32 replies to this topic

[dreamwolf]

I was wondering if wellbutrin/bupropion conflicted with taking bacopa and ashwagandha first.

Second; I was wondering if there were any conflicts between bupropion and the following:

Yohimbe
Epimedium grandiflorum (Horny Goat Weed)
Tribulus terrestris
Mucuna pruriens
Garlic
Erycoma longifolia (Tongkat ali)
Ginko Biloba
One Source Multivitamin
Fish Oil
5-HTP (One day only)
Paxil (Paroxitine 10mg 1x - for the last week only)
Lisinopril (5mg 1x - First 1.5 weeks)

As far as the previous 'stack' - one can probably guess the purpose [wis] This was taken by myself during the month of may off and on with the bupropion being taken consistently at 150mg SR/daily - 75mg daily of wellbutrin by splitting the pills the last couple days. I started seeing myself slipping into a depression so I had a doctor friend write a script for wellbutrin at the beginning of may. I felt I started becoming more forgetful during the month of may....and became much worse after getting off of the wellbutrin. Seriously; I am paranoid about the wellbutrin - by itself or in combination with the other things - has caused some sort of brain damage of the type that might typically occur with MDMA.

ie:

http://www.geocities...Letter32001.htm
http://www.unboundme...ss_spectrometry


As far as what I am presently taking:

Vitamin C 1000mg 3x Daily
Creatine 4500mg 3x
Arginine 1000mg 3x
ALCAR 500mg 3x
Bacopa (100mg bacosides a,b 345mg total bacopa) 3x
Glycine 1500mg 3x
Ashwagandha 500mg 2x
Fish Oil (450mg DHA 90mg EPA Other Omega3 40mg Omega9 24mg) 2x
Escitalopram (Lexapro) 5mg 1x
Aripiprazole (Abilify - Off label anxiety/OCD) 5-10mg 1x
One Source Multivitamin 2x

What I want is my libido back on a consistent basis; as well as my cognitive abilities to return.
And do inform me if we can chalk all my difficulties up to depression/anxiety and that I shouldn't be worrying about the bupropion.

I was considering taking wellbutrin again (150 XL Non-generic)....if only to regain my libido.

Thank you!

[niner]

Are you splitting the Wellbutrin SR? If so, you are probably defeating the time-release formulation and not getting 24 hour coverage.

[graatch]

You can expect possible nervous overstimulation/possible cardiovascular problems with the yohimbe + bupropion.

I'd be a little worried about the lisinopril in combination with the other things in general; that seems like a powerful medication, but maybe someone else knows more than me here.

>Seriously; I am paranoid about the wellbutrin - by itself or in combination with the other things - has caused some sort of brain damage of the type that might typically occur with MDMA.

I seriously doubt it.

However, users of bupropion often report anticholinergic side effects, and a feeling of dullness/muddled thinking. This is temporary, may go away with extended use, and leaves with the medication's last metabolites.

[spacey]

Interestingly enough, do you find that Wellbutrin reduces your libido? Because for me it was the only anti-depressant that did the exact opposite thing, it severly increased my libido, duration of orgasms and generally just made sex a lot better, but maybe that's just for me.

Also I wouldn't mix Yohimbe with Wellbutrin, I have a bad experience with mixing stimulants with Yohimbe.

[FunkOdyssey]

If bupropion has any anticholinergic effects, I haven't seen any personally. I've been studying 6+ hours a day, then taking and passing an IT certification exam at the rate of one every few weeks. I feel as sharp as ever and memory formation / recall are definitely not impaired. However, I am also taking acetyl-l-carnitine, lithium orotate, ashwagandha, and relatively high-dose fish oil, so there are some confounding factors.

Yohimbe + bupropion is pretty unpleasant in my experience. Yohimbe induces noradrenaline secretion, so when you combine that with noradrenaline reuptake inhibition, that is some potentially dangerous synergy. I observed my heart racing after the slightest physical activity (walking upstairs), increased sweating, and random chills. Not recommended.

[luv2increase]

If bupropion has any anticholinergic effects, I haven't seen any personally.  I've been studying 6+ hours a day, then taking and passing an IT certification exam at the rate of one every few weeks.  I feel as sharp as ever and memory formation / recall are definitely not impaired.  However, I am also taking acetyl-l-carnitine, lithium orotate, ashwagandha, and relatively high-dose fish oil, so there are some confounding factors.

Yohimbe + bupropion is pretty unpleasant in my experience.  Yohimbe induces noradrenaline secretion, so when you combine that with noradrenaline reuptake inhibition, that is some potentially dangerous synergy.  I observed my heart racing after the slightest physical activity (walking upstairs), increased sweating, and random chills.  Not recommended.

What is your reasoning behind taking lithium orotate? Improving brain function or legitimate disorder?

Thanks!

[FunkOdyssey]

I'm using it for its neuroregenerative properties (not bipolar). AOR put together a good article advocating its use:

http://aor.ca/int/re...ium_orotate.php

[luv2increase]

Do you just take 5mg a day? How long have you been taking it and have you noticed anything different?

I appreciate your response!

[edward]

With regards to Welbutrin/ bupropion

I took it on and off for many years and finally came to the conclusion that although it was great at making me happy and giving me energy it did have some effects on my cognition. Especially with regards to my verbal fluency and certain aspects of memory. I researched this extensively and found no official anticholinergic effects, however the effects were very noticeable for me over time. I could still get good grades and perform at work but it took twice as much effort, which in general on Welbutrin was no problem as it did remarkably increase my ability to get work done.

In the end I found that the weird cognitive problems were just too much to deal with so I switched to 1-2 mg of liquid deprenyl to fulfill the dopamine part of my brain regimine. I am much happier and my memory is much better.

[luv2increase]

With regards to Welbutrin/ bupropion

I took it on and off for many years and finally came to the conclusion that although it was great at making me happy and giving me energy it did have some effects on my cognition. Especially with regards to my verbal fluency and certain aspects of memory. I researched this extensively and found no official anticholinergic effects, however the effects were very noticeable for me over time. I could still get good grades and perform at work but it took twice as much effort, which in general on Welbutrin was no problem as it did remarkably increase my ability to get work done.

In the end I found that the weird cognitive problems were just too much to deal with so I switched to 1-2 mg of liquid deprenyl to fulfill the dopamine part of my brain regimine. I am much happier and my memory is much better.

Hey edward, I forgot how old you were again. I have some liquid deprenyl (cyprenyl) on its way. I'm 24, so I was just think of doing 1mg EOD or maybe even twice weekly just to play it safe. So, it effects your mood positively? That is good to hear. I am looking forward to trying it.

[FunkOdyssey]

Do you just take 5mg a day? How long have you been taking it and have you noticed anything different?

Just 5mg a day, or 6mg including Ortho-Core. I have noticed some mood stabilization effects, although this may be placebo because it is exactly what you would expect to see. In combination with the wellbutrin, the result is a persistently elevated good mood compared to baseline.

[luv2increase]

Thanks for the input! I will be adding this to the regimen also. I read the lit on it and like all I see. Especially the parts about brain repair.

[dreamwolf]

With regards to Welbutrin/ bupropion

I took it on and off for many years and finally came to the conclusion that although it was great at making me happy and giving me energy it did have some effects on my cognition. Especially with regards to my verbal fluency and certain aspects of memory. I researched this extensively and found no official anticholinergic effects, however the effects were very noticeable for me over time. I could still get good grades and perform at work but it took twice as much effort, which in general on Welbutrin was no problem as it did remarkably increase my ability to get work done.

In the end I found that the weird cognitive problems were just too much to deal with so I switched to 1-2 mg of liquid deprenyl to fulfill the dopamine part of my brain regimine. I am much happier and my memory is much better.

If you don't mind me asking - how long did it take to 'recover' your cognitive capabilities? Did they recover to baseline or better than baseline? What was your conclusion as to why the Wellbutrin/Bupropion was causing these 'anticholinergic' effects?

No I really didn't notice a reduction in libido - actually towards the end of the time I took wellbutrin my libido was noticeably increased for a day or two. I did seem to be 'happier' towards the end - however I found it intolerable to live without my cognitive abilities.

How long have those whom have taken Wellbutrin/Bupropion together with Yohimbine taken them concurrently for?

My other theory is along the lines of a 'dopamergenic overload' induced by the combination of the Wellbutrin with the various other things I was taking at the time; being that dopamine (according to various research encountered on the 'net) has much to do with working memory, verbal function, motor function, and a host of other things. If true - how long would it take to 'readapt' from this state?

Thank you!

Edited by dreamwolf, 18 September 2007 - 04:04 AM.

[FunkOdyssey]

I'm really surprised by these reports of anti-cholinergic effects / cognitive deficits associated with bupropion. I've read ALOT about the drug and this is the first I've heard of it. I wonder if the pro-cholinergic 2.25g/daily Acetyl-L-Carnitine I'm taking is preventing me from experiencing this. Honestly, my memory has never been better than it is right now.

You might be experiencing a rare side effect or it may be related to other items in your stack. There are several neurochemistry-tweaking substances on your list -- you might be blaming the wrong one, especially if the problems are persisting after discontinuing bupropion.

[krillin]

The title says it all.

J Pharmacol Exp Ther. 2000 Oct;295(1):321-7.
Bupropion is a nicotinic antagonist.
Slemmer JE, Martin BR, Damaj MI.
Department of Pharmacology and Toxicology, Medical College of Virginia of Virginia Commonwealth University, Richmond, Virginia, USA.

Neuronal nicotinic receptors are ligand-gated ion channels of the central and peripheral central nervous system that regulate synaptic activity from both pre- and postsynaptic sites. The present study establishes the acute interaction of bupropion, an antidepressant agent that is also effective in nicotine dependence, with nicotine and nicotinic receptors using different in vivo and in vitro tests. Bupropion was found to block nicotine's antinociception (in two tests), motor effects, hypothermia, and convulsive effects with different potencies in the present investigation, suggesting that bupropion possesses some selectivity for neuronal nicotinic receptors underlying these various nicotinic effects. In addition, bupropion blocks nicotine activation of alpha(3)beta(2), alpha(4)beta(2), and alpha(7) neuronal acetylcholine nicotinic receptors (nAChRs) with some degree of selectivity. It was approximately 50 and 12 times more effective in blocking alpha(3)beta(2) and alpha(4)beta(2) than alpha(7.) This functional blockade was noncompetitive, because it was insurmountable by increasing concentration of ACh in the nAChRs subtypes tested. Furthermore, bupropion at high concentration failed to displace brain [(3)H]nicotine binding sites, a site largely composed of alpha(4)beta(2) subunit combination. Given the observation that bupropion inhibition of alpha(3)beta(2) and alpha(4)beta(2) receptors exhibits voltage-independence properties, bupropion may not be acting as an open channel blocker. These effects may explain in part bupropion's efficacy in nicotine dependence. Our present findings suggest that functional blockade of neuronal nAChRs are useful in nicotine dependence treatment.

PMID: 10991997

[FunkOdyssey]

That is interesting and might explain the negative effects reported here. However, this nAChR blockade clearly does not cause reduced cognitive function in the majority of users -- I'm guessing the nACh receptors either become more sensitive or multiply in number to effect homeostasis. In comparison to other popular antidepressants, bupropion produces better cognitive performance than any of the others (at least in depressed patients):

From: Bupropion Normalizes Cognitive Performance in Depressed Patients

Patients with depression are subject to neuropsychological deficits in attention, memory, psychomotor speed, processing speed, and executive function. When they are treated, they perform better, but they do not perform as well as normal controls.[1,17] They improve, at least to a degree, but do not “normalize.” The data reported here suggest that how well they perform on neurocognitive testing may be a function of the antidepressant with which they are treated. What our data show is that depressed patients on bupropion perform as well as normals do on a battery of neurocognitive tests. Patients on venlafaxine and SSRIs do not.

These results are consistent with the hypothesis that cognitive benefit may occur relative to an antidepressant's norepinephrine activity, while lack of benefit may relate to its serotonergic activity. The noradrenergic/dopaminergic antidepressant bupropion is associated with normal function. The mixed serotonin/norepinephrine reuptake venlafaxine performs less well than bupropion but better than the SSRIs (Figure). This is consistent with the principle that enhanced norepinephrine metabolism is associated with better cognitive performance of a variety of neurocognitive tasks.

[edward]

With regards to Welbutrin/ bupropion

I took it on and off for many years and finally came to the conclusion that although it was great at making me happy and giving me energy it did have some effects on my cognition. Especially with regards to my verbal fluency and certain aspects of memory. I researched this extensively and found no official anticholinergic effects, however the effects were very noticeable for me over time. I could still get good grades and perform at work but it took twice as much effort, which in general on Welbutrin was no problem as it did remarkably increase my ability to get work done.

In the end I found that the weird cognitive problems were just too much to deal with so I switched to 1-2 mg of liquid deprenyl to fulfill the dopamine part of my brain regimine. I am much happier and my memory is much better.

Hey edward, I forgot how old you were again. I have some liquid deprenyl (cyprenyl) on its way. I'm 24, so I was just think of doing 1mg EOD or maybe even twice weekly just to play it safe. So, it effects your mood positively? That is good to hear. I am looking forward to trying it.

I am 29. For the past year or so I have been using 1 mg per day and it has been great. Recently I have been trying 1 mg one day and 2 mg the next day to see if I can increase my energy level a little bit more. So far so good. Again I do have depression issues hence the every day use. If I didnt have depression issues I would consider 1mg every other day for general health, energy and life extension. But even 1-2mg per day for someone in their 20s or 30s seems reasonable.

[edward]

If you don't mind me asking - how long did it take to 'recover' your cognitive capabilities?  Did they recover to baseline or better than baseline?  What was your conclusion as to why the Wellbutrin/Bupropion was causing these 'anticholinergic' effects?

No I really didn't notice a reduction in libido - actually towards the end of the time I took wellbutrin my libido was noticeably increased for a day or two.  I did seem to be 'happier' towards the end - however I found it intolerable to live without my cognitive abilities. 

How long have those whom have taken Wellbutrin/Bupropion together with Yohimbine taken them concurrently for? 

My other theory is along the lines of a 'dopamergenic overload' induced by the combination of the Wellbutrin with the various other things I was taking at the time; being that dopamine (according to various research encountered on the 'net) has much to do with working memory, verbal function, motor function, and a host of other things.  If true - how long would it take to 'readapt' from this state?

Thank you!

I came to the conclusion based upon the fact that a number of times (at least 4) I went off Welbutrin for a number of months and the cognitive issues went away after only a few weeks (returned to baseline). The cognitive issues always came back within a month of starting to take Welbutrin again. As far as sexual side effects, Welbutrin was great in that area. It definitely increased my sex drive. But then again most pro dopamine things will, including deprenyl.

Again I found that deprenyl (only the liquid citrate) has been a very positive alternative to Welbutrin (ie increased energy, concentration, cognition, mood etc.) without the side effects, and of course neuroprotection, increased lifespan and other benefits that Welbutrin doesn't have

Edited by edward, 18 September 2007 - 08:24 PM.

[dopamine]

Bupropion antagonizes nicotinic acetylcholine receptors (which plays a large role in dopamine release), though it is speculated that use in smoking cessation is due to DA/NE uptake inhibition.

Addict Biol. 2005 Sep;10(3):219-31.

How does bupropion work as a smoking cessation aid?

Warner C, Shoaib M.

School of Neurology, Neurobiology and Psychiatry, Faculty of Medical Sciences, University of Newcastle upon Tyne, UK.

Bupropion exhibits reasonable efficacy as a smoking cessation aid, yet its precise mechanisms of action remain unclear. This review evaluates the mechanism of action of bupropion by considering the clinical evidence in combination with results from pre-clinical experiments in vivo and in vitro. Bupropion is a weak inhibitor of dopamine and noradrenaline reuptake, and has also been shown to antagonise nicotinic acetylcholine receptor function. It is extensively metabolized in humans, its major metabolites reaching levels higher than those of bupropion itself. These metabolites share many of the pharmacological properties of bupropion, so they may play an important role in its clinical activity, yet they have been neglected in investigations into bupropion action. This review led to several conclusions: (1) the principal mode of bupropion action is upon the withdrawal symptoms following smoking cessation; (2) during withdrawal, bupropion may attenuate symptoms by mimicking nicotinic effects on dopamine and noradrenaline; (3) its ability to antagonize nicotinic receptors may prevent relapse by attenuating the reinforcing properties of nicotine, but probably cannot acutely reduce smoking; and (4) further exploration of bupropion metabolites and its role in withdrawal and relapse, within more appropriate animal models, could be crucial in the determination of the precise mechanisms by which bupropion exerts its activity in smoking cessation. Greater elucidation of the exact mechanisms of action of bupropion could lead to the development of new drugs even more beneficial in promoting smoking abstinence.

PMID: 16109583

[graatch]

Dudes,

What I think I'll going to start trying to dig up info on is the assertion I heard somewhere that adrenergic activity in general will lead to anticholinergic activity "downstream".

This makes gut sense to me if you look at the experienced similarities between amphetamine psychosis and similarly too-high doses of anticholinergics like diphenhydramine, and the tropanes.

Does anyone know anything about this?

I also know that amphetamine, at least, is a modest stimulant to acetylcholine at certain doses.

[luv2increase]

Dudes,

What I think I'll going to start trying to dig up info on is the assertion I heard somewhere that adrenergic activity in general will lead to anticholinergic activity "downstream".

This makes gut sense to me if you look at the experienced similarities between amphetamine psychosis and similarly too-high doses of anticholinergics like diphenhydramine, and the tropanes.

Does anyone know anything about this?

I also know that amphetamine, at least, is a modest stimulant to acetylcholine at certain doses.

Looking at a PDR in school yesterday, I thought it was odd to see deprenyl listed as an anticholinergic.

[edward]

That is a ludicrous notion. What PDR? "The PDR"? how old? I would discount that a major error.

Now there is the theory that dopamine and acetylcholine levels have an inverse relationship when talking about high levels. That is if you boost dopamine up very high in certain parts of the brain then acetylcholine production and release will go down... and vica versa. So theoretically any dopamine enhancing compound could have this effect in large doses. That is hardly the same as calling it anticholinergic.

I know what anticholinergic is, I took the old tricyclic antidpressants before moving on to SSRI's combined first with Welbutrin (which proved anticholinergic-ish) then Deprenyl which is definitely not anticholinergic. If anything it improves my memory.

[kottke]

Edward also posted earlier

Brain Res. 2001 Mar 9;894(1):74-87.
Amphetamine-stimulated cortical acetylcholine release: role of the basal forebrain.
Arnold HM, Fadel J, Sarter M, Bruno JP.
Department of Psychology, 31 Townshend Hall, The Ohio State University, Columbus, OH 43210, USA.

Systemic administration of amphetamine results in increases in the release of acetylcholine in the cortex. Basal forebrain mediation of this effect was examined in three experiments using microdialysis in freely-moving rats. Experiment 1 examined whether dopamine receptor activity within the basal forebrain was necessary for amphetamine-induced increase in cortical acetylcholine by examining whether intra-basalis perfusion of dopamine antagonists attenuates this increase. Systemic administration of 2.0 mg/kg amphetamine increased dopamine efflux within the basal forebrain nearly 700% above basal levels. However, the increase in cortical acetylcholine efflux following amphetamine administration was unaffected by intra-basalis perfusions of high concentrations of D1- (100 microM SCH 23390) or D2-like (100 microM sulpiride) dopamine receptor antagonists. Experiments 2 and 3 determined whether glutamatergic or GABAergic local modulation of the excitability of the basal forebrain cholinergic neurons influences the ability of systemic amphetamine to increase cortical acetylcholine efflux. In Experiment 2, perfusion of kynurenate (1.0 mM), a non-selective glutamate receptor antagonist, into the basal forebrain attenuated the increase in cortical acetylcholine produced by amphetamine. Experiment 3 revealed that positive modulation of GABAergic transmission by bilateral intra-basalis infusion of the benzodiazepine receptor agonist chlordiazepoxide (40 microg/hemisphere) also attenuated the amphetamine-stimulated increase in cortical acetylcholine efflux. These data suggest that amphetamine increases cortical acetylcholine release via a complex neuronal network rather than simply increasing basal forebrain D1 or D2 receptor activity.

PMID: 11245817

From what i get dopamine helps memory through some mechanism and whether it is direct in the process or modulates Ach or other neurotransmitters indirectly I'm not sure.

Deprenyl has personally enhanced working memory and word recall dramatically.

[krillin]

Edward also posted earlier

That was me.

[sp0sp0]

http://crazymeds.org...hiumorotate.htm

[dreamwolf]

Thanks for all of your quality replies!

However it still does not address one of my concerns - that some of the lesser known metabolites of welbutrin share commonalities with substances such as p-chloroamphetamine which is neurotoxic and as such has been shown to destroy fine serotonin axons (such as those that cannot be regenerated properly that innervate the forebrain areas because of the distance any new axons formed would have to traverse). Please see the links posted at the start of this thread.

I am honestly hoping that the metabolites of welbutrin are disimilar enough from p-chloroamphetamine and related compounds that my concerns are moot; as otherwise I would like to get a pet/spect scan to determine how much I have been damaged by bupropion.

Any other theories as to my condition are welcome - I want to know if I will honestly recover to my baseline performance! I suffer from reduced concentration, memory, poor/fluctuating sexual performance, loose train of thought often. I've also had odd things with listening to music in that it will take 30 or so seconds for my mind to sync and recognize it as music rather than random garbled noise. This has become worse in that it now happens with people speaking to me. And of course I just feel generally 'fuzzy'....and not in a good way.

I have started taking cymbalta again; being that it was an ad I have previously took that seemed to have good results/almost no side effects. In addition I have added 5mg/daily deprenyl and 500mg daily phenelalaine (looking to increase phenylethylamine levels). All this should provide a generous boost to the big three - serotonin, dopamine, and norepherine.

With the suppliments and welbutrin I took back in may is there any possibility that my condition is due to a 'dopamine/norepherine overload' and resultant downregulation/compensation? There have been studies done with monkeys that were administered cocaine where it took several months for their dopamine receptors to recover to baseline levels. Also I have read another study that suggests that smoking/nicotine may reduce the reregulation of dopamine receptors (this was in regard to neuroleptic administation and incidence of extrapyamidal effects). Since I do smoke (and have actually smoked more since taking welbutrin/zyban) could this be prolonging my suffering?

Welbutrin, being an agent that modulates dopamine levels - would it cause extrapyamidal effects as well?

Thank you!

[luv2increase]

You are taking a lot of stuff. Does your doctor know about the deprenyl and phenylalanine?

I have a sincere suggestion to you. I think you should talk to your doctor about slowly getting off of everything. You really ought to rid yourself of the cigarettes also.

After you are off of everything for awhile, your brain will be able to repair itself. The problems you are having with music and communication are very troubling. It doesn't sound like anything is working right for you. Instead of cooling down off of stuff, you throw more at it.

You are probably right. You may have super elevated neurotransmitter levels. You are taking drugs with difference modes of action which is dangerous and makes your situation more complex. The variables just keep rising, and you are getting worse.

This is evidence IMO that you are not thinking correctly. Your logical conclusion should have been to lower or eliminate your meds, but instead you throw in deprenyl and phenylalanine.

More is not always better. Don't forget that.

[dreamwolf]

Indeed.

I feel my memory has improved to a degree but has still not returned to baseline. The 'sound' issues at the present seem to fluctuate - some days/times are better than others. That issue originally appeared probably back in November-December 2006 before I had ever touched the Welbutrin. At that point it was just noticed with music when I would first turn something on. In June of this year it became worse.

I have had the thought that I may just not be giving my systems time to adapt - I did probably get on St. John's Wort less than three weeks after discontinuing bupropion. Given other's previous experience in this thread and others elsewhere 3-4 clean weeks may be needed to readapt one's systems - assuming it's just not drug metabolites hanging around for more than a week. I assume there are certain items in my 'regiment' that are innocuous however? I have been focusing on neurogenesis as well as bludgeoning (heh - I would call that the difference between an SSRI and tianeptine) my systems to function better but not necessarily more efficient.

I would still really like to further examine the issue of the potential toxicity of the lesser known metabolites of welbutrin. Has anyone looked at the links I originally posted and point to the flaw in the logic or prove that none of the metabolites of welbutrin are neurotoxic (as in destruction of axons). I have not been able to accept the statistical evidence of the safety of the drug - I want something solid. Of course - maybe I should just accept that the drug has been on the market for many years and with the exceptions of being pulled once for causing seizures...it is still on the market.

Is there anything you would keep in my regimen? Now consisting of:

Glycine
Fish Oil
Phosphatidysetine-docosahexaenoic acid
Phenylalanine
Bacopa
Ashwaganda
Multivitamin
Arginine
Cymbalta
Vitamin C
Deprenyl

Thank you!

[FunkOdyssey]

Were you on the glycine at the same time as the Wellbutrin? I've been meaning to post about the interaction between the two. Specifically, taking glycine and wellbutrin together will produce symptoms of wellbutrin overdose, at least in my experience.

What I was doing was taking 3g of glycine at bedtime, which was suggested to be beneficial for sleep quality in some recent studies. I began to notice that I was feeling extremely, uncomfortably alert and overaroused (best way I can describe it) in the 2-5 hour range after dosing wellbutrin. This progressed and began to include weird tingling feelings in my head, anxiety, increased intraocular pressure (literally felt like my eyes were bugging out, think Arnold in Total Recall on the Mars surface), elevated heart rate, and nearly feinting at times. Most of these are symptoms of wellbutrin overdose or in mechanistic terms, super elevated norepinephrine levels.

Turns out that glycine inhibits norepinephrine release, and this is probably why it improves sleep quality. I theorized that taking a large dose of glycine in one shot every night had desensitized my glycine receptors and was exaggerating the effects of the wellbutrin. I took a gram of glycine in the middle of the day when all of the above symptoms were starting to kick in again, and sure enough it staved them off and returned me to normal in about 15 minutes. I then began to wean myself off the glycine at night, and take small 300-500mg doses during the day to ward off the "NE attacks". A week later I'm glycine free and back to enjoying the usual wellbutrin benefits without feeling like I'm having a stroke/seizure/panic attack simultaneously.

So the moral of the story is, don't take glycine if you're on wellbutrin. [tung]

Edited by FunkOdyssey, 04 October 2007 - 09:17 PM.

[dreamwolf]

I started taking the glycine sometime late June as well when I was really bugging out about the welbutrin - so not taken concurrently with the glycine. I started taking the glycine due to the paper I read (linked at the start of the thread) thinking it would help clear my system of the welbutrin. Later on I discovered an article on how Glycine at certain concentrations stimulates dopamine release - I did not discover anything about glycine increasing NE as a withdrawal effect.

Given what you have said it allows me to theorize that bupropion - depending on metabolism (if possibly the bupropion was quickly metabolized to hydroxybupropion that reaches 800% concentrations of the parent drug in the body) and what it's combined with has a great tendency to cause a NE overload. Add the yohimbe and other sexual supplements I (inadvertently - stupid didn't read the back label of the 'Super Horny Goat Weed' to see what else it contained besides Horny Goat Weed) Yeah....I probably had some elevated NE levels. I also theorize that my 'sound' issues are due to low NE levels/desensitized receptors - also giving a neat explanation as to why that problem became worse after ceasing welbutrin. Could cognition be made overall worse by reduced NE levels/NE desensitization?

I'm back to boosting NE levels along with DA and HT. Deprenyl/Phenylalaine will definitely boost NE - through being partly metabolized to L-Amphetamine, increased phenylethylamine production, inhibition of phenylethylamine breakdown. Cymbalta will boost NE activity as well. Anyone know by how much I am presently spiking my NE?

How long does it typically take for DA and NE receptors to reregulate themselves after being overstimulated?

Glycine seems to work well for maintaining some libido whilst on SSRIs such as escitalopram. Initially when starting escitalopram (and only when taking the glycine in addition) I had a boosted sex drive/erectile response - going so far as to be able to keep going after the initial climax. This effect seemed to fade over time.

Thank you!