![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 25 of 164. This is the beginning of the thread.
Posted by JohnB. on April 8, 1999, at 23:24:43
There's very promising information on a drug/neurotransmitter approach to treating chronic long term/ intractable depressive illness. The dopaminergic system has long been suspected as a biochemical part of the affective disorder problem (either directly or indirectly) and more evidence mounts that that dopamine receptors play a critical role not just in terms of mood state but just as critically in the prolongation/inescapability of this illness as it relates to memory, specifically emotional memory. It seems that what we call chronic, recurrent, or dysthymic depression may just be the mysteriously caused and tormentingly intrusive omnipresence of negative/stress related emotional memories. Somehow, the sufferer's perceptive awareness, or consciousness, is quite literally unable to break away from this unbearable onslaught of exclusively aversive emotive memories; the learned helplessness paradigm seems to fit in critically with this hypothesis.
At any rate, interesting things are happening in studies of a relatively new European "anti-psychotic" called Amisulpride (SOLIAN) as it relates to chronic depressive illness, not psychosis. This unique drug selectively blocks two subtypes of dopamine receptors (D2 and D3) and almost exclusively acts in the mesolimbic brain, unlike most other anti-psychotic meds. Intruigingly, amisulpride only blocks pre-synaptically, which means that in small doses, it actually increases dopaminergic (2 & 3) neurotransmission; this selectivity is amazing enough, but what makes this medication so potentially meaningful for treatment resistant and chronic depressives is the fact that it seems to potentiate D2 and D3 transmission primarily at certain sites WITHIN ONLY THE LIMBIC SYSTEM, the "birthplace" of emotional (mood) states and crucially implicated in memory storage and retreival. Unnecessary stimulation of dopaminergic receptors elsewhere in the brain involving locomotion and general attention/arousal seem to be larely bypassed, eliminating sleep disturbances, anxiety exascerbations, the jitters, and scattered and/or hyperattentiveness. Also, the extrapyramidal side effects (atkinesias and dyskinesias) are practically nonexistent at these non-pschotic doses. My guess is that drugs directed specifically for neuroaction in the limbic structures (whether dopaminergic, noradrenergic, serotonergic, or whatever) are going to be the critical links toward the most effective treatments for the core dysfunctions causing affective illness. Never use the word cure, but keep your eyes this and like-acting meds to come.
Posted by nick on April 9, 1999, at 7:37:32
In reply to Dysthymia/Treatment Resistant Depressions, posted by JohnB. on April 8, 1999, at 23:24:43
> Amisulpiride has been used in France for the treatment of dysthymis for sometime. Flupenthixol is licensed for 'mild depression' in the UK. Venlafaxine at high dosage has some DA reuptake blockade, and paroxetine also has some pro-dopaminergic action. The Hospital trials in the 1960s sugest chlorpromazine to be superior to placebo as an antidepressant.
Clinical experience suggests however that neuroleptics are not as potent an antidepressant as more usual drugs, and that they can cause profound dysphoria (David Healy's work - not sure if it's been published yet.) Still, interesting developments.
Nick
Posted by Jim on April 9, 1999, at 7:57:08
In reply to Dysthymia/Treatment Resistant Depressions, posted by JohnB. on April 8, 1999, at 23:24:43
Thanks, John. I'm usually pretty skeptical of these kind of claims with meds I don't know very well, so I did some checking around on the Psych-info database. Sure enough, there's some strong evidence on using the novel antipsychotic amisulpride as an antidepressant. Out of many studies, I've listed two of the non-technical ones below. -- Jim
TITLE: Amisulpride versus fluoxetine in patients with dysthymia or major depression in partial remission: A double-blind, comparative study.
AUTHOR: Smeraldi,-Enrico
SOURCE: Journal-of-Affective-Disorders. 1998 Feb; Vol 48(1): 47-56
ABSTRACT: In a multicentre, double blind, parallel group study, 281 patients (aged 18-70 yrs) with Diagnostic and Statistical Manual of Mental Disorders-III-Revised (DSM-III-R) diagnosis of dysthymia or a single episode of major depression in partial remission were randomised to 3 mo of treatment with amisulpride 50 mg/day or fluoxetine 20 mg/day. The baseline Montgomery-Asberg Depression Rating Scale (MADRS) total score was reduced by at least 50% in 74.1% of patients with amisulpride and 67.4% with fluoxetine. No significant differences between treatment groups were found in the reductions in mean total score with the MADRS, Widloecher psychomotor retardation scale, Sheehan disability scale, and CGI. Anxiety measured by the Hamilton Rating Scale for Anxiety total mean score decreased significantly more with amisulpride (63%) than with fluoxetine (54%). There were 13 dropouts due to adverse events with amisulpride and 10 with fluoxetine. The number of patients reporting at least one adverse event was similar in the 2 groups (amisulpride 47.5%; fluoxetine 40.9%). As expected, in the amisulpride group endocrine-like adverse events in female patients were the most common, while nausea, dyspepsia, anorexia and insomnia occurred more frequently with fluoxetine. ((c) 1998 APA/PsycINFO, all rights reserved)
TITLE: Amisulpride in dysthymia: Results of a naturalistic study in general practice.
SOURCE: European-Psychiatry. 1996; Vol 11(Suppl 3): 145s-147s
ABSTRACT: A naturalistic study was conducted on the efficacy and tolerance of low doses of amisulpride in the treatment of dysthymia. A total of 109 patients (aged 17-81 yrs) received low doses (50-100 mg) of amisulpride for 4-wks. A global evaluation showed good or very good efficacy and tolerance in more than 80% of the patients. The social disability observed at baseline was significantly improved after the 4-wk treatment period. Few adverse events were observed and only 4 patients dropped out due to side effects. The results suggest that low doses of amisulpride might be a safe and effective treatment for dysthymia in clinical practice. ((c) 1997 APA/PsycINFO, all rights reserved)
Posted by Nancy on April 9, 1999, at 20:12:24
In reply to Dysthymia/Treatment Resistant Depressions, posted by JohnB. on April 8, 1999, at 23:24:43
> There's very promising information on a drug/neurotransmitter approach to treating chronic long term/ intractable depressive illness. The dopaminergic system has long been suspected as a biochemical part of the affective disorder problem (either directly or indirectly) and more evidence mounts that that dopamine receptors play a critical role not just in terms of mood state but just as critically in the prolongation/inescapability of this illness as it relates to memory, specifically emotional memory. It seems that what we call chronic, recurrent, or dysthymic depression may just be the mysteriously caused and tormentingly intrusive omnipresence of negative/stress related emotional memories. Somehow, the sufferer's perceptive awareness, or consciousness, is quite literally unable to break away from this unbearable onslaught of exclusively aversive emotive memories; the learned helplessness paradigm seems to fit in critically with this hypothesis.
> At any rate, interesting things are happening in studies of a relatively new European "anti-psychotic" called Amisulpride (SOLIAN) as it relates to chronic depressive illness, not psychosis. This unique drug selectively blocks two subtypes of dopamine receptors (D2 and D3) and almost exclusively acts in the mesolimbic brain, unlike most other anti-psychotic meds. Intruigingly, amisulpride only blocks pre-synaptically, which means that in small doses, it actually increases dopaminergic (2 & 3) neurotransmission; this selectivity is amazing enough, but what makes this medication so potentially meaningful for treatment resistant and chronic depressives is the fact that it seems to potentiate D2 and D3 transmission primarily at certain sites WITHIN ONLY THE LIMBIC SYSTEM, the "birthplace" of emotional (mood) states and crucially implicated in memory storage and retreival. Unnecessary stimulation of dopaminergic receptors elsewhere in the brain involving locomotion and general attention/arousal seem to be larely bypassed, eliminating sleep disturbances, anxiety exascerbations, the jitters, and scattered and/or hyperattentiveness. Also, the extrapyramidal side effects (atkinesias and dyskinesias) are practically nonexistent at these non-pschotic doses. My guess is that drugs directed specifically for neuroaction in the limbic structures (whether dopaminergic, noradrenergic, serotonergic, or whatever) are going to be the critical links toward the most effective treatments for the core dysfunctions causing affective illness. Never use the word cure, but keep your eyes this and like-acting meds to come.Thanks for the detailed info. :) Nancy
Posted by anne on April 9, 1999, at 22:24:58
In reply to Dysthymia/Treatment Resistant Depressions, posted by JohnB. on April 8, 1999, at 23:24:43
Unquestionably DA has mood altering affects. While I suffer from depression, I have a concomitant neurologic disorder, multifocal dystonia. One of the treatments tried for my dystonia was Sinemet (a form of DA which crosses the blood/brain barrier). When the first dose would *hit* in the morning I felt wonderful like I never had in my life. Unfortunately, it only lasted a few hours as Sinemet has a short half-life and subsequent doses during the day were never as mood-altering. While my neuologist recognized my depression before I started the Sinemet, it wasn't until I stopped taking Sinemet 4 months later I recognized how badly I really felt. The contrast was striking without the Sinemet. I am not advocating this particular drug for depression, the side-effects are hard to live with and the short half-life makes it a roller coaster ride. I think the dopamine theory has merit for some types of depression and welcome further research in this area. I'm a little confused about Nick's remarks lumping Effexor and Paxil into the neuroleptic category and would appreciate clarification here. I thought the action of neuroleptics was to decrease DA in the brain.
Posted by Elaine on April 9, 1999, at 23:16:52
In reply to Dysthymia/Treatment Resistant Depressions, posted by JohnB. on April 8, 1999, at 23:24:43
Typically, ADs do not work very well or very long for Bipolar disorder. I have been dx'd bipolar (NOS) but also have dysthymia. Do you know if this type of medication is supposed to be effective for depression in bipolars, particularly acute depressions?
Posted by JohnB. on April 10, 1999, at 3:02:23
In reply to Re: Dysthymia/Treatment Resistant Depressions, posted by Elaine on April 9, 1999, at 23:16:52
Thanks for the interest in Dysthymia/Treatment Resistant Depression. I'm 37 and have had excruiting, chronic depression since age 15; needless to say, it's a subject near and dear to me. I've been trying different meds/cocktails for a dozen years with minor success. I've been involved in psychotherapy as well, which has been helpful. But, as many of you know, meds can help some but often never touch the core feelings of emptiness, hopelessness, and total inability to experience emotional satisfaction or pleasure. Joy and contentment are completely unknowable (unfeelable?) to me. So, I really latch on to any new medical stuff aimed at treating these "inner peace" symptoms.
Nick: Thanks for the info. I must say that I would agree that the classic neuroleptics aren't good choices for treating depression for the reasons you stated. However, the important point about the AYTYPICAL neuroleptic Amisulpride is its ability to enhance dopaminergic action at LOW doses and block dopaminergic action at HIGH doses, unlike the traditional anti-psychotics which block dopamine receptors generally. Dysphoric states would be expected from any dopamine blocker. Because Amisulpride doesn't block dopamine receptors at low doses and because it targets its dopamine enhancing action in specific emotion centers only, its action as a pharm at this dose is more targeted for mood disorders than for psychotic illness. Of course, chlorpromazine would be superior to placebo for depression; almost any drug would. But Amisulpride would clearly be superior to Chlorpromazine for treating depression because low dose Amis. enhances dop. where it counts and CHLORP. blocks dop. generally. I suppose you could say that Amisulpride (at low doses) wouldn't qualify being called a neuroleptic. We'll have to wait and see for further studies.
Elaine: I haven't read anything about Amulsipride and mania. My guess is that targeting dopamine receptors in the Limbic brain only might bypass any mania-triggering which seems to be more of an attentional/organizational/flow problem in moment-to-moment consciousness controlled at other sites in the brain. Just a guess, though. Most of this is just guesswork anyway, isn't it?
Anne: Nick wasn't lumping Effexor and Pazil into the neuroleptic class of drugs; he was merely listing AD drugs that had some indirect dopamine enhancing properties. The best way I know how to explain the seemingly contradictory dopamine enhancing abiltity of an otherwise dopamine blocking drug is that Amisulpride acts on dopamine differently at neuro-receptor sites. Some drugs stimulate the production of dopamine, some drugs block actions by agents that would otherwise remove available dopamine (re-uptake inhibitors), some drugs block dopamine receptors to prevent/reduce neurotransmission, and others act in other ways to facilitate the dopamine system. Amulsipride, like several new AD's, seems to target it's action even more specifically, in this case to dopamine receptors of the pre-synaptic neuron (as opposed to the neuron receiving the impulse, ie post--synaptic) The idea to remember here is that the drug is not doing its thing broadly/everywhere, so to speak. So, apparently when Amisulpride is taken a lower does, it's blockade of dopamine is limited to one neuron (pre-synapse only) which actually stimulates an increase in dopamine to compensate. At higher doses, this phenomenon doesn't occur and dopamine blockade is the result. HOW and EXACTLY WHERE a med acts at nerve receptor sites seems to be crucial, not so much for what the meds do but for how the nerons compensate for what the meds are doing.(which might make things worse) I hope I've helped some. It's all too complicated for me and there's so much science doesn't know!
Anyway, thanks again. Any more new information from anyone out there would be greatly appreciated.
Posted by Wayne R. on April 10, 1999, at 8:07:41
In reply to Re: Dysthymia/Treatment Resistant Depressions, posted by JohnB. on April 10, 1999, at 3:02:23
I am fascinated by the speculations about how these meds work. I am 51 and have suffered from intractable depression since I was 14. In November of last year a miracle happened which was the augmentation of Prozac with Naltrexone. After 25 years on the merry-go-round, three hospitalizations and 14 ECT’s I can’t express the relief I feel on this augmentation. However, nobody has been able to give me a hint as to why this combination should work. Can anyone speculate about this? Wayne
Posted by Nick on April 10, 1999, at 13:27:22
In reply to Re: Dysthymia/Treatment Resistant Depressions, posted by Wayne R. on April 10, 1999, at 8:07:41
> In November of last year a miracle happened which was the augmentation of Prozac with Naltrexone..... However, nobody has been able to give me a hint as to why this combination should work. Can anyone speculate about this? Wayne
OK big guess coming up! There is cross - talk between Opiate systems and Noradrenergic systems - it MAY be (wild guess) that naltrexone operating through the opiate system somehow activates noradrenergic transmission, lifting mood. There you are, speculation!
Posted by Nick on April 10, 1999, at 13:37:54
In reply to Re: Dysthymia/Treatment Resistant Depressions, posted by Elaine on April 9, 1999, at 23:16:52
> I have been dx'd bipolar (NOS) but also have dysthymia. Do you know if this type of medication is supposed to be effective for depression in bipolars, particularly acute depressions?
I don't know of anything yet BUT both risperidone and olanzapine have mood lifting properties and can also be useful for the treatment of mania/hypomania. However, they have a different mechanism of action to amisulpride (D2, D3 blocker, although potentiates DA transmission at low dose) Risperidone MAY be undergoing trials in bipolar disorder as a single therapeutic agent. I would have thought that amisulpiride might be a reasonable experiment, although at low dose with potentiation of DA transmission there is a risk (theoretically) of precipitating mania.
Posted by Nick on April 10, 1999, at 13:50:01
In reply to Re: Dysthymia/Treatment Resistant Depressions, posted by anne on April 9, 1999, at 22:24:58
> I'm a little confused about Nick's remarks lumping Effexor and Paxil into the neuroleptic category and would appreciate clarification here. I thought the action of neuroleptics was to decrease DA in the brain.
Sorry for the confusion! Effexor & paxil are not neuroleptics - nor is amisulpiride at low dose. I was simply tring to list a few drugs that have mood altering proerties and also an action on DA transmission. I should have mentioned amphetamines, which have powerful effects on DA release.
The difficulty with 'simple' i.e. one step theories like the monoamine hypothesis and also with our simplistic explanations of how the drugs work is that they often ignore the fact that if you do something to the brain - alter a transmitter release rate, for instance - it does something back - like modify receptor sensitivity. The theories also take no notice of the fact that monoamine systems talk not only to each other, but to other chemical systems, both between neurones and intraneuronally. I fear we are a long way from understanding it in any real way.
Posted by Jim on April 10, 1999, at 17:21:26
In reply to Re: Dysthymia/Treatment Resistant Depressions, posted by Wayne R. on April 10, 1999, at 8:07:41
Wayne--
While we're off in speculation-land, here's
my two cents on why naltrexone augmentation might
work for some people. Since naltrexone is an
opiate antagonist that can also help with drug and
alcohol cravings as well as impulse disorders
(gambling, cutting, etc.), I'd reckon that some
depressive states might also involve a counter-
productive "addiciton" to the body's own opiate
peptides. This addiction might be strong enough
to keep somebody chronically depressed by the way
the opiate system interacts with noradrenaline and
especially dopamine, among other things. Just my
personal hypothesis of course, awaiting
refutation!For the record, I recently tried adding very low
dose naltrexone to my Tofranil to see if I could
get your great results. Unforch, all I got were
some VERY unpleasant dreams before I threw in the
towel, perhaps prematurally...--Jim
Posted by Nancy on April 10, 1999, at 17:53:39
In reply to Re: Dysthymia/Treatment Resistant Depressions, posted by Elaine on April 9, 1999, at 23:16:52
> Typically, ADs do not work very well or very long for Bipolar disorder. I have been dx'd bipolar (NOS) but also have dysthymia. Do you know if this type of medication is supposed to be effective for depression in bipolars, particularly acute depressions?
??ACUTE/TREATMENT REFRACTIVE/DISABLING?? If it continues beyond 6months and you're suicidal, DON'T WAIT ANY LONGER!!! Get ECT done (it's 90% effective). Don't end up DOA at the ER like I did, then, on life support for days!
After the ECT, my 18 months of chronically suicidal, totally disabling, treatment resistive, absolutely intolerably painful/anguishing bipolar depression was stopped DEAD in ITS tracks (instead of ME being dead)!
Respectfully,
Nancy
Posted by Nancy on April 10, 1999, at 18:15:46
In reply to Re: Dysthymia/Bipolar Depression (Elaine), posted by Nick on April 10, 1999, at 13:37:54
However, Respiradone and Zyprexa didn't work for me (a severely bipolar 1, rapid cycler and treatment resistive). Recent augmentation of my treatments with T3 and T4 (to get the thyroid function into the upper-quartile range of "normal") have miraculously improved physiological responsiveness to AD and mood stabilizing meds.
> > I have been dx'd bipolar (NOS) but also have dysthymia. Do you know if this type of medication is supposed to be effective for depression in bipolars, particularly acute depressions?
>
> I don't know of anything yet BUT both risperidone and olanzapine have mood lifting properties and can also be useful for the treatment of mania/hypomania. However, they have a different mechanism of action to amisulpride (D2, D3 blocker, although potentiates DA transmission at low dose) Risperidone MAY be undergoing trials in bipolar disorder as a single therapeutic agent. I would have thought that amisulpiride might be a reasonable experiment, although at low dose with potentiation of DA transmission there is a risk (theoretically) of precipitating mania.
Posted by Nick on April 11, 1999, at 15:37:55
In reply to Re: Dysthymia/Bipolar Depression (Elaine), posted by Nancy on April 10, 1999, at 18:15:46
> Recent augmentation of my treatments with T3 and T4 (to get the thyroid function into the upper-quartile range of "normal") have miraculously improved physiological responsiveness to AD and mood stabilizing meds.
>Nancy - I'm delighted to hear thyroid augmentation was effective. It's a treatment that a lot of psychiatrists balk at. For my own education: how long did you have to wait for an effect, what doses of T3 and T4 were used, and did you get any side effects? I've had people complain of hair loss as well as sweats and diarrhoea. Thanks, Nick
Posted by Wayne R. on April 12, 1999, at 7:50:08
In reply to Re: Refractory depression--naltrexone theories?, posted by Jim on April 10, 1999, at 17:21:26
> Since naltrexone is an opiate antagonist that can also help with drug and alcohol cravings as well as impulse disorders (gambling, cutting, etc.), I'd reckon that some depressive states might also involve a counter-productive "addiciton" to the body's own opiate peptides. This addiction might be strong enough to keep somebody chronically depressed by the way the opiate system interacts with noradrenaline and especially dopamine, among other things…
Jim, I am just an interested patient and have no training in any of this. My question is why there would be no evidence of Naltrexone being an effective AD in its own right if this was the case? Everything I have seen points to it only being effective as an augmentation and even then only for the SSRI family. Wayne
Posted by Wayne R. on April 12, 1999, at 7:55:50
In reply to Re: Refractory depression--naltrexone theories?, posted by Jim on April 10, 1999, at 17:21:26
The onset of my depression is strongly linked to an Epstein-Barr infection. Does Epstein-Barr have known pathology in the systems that have been referred to? Could Epstein-Barr markers potentially be used to provide some measure as to whether a person might respond to SSRI with Naltrexone? Wayne
Posted by Wayne R. on April 12, 1999, at 8:00:51
In reply to Re: Refractory depression--naltrexone theories?, posted by Jim on April 10, 1999, at 17:21:26
> For the record, I recently tried adding very low dose naltrexone to my Tofranil to see if I could get your great results. Unforch, all I got were some VERY unpleasant dreams before I threw in the towel, perhaps prematurally...
I have been disheartened that I have not yet had postings or emails indicating a duplication of my results. In my last exchange with Dr Dante he indicated that he has had over 200 successes with Naltrexone. I sure wish there was a litmus test… Wayne
Posted by Elizabeth on April 12, 1999, at 8:38:39
In reply to Re: Dysthymia/Treatment Resistant Depressions, posted by Elaine on April 9, 1999, at 23:16:52
> Typically, ADs do not work very well or very long for Bipolar disorder. I have been dx'd bipolar (NOS) but also have dysthymia. Do you know if this type of medication is supposed to be effective for depression in bipolars, particularly acute depressions?
Elaine, I'm curious about this: what does the "NOS" mean in your case? I know it stands for "not otherwise specified," I mean why did you receive this diagnosis instead of bipolar I or II.
(I had a single mixed episode and recurring major depression, but my dx is bipolar NOS rather than bipolar I because it wasn't clear whether the mixed episode was spontaneous, or whether it was an idiosyncratic reaction to an antidepressant. My assumption has been the latter.)
Posted by Elizabeth on April 12, 1999, at 9:11:33
In reply to Re: Bipolar/Treatment Resistant Depressions/ECT!!!, posted by Nancy on April 10, 1999, at 17:53:39
Nancy,
I agree that ECT is a good choice in some emergencies, but I also seem to recall that some subtypes of depression don't respond well to it. Anyone know anything about this? (My recollection is that it was more effective in severe or delusional depression and less effective (or ineffective) in dysthymic or atypical depression.)
I'd actually say that for resistant dysthymia, if there's a need for immediate results (which wasn't the impression I got from Elaine's post...Elaine, could you elaborate?), amphetamines (e.g., methylphenidate or d-amphetamine) might be a good thing to try, as they tend to work fast (when they do work).
For long-term treatment of bipolar depression, the atypical antipsychotics are worth a try, as they seem to act as antidepressants in some people. (Not everybody, though.)
Posted by Nancy on April 12, 1999, at 16:40:45
In reply to Re: Dysthymia/Bipolar Depression (Elaine), posted by Nick on April 11, 1999, at 15:37:55
> > Recent augmentation of my treatments with T3 and T4 (to get the thyroid function into the upper-quartile range of "normal") have miraculously improved physiological responsiveness to AD and mood stabilizing meds.
> >
>
> Nancy - I'm delighted to hear thyroid augmentation was effective. It's a treatment that a lot of psychiatrists balk at.***NO KIDDING!!! I went through hell and high water to get T-three and T4!!!!!!!!!!! In just the first 7 days of taking T-three, you will begin to feel more energetic. ??i have to spell out the word "three" because my keyboard just lost it's mind...the numeral three isn't working at the moment(33333...see?)...oh, well.
Anyway, (oh, i love to tell my stories....Thank You!) my pdoc and gp were totally against using thyroid augmentation BECAUSE MY TEST RESULT CAME BACK "NORMAL". I finally began asking where on the range of "normal" was I???? GET THIS: Doctors say that your thyroid levels are normal, even when those levels are in the "low end of normal". Which, by the way, IS NOT sufficient thyroid level for treatment refractory patients!
The pdoc who had read literature (even after graduating from med school) important for prescribing drugs for severly treatment resistive bipolar patients (like me), was the pdoc who ended my 18 months of agonizing and totally disabling depression.
:) ok next question (deep breath)
For my own education: how long did you have to wait for an effect, what doses of T3 and T4 were used, and did you get any side effects?****Dosage begins at 0.05mgs/ A.M./ empty stomach. An ultra sensitive thyroid blood test is done two weeks later. Increase dosage by 0.05mgs, as before, until both T3three and T4 levels are in the upper-quartile of the "normal" range.
Personally??? the doses of thyroid meds I take...T4 = 0.15mgs and T3three = 0.05mgs...at the present time
Side Efeects??? be careful that you don't drink enough caffienated drinks to cause a pounding heart...you may have some flushing (turning a little pinkish) of your skin, rather than the pale sickly color of the skin when your thyroid is "low normal"...oh, also, you may feel a lot better than you ever have since this awful depression began!
I've had people complain of hair loss as well as sweats and diarrhoea. Thanks, NickOh yea, the thyroid meds will make you feel warmer. Which is a great benefit to those of us who always felt cold all the time. Haven't noticed hair loss. But, I have very long, curly blonde hair. It would probably take a long time for me to notice much of my hair missing...hee hee hee :) Nancy
Posted by Danielle on April 12, 1999, at 17:37:10
In reply to Re: Dysthymia/Bipolar Depression (Elaine), posted by Nancy on April 12, 1999, at 16:40:45
> > > Recent augmentation of my treatments with T3 and T4 (to get the thyroid function into the upper-quartile range of "normal") have miraculously improved physiological responsiveness to AD and mood stabilizing meds.
> > >
> >
> > Nancy - I'm delighted to hear thyroid augmentation was effective. It's a treatment that a lot of psychiatrists balk at.
>
> ***NO KIDDING!!! I went through hell and high water to get T-three and T4!!!!!!!!!!! In just the first 7 days of taking T-three, you will begin to feel more energetic. ??i have to spell out the word "three" because my keyboard just lost it's mind...the numeral three isn't working at the moment(33333...see?)...oh, well.
>
> Anyway, (oh, i love to tell my stories....Thank You!) my pdoc and gp were totally against using thyroid augmentation BECAUSE MY TEST RESULT CAME BACK "NORMAL". I finally began asking where on the range of "normal" was I???? GET THIS: Doctors say that your thyroid levels are normal, even when those levels are in the "low end of normal". Which, by the way, IS NOT sufficient thyroid level for treatment refractory patients!
>
> The pdoc who had read literature (even after graduating from med school) important for prescribing drugs for severly treatment resistive bipolar patients (like me), was the pdoc who ended my 18 months of agonizing and totally disabling depression.
> :) ok next question (deep breath)
>
>
> For my own education: how long did you have to wait for an effect, what doses of T3 and T4 were used, and did you get any side effects?
>
> ****Dosage begins at 0.05mgs/ A.M./ empty stomach. An ultra sensitive thyroid blood test is done two weeks later. Increase dosage by 0.05mgs, as before, until both T3three and T4 levels are in the upper-quartile of the "normal" range.
>
> Personally??? the doses of thyroid meds I take...T4 = 0.15mgs and T3three = 0.05mgs...at the present time
>
> Side Efeects??? be careful that you don't drink enough caffienated drinks to cause a pounding heart...you may have some flushing (turning a little pinkish) of your skin, rather than the pale sickly color of the skin when your thyroid is "low normal"...oh, also, you may feel a lot better than you ever have since this awful depression began!
>
>
>
> I've had people complain of hair loss as well as sweats and diarrhoea. Thanks, Nick
>
> Oh yea, the thyroid meds will make you feel warmer. Which is a great benefit to those of us who always felt cold all the time. Haven't noticed hair loss. But, I have very long, curly blonde hair. It would probably take a long time for me to notice much of my hair missing...hee hee hee :) NancyHi Nancy:
Same for me, only I was also losing big globs of hair. Finally got hold of a endocrinologist - ob/gyn who said the others were silly, low end of normal wasn't normal for me! Ranges aren't absolutes.
Danielle
Posted by Jim on April 12, 1999, at 19:02:34
In reply to Re: Refractory depression--naltrexone theories?, posted by Wayne R. on April 12, 1999, at 8:00:51
Wayne,
On your questions about who naltrexone
works for and why, I too am just an
interested (perhaps too interested!)
patient. I agree that most reports
(especially Lee Dante's) see it working
only as an augmentation strategy with
things like SSRIs (and also sometimes
tricyclics). But when I did some of my own
research on naltrexone use across
the board, I did find a bunch of places
in the alcholism & autism literature where
there was some question about whether it
might have an antidepressant effect in its
own right. This has not really been
formally researched so you're right to see
naltrexone as remaining basically an
augmentation strategy for the time being.
(My *theory* that I posted was basically
the best one that I as a non-specialist could
come up with!) If there are other people
that naltrexone has helped, I'd be interested
to see them come out of the woodwork too!
-Jim
Posted by Elaine on April 12, 1999, at 21:53:30
In reply to bipolar NOS - Elaine, posted by Elizabeth on April 12, 1999, at 8:38:39
It's the same thing - Not Otherwise Specified. Since not everything fits a clean diagnosis, they always have to leave an 'out'. In my case, I don't have mania, per se; my psychiatrist feels that the anger flashes I sometimes get fits into a bipolar dx, particular since, again, AD's haven't helped my bouts of depression as well as should. Since she tried several over the years and one characteristic of bipolar is not responding well or for very long to AD's...
I'm still not entirely convinced about the bipolar dx, but it's just a name as long as she knows what meds are helping. Again, though, I do not suffer from mania (although it might be nice just once, just for a little while?), so it really throws me into a strange category. I believe there is research about bipolar of a more dysthymic nature.
Is this anything you were looking for?
Posted by Elaine on April 12, 1999, at 22:02:04
In reply to Re: Dysthymia/Bipolar Depression (Elaine), posted by Nancy on April 12, 1999, at 16:40:45
My pdoc DID prescribe thyroid augmentation even though the doc's lab tests came back "Normal". She told me that a psych's range of "normal" can be different from a gp. I don't always know what helps, but she says it has. I guess I should consider myself fortunate that she doesn't simply go with the standard results.
Excuse me, did someone say "be careful you don't drink enough caffienated drinks"? I assume you mean "too much"? Does that apply to all thyroid meds? It seems I wake up sometimes with a pounding heart - (no, NOT anxiety or nightmares) - how long can the combination take before the side effect shows up? I never really thought about side effects with thyroid meds.
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