I will not bore you with the details.
Five months ago I went to my pdoc for my regularly scheduled visit. At the time, I was only taking Lithobid because of the AD side effects and, therefore, depression was a problem. My pdoc had recently reviewed several studies showing success in treating depression using SAM-e in conjunction with an AD and success using SAM-e alone. He suggested that I take 400 mg/day of SAM-e in conjunction with 25 mg/day of Zoloft. (I am hypersensitive to most medication so I take small SSRI doses). Initially, I was skeptical because over the years I have taken a lot of over-the-counter supplements, most of which did very little to ease my depression. But I told my pdoc that I would give it a try.
Initially I could only take one 200 mg tablet of SAM-e every other day. If I took more, I would experience side effects (flush, nausea, confused thinking, general ill feeling, "skin crawling"). However, within about five days, my depression began to lift.
Currently, I take 200 mg/day of SAM-e without any adverse side effects. Also, I recently dumped the Zoloft because even at the micro dose of 12.5 mg/day, I began to experience breakthrough anergy and anhedonia. When I dumped the Zoloft I increased the SAM-e to 400 mg/day thinking that I needed to compensate for the loss of the SSRI effect with additional SAM-e. However, as I mentioned above, the higher dose of SAM-e induced hypomania. Therefore, all I take is 600 mg Lithobid and 200 mg SAM-e daily. And it is GREAT!!
Bottom line: 200 mg SAM-e daily has helped me more than any of the many ADs I've tried over the years. For me personally, SAM-e has turned out to be a lifesaver! So far I have five months of excellent results and absolutely no hint of poop out.
My layman's opinion regarding the mechanism by which SAM-e helps me is that it raises the serotonin and dopamine levels in my brain in a "balanced" fashion.
It is very important to take plenty of B-6, B-12 (use sublingual form) and folate with the SAM-e to prevent the build up of homocystiene. Also, SAM-e is absorbed more efficiently by the small intestines when it is taken on an empty stomach. However, I usually eat a small bite of food to reduce nausea.
> 5. Is it safe to combine S-AMe with a MAO-inhibitor?I do not know, Scott. The package insert for SAM-e does not warn against use with MAOI, while at the same time it does warn against bipolar patients taking it without being on a mood stabilizer to avoid mania. In all I have read on SAM-e, I have never seen it stated that it is incompatible with an MAOI. But better to be safe and ask your pdoc.
> > For you, it might be 300 mg/day Lamictal and 400 mg/day SAM-e (or as high as 1600 mg/day SAM-e if needed). Start by using 100 or 200 mg/day of SAM-e as an add-on to your current cocktail, then play it by ear to see if you can discontinue your AD.
>
> > PLEASE read the very well written and technically informative SAM-e article (posted previously by davex) linked below. All I can do is put out the bread; it's up to you to decide whether or not to eat.
>
> Thank you very much. I think I'll move S-AMe near the top of my list. At this point in time, I am planning to:
>
> 1. Try to find an optimum dosage of nortriptyline that will maintain a partial response.
>
> 2. Add Nardil, titrating to perhaps 90mg.
>
> Perhaps this would be a good point to try adding S-AMe. What do you think?
>
> 3. Retry an atypical neuroleptic. Previous trials produced mild transient improvements followed by the emergence of unacceptable cognitive side effects at higher dosages.
> - Zyprexa (olanzapine)
> - Geodon (ziprasidone)
> - Abilitat (aripiprazole)
>
> 4. Add Mirapex.
>
> 5. Finish reading your S-AMe article. :-)
Move #5 to #1. Move #5 to #1. Move #5 to #1. Move #5 to #1. Move #5 to #1. Move #5 to #1. Move #5 to #1. Move #5 to #1. Move #5 to #1.
Move #5 to #1. Move #5 to #1. Move #5 to #1.
Move #5 to #1.-- Ron
---------------------------------------------
Posted by MoQ on December 19, 2002, at 16:39:59
In reply to Re: treatment resistant depression -Suggestions? » SLS, posted by shelliR on March 18, 2002, at 20:39:09
Hi there! I am new to posting on this board, although have been reading it at length over the past month or so. I won't go into my 10+ year of treatment-resistant depression, but will say that I was extremely relieved (and, I must admit, excited) to find this site. I am coming in a different door, I know, because I am still unsure of my navigational skills in here, but Shelli, I really wanted to make sure I was in contact with you as you have the same views I do with regard to using Vicodin (or other opiates) in the treatment of depression that has just not responded to several different trials of anti-depression meds. I thought I was the only one who experienced incredible symptom relief with the use of two one-half tablet doses of Vicodin daily. I found out how well I responded to this opiate several years ago and have used it off and on (in very small amounts) in connection with injuries and hospital stays for a couple of surgeries. I am very fortunate to have a psychiatrist I have been going to for ten years that respects my opinion and really listens to my concerns. After sending her quite a bit of information (mainly from this site), she referred me to a psychopharmacologist. My initial consult with him is in January (2003). My question is this: Does anyone know of any other research articles/links I can go to in order to be as well prepared and informed as possible when I have my appointment? Thank you in advance to any and all who can assist me in this regard!
Posted by ShelliR on December 19, 2002, at 21:15:51
In reply to Use of opiates in treating depression, posted by MoQ on December 19, 2002, at 16:39:59
Dear MoQ,
I was very much like you when I first started taking vicodin: for several years a very small amount took care of my depression when my AD didn't work. First only premenstrually, then all the time. But my story sort of goes downhill, so be careful.
I was put on oxycontin instead of vicodin, because this new psychiatrist thought it was better because it lasted longer. I got habituated very quickly and had to go up and up until I no longer could afford it. Now I'm on methadone, which doesn't have as good an effect, but is a lot cheaper. But even with the methadone, in order for it to be effective, I'm on a large dose, and unless I keep increasing, it loses its effectiveness for my depression.
If I had to do it all over again, I wouldn't bother finding a psychiatrist to prescribe opiates. I'd get it from a pain doctor and I would stick with the vicodin--the very least I could get away with. I think the oxycontin really messed me up because now even a large dose of vicodin does nothing.
There's a woman on this board, Elizabeth. I'm sure you've run into her posts about buprenorphine if you're doing searches on opiates and depression. She was able to get it from her psychiatrists, but it is only available in liquid form for injections. She uses it intranasally. It was supposed to go on the market here in a sublingual form as an alternative to methadone, but they've put it off at least a year. It's a partial opiate and seems to help people not crave heroin--like methadone. There was a small study on it http://www.biopsychiatry.com/bupref.html-that's an abstract, but I know the whole study is on the internet. Buprenorphine is also "addictive", really the right word is "habituating".
The other bad thing about using opiates for depression is that if you have to go into a hospital, they treat you like shit, like you are a street addict. I kept blacking out from the large doses of effexor they were giving me, but they blamed it on coming off the oxycontin, so they couldn't care less. Anyway, if it's the only thing that works for you, I would go for it, but I'd be surprised if you'll get any support from a psychopharmacologist. The guys from the study no longer prescribe it because they were sued by someone who blamed their dependence on buprenorphine on them.
Sorry, for the bad news, but it's important to know what you may be getting yourself in to. Still, while I am trying other ADs, and homeopothy and acupuncture, I am still taking methadone, because it has kept me alive. Just be careful.
Shellli
Posted by linkadge on December 20, 2002, at 9:29:32
In reply to Re: Use of opiates in treating depression » MoQ, posted by ShelliR on December 19, 2002, at 21:15:51
Are you in a place where you can
do an intense physical workout?I knew from the beginning that opiates
were very effective for my mood. Tylenol
3 (codine) for wizdom teeth was very mood elevating. I really think some people have
a disturbance in the endorphin system,
hense my hypersensitivity to pain. I feel
like I will just fall apart all the time.While the Celexa really helps, the only thing
that has put me in a place of feeling very
good, was extreme arobic excercise. It sounds
basic, but research shows heroin habits are
very rarely broken without some type of
intense physical workout.Linkadge
Posted by BrittPark on December 20, 2002, at 23:52:22
In reply to This may sound trivial but, posted by linkadge on December 20, 2002, at 9:29:32
A large percentage of people respond well to opioids, depressed or not. I've generally looked forward to things like wisdom teeth being pulled because I know I'll be on vicodin for a day or two. The improvement in mood that I get (and I believe many others get) is remarkable. Indeed before the discovery of the first antidepressants opioids were commonly prescribed for depression.
The problem with opioids is tolerance. Almost everyone develops it sooner or later. So if you're going to use opioids to treat depression, take as little as possible and as mild as possible an opiod. In addition take opioid holidays. I don't know how long they would have to be, and they wouldn't feel like holidays. Other possibilities are mixed agonist antagonists like buprenorphine, which is supposed to produce less tolerance, or tramadol a very week opioid that is also supposed to produce less tolerance.
There is some possibly very good news coming from a company called Pain Therapeutics who are in clinical trials of two drugs, one a morphine formulation and one an oxycodone formulation. The trick of these new drugs is they contain very small amounts of an opioid antagonist (I'm not sure whether it is naloxone or naltrexone). On the surface it sounds silly, but the researchers who founded the company found that the addition of microdoses of antagonists with opiod agonists not only improved analgesia in rats but seemed to block the development of tolerance. Now Murphy's law says that along with the lack of tolerance will come lack of euphoria :( I hope not though.
By the way I do take vicodin for depression at 5/500 in the evening. My psychiatrist prescribes it. I think that if I could take 3 or 4 5/500s a day without becoming tolerant it would eliminate the rest of my depression. Alas, vicodin doesn't work that way, at least for me.
In hopes of better living through better chemistry,
Britt
Posted by judy1 on December 21, 2002, at 11:05:54
In reply to Use of opiates in treating depression, posted by MoQ on December 19, 2002, at 16:39:59
I'm glad you have found relief with such a small dose of hydrocodone daily- it is what my shrink prescribes for some of his panic/depressed patients. Personally I couldn't agree more with Shelli's post- it is a LOT easier going through a pain doc, I get ms contin (morphine) that way. Because I have bipolar disorder, my depresssions tend to be self-limiting and opiate treatment works really well in that setting because I don't have to keep upping the dose to get the same effect. I wonder if you have anxiety symptoms?, I ask because hydrocodone (vicodin) is a great anxiolytic drug too, and since you are getting such a robust response from a relatively low dose perhaps that is why. take care, judy
Posted by jimmygold70 on December 21, 2002, at 12:21:01
In reply to Use of opiates in treating depression, posted by MoQ on December 19, 2002, at 16:39:59
Why mess with opiates? I'd bet you didn't try all treatment options.
My protocol:
1) SSRI
2) Raise Dose
3) Switch SSRI with same higher dose
4) Add Edronex (or if not tolerated, move to high dose Effexor)
5) SSRI+Edronax+Remeron or Effexor+Remeron
6) Add Lamictal
7) Add Lithium
8) Add amantadine (Symmestrel)
9) ECT
10) MAO Inhibitor (Nardil/Parnate)
11) Going to a well known psychopharmacologist and staying there for a year+This works for 98% of depressed...
Jimmy
10)
Posted by MoQ on December 29, 2002, at 10:31:40
In reply to Re: Use of opiates in treating depression » MoQ, posted by ShelliR on December 19, 2002, at 21:15:51
> Dear MoQ,
>
> I was very much like you when I first started taking vicodin: for several years a very small amount took care of my depression when my AD didn't work. First only premenstrually, then all the time. But my story sort of goes downhill, so be careful.
>
> I was put on oxycontin instead of vicodin, because this new psychiatrist thought it was better because it lasted longer. I got habituated very quickly and had to go up and up until I no longer could afford it. Now I'm on methadone, which doesn't have as good an effect, but is a lot cheaper. But even with the methadone, in order for it to be effective, I'm on a large dose, and unless I keep increasing, it loses its effectiveness for my depression.
>
> If I had to do it all over again, I wouldn't bother finding a psychiatrist to prescribe opiates. I'd get it from a pain doctor and I would stick with the vicodin--the very least I could get away with. I think the oxycontin really messed me up because now even a large dose of vicodin does nothing.
>
> There's a woman on this board, Elizabeth. I'm sure you've run into her posts about buprenorphine if you're doing searches on opiates and depression. She was able to get it from her psychiatrists, but it is only available in liquid form for injections. She uses it intranasally. It was supposed to go on the market here in a sublingual form as an alternative to methadone, but they've put it off at least a year. It's a partial opiate and seems to help people not crave heroin--like methadone. There was a small study on it http://www.biopsychiatry.com/bupref.html-that's an abstract, but I know the whole study is on the internet. Buprenorphine is also "addictive", really the right word is "habituating".
>
> The other bad thing about using opiates for depression is that if you have to go into a hospital, they treat you like shit, like you are a street addict. I kept blacking out from the large doses of effexor they were giving me, but they blamed it on coming off the oxycontin, so they couldn't care less. Anyway, if it's the only thing that works for you, I would go for it, but I'd be surprised if you'll get any support from a psychopharmacologist. The guys from the study no longer prescribe it because they were sued by someone who blamed their dependence on buprenorphine on them.
>
> Sorry, for the bad news, but it's important to know what you may be getting yourself in to. Still, while I am trying other ADs, and homeopothy and acupuncture, I am still taking methadone, because it has kept me alive. Just be careful.
>
> ShellliThanks so much for your kind response. I was a bit hurt by the first response I saw from someone who basically accused me of not doing everything I could, by using the words "I bet you haven't...." Wow, that was kind of a shocker because it took up quite a bit of courage to post anything at all and everyone had seemed so supportive. Anyway, it made me feel better to get your response (who needs to be kicked when they're down, right?). Anyway, the only thing I am open to at this point is the Vicodin in small doses. I do not want to get involved with OxyContin or Methadone as I know there is an extremely high risk of the negatives far outweighing the positives. Thanks again and all my best to you and your ongoing recovery.
Posted by MoQ on December 29, 2002, at 10:50:34
In reply to Re: Use of opiates in treating depression » MoQ, posted by judy1 on December 21, 2002, at 11:05:54
> I'm glad you have found relief with such a small dose of hydrocodone daily- it is what my shrink prescribes for some of his panic/depressed patients. Personally I couldn't agree more with Shelli's post- it is a LOT easier going through a pain doc, I get ms contin (morphine) that way. Because I have bipolar disorder, my depresssions tend to be self-limiting and opiate treatment works really well in that setting because I don't have to keep upping the dose to get the same effect. I wonder if you have anxiety symptoms?, I ask because hydrocodone (vicodin) is a great anxiolytic drug too, and since you are getting such a robust response from a relatively low dose perhaps that is why. take care, judy
Thank you, thank you, thank you! I had just responded to Shelli, indicating my appreciation of how supportive she was. The first response I opened had come across (at least to me) as accusatory rather than offering suggestions. I do have anxiety disorder with panic attacks, as well as depersonalization (which is the most horrible experience ever!! Luckily this doesn't happen as much). I haven't had to up the dosage at all. I do have benzos, which I have never abused, and my husband recreationally smokes pot, but I have absolutely no interest in that. I also drink maybe four times a year, two drinks each occasion. My point that I am trying to make to people (without being judged--and you and Shelli have certainly NOT judged me), is that I am not on a search for a legal high. I read somewhere that someone indicated doctors are afraid someone will become addicted to a narcotic, but aren't we all addicted to antidepressants? If something is available that improves my quality of life and takes away the terrible suffering and feelings of suicide, then why on earth is it not available? Anyway, your feedback was much appreciated! Take care!
Posted by MoQ on December 29, 2002, at 10:55:39
In reply to This may sound trivial but, posted by linkadge on December 20, 2002, at 9:29:32
> Are you in a place where you can
> do an intense physical workout?
>
> I knew from the beginning that opiates
> were very effective for my mood. Tylenol
> 3 (codine) for wizdom teeth was very mood elevating. I really think some people have
> a disturbance in the endorphin system,
> hense my hypersensitivity to pain. I feel
> like I will just fall apart all the time.
>
>
>
> While the Celexa really helps, the only thing
> that has put me in a place of feeling very
> good, was extreme arobic excercise. It sounds
> basic, but research shows heroin habits are
> very rarely broken without some type of
> intense physical workout.
>
> Linkadge
>
>Nothing is trivial, I appreciate any and all information! I know that exercise is supposed to produce endorphins, and I agree that I should indeed get more exercise. I am deconditioned but am in good physical shape for working out (low cholesterol, low blood pressure, normal body weight, etc.). I did want to comment on one thing, however, and that is how odd I find it that THE ONLY THING that elevates my mood is the Vicodin. Tylenol with codeine does absolutely nothing. Isn't that weird? I am just becoming convinced that people's brains can be wired very differently and in some cases respond differently to certain medications. Thanks again for your always welcome input!
>
>
>
Posted by MoQ on December 29, 2002, at 10:58:39
In reply to Re: opioids, posted by BrittPark on December 20, 2002, at 23:52:22
> A large percentage of people respond well to opioids, depressed or not. I've generally looked forward to things like wisdom teeth being pulled because I know I'll be on vicodin for a day or two. The improvement in mood that I get (and I believe many others get) is remarkable. Indeed before the discovery of the first antidepressants opioids were commonly prescribed for depression.
>Thanks for your response! Until I found this site I thought I was completely alone in this reaction. Take care!
> The problem with opioids is tolerance. Almost everyone develops it sooner or later. So if you're going to use opioids to treat depression, take as little as possible and as mild as possible an opiod. In addition take opioid holidays. I don't know how long they would have to be, and they wouldn't feel like holidays. Other possibilities are mixed agonist antagonists like buprenorphine, which is supposed to produce less tolerance, or tramadol a very week opioid that is also supposed to produce less tolerance.
>
> There is some possibly very good news coming from a company called Pain Therapeutics who are in clinical trials of two drugs, one a morphine formulation and one an oxycodone formulation. The trick of these new drugs is they contain very small amounts of an opioid antagonist (I'm not sure whether it is naloxone or naltrexone). On the surface it sounds silly, but the researchers who founded the company found that the addition of microdoses of antagonists with opiod agonists not only improved analgesia in rats but seemed to block the development of tolerance. Now Murphy's law says that along with the lack of tolerance will come lack of euphoria :( I hope not though.
>
> By the way I do take vicodin for depression at 5/500 in the evening. My psychiatrist prescribes it. I think that if I could take 3 or 4 5/500s a day without becoming tolerant it would eliminate the rest of my depression. Alas, vicodin doesn't work that way, at least for me.
>
> In hopes of better living through better chemistry,
>
> Britt
>
Posted by MoQ on December 29, 2002, at 11:09:56
In reply to Re: Use of opiates in treating depression, posted by jimmygold70 on December 21, 2002, at 12:21:01
> Why mess with opiates? I'd bet you didn't try all treatment options.
>
> My protocol:
> 1) SSRI
> 2) Raise Dose
> 3) Switch SSRI with same higher dose
> 4) Add Edronex (or if not tolerated, move to high dose Effexor)
> 5) SSRI+Edronax+Remeron or Effexor+Remeron
> 6) Add Lamictal
> 7) Add Lithium
> 8) Add amantadine (Symmestrel)
> 9) ECT
> 10) MAO Inhibitor (Nardil/Parnate)
> 11) Going to a well known psychopharmacologist and staying there for a year+
>
> This works for 98% of depressed...
>
> Jimmy
>
> 10)Just a quick FYI: I have tried #1, #2, #3, #4, #5, #6, and am now trying #11. The rest of the options (#7, 8, 9 and 10) were discussed with my psychiatrist of 11 years and her colleagues, and THEY recommended those were roads not to travel down. I am wondering if you are familiar at all with all of the studies that have been conducted regarding the positive anti-depressant effect(s) produced by SMALL AMOUNTS of opiates? (i.e., the fact that they were the medication of choice for depression up until the 1960's; that there has been extensive research conducted at hospitals such as one in Boston; and that there are researchers who are in the process of trying to develop medicinal agents that work with the use of an opiate ingredient). I am not "messing with opioids," I am trying to become as educated as possible on my condition and, after 11 years of suffering, am going through PROPER, MEDICAL channels to explore other treatment options, with the assistance of my doctor, psychiatrist, and now a psychopharmacologist. Perhaps you didn't mean to come across the way you did in your message, but, to say the least, I felt a bit attacked. You do not know my background or what courses of treatment I have undergone, and your tone was rather judgmental. I am just thankful there were other people who provided input, or I would have abruptly stopped looking for help on this site.
Posted by MoQ on December 29, 2002, at 11:21:07
In reply to Re: Use of opiates in treating depression » MoQ, posted by ShelliR on December 19, 2002, at 21:15:51
> Dear MoQ,
>
> I was very much like you when I first started taking vicodin: for several years a very small amount took care of my depression when my AD didn't work. First only premenstrually, then all the time. But my story sort of goes downhill, so be careful.
>
> I was put on oxycontin instead of vicodin, because this new psychiatrist thought it was better because it lasted longer. I got habituated very quickly and had to go up and up until I no longer could afford it. Now I'm on methadone, which doesn't have as good an effect, but is a lot cheaper. But even with the methadone, in order for it to be effective, I'm on a large dose, and unless I keep increasing, it loses its effectiveness for my depression.
>
> If I had to do it all over again, I wouldn't bother finding a psychiatrist to prescribe opiates. I'd get it from a pain doctor and I would stick with the vicodin--the very least I could get away with. I think the oxycontin really messed me up because now even a large dose of vicodin does nothing.
>
> There's a woman on this board, Elizabeth. I'm sure you've run into her posts about buprenorphine if you're doing searches on opiates and depression. She was able to get it from her psychiatrists, but it is only available in liquid form for injections. She uses it intranasally. It was supposed to go on the market here in a sublingual form as an alternative to methadone, but they've put it off at least a year. It's a partial opiate and seems to help people not crave heroin--like methadone. There was a small study on it http://www.biopsychiatry.com/bupref.html-that's an abstract, but I know the whole study is on the internet. Buprenorphine is also "addictive", really the right word is "habituating".
>
> The other bad thing about using opiates for depression is that if you have to go into a hospital, they treat you like shit, like you are a street addict. I kept blacking out from the large doses of effexor they were giving me, but they blamed it on coming off the oxycontin, so they couldn't care less. Anyway, if it's the only thing that works for you, I would go for it, but I'd be surprised if you'll get any support from a psychopharmacologist. The guys from the study no longer prescribe it because they were sued by someone who blamed their dependence on buprenorphine on them.
>
> Sorry, for the bad news, but it's important to know what you may be getting yourself in to. Still, while I am trying other ADs, and homeopothy and acupuncture, I am still taking methadone, because it has kept me alive. Just be careful.
>
> Shellli
By the way, thank you so much for the link you provided. I was able to garner a lot of information that may be useful in my ongoing quest. Thanks again!
Go forward in thread:
Psycho-Babble Medication | Extras | FAQ
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.org
Script revised: February 4, 2008
URL: http://www.dr-bob.org/cgi-bin/pb/mget.pl
Copyright 2006-17 Robert Hsiung.
Owned and operated by Dr. Bob LLC and not the University of Chicago.