Psycho-Babble Medication Thread 818442

Shown: posts 1 to 10 of 10. This is the beginning of the thread.

 

Nardil plus PEA or DLPA

Posted by Carlton on March 17, 2008, at 13:08:14

First, I am aware that taking any supplements with Nardil is dangerous and can, ultimately, be fatal. For that matter, it is my understanding that having a glass of wine and cheese can be fatal for uses of phenelzine.

With that said, I am aware that there have been studies which tested very low dosages of PEA with certain MAO inhibitors, who had been administered selegiline (L-deprenyl). I am not aware of any studies which combined PEA or DLPA as an adjunct treatment with Phenelzine for depression. I quote from one study, below, but the information regarding PEA with Phenelzine is sparse, to say the least.

Is there a difference between Nardil and selegiline (L-deprenyl)?

And, secondly, has anyone tried to supplement Phenelzine (nardil) with PEA or DLPA (DL-phenylalanine).

If so, what dosage of PEA or DLPA and Nardil?

What were the effects?

"Phenylethylamine (PEA), an endogenous neuroamine,
increases attention and activity in animals
and has been shown to relieve depression in 60% of
depressed patients." See Sabelli H, Fink P, Fawcett J, et al. Sustained antidepressant effects of PEA replacement. J Neuropsychiatry
1996;8:16871


"In depressed subjects treated with an MAOI, PEA markedly improves mood (because PEA is rapidly metabolized. PEA alone produces no noticeable effects). The addition of 10 to 30 mg/day of PEA to current treatment withamitriptyline plus phenelzine terminated the episode of depression in 2 of the 3 inpatients with MOD who had not achieved any significant recovery with tricyclic antidepressants, MAOI, or their combination.
98 No significant side effects were noted. Patients noted a reduction of appetite, which had been increased by the antidepressants used." Sabelli H, Javaid J. Phenylethlyamine modulation of affect: therapeutic and diagnostic implications. J Neuropsychiatry Clin Neuroscience 1995;7:614

 

Re: Nardil plus Phenylethylamine (PEA) Carlton

Posted by Ron Hill on March 18, 2008, at 23:37:25

In reply to Nardil plus PEA or DLPA, posted by Carlton on March 17, 2008, at 13:08:14

> First, I am aware that taking any supplements with Nardil is dangerous and can, ultimately, be fatal. For that matter, it is my understanding that having a glass of wine and cheese can be fatal for uses of phenelzine.

> With that said, I am aware that there have been studies which tested very low dosages of PEA with certain MAO inhibitors, who had been administered selegiline (L-deprenyl). I am not aware of any studies which combined PEA or DLPA as an adjunct treatment with Phenelzine for depression. I quote from one study, below, but the information regarding PEA with Phenelzine is sparse, to say the least.

> Is there a difference between Nardil and selegiline (L-deprenyl)?

Yes, there is a very important difference. Selegiline is a selective MAOI-B at 10 mg/day or less. However, Nardil is an MAOI-A and MAOI-B.

MAO-A occurs mainly in the intestine and brain, and the enzyme preferentially oxidizes (inactivates) serotonin, epinephrine, norepinephrine, and octopamine.

MAO-B occurs in the brain and in platelets as well as in other tissues, and it inactivates phenylethylamine (PEA), phenylethanolamine, N-methyl-histamine, and benzylamine. Both enzymes (MAO-A and MAO-B) metabolize tyramine, tryptamine and dopamine.

Elevated levels of norepinephrine and other catecholamines can cause a hypertensive crisis.

A selective MAOI-B, like selegiline at a dosage of 10 mg/day or less, does not inhibit the MAO-A enzymes and, therefore, norepinephrine and epinephrine levels are held in check and not allowed to elevate in concentration.

However, Nardil inhibits MAO-A as well as MAO-B. Therefore, anything that causes an elevation in norepinephrine or epinephrine goes unchecked and the concentrations increase. This can cause a hypertensive crisis.

> And, secondly, has anyone tried to supplement Phenelzine (nardil) with PEA or DLPA (DL-phenylalanine).

PEA, yes. But, there is no way in heck that I would try adding DLPA or LPA to Nardil because I deem it way too risky. Adding DLPA or LPA to selegiline is fine, but I would never add either of them to Nardil.

L-phenylalanine is the precursor to PEA. However, L-phenylalanine IS ALSO the precursor to tyrosine which then continues on as follows; tyrosine > L-dopa > dopamine > norepinephrine > epinephrine. The L-dopa and the three catecholamines (DA, NE, and epinephrine) scare the heck out of me as a Nardil user. DLPA or LPA combined with Nardil is a hypertensive crisis waiting to happen as I see it. Way too risky in my book.

> If so, what dosage of PEA or DLPA and Nardil?

A couple of days ago I began my second trial of PEA with Nardil. It is important to begin with a very low dosage of PEA. Take too much and it can cause a hypertensive crisis. Please be very careful. I am currently taking 10 mg/day of PEA with 75 mg/day of Nardil. It is too early in the trial to discuss its efficacy.

I have found that I need to take a couple of milligrams of PEA every two hours otherwise the beneficial effect begins to wear off. The PEA product that I bought comes in 250 mg capsules, so measuring out two milligrams requires an accurate scale or some alternative measuring method. What I do is empty one 250 mg capsule into two gallons of water and shake thoroughly. Each day I fill my personal water bottle from this two gallon standardized solution. My personal water bottle has graduated milliliter markings on the outside of the see-through bottle. Therefore, I can calculate the amount of PEA that I take by recording the amount drank from my water bottle. Make sense?

Carlton, if you decide to try this cocktail, monitor your blood pressure frequently and keep your nifedipine (hypertensive anecdote) handy. My experience is that even with low dosages of PEA added to Nardil my blood pressure rises. A little too much PEA and it will cause anxiety and uneasiness.

> What were the effects?

Read my post regarding my first trial at: http://www.dr-bob.org/babble/neuro/20080204/msgs/813379.html

Carlton, please list all of the medications that you are on, and the dosages of each.

Be safe.

-- Ron

dx: Bipolar II, with ultra rapid cycling (15 days for one complete cycle), and mild OCPD

300 mg/day Trileptal (Note: Trileptal is my antimanic med. If I get hypomanic, I jump it up to 600 or 900.)
200 mg/day Lamictal
250 mg/day Keppra
75 mg/day Nardil
1.875 mg/day Deplin
10 mg/day Phenylethylamine (PEA)


> "Phenylethylamine (PEA), an endogenous neuroamine, increases attention and activity in animals and has been shown to relieve depression in 60% of depressed patients." See Sabelli H, Fink P, Fawcett J, et al. Sustained antidepressant effects of PEA replacement. J Neuropsychiatry
> 1996;8:16871


> "In depressed subjects treated with an MAOI, PEA markedly improves mood (because PEA is rapidly metabolized. PEA alone produces no noticeable effects). The addition of 10 to 30 mg/day of PEA to current treatment withamitriptyline plus phenelzine terminated the episode of depression in 2 of the 3 inpatients with MOD who had not achieved any significant recovery with tricyclic antidepressants, MAOI, or their combination.

> 98 No significant side effects were noted. Patients noted a reduction of appetite, which had been increased by the antidepressants used." Sabelli H, Javaid J. Phenylethlyamine modulation of affect: therapeutic and diagnostic implications. J Neuropsychiatry Clin Neuroscience 1995;7:614

 

Re: Nardil plus Phenylethylamine (PEA) Ron Hill

Posted by SLS on March 19, 2008, at 5:05:43

In reply to Re: Nardil plus Phenylethylamine (PEA) Carlton, posted by Ron Hill on March 18, 2008, at 23:37:25

> 300 mg/day Trileptal (Note: Trileptal is my antimanic med. If I get hypomanic, I jump it up to 600 or 900.)

My knee-jerk reaction to this is that it is the worst thing you can do with this medication. Pulsing any psychotropic is considered counterproductive and often yields treatment-resistance. Perhaps more important is that allowing the mania to appear at all just reinforcing the cycle. After mania comes depression. Stop the mania, and you might also avoid the depressive rebound that occurs during a switch from mania to depression. Since Trileptal is so useful to you episodically, it might act to penetrate your cycle and prevent mood swings if used chronically. It very often takes 6 months or longer for mood-stabilizer treatment to effect a significant reduction of ultra-rapid cycling.

Great post, by the way.


- Scott

 

Re: Nardil plus Phenylethylamine (PEA) Ron Hill

Posted by carlton on March 19, 2008, at 11:57:08

In reply to Re: Nardil plus Phenylethylamine (PEA) Carlton, posted by Ron Hill on March 18, 2008, at 23:37:25

Ron,

Thanks for your post. Very informative.
Instead of nifedipine, doc prescribed clonidine to be used only in event of hypertensive crisis.

I am taking

Provigil 100mg
Lunesta 2 mg (night time)
Nardil 60mg
Multi-vitamin
Fish Oil 4 grams

 

Re: Nardil plus Phenylethylamine (PEA)

Posted by undopaminergic on March 19, 2008, at 14:51:37

In reply to Re: Nardil plus Phenylethylamine (PEA) Carlton, posted by Ron Hill on March 18, 2008, at 23:37:25

>
> > And, secondly, has anyone tried to supplement Phenelzine (nardil) with PEA or DLPA (DL-phenylalanine).
>
> PEA, yes. But, there is no way in heck that I would try adding DLPA or LPA to Nardil because I deem it way too risky.

PEA is considerably more risky than phenylalanine (PA), because it can rapidly release noradrenaline from storage vesicles in sympathetic nerve terminals, whereas PA first has to be converted into an active compound.

>
> L-phenylalanine is the precursor to PEA. However, L-phenylalanine IS ALSO the precursor to tyrosine which then continues on as follows; tyrosine > L-dopa > dopamine > norepinephrine > epinephrine. The L-dopa and the three catecholamines (DA, NE, and epinephrine) scare the heck out of me as a Nardil user.

DA is more hypotensive than hypertensive (except perhaps at very high concentrations), so any risk it may present is likely to be through its conversion into noradrenaline.

More importantly, it should be emphasised that the conversions of phenylalanine to tyrosine and tyrosine to L-dopa are relatively slow processes. L-dopa synthesis is the rate-limiting step in the production of catecholamines. Additionally, excessive concentrations of PA can further slow down the synthesis of L-dopa due to competitive inhibition of tyrosine hydroxylase (TH).

Catecholamines are also metabolised by catechol-O-methyltransferase (COMT), so they can be broken down even without MAO, albeit at a reduced rate.

> Carlton, if you decide to try this cocktail, monitor your blood pressure frequently and keep your nifedipine (hypertensive anecdote) handy. My experience is that even with low dosages of PEA added to Nardil my blood pressure rises. A little too much PEA and it will cause anxiety and uneasiness.

Depending on your baseline blood pressure, it might be interesting to try adding some guanfacine or guanabenz - alpha2-adrenergic agonists that reduce dopamine beta-hydroxylase (DBH) activity, slowing the conversion of DA to noradrenaline, and perhaps improving working memory as a bonus.

 

Re: Trileptal Dosage SLS

Posted by Ron Hill on March 19, 2008, at 21:51:16

In reply to Re: Nardil plus Phenylethylamine (PEA) Ron Hill, posted by SLS on March 19, 2008, at 5:05:43

Scott,

I hear what you are saying, Scott.

I've been taking Trileptal for four years. Throughout this time I held steady at the higher dosage. However, I recently reduced my Trileptal dosage because it seemed to be holding me in my depressive phase to some extent. Only on very rare occasions have I found it necessary to pulse up my Trileptal dosage.

I never get manic, and the only time I get hypomanic these days is if I use sleep deprivation to snap myself out of depression.

Consistent sleep habits are where I have been failing badly for the past several months. And, you are absolutely right; to the extent that I allow myself to keep erratic sleep times and, thereby, screw up my circadian clock, the more instability I invite into my rapid cycling.

-- Ron

-----------------------------

> > 300 mg/day Trileptal (Note: Trileptal is my antimanic med. If I get hypomanic, I jump it up to 600 or 900.)
>
> My knee-jerk reaction to this is that it is the worst thing you can do with this medication. Pulsing any psychotropic is considered counterproductive and often yields treatment-resistance. Perhaps more important is that allowing the mania to appear at all just reinforcing the cycle. After mania comes depression. Stop the mania, and you might also avoid the depressive rebound that occurs during a switch from mania to depression. Since Trileptal is so useful to you episodically, it might act to penetrate your cycle and prevent mood swings if used chronically. It very often takes 6 months or longer for mood-stabilizer treatment to effect a significant reduction of ultra-rapid cycling.
>
> Great post, by the way.
>
>
> - Scott

 

Re: Nardil plus Phenylethylamine (PEA) carlton

Posted by Ron Hill on March 19, 2008, at 22:00:20

In reply to Re: Nardil plus Phenylethylamine (PEA) Ron Hill, posted by carlton on March 19, 2008, at 11:57:08

Carlton,

Please keep us posted if you decide to conduct a trial of PEA.

Be safe, my friend.

Have you seen this document:
http://www.freepatentsonline.com/5455276.html
(scroll down in the document)

-- Ron
-------------------------------

> Ron,
>
> Thanks for your post. Very informative.
> Instead of nifedipine, doc prescribed clonidine to be used only in event of hypertensive crisis.
>
> I am taking
>
> Provigil 100mg
> Lunesta 2 mg (night time)
> Nardil 60mg
> Multi-vitamin
> Fish Oil 4 grams

 

Re: Nardil plus Phenylethylamine (PEA) undopaminergic

Posted by Ron Hill on March 19, 2008, at 23:39:29

In reply to Re: Nardil plus Phenylethylamine (PEA), posted by undopaminergic on March 19, 2008, at 14:51:37

undopaminergic,

Thank you for your post. I respect your knowledge of neurochemistry.

> PEA is considerably more risky than phenylalanine (PA), because it can rapidly release noradrenaline from storage vesicles in sympathetic nerve terminals, whereas PA first has to be converted into an active compound.

At what dosage level does PEA release NE from storage vesicles in sympathetic nerve terminals? Can you point me to a research document discussing this issue? I've not seen this stated anywhere in the literature. Thanks for your help.

> DA is more hypotensive than hypertensive (except perhaps at very high concentrations), so any risk it may present is likely to be through its conversion into noradrenaline.

Exactly, NE is the issue.

> More importantly, it should be emphasised that the conversions of phenylalanine to tyrosine and tyrosine to L-dopa are relatively slow processes. L-dopa synthesis is the rate-limiting step in the production of catecholamines. Additionally, excessive concentrations of PA can further slow down the synthesis of L-dopa due to competitive inhibition of tyrosine hydroxylase (TH).

Thanks for the information. But, why then, on page 2 of the Nardil Prescribing Information (Pfizer) document, is PA specifically contraindicated for the same reasons I put forth in my original post?

http://www.pfizer.com/files/products/uspi_nardil.pdf

On the other hand, PEA has been used safely with Nardil in small open trials. PEA must be treated with care and respect, but it can be done.

Others can do what they deem appropriate. But, for me, I'll follow Pfizer's warning and use PEA directly, yet carefully.

> Catecholamines are also metabolised by catechol-O-methyltransferase (COMT), so they can be broken down even without MAO, albeit at a reduced rate.

Clearly, catecholamines are not metabolized fast enough by COMT to avoid a hypertensive crisis in all situations.

Thanks again for your thought provoking post.

-- Ron

 

Re: Trileptal Dosage

Posted by SLS on March 21, 2008, at 10:02:50

In reply to Re: Trileptal Dosage SLS, posted by Ron Hill on March 19, 2008, at 21:51:16

> I hear what you are saying, Scott.

I hear what you are saying, too. I have a great respect for your powers of logic and observation. You know yourself better than I do. If you have already tried a higher dose of Trileptal for an extended period of time, you have thus already tried my suggestion. I am relieved to know that you pulse the drug only rarely.

Have you ever tried nifedipine or nimodipine? The NIMH was looking into these CA channel blockers. I think the results of nimodipine were disappointing, but they tried using it as a monotherapeutic treatment.

By the way, which antipsychotics have you tried, and at what doses?


- Scott


>
> I've been taking Trileptal for four years. Throughout this time I held steady at the higher dosage. However, I recently reduced my Trileptal dosage because it seemed to be holding me in my depressive phase to some extent. Only on very rare occasions have I found it necessary to pulse up my Trileptal dosage.
>
> I never get manic, and the only time I get hypomanic these days is if I use sleep deprivation to snap myself out of depression.
>
> Consistent sleep habits are where I have been failing badly for the past several months. And, you are absolutely right; to the extent that I allow myself to keep erratic sleep times and, thereby, screw up my circadian clock, the more instability I invite into my rapid cycling.
>
> -- Ron
>
> -----------------------------
>
> > > 300 mg/day Trileptal (Note: Trileptal is my antimanic med. If I get hypomanic, I jump it up to 600 or 900.)
> >
> > My knee-jerk reaction to this is that it is the worst thing you can do with this medication. Pulsing any psychotropic is considered counterproductive and often yields treatment-resistance. Perhaps more important is that allowing the mania to appear at all just reinforcing the cycle. After mania comes depression. Stop the mania, and you might also avoid the depressive rebound that occurs during a switch from mania to depression. Since Trileptal is so useful to you episodically, it might act to penetrate your cycle and prevent mood swings if used chronically. It very often takes 6 months or longer for mood-stabilizer treatment to effect a significant reduction of ultra-rapid cycling.
> >
> > Great post, by the way.
> >
> >
> > - Scott
>
>

 

Re: Nardil plus Phenylethylamine (PEA)

Posted by undopaminergic on March 23, 2008, at 2:43:00

In reply to Re: Nardil plus Phenylethylamine (PEA) undopaminergic, posted by Ron Hill on March 19, 2008, at 23:39:29

>
> At what dosage level does PEA release NE from storage vesicles in sympathetic nerve terminals? Can you point me to a research document discussing this issue? I've not seen this stated anywhere in the literature. Thanks for your help.

According to this abstract, a concentration of 4-6 micrograms/ml is required:
http://www.ncbi.nlm.nih.gov/pubmed/8649195

Assuming the above is accurate not only for rabbits but also humans in general, the oral dose required to achieve that concentration still depends on a number of factors, such as rate and completeness of absorption of the dose into the blood stream, how fast it is metabolised, and so on. Your guess is better than mine, since you have already determined, empirically, the approximate dose required to elicit a pressor effect.

Also note that it compares PEA to tyramine, which is responsible for the famous cheese effect.

>
> > More importantly, it should be emphasised that the conversions of phenylalanine to tyrosine and tyrosine to L-dopa are relatively slow processes. L-dopa synthesis is the rate-limiting step in the production of catecholamines. Additionally, excessive concentrations of PA can further slow down the synthesis of L-dopa due to competitive inhibition of tyrosine hydroxylase (TH).
>
> Thanks for the information. But, why then, on page 2 of the Nardil Prescribing Information (Pfizer) document, is PA specifically contraindicated for the same reasons I put forth in my original post?

Note that I did not say PA is necessarily safe - only safer than PEA. Also note that they caution against excessive consumption of chocolate, which is commonly a primary dietary source of PEA for many people. Besides, as I'm sure you realise, only some of the most common and probable dangers can be listed.

>
> http://www.pfizer.com/files/products/uspi_nardil.pdf
>
> On the other hand, PEA has been used safely with Nardil in small open trials. PEA must be treated with care and respect, but it can be done.

Precisely! Amphetamine would be safe, too, if taken in safe amounts - and I suspect it has been tried, considering the number of people who have been treated with MAOIs.

> Clearly, catecholamines are not metabolized fast enough by COMT to avoid a hypertensive crisis in all situations.

Even those who not using MAOIs can experience hypertensive crises. The point is that catecholamine synthesis, uptake, release and degradation are all part of normal function, even with MAOI treatment. Regular protein-rich foods - which contain phenylalanine and tyrosine - are not contraindicated because they don't overwhelm the system with freshly synthesised catacholamines. Precursors that are more rapidly converted into catecholamines - such as L-dopa - are more risky. Agents capable of rapidly releasing existing stores of monoamine neurotransmitters are still more potent dangers, and PEA is one of those, along with tyramine, ephedrine, amphetamines and others.


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