![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
[email protected]Shown: posts 18 to 42 of 72. Go back in thread:
Posted by Ines on March 3, 2007, at 12:44:50
In reply to Re: Atypical depression MERI, posted by gardenergirl on March 3, 2007, at 12:26:08
> When my therapist diagnosed me with atypical depression, it was like a god-send for me. No one else had ever picked up on that, and knowing what I was dealing with led directly to trying Nardil and finally to remission.
>
> Given how prevalent it is, you would think it would fall regularly off the lips of docs.
>
> namaste
>
> ggGood for you! I wish I could find a doc that would do that for me over here... As it is it looks like I'll have to go through every other med before someone will let me try a MAOI. Argghh!
Posted by Meri-Tuuli on March 3, 2007, at 13:18:41
In reply to Re: Atypical depression MERI, posted by Ines on March 3, 2007, at 11:32:23
Hello
Yeah I know, I remember when I first got diagnoised with depression I was reading this book and it was all like 'you can't sleep, you can't eat' blah blah, and I was like, 'um, I'm sleeping too much and eating too much too' whats wrong with me? And then I came across the atypical stuff. Yeah you would really think it'd be alot more 'out there'.
Anyway, I bet your GP has used wellbutrin - its actually called Zyban and its only licensed for smoking cessation - so perhaps he actually didn't want you to take it, as he'd have to use it 'off-label' although its perfectly 'on-label' in the states. You know covering he's own back should anything nasty happen. I'm surprised he'd let you use moclebomide and not zyban. Anyway.
Someone at the practice will have used Zyban, its routinely used to help people quit smoking. Anyway. And with the moc, just because it isn't effective for most people, doesn't mean it might not be effective for you, if you see what I mean.
I'm fairly certain your GP won't let you try a MAOI, but your pdoc might be more willing to give it a go, although s/he might take some convincing. Just go armed with print-outs, scientific studies, the diet list and sort of give the impression you're knowledgble about it. I find that works.
I haven't tried many things compared to most people here on babble. Are you taking anything at the moment? What have you taken?
Kind regards
Meri
Posted by Phillipa on March 3, 2007, at 18:27:39
In reply to Re: Atypical depression MERI, posted by Ines on March 3, 2007, at 12:44:50
Here's a link. Love Phillia
Outpatient Psychiatry Center, Ravenna and Forli, Italy.BACKGROUND: The definition of atypical depression (AD) has recently seen a rebirth of studies, as the evidence supporting the current DSM-IV atypical features criteria is weak. Study aim was to compare a definition of AD requiring only oversleeping and overeating (reversed vegetative symptoms) to the DSM-IV AD definition (always requiring mood reactivity, plus overeating/weight gain, oversleeping, leaden paralysis, and interpersonal sensitivity [at least 2]). METHODS: Consecutive 202 major depressive disorder (MDD) and 281 bipolar II outpatients were interviewed, during a major depressive episode (MDE), with the Structured Clinical Interview for DSM-IV. The DSM-IV criteria for AD were compared to a new AD definition based only on oversleeping and overeating, which was the one often used in community studies. Associations were tested by univariate logistic regression. RESULTS: The frequency of DSM-IV AD was 42.8 %, and that of the new AD definition was 38.7 %. DSM-IV AD, and the new AD definition, had almost all the same significant associations: bipolar II, female gender, lower age, lower age of onset, axis I comorbidity, depressive mixed state, MDE symptoms lasting more than 2 years, and bipolar family history. DSM-IV AD was present in 86 % of the new AD definition sample. The new definition of AD was significantly associated with all the other DSM-IV AD symptoms not included in it. The new AD definition was strongly associated with DSM-IV AD (odds ratio = 17.8), and had sensitivity = 77.7 %, specificity = 90.5 %, positive predictive value = 86.1 %, negative predictive value = 84.4 %, and ROC area curve = 0.85, for predicting DSM-IV AD. CONCLUSIONS: Results support a simpler definition of AD, requiring only oversleeping and overeating, and support the similar AD definition previously used in community studies. This definition is easier and quicker to assess by clinicians than the DSM-IV definition (mood reactivity and interpersonal sensitivity are more difficult to assess). Some pharmacological studies support this new AD definition (by showing better response to MAOI than to TCA, as shown in DSM-IV AD).
PMID: 12563537 [PubMed
Posted by Declan on March 3, 2007, at 22:55:03
In reply to Re: Atypical depression, posted by Maxime on March 2, 2007, at 23:34:20
Hi Maxi
Your doc's worried about addiction with you? Astonishing.
Of course bupe might not work for you, but (given your history) it surely should be an option.
Posted by River1924 on March 3, 2007, at 23:56:52
In reply to Re: Atypical depression » Maxime, posted by Declan on March 3, 2007, at 22:55:03
Yeah, I don't get it. A person has a potentially fatal illness but the doc isn't willing to try every available option.
Aren't they responsible for a suicide by refusing to use a potential medication? If the options are addiction, a potential hypertensive crisis, or a gunshot to the head... wouldn't a doc choose the lesser of evils?
Perhaps someone on this site should create a legal form which we can give to docs saying... your refusal to consider all options available makes you liable for any injury I may incur do to your ignorance and/or indifference.
River.
Posted by snapper on March 4, 2007, at 2:53:56
In reply to Re: Atypical depression MERI, posted by Phillipa on March 3, 2007, at 18:27:39
OKay , so we pretty much all agree or concur....like I have felt and beleived for years.... Atyp Dep. Is much more common than the "leaded" type of depression. It also seems most of us on this board appear to be BP II mixed-rapid cycling and or TRD and a smidge or more of BP "what ever" ---- all we can really do is therapy......(sorry...In my HMO does nothing" or keep fighting for better MAOI's ---- If there are this many sick people out there or here...what are they gonna do. I truly beleive it is a spectrum in which they ( Dr.s or Scientists) could have not seen coming 40 to 60 years ago. It is time to go back to the lab....re-tool. refit. and maybe by the end of the decade we will hopefully see more "wellness" than sickness. Even though many of us fit snuggly in to the BP II mixed....cycling...........category. It is no excuse. There surely must be a reason Nardil and Parnate and Moclebemide and the others worked ....... I know this may sound glib, but if 50 years ago we could send a man to the moon and back, I am sure and confident that our mental plights are not new to the "ssri" era and they can come up with chemicals that will or at least have the ability to at least make us feel like life is worth living or not. The moon is one thing...the Human brain is quite the othe...but not really... if anyone does not understand this post or any parts therin, I will do my best to explain my thoughts and feelings.
--Snapper
Posted by laima on March 4, 2007, at 7:44:39
In reply to Re: Atypical depression » Declan, posted by River1924 on March 3, 2007, at 23:56:52
Wikipedia also seems to have some helpful and basic info on atypical depression. Here's a link, and some of the text. (Of course, as usual, they have tons of other links and stuff there, too.)http://en.wikipedia.org/wiki/Atypical_depression
Atypical depression
From Wikipedia, the free encyclopediaAtypical Depression (AD) is a subtype of Major Depression characterized by mood reactivity — being able to experience improved mood in response to positive events. In contrast, sufferers of "melancholic" depression generally cannot experience positive moods, even when good things happen. Additionally, atypical depression is characterized by reversed vegetative symptoms, namely over-eating and over-sleeping.
Despite its name, "atypical" depression is actually the most common subtype of depression[1][2] — up to 40% of the depressed population may be classified as having atypical depression.Diagnostic criteria (DSM-IV-TR)
The DSM-IV-TR, a widely used manual for diagnosing mental disorders, defines Major Depressive Disorder with Atypical Features as a subtype of depression characterized by:
A. Mood reactivity (i.e., mood brightens in response to actual or potential positive events)
B. At least two of the following:
Significant weight gain or increase in appetite
Hypersomnia (sleeping too much, as opposed to the insomnia present in melancholic depression)
Leaden paralysis (i.e., heavy, leaden feelings in arms or legs)
long-standing pattern of interpersonal rejection sensitivity (not limited to episodes of mood disturbance) that results in significant social or occupational impairment
C. Criteria are not met for Melancholic Depression or Catatonic Depression during the same episode.
By the ICD-10 classification, it will fall in the category of F32 or F39.
ResearchIn general, atypical depression tends to cause greater functional impairment than other forms of depression.[3] Atypical depression tends to occur earlier in life than other forms of depression — usually beginning in teenage years. Similarly, patients with atypical depression are more likely to suffer from other mental illnesses such as social phobia, avoidant personality disorder, or body dysmorphic disorder. Atypical depression is more common in females — nearly 70% of the atypical population are women.
It is not yet entirely clear how atypical depression responds to treatment as compared with melacholic depression. Some studies suggest that an older class of drugs, MAOIs, may be more effective at treating atypical depression than the more modern tricyclic antidepressant and SSRIs.
It has been noted that patients with atypical depression often suffer from intense cravings for carbohydrates. A mineral supplement, chromium picolinate, was found to assuage these cravings in one study, though the conclusion reached has not been replicated.
It has been hypothesized that atypical depression may be related to thyroid dysregulation. Some studies have found subtle thyroid abnormalities in people with atypical depression. Another study suggests that patients may benefit from triiodothyronine, a medication used to treat hypothyroidism.
Posted by laima on March 4, 2007, at 8:54:01
In reply to Atypical depression, posted by Ines on March 1, 2007, at 17:03:02
Hi,Yes, mine is atypical depression, too.
There HAS been research showing good results from combining deprenyl (a brand or alternate name for oral selegeline, I gather) with various versions of phenylalanine, and that of course includes dlpa. I've seen a number of references on internet. Can you get deprenyl where you live? I even recall reading that as little as 5-10mg oral selegeline plus l-phenylalanine can be efective, though I later heard that the d version is more potent as an anti-depressent. Regardless, before Emsam, I got a decent result by adding some l-phenylalanine to my 10-15 mg of oral selegeline, which was in the process of being stepped up, when lo and behold Emsam came out. And, apparently dietary restrictions are pretty darn loose, perhaps not even necessary, with oral selegeline at 10 mg and under. I've even seen some claims that even at 15-20mg and under don't require dietary restrictions- but don't know if that's in fact true or not. I do understand drug restrictions DO need to be heeded at any dose, though.
Yes- maois said to be preferred treatment for atypical depression.
St. John's Wort more seratonin-ish- maybe that's why not as helpful?
SSRIs worked for me only for a short time- and the only reason I ever was on them in first place was due to the ssri craze of the late 80's-1990's. The doctors I saw then confused "best new antidepressent breakthrough" with "best antidepressent"- if you get what I mean.
I've also found stims helpful- interesting to me that there is some kind of relationship between phenylalanine and amphetamine- but what that exactly is I don't quite understand at this point. I plan to try to read more eventually, out of curiosity. I also find it interesting that Emsam is said to break down into amphetamine-like substances as it metabolizes. Well, this info may or may not be practical- I just find it intriquing and a bit tantalizing.
I personally have never felt any agitation from oral selegeline or Emsam; if anything, they made me a little tired, even lethargic, probably because they can lower blood pressure, and they did/do for me. But, addition of stimulant, or presumabley by tweaking amount of phenylalanine, this can be corrected.
I do vouch for effectiveness of the combo!
Anyway, here are a few brief references from a dig-able site that has loads of interesting stuff on it. (You can click from link to link to link- getting loads of new links each time.)
http://www.selegiline.com/depplus.html
L-deprenyl plus L-phenylalanine
in the treatment of depression
by Birkmayer W, Riederer P, Linauer W, Knoll J
J Neural Transm 1984; 59(1):81-7ABSTRACT
The antidepressive efficacy of 1-deprenyl (5-10 mg daily) plus 1-phenylalanine (250 mg/day) has been evaluated in 155 unipolar depressed patients. Both oral and intravenous administration showed beneficial effects in 90% of outpatients and 80.5% of inpatients. It is concluded that this combined treatment has a potent antidepressive action based on the accumulation of 1-phenylethylamine in the brain.
http://www.selegiline.com/pea.html
Sustained antidepressant effect of PEA replacement
by Sabelli H, Fink P, Fawcett J, Tom C
Rush University and the
Center for Creative Development,
Chicago, Illinois, USA.
J Neuropsychiatry Clin Neurosci 1996 Spring; 8(2):168-71ABSTRACT
Phenylethylamine (PEA), an endogenous neuroamine, increases attention and activity in animals and has been shown to relieve depression in 60% of depressed patients. It has been proposed that PEA deficit may be the cause of a common form of depressive illness. Fourteen patients with major depressive episodes that responded to PEA treatment (10-60 mg orally per day, with 10 mg/day selegiline to prevent rapid PEA destruction) were reexamined 20 to 50 weeks later. The antidepressant response had been maintained in 12 patients. Effective dosage did not change with time. There were no apparent side effects. PEA produces sustained relief of depression in a significant number of patients, including some unresponsive to the standard treatments. PEA improves mood as rapidly as amphetamine but does not produce tolerance.
2-Phenylethylamine-induced changes in catecholamine receptor density: implications for antidepressant drug action
by
Paetsch PR, Greenshaw AJ
Department of Psychiatry,
University of Alberta,
Edmonton, Canada.
Neurochem Res 1993 Sep; 18(9):1015-22ABSTRACT
It is now established that (1) concentrations of 2-phenylethylamine (PEA) are greatly increased in brain following administration of monoamine oxidase inhibitor (MAOI) antidepressants; (2) PEA is a metabolite of the MAOI antidepressant phenelzine; and (3) PEA may be a neuromodulator of catecholamine activity. On the basis of these observations, the effects of long term increases in brain PEA on catecholamine receptors have been assessed. Both PEA and antidepressants induced a reduction in the behavioural response to the beta 2 adrenoceptor agonist salbutamol. Radioligand binding measurements revealed that 28 day administration of PEA in combination with the type B MAOI (-)-deprenyl results in a decrease in the density of beta 1 adrenoceptors but not beta 2 adrenoceptors in rat cerebral cortex and cerebellum. (-)-Deprenyl alone also induced a significant decrease in beta 1-adrenoceptors but when PEA was added to this treatment there was a further decrease in beta 1-adrenoceptor density. Only changes in beta 1 adrenoceptor density were evident following 28 day administration of MAOI antidepressants. PEA also induced a decrease in the density of D1-like dopamine (DA) receptors in the rat striatum. MAOI antidepressants induced a decrease in the density of both D1-like and D2-like DA receptors. These data are discussed in terms of a possible role of PEA-catecholamine interactions in antidepressant drug action.
(Sorry- no idea what that just said, other than phenylethylamine can help.)
http://chocolate.org/pea.html
Does phenylethylamine act as an
endogenous amphetamine in some patients?
by
Janssen PA, Leysen JE, Megens AA, Awouters FH.
Centre for Molecular Design,
Janssen Research Foundation,
B-2340 Beerse, Belgium.
Int J Neuropsychopharmcol 1999 Sep; 2(3):229-240ABSTRACT
In brain capillary endothelium and catecholaminergic terminals a single decarboxylation step effected by aromatic amino-acid decarboxylase converts phenylalanine to phenylethylamine, at a rate comparable to that of the central synthesis of dopamine. Phenylethylamine, however, is not stored in intra-neuronal vesicles and is rapidly degraded by monoamine oxidase-B. Despite its short half-life, phenylethylamine attracts attention as an endogenous amphetamine since it can potentiate catecholaminergic neurotransmission and induce striatal hyperreactivity. Subnormal phenylethylamine levels have been linked to disorders such as attention deficit and depression; the use of selegiline (Deprenyl) in Parkinson's disease may conceivably favour recovery from deficient dopaminergic neurotransmission by a monoamine oxidase-B inhibitory action that increases central phenylethylamine. Excess phenylethylamine has been invoked particularly in paranoid schizophrenia, in which it is thought to act as an endogenous amphetamine and, therefore, would be antagonized by neuroleptics. The importance of phenylethylamine in mental disorders is far from fully elucidated but the evolution of phenylethylamine concentrations in relation to symptoms remains a worthwhile investigation for individual psychotic patients.
You get the idea- they have TONS of these sorts of abstracts, losely grouped together by relevence.And be sure to check out this site:
http://www.selegiline.com/
Good luck, Ines!!And in the meanwhile, before you get back with your doctor, maybe some dark chocolate? :)
*Note to Emsam users- WOW- there is a new bit on there, in the relatively recent Emsam section:"A restricted "MAOI diet" is prudently advised for the higher dosage EMSAM 9 mg/24 hr patch and the 12 mg/24 hr patch to avoid any risk of hypertensive crisis. But it's worth noting that (as of 2007) no hypertensive crises following dietary indiscretions have been reported even in users of the high strength patches."
> Hello again everyone,
>
> I thought I'd start a thread on atypical depression. I only recently foud out about this subtype of depression, and I seem to fit all the criteria, i.e. mood reactivity, oversleeping, overeating, chronic fatigue and rejection sensitivity, early onset.
>
> I've been on escitalopram and St John's Wort with no success whatsoever. Had a bried trial with mirtazapine that left me feeling like a zombie, and am currently trying reboxetine (early days yet). Given all the literature suggesting that MAOIs work best in atypical depression I would like to give that a go, but doctor won't hear of it.
>
> Just thought it would be useful to share experiences with anyone who's up againts the same sort of symptoms. I've read quite a bit on the net about the possibility of combining low dose deprenyl with DLPA- anyone had success with that?
>
> Bye for now,
> Ines
Posted by Ines on March 4, 2007, at 9:01:02
In reply to Re: Atypical depression, posted by laima on March 4, 2007, at 7:44:39
I think a problem with atypical depression is that a lot (obviously not all) of sufferers are 'high functioning'- they can function reasonably in day to day life, and it stops other people (and doctors) from realising how bad it is. That could be why 'typical' depression has had so much more medical attention- when someone is going through a bout of typical depression it is obvious that help is a matter of life or death. For an atypical depressive it might not be obvious to anyone but the person that the level of suffering is actually very high. River's post about his niece Jessica struck me as so sad, and so typical of an atypical depressive... I can certainly understand her but like he said, most people wouldn't understand it at all.
In defense of those involved in medical research, noone really knows what is the biological cause of this disease, and what it is about MAOI's that makes them so much more effective in these cases; without that sort of knowledge developing effective treatments is a long process of trial and error... I just think that if it was more obvious to society at large how much suffering this causes, there would be more money going into the research, so the chances of finding something that works would be higher.
Having a blue day as you can probably see....
I.
Posted by gardenergirl on March 4, 2007, at 10:42:20
In reply to Re: Atypical depression, posted by Ines on March 4, 2007, at 9:01:02
Perhaps if we could identify one or two, we could ask Dr. Bob to invite them to be a guest expert here.
namaste
gg
Posted by bulldog2 on March 4, 2007, at 14:23:29
In reply to Re: Atypical depression, posted by Ines on March 4, 2007, at 9:01:02
By the way rn320 suffered a bad hypertensive crisis on emsam 12 mg. So if your an emsam user and you're up to 12 mg be as careful as if you're on nardil or parnate.
Maybe the reason that maois are effective in atypical depression is they're the only ads that boost serotonin and dopamine which is the amine of pleasure. Maybe atypicals have some disruption of their dopamine pathways or levels. I've also read that ssris lower dopamine. No wonder many complain that they feel numb on ssris.
Posted by Maxime on March 4, 2007, at 17:27:29
In reply to Re: Atypical depression » Maxime, posted by Declan on March 3, 2007, at 22:55:03
> Hi Maxi
>
> Your doc's worried about addiction with you? Astonishing.
>
> Of course bupe might not work for you, but (given your history) it surely should be an option.Declan:
I can't tell if your first sentence is sarcasm or not. You've never been sarcastic with me before though.
I believe that I am prediposed to addiction. Look at what I have done to myself with anorexia. Luckily, I made choices NOT to try certain things (illegal) because I know I would get hooked.
xxx
Maxime
Posted by Ines on March 4, 2007, at 17:29:32
In reply to Re: Atypical depression » Ines, posted by laima on March 4, 2007, at 8:54:01
Hi Laima,
Thanks for that awesome message-really helpful. I knew a bit about selegiline- I asked doc for a trial but didn't get it- but not that much. I'm gonna check the articles out properly. I'm on reboxetine at the mo, not working all that well but I'm giving it a proper chance. If this doesn't work I'm going to really push for the selegiline/ DLPA combo. Like Meri suggested, I'll try and go in armed with papers and knowledge. GP is keen on having me try paroxetine or venlafaxine but dismisses seleginline or wellbutrin! I don't get it, but perhaps he's got access to secret research we don't
know about ;-)I've read about the amphetamine / d-phenylalanine connection somewhere. I think the end product in the brain is the same and it's possible that atypical dps don't produce a lot of it. PEA I think? I'll see if I can dig that out.
Meri, thanks for advice on how to prep for meeting with GP/ pdoc. It really got me thinking and I'll definitely try that for next time. Show you know what you're talking about and the risks involved. We were talking about meds I've tried- not much at all. An SSRI, St John's Wort and mirtazapine- no luck with any. So I guess I've got loads of options still.
I'm glad I found this board- it really helps to feel you are not isolated...
BTW Laima, dark chocolate features heavily on my menu ! :-)
Cheers I.
Posted by Ines on March 4, 2007, at 17:33:40
In reply to Any atypical depression experts/researchers?, posted by gardenergirl on March 4, 2007, at 10:42:20
> Perhaps if we could identify one or two, we could ask Dr. Bob to invite them to be a guest expert here.
>
> namaste
>
> ggWhat a great idea!! I don't know of any, but will look into it during the week. If nothing else we'll know of research to watch out for.
I.
Posted by laima on March 4, 2007, at 17:52:13
In reply to Any atypical depression experts/researchers?, posted by gardenergirl on March 4, 2007, at 10:42:20
That would be awesome! But how/where to identify one?
> Perhaps if we could identify one or two, we could ask Dr. Bob to invite them to be a guest expert here.
>
> namaste
>
> gg
Posted by laima on March 4, 2007, at 17:53:32
In reply to Re: Atypical depression, posted by bulldog2 on March 4, 2007, at 14:23:29
Thanks for mentioning this- good reminder one can't believe everything one reads. Sorry to hear about it though.
> By the way rn320 suffered a bad hypertensive crisis on emsam 12 mg. So if your an emsam user and you're up to 12 mg be as careful as if you're on nardil or parnate.
> Maybe the reason that maois are effective in atypical depression is they're the only ads that boost serotonin and dopamine which is the amine of pleasure. Maybe atypicals have some disruption of their dopamine pathways or levels. I've also read that ssris lower dopamine. No wonder many complain that they feel numb on ssris.
>
Posted by Ines on March 4, 2007, at 18:09:26
In reply to Re: Atypical depression, posted by bulldog2 on March 4, 2007, at 14:23:29
> By the way rn320 suffered a bad hypertensive crisis on emsam 12 mg. So if your an emsam user and you're up to 12 mg be as careful as if you're on nardil or parnate.
> Maybe the reason that maois are effective in atypical depression is they're the only ads that boost serotonin and dopamine which is the amine of pleasure. Maybe atypicals have some disruption of their dopamine pathways or levels. I've also read that ssris lower dopamine. No wonder many complain that they feel numb on ssris.
>I believe wellbutrin is the only non MAOI AD that acts directly on dopamine? It acts on dopamine+noradrenaline/epinephrine. If it was the dopamine+ serotonin factor that made MAOIs effective then it could be that a combination of wellbutrin and an ssri would be effective as well. Any experiences? (I seem to remember reading that venlafaxine above a certain dose also acts on dopamine, but not sure about that)
I.
Posted by Declan on March 4, 2007, at 19:10:40
In reply to Re: Atypical depression » Declan, posted by Maxime on March 4, 2007, at 17:27:29
No Maxi, not at all scarcastic or ironic.
I meant given the seriousness of your situation, the problems with bupe pale in comparison should it be of use to you.
Does that make sense?
Posted by FredPotter on March 4, 2007, at 19:10:57
In reply to Re: Atypical depression » bulldog2, posted by Ines on March 4, 2007, at 18:09:26
> > By the way rn320 suffered a bad hypertensive crisis on emsam 12 mg. So if your an emsam user and you're up to 12 mg be as careful as if you're on nardil or parnate.
> > Maybe the reason that maois are effective in atypical depression is they're the only ads that boost serotonin and dopamine which is the amine of pleasure. Maybe atypicals have some disruption of their dopamine pathways or levels. I've also read that ssris lower dopamine. No wonder many complain that they feel numb on ssris.
> >
>
> I believe wellbutrin is the only non MAOI AD that acts directly on dopamine? It acts on dopamine+noradrenaline/epinephrine. If it was the dopamine+ serotonin factor that made MAOIs effective then it could be that a combination of wellbutrin and an ssri would be effective as well. Any experiences? (I seem to remember reading that venlafaxine above a certain dose also acts on dopamine, but not sure about that)
> I.
>
>
I've heard that too but the dose has to be high. Strangely I didn't find Wellbutrin effective. When I asked the pdoc if too much SSRI caused degradation of dopamine system he waved his hands about a lot, but as it was a hot day managed to keep the room really cool. But he did nothing about it.I want to try to persuade my GP to give me Nardil or buprenorphine. The alternative would be things that don't work, or ECT which they'd say I'm not bad enough for
Fred
Posted by bulldog2 on March 4, 2007, at 19:30:53
In reply to Re: Atypical depression » bulldog2, posted by Ines on March 4, 2007, at 18:09:26
Wellbutrin is primarily norandregenic. It's effect on dopamine is very weak. The stimulants do hit dopamine.
Posted by Maxime on March 4, 2007, at 20:43:18
In reply to Re: Atypical depression » Maxime, posted by Declan on March 4, 2007, at 19:10:40
> No Maxi, not at all scarcastic or ironic.
>
> I meant given the seriousness of your situation, the problems with bupe pale in comparison should it be of use to you.
>
> Does that make sense?Yes, it DOES make sense. I didn't think you were being sarcastic. But I am on other board for eating disorders and the environment there is a lot different than here.
Thanks Declan. I did ask my pdoc about it and he said no. Wonder if he would reconsider?
Maxime
Posted by Maxime on March 4, 2007, at 20:52:30
In reply to Re: Atypical depression, posted by FredPotter on March 4, 2007, at 19:10:57
>
> I've heard that too but the dose has to be high. Strangely I didn't find Wellbutrin effective. When I asked the pdoc if too much SSRI caused degradation of dopamine system he waved his hands about a lot, but as it was a hot day managed to keep the room really cool. But he did nothing about it.
>
> I want to try to persuade my GP to give me Nardil or buprenorphine. The alternative would be things that don't work, or ECT which they'd say I'm not bad enough for
> Fred
>I love the description of what you pdoc doc did.
How can you not be bad enough for ECT when nothing works. I love how they decide that for you. Sigh. It's not fair.
I hope you find that something works Fred.
Maxime
Posted by River1924 on March 5, 2007, at 4:18:02
In reply to Re: Atypical depression » FredPotter, posted by Maxime on March 4, 2007, at 20:52:30
http://www.mcmanweb.com/rapid-cycling.htm
For me, although I'm never up (much above normal), I was really surprised when mood swings were not included with the diagnosis of depression. I was on one med (geodon or zonegran or it may have been another) that made me giddy and then turn suicidal the second I stopped. Sometimes I'd be having a blast and feel suicidal at exactly the same time. That was far worse than being unmotivated and blah on zoloft. Plus I am always much more outgoing and full of possibilities just before bed than when I awaken.
Anybody else like this?
Posted by Ines on March 5, 2007, at 11:50:05
In reply to Re: Atypical depression, posted by River1924 on March 5, 2007, at 4:18:02
> http://www.mcmanweb.com/rapid-cycling.htm
>
> For me, although I'm never up (much above normal), I was really surprised when mood swings were not included with the diagnosis of depression. I was on one med (geodon or zonegran or it may have been another) that made me giddy and then turn suicidal the second I stopped. Sometimes I'd be having a blast and feel suicidal at exactly the same time. That was far worse than being unmotivated and blah on zoloft. Plus I am always much more outgoing and full of possibilities just before bed than when I awaken.
>
> Anybody else like this?
>
Yes, I can have very quick and dramatic mood changes, but they are usually triggered by something external (often something completely unsignificant like bus driver being unfriendly etc). I'm on reboxetine right now and that aspect of things has got worse- like you on that med I can actually feel elated one moment and hopeless the next, sometimes they overlap. With respect to cycling during the day though, I've heard that atypical depressives usually feel best in the morning straight after waking up, and for typical depressives the depression is worst in the morning. No idea if that's actually documented in some way. It's tue for me- I tend to feel more hopeful in am.
Posted by FredPotter on March 5, 2007, at 13:47:01
In reply to Re: Atypical depression » River1924, posted by Ines on March 5, 2007, at 11:50:05
Me too. I feel best in the morning, the earlier the better, unless I've been drinking the night before, which I don't usually do. Even then I sometimes feel best in the morning. Worst probably evening. Often I feel better come bed time
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