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
poster:laima
thread:737405
URL: http://www.dr-bob.org/babble/20070302/msgs/738143.html