![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 9 of 9. This is the beginning of the thread.
Posted by Jason911 on March 4, 2002, at 19:17:10
Felt I should post this again. I just don't see how this could not be true. I'd believe a man as smart as Dr Joseph Knoll. He knows his shit.
"deprenyl's discoverer, Dr. Joseph Knoll, and the uses of the medicine. It explained basically everything I spent hours researching on in a single report which I have printed out and am bringing to my visit next week. It talks about it's unique selective MAO-B inhibiting properties, catecholamine activity enhancing ability, neuroprotection from various neurotoxins, anti-aging possibilities, and most importantly its effectiveness in teating depression.
I brought it up the last time I met with the doctor but he said that, to his knowledge, it didn't work very well with depression and that he'd never heard of it used for this in quite some time and was mainly used as a medicine for Parkinsons and that it wasn't the best choice, in his opinion. Knowing as much as I know now, I believe he is unaware of some of deprenyl (selegiline HCL - Eldepryl in the US)'s potential benefits and recent findings. Who could blame him? He deals with psychotropic drugs that deal with depression and few doctors use deprenyl for this purpose. All that he knew was that at MAO-B selective doses (above 15mg, it becomes a full MAOI) it was not SOLELY effective at treating depression. My paper describes the studies that were done on atypical depressives, tretment-resistant depressives, and major despressives, and that effective treatment levels required dosages in the 20-30, even 60mg range. Well above MAO-B selective doses. Even though the treatments were effective and had low side-effects, there are risks involved with all-out MAOI's like diet restrictions (such as the "cheese effect"). So I can see where he's coming from in this light. But, there were three studies that suggested effective antidepressant action at selective MAO-B inhibiting doses.
That study was just the beginning of the paper's deprenyl-depression studies. What's eye-catching is what followed: "In 1978 Mendelwicz and Youdim treated 14 depressed patients with low-dose deprenyl (< or =10mg) plus 300mg 5-HTP 3 times daily for 32 days. Deprenyl potentiated the antidepressant effect of 5-HTP in 10/14 patients. 5-HTP enhances brain serotonin metabolism, which is frequently a problem in depression, while deprenyl enhances dopamine/noradrenalin activity" (how? - I'll explain in a bit). "Under activity of brain dopamine, noradrenalin (norepinephrine), and serototin neural systems are the most frequently cited biochemical causes of depression. So, deprenyl plus 5-HTP would seem a natural antidepressant combination."
The next one gets even more promising! "In 1984 Birkmayer, Knoll, and colleagues published their successful results in 155 unipolar depressed patients who were extremely treatment-resistant. Patients were given 5-10mg deprenyl plus 250mg phenylalanine daily. Approximately 70% of their patients achieved full remission, typically within 1-3 weeks. Some patients were continued up to 2 years on treatment without loss of antidepressant action. The combination of deprenyl plus phenylalanine enhances brain PEA activity, while both deprenyl and PEA enhance brain catecholamine activity. Thus deprenyl plus phenylalanine is also a natural antidepressant combination."
Almost equally impressive: "In 1991 H. Sabelli reported successful results treating 10 drug-resistant major depressive disorder patients. Sabelli used 5mg deprenyl daily along with 100mg vitamin B6, and 1-3 grams phenylalanine twice daily as treatment. 6 of 10 patients viewed their depressive episodes terminated within 2-3 days! Global Assessment Scale scores confirmed the patients' subjective experiences. Vitamin B6 activates the enzyme that converts phenylalanine to PEA, so the combination of the three is a bio-logical way to enhance both PEA and catecholamine brain function, and thus to diminish depression."
Here is why the catecholamine enhancement is so important in treating depression, especially in those whose depression can be related directly to dopamine under-activity (as in my case). You see, even if deprenyl's oringinally hypothesized mode of action - directly increasing synaptic dopamine levels through MAO-B inhibition - is false, deprenyl's MAO-B inhibition still provides part of its benefit.
It wasn't until the 1990s that Knoll's deprenyl research took a new direction. Working with rat brain stems, rabbit pulmonary and ear arteries, frog hearts and rats in shuttle boxes, Knoll discovered a new mode of action of deprenyl that he believes explains its widespread clinical utility. Knoll discovered that deprenyl [selegiline] (and it's cousin, PEA) are "catecholamine enhancers". Catecholamines refers to the inter-related neurotransmitters dopamine, noradrenaline, and adrenaline. Catecholamines are the transmitters for key activating brain circuits - the mesolimbic-cortical circuit and the locus coeruleus. The neurons from these two brain circuits project from the brain stem, through the mid-brain, to the cerebral cortex. They help to maintain focus, concentration, alertness and effortful attention. One of the reasons the doctor put me on Adderall! - but it seems obvious Adderall is only a temporary fix as it is well documented that the human body develops tolerance (whether it's 6 days or 2 years, everyone's different) to amphetamines, including d-amphetamine, quite quickly. Plus, amphetamines are known to damage dopamine cells but whether or not the damage is done at clincally prescribed doses is not yet known and that scares me especially after long term use AND from what I hear, discontinuing use just sends the person right back into the hole it once lifted them out of). Deprenyl would seem much better (it even protects your dopamine cells from damage/neurotoxicity) :) Dopamine is also the transmitter for a brainstem circuit - the nigrostriatal tract - which connects the the substantia nigra (which deprenyl enhances) and the striatum, a nerve tract that helps control bodily movement.
Here's how it works: when an electrical impulse travels down the length of a neuron - from the recieving dendrite, through the cell body, and down the transmitting axon - it triggers the release of packets of nerotransmitters into the synaptic gap. These transmitters hook onto receptors of the next neuron, triggering an electrical impulse which then travels down that neuron , causing yet another transmitter release. What Knoll and colleagues discovered through their highly technical experiments is that deprenyl and PEA act to more efficiently couple the release of neurotransmitters to the electrical impulse that triggers their release. In other words, deprenyl (and PEA) cause a larger release of transmitters in response to a given electrical impulse. It's like "turning up the volume" on catecholamine nerve cell activity. And this may be clinically very useful in depression where there may be under-activity of both dopamine and noradrenalin neurons. And the key here is the addition of the supplement phenylalanine to the deprenyl to help significantly increase PEA levels (one need only look to the results of the above studies to come to that conclusion). Even deprenyl in itself has shown in autopsy studies to not only increase dopamine levels by 40-70% in Parkinson patients but increase PEA levels 1300-3500%! You see, PEA is the preferred substrate for MAO-B, the MAO that deprenyl inhibits. PEA has an extremely rapid turnover due to its rapid and continuous breakdown by MAO-B. Thus deprenyl's catecholamine activity enhancer has a dual mode of action. At MAO-B inhibiting doses, deprenyl has a huge catecholamine enhancing effects due to the major increases in PEA levels. Many authors have pointed out the probable dopamine neuron activity enhancing effect of PEA in Parkinson patients taking deprenyl. Knoll's discovery of PEA's catecholamine activity enhancer effect now explains this PEA dopamine-enhancing effect.
So my proposal on Wednesday will be to take 10mg a day of selegiline, 600mg of phenylalanine supplement, as well as a good amount of vitamin's C and E, and 1000mg of NAC. The reason for the latter is that deprenyl increases only 2 of the 3 main antioxidants made in the brain. SOD, and catalase to a lesser extent. But the third, glutathione isn't raised at all so it is recommended by Knoll that one take around 1000mg NAC (which increases glutathione levels) to normalize these levels. Good amounts of vitamin C and E help very much as antioxidants themselves. I will ask to discontinue Adderall and taper off the Wellbutrin as well. Wellbutrin is now said to be mainly a noradrenalin reputake inhibitor while only mildly binding to the dopamine uptake sites and actually decreasing the amount of dopamine that is manufactured! I believe that Eldepryl and around 600mg/day of phenylalaine will take care of the noradrenalin AND dopamine especially."
This is why I preach so much about selegiline AND phenylalanine as the cure for depression that so many people don't know about and are missing out on. Just look at the people who have posted on the forum with positive results. I don't see how it could do anything bad other than "over-activate" those who's problems lie else where. Those that don't have MAJOR DEPRESSION I think will almost definately benefit, especially with Klonopin for those who can't get to sleep. -Jason911
Posted by Jason911 on March 4, 2002, at 19:30:29
In reply to Just look. Take it or leave it. SELEGLINE COMBO!!!, posted by Jason911 on March 4, 2002, at 19:17:10
Posted by Lorraine on March 4, 2002, at 23:28:10
In reply to Just look. Take it or leave it. SELEGLINE COMBO!!!, posted by Jason911 on March 4, 2002, at 19:17:10
Jason: Good analysis and it is always nice to have people beating the drum about any med combo. I hope it works for you. I can't stand 5HTP or phenylalamine. 5HTP makes me sleepy, sedated and thick headed; while phenylalmine makes me feel "pressure". Anyway, tried phenylalamine with selegiline, did nothing for me, but then I wasn't on Klonopin. Like selegiline generally, but makes me too anxious and has no real antidepressant effect for me.
Good luck. If Selegiline comes out in patch form and I'm not "fixed", I may try your 5HTP selegiline combo (though I'll have to check my records, I might have tried that too.)
Lorraine
Posted by Eloy on March 5, 2002, at 4:35:30
In reply to Just look. Take it or leave it. SELEGLINE COMBO!!!, posted by Jason911 on March 4, 2002, at 19:17:10
Sounds deep, so are you saying that there's a kinda combination medicine that could work better then the common SSRI's and AD's? Without using the big chemical jargon could you please break it down into laymens terms for me to understand, i'm sorry, it's just that i'm a true blond. In short, what is the panacea combo you discovered, and how is it better, and can it really slow down a persons degenerative aging too?
Posted by Jason911 on March 5, 2002, at 10:52:31
In reply to Re: Just look. Take it or leave it. SELEGLINE COMBO!!!, posted by Eloy on March 5, 2002, at 4:35:30
About the aging, it won't be proven until another 30-40 or more years because the people didn't take the selegiline for life extention until the 1980's, so only time will tell. If the studies are any indication, it should increase life-span via keeping your brain healthy and slow down it's dopaminergic decline with age. It protects these cells. Like scientists know, after the age of 50 people's dopamine counts declines by anout 13% per year!! This is why you see the typical 75 year old slow (mentally) to recognize, react, and so on. Well in theory, at the age of 80 you should be mentally capable of a person in his 50's! Death occurs normally when the dopamine cells' count is at about 30% of what it was when you were younger. Not to say you wil live forever, you can just die for other reasons (heart attack (which Omega-3 can help considerably, accident, etc.). Dopamine plays a critical role in concentration, alertness, and drive; our ability to distiguish 'experience'. Now, as for a substitution for AD's and especially those dreaded SSRI's the selegiline+phenylalanine is a wise decision before resorting to these meds as the S&P combo is less-likly to cause any side-effects. The only way one should experience side-effects is if one's problem is not dopamine related, i.e serotonin related. If you don't experience constant sadness, suicidal thoughts, sleep all the time, then the selegiline combo could work quite well for you. Like the posts recently put on this board about people on Effexor (another SSRI) and having sexual dysfunction even after quitting the meds for quite some time is just a scary thought. You won't have to worry about any of this on the combo (probably an increase in libido, sex drive). It is relatively harmless, especially when taken at low dose and does so much good for not only your mood, possibly, but your brain itself! In addition to selegline partially preventing the breakdown of dopamine (MAO-A also breaks it down a little) it's the PEA that seems to have the real mood brightening effect in people. PEA is the chemical that is released when we fall in love and walk around all day in a great mood and well.... in love! The selegiline stimulates (especially with the l-phenylalanine combo) the part of our brain that affects drive, motivation, and memory. It put that spark back into our live's that we have been lacking for so long! Knoll's deprenyl discovery occured in the 60's in Bulgaria. It was originally developed as an anti-depressant with the mindset of increasing dopamine levels through MAO-B inhibition alone as it was thought that dopamine was broken down by MAO-B only. Well that was not the case as MAO-A plays a part in this as well. But Knoll did not give up and eventually found it's reall amazing potential. The US has yet to acknowledge it's anti-depressant effect. It wasn't until the 1990's that Knoll discovered it's true clinical use for us depressed people. It's worth a try. I don't want to see you get into all of those side-effect problems with all of those other anti-dpressants and it's worth giving it a shot! You should find it quite activating and mentally stimulating and sexually stimulating. Hell, Somerset (the company that makes Eldepryl (selegiline)) recently did a trial on a Selegiline patch to treat depression, and people on this very board reported amazing benefits. The purpost of the patch was to release higher amounts of deprenyl into the bloodstream while also allowing the patient to not have to observe dietary restrictions that accompany MAOI's. The FDA will make it's approval a long and drwn out process and won't be seen in the near future. But now, right now, there is an answer. Give it a try. -Jason911
> Sounds deep, so are you saying that there's a kinda combination medicine that could work better then the common SSRI's and AD's? Without using the big chemical jargon could you please break it down into laymens terms for me to understand, i'm sorry, it's just that i'm a true blond. In short, what is the panacea combo you discovered, and how is it better, and can it really slow down a persons degenerative aging too?
Posted by Jason911 on March 5, 2002, at 10:56:10
In reply to Re: Just look. Take it or leave it. SELEGLINE COMBO!!!, posted by Eloy on March 5, 2002, at 4:35:30
Posted by Psydoc on March 13, 2002, at 21:42:38
In reply to Re: Just look. Take it or leave it. SELEGLINE COMBO!!!, posted by Eloy on March 5, 2002, at 4:35:30
Here are a few MEDLINE abstracts on Selegline:
1: Arch Gen Psychiatry 1994 Aug;51(8):607-15
High-dose selegiline in treatment-resistant older depressive patients.
Sunderland T, Cohen RM, Molchan S, Lawlor BA, Mellow AM, Newhouse PA, Tariot PN,
Mueller EA, Murphy DL.Section on Geriatric Psychiatry, National Institute of Mental Health, Bethesda,
Md.BACKGROUND: We examined the effect of high-dose selegiline in 16
treatment-resistant older depressive patients. We hypothesized that selegiline,
at a dosage of 60 mg/d, would be at least partially effective but that the
higher doses would not maintain the monoamine oxidase B selectivity observed
with the lower doses of selegiline. METHODS: Sixteen treatment-resistant
subjects (mean [ SD] age, 65.6 9.3 years) entered a double-blind,
randomized, crossover study of placebo vs 3 weeks of selegiline at a dosage of
60 mg/d. Objective measures of mood and behavior were obtained in all subjects,
and 10 of the subjects underwent repeated lumbar punctures for analysis of
monoamine metabolites in the cerebrospinal fluid. RESULTS: Objective measures of
mood and behavior revealed significant improvement in the Hamilton Depression
Rating Scale score (37.4% decrease), the Global Depression score (22.7%
decrease), and the Brief Psychiatric Rating Scale score (19.3% decrease);
subjective behavioral measures, however, did not show significant improvement
during the 3-week medication trial. Cerebrospinal fluid values revealed a
statistically significant drop in 3-methoxy-4-hydroxyphenylglycol (51%) and
5-hydroxyindoleacetic acid (17%) levels, and there was a significant lowering of
systolic blood pressure on standing (15%), but these changes were not
accompanied by clinical side effects. CONCLUSIONS: Our results suggest that
high-dose selegiline can be an effective antidepressant in treatment-resistant
older depressive patients. While the selegiline dose required has nonselective
monoamine oxidase effects and thus would not be free of possible tyramine
interactions, other advantages suggest that further investigations with
selegiline are warranted in this population.Publication Types:
Clinical Trial
Randomized Controlled TrialPMID: 7519005 [PubMed - indexed for MEDLINE]
2: Arch Gen Psychiatry 1989 Jan;46(1):45-50
A controlled study of the antidepressant efficacy and side effects of
(-)-deprenyl. A selective monoamine oxidase inhibitor.Mann JJ, Aarons SF, Wilner PJ, Keilp JG, Sweeney JA, Pearlstein T, Frances AJ,
Kocsis JH, Brown RP.Department of Psychiatry, Cornell University Medical College, New York, NY
10021.Monoamine oxidase (MAO) inhibitors are effective antidepressants whose use is
limited because of unwanted side effects and the possibility of a
tyramine-induced hypertensive crisis (cheese reaction). (-)-Deprenyl (the
official nonproprietary name for this substance is selegiline), a selective MAO
type B inhibitor, may be safer and have fewer side effects, but its
antidepressant efficacy is uncertain. A double-blind placebo-controlled study
was carried out in depressed outpatients who were treated with (-)-deprenyl in
an MAO type B selective dose range and at a higher nonselective dose range.
(-)-Deprenyl did not have a statistically significant antidepressant effect
after three weeks of treatment at doses of 10 mg/d. However, after six weeks and
at higher doses (averaging about 30 mg/d for the second three weeks),
(-)-deprenyl was superior to placebo in antidepressant effect with a positive
response rate of 50% vs 13.6% and with a 41% reduction in the Hamilton
Depression Rating Scale mean score vs 10% in the placebo-treated group. No
hypertensive crises were seen. The rate of occurrence of side effects with
(-)-deprenyl was no greater than with placebo. It was concluded that
(-)-deprenyl is an effective antidepressant in a dose range where it is
distinguished by the absence of many of the side effects typical of nonselective
MAO inhibitors.Publication Types:
Clinical Trial
Controlled Clinical TrialPMID: 2491941 [PubMed - indexed for MEDLINE]
3: Biol Psychiatry 1985 May;20(5):558-65
Biochemical effects of L-deprenyl in atypical depressives.
Liebowitz MR, Karoum F, Quitkin FM, Davies SO, Schwartz D, Levitt M, Linnoila M.
To examine the biochemical effects of 10-30 mg/day L-deprenyl, measurement of
24-hr urinary output of phenylethylamine (PEA), 3-methoxy 4-hydroxy
phenylethyleneglycol (MHPG), and L-deprenyl's amphetamine metabolites were
carried out before and during the treatment of atypical depressives. Platelet
monoamine oxidase (MAO) activity was also assessed. With L-deprenyl 10-30
mg/day, the expected MAO B inhibition occurred, as indicated by significant
increase in urinary PEA excretion and virtual disappearance of platelet MAO
activity. Twenty-five to 33% of the daily dose of L-deprenyl was recovered as
urinary methamphetamine or amphetamine. Excretion of MHPG was significantly
decreased with L-deprenyl 10-20 mg/day. Overall, the results suggest that
L-deprenyl's antidepressant effects are mediated by some mechanism other than,
or in addition to, MAO B inhibition.Publication Types:
Clinical TrialPMID: 3921065 [PubMed - indexed for MEDLINE]
4: Br J Psychiatry 1983 May;142:508-11
L-Deprenil, a selective monoamine oxidase type B inhibitor, in the treatment of
depression: a double blind evaluation.Mendlewicz J, Youdim MB.
In a double blind controlled study, 14 affectively ill patients (2 bipolars, 12
unipolars) were randomly allocated to L-Deprenil treatment (an irreversible
selective MAO-B inhibitor without "cheese effect") and 13 patients (3 bipolars,
10 unipolars) to placebo only. Patients on L-Deprenil showed a significantly
greater clinical improvement than placebo patients. A positive relationship was
found between clinical improvement and degree of platelet MAO inhibition in
patients treated with L-Deprenil.Publication Types:
Clinical Trial
Randomized Controlled TrialPMID: 6409196 [PubMed - indexed for MEDLINE]
Best regards . . .
Ivan
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%
Posted by djmmm on March 14, 2002, at 13:46:23
In reply to SELEGLINE Abstracts, posted by Psydoc on March 13, 2002, at 21:42:38
Here are some more...
http://www.deprenyl.net/
Posted by katz on September 16, 2002, at 23:05:08
In reply to Just look. Take it or leave it. SELEGLINE COMBO!!!, posted by Jason911 on March 4, 2002, at 19:17:10
>Hi Jason! I don't know if you're still out there. If you are, I was wondering how your slegeline/phenylalanine trial turned out. Was it successful? I would be really interested to here what the outcome was and if you are currently still using this combo.
Kathy
Felt I should post this again. I just don't see how this could not be true. I'd believe a man as smart as Dr Joseph Knoll. He knows his shit.
>
> "deprenyl's discoverer, Dr. Joseph Knoll, and the uses of the medicine. It explained basically everything I spent hours researching on in a single report which I have printed out and am bringing to my visit next week. It talks about it's unique selective MAO-B inhibiting properties, catecholamine activity enhancing ability, neuroprotection from various neurotoxins, anti-aging possibilities, and most importantly its effectiveness in teating depression.
>
> I brought it up the last time I met with the doctor but he said that, to his knowledge, it didn't work very well with depression and that he'd never heard of it used for this in quite some time and was mainly used as a medicine for Parkinsons and that it wasn't the best choice, in his opinion. Knowing as much as I know now, I believe he is unaware of some of deprenyl (selegiline HCL - Eldepryl in the US)'s potential benefits and recent findings. Who could blame him? He deals with psychotropic drugs that deal with depression and few doctors use deprenyl for this purpose. All that he knew was that at MAO-B selective doses (above 15mg, it becomes a full MAOI) it was not SOLELY effective at treating depression. My paper describes the studies that were done on atypical depressives, tretment-resistant depressives, and major despressives, and that effective treatment levels required dosages in the 20-30, even 60mg range. Well above MAO-B selective doses. Even though the treatments were effective and had low side-effects, there are risks involved with all-out MAOI's like diet restrictions (such as the "cheese effect"). So I can see where he's coming from in this light. But, there were three studies that suggested effective antidepressant action at selective MAO-B inhibiting doses.
>
> That study was just the beginning of the paper's deprenyl-depression studies. What's eye-catching is what followed: "In 1978 Mendelwicz and Youdim treated 14 depressed patients with low-dose deprenyl (< or =10mg) plus 300mg 5-HTP 3 times daily for 32 days. Deprenyl potentiated the antidepressant effect of 5-HTP in 10/14 patients. 5-HTP enhances brain serotonin metabolism, which is frequently a problem in depression, while deprenyl enhances dopamine/noradrenalin activity" (how? - I'll explain in a bit). "Under activity of brain dopamine, noradrenalin (norepinephrine), and serototin neural systems are the most frequently cited biochemical causes of depression. So, deprenyl plus 5-HTP would seem a natural antidepressant combination."
>
> The next one gets even more promising! "In 1984 Birkmayer, Knoll, and colleagues published their successful results in 155 unipolar depressed patients who were extremely treatment-resistant. Patients were given 5-10mg deprenyl plus 250mg phenylalanine daily. Approximately 70% of their patients achieved full remission, typically within 1-3 weeks. Some patients were continued up to 2 years on treatment without loss of antidepressant action. The combination of deprenyl plus phenylalanine enhances brain PEA activity, while both deprenyl and PEA enhance brain catecholamine activity. Thus deprenyl plus phenylalanine is also a natural antidepressant combination."
>
> Almost equally impressive: "In 1991 H. Sabelli reported successful results treating 10 drug-resistant major depressive disorder patients. Sabelli used 5mg deprenyl daily along with 100mg vitamin B6, and 1-3 grams phenylalanine twice daily as treatment. 6 of 10 patients viewed their depressive episodes terminated within 2-3 days! Global Assessment Scale scores confirmed the patients' subjective experiences. Vitamin B6 activates the enzyme that converts phenylalanine to PEA, so the combination of the three is a bio-logical way to enhance both PEA and catecholamine brain function, and thus to diminish depression."
>
> Here is why the catecholamine enhancement is so important in treating depression, especially in those whose depression can be related directly to dopamine under-activity (as in my case). You see, even if deprenyl's oringinally hypothesized mode of action - directly increasing synaptic dopamine levels through MAO-B inhibition - is false, deprenyl's MAO-B inhibition still provides part of its benefit.
>
> It wasn't until the 1990s that Knoll's deprenyl research took a new direction. Working with rat brain stems, rabbit pulmonary and ear arteries, frog hearts and rats in shuttle boxes, Knoll discovered a new mode of action of deprenyl that he believes explains its widespread clinical utility. Knoll discovered that deprenyl [selegiline] (and it's cousin, PEA) are "catecholamine enhancers". Catecholamines refers to the inter-related neurotransmitters dopamine, noradrenaline, and adrenaline. Catecholamines are the transmitters for key activating brain circuits - the mesolimbic-cortical circuit and the locus coeruleus. The neurons from these two brain circuits project from the brain stem, through the mid-brain, to the cerebral cortex. They help to maintain focus, concentration, alertness and effortful attention. One of the reasons the doctor put me on Adderall! - but it seems obvious Adderall is only a temporary fix as it is well documented that the human body develops tolerance (whether it's 6 days or 2 years, everyone's different) to amphetamines, including d-amphetamine, quite quickly. Plus, amphetamines are known to damage dopamine cells but whether or not the damage is done at clincally prescribed doses is not yet known and that scares me especially after long term use AND from what I hear, discontinuing use just sends the person right back into the hole it once lifted them out of). Deprenyl would seem much better (it even protects your dopamine cells from damage/neurotoxicity) :) Dopamine is also the transmitter for a brainstem circuit - the nigrostriatal tract - which connects the the substantia nigra (which deprenyl enhances) and the striatum, a nerve tract that helps control bodily movement.
>
> Here's how it works: when an electrical impulse travels down the length of a neuron - from the recieving dendrite, through the cell body, and down the transmitting axon - it triggers the release of packets of nerotransmitters into the synaptic gap. These transmitters hook onto receptors of the next neuron, triggering an electrical impulse which then travels down that neuron , causing yet another transmitter release. What Knoll and colleagues discovered through their highly technical experiments is that deprenyl and PEA act to more efficiently couple the release of neurotransmitters to the electrical impulse that triggers their release. In other words, deprenyl (and PEA) cause a larger release of transmitters in response to a given electrical impulse. It's like "turning up the volume" on catecholamine nerve cell activity. And this may be clinically very useful in depression where there may be under-activity of both dopamine and noradrenalin neurons. And the key here is the addition of the supplement phenylalanine to the deprenyl to help significantly increase PEA levels (one need only look to the results of the above studies to come to that conclusion). Even deprenyl in itself has shown in autopsy studies to not only increase dopamine levels by 40-70% in Parkinson patients but increase PEA levels 1300-3500%! You see, PEA is the preferred substrate for MAO-B, the MAO that deprenyl inhibits. PEA has an extremely rapid turnover due to its rapid and continuous breakdown by MAO-B. Thus deprenyl's catecholamine activity enhancer has a dual mode of action. At MAO-B inhibiting doses, deprenyl has a huge catecholamine enhancing effects due to the major increases in PEA levels. Many authors have pointed out the probable dopamine neuron activity enhancing effect of PEA in Parkinson patients taking deprenyl. Knoll's discovery of PEA's catecholamine activity enhancer effect now explains this PEA dopamine-enhancing effect.
>
> So my proposal on Wednesday will be to take 10mg a day of selegiline, 600mg of phenylalanine supplement, as well as a good amount of vitamin's C and E, and 1000mg of NAC. The reason for the latter is that deprenyl increases only 2 of the 3 main antioxidants made in the brain. SOD, and catalase to a lesser extent. But the third, glutathione isn't raised at all so it is recommended by Knoll that one take around 1000mg NAC (which increases glutathione levels) to normalize these levels. Good amounts of vitamin C and E help very much as antioxidants themselves. I will ask to discontinue Adderall and taper off the Wellbutrin as well. Wellbutrin is now said to be mainly a noradrenalin reputake inhibitor while only mildly binding to the dopamine uptake sites and actually decreasing the amount of dopamine that is manufactured! I believe that Eldepryl and around 600mg/day of phenylalaine will take care of the noradrenalin AND dopamine especially."
>
> This is why I preach so much about selegiline AND phenylalanine as the cure for depression that so many people don't know about and are missing out on. Just look at the people who have posted on the forum with positive results. I don't see how it could do anything bad other than "over-activate" those who's problems lie else where. Those that don't have MAJOR DEPRESSION I think will almost definately benefit, especially with Klonopin for those who can't get to sleep. -Jason911
>
>
This is the end of the thread.
Psycho-Babble Medication | Extras | FAQ
Dr. Bob is Robert Hsiung, MD,
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