72 replies to this topic

[nezxon]

Do I need to wait longer than 2 months?

If you don't like the effects after 2 months it's unlikely to get better, but it may be worth the effort to hang in there another month, it's still in the realm of possibility for some of your negative side effects to lessen.

I was on Lexapro (20mg/daily) + Bupropion (150mg twice daily) for a couple years for moderate depression and the combination worked well, while Lexapro alone was only helping slightly. I never quite felt "up" but they kept some of the extreme lows at bay. I was able to socialize more than I'm normally comfortable with.

I'd like to at least give Bupropion a try again, I'll need to talk to a doctor about my nootropic stack just to make sure it will be safe though.

[nupi]

Been taking 150mg SR for 5 days now for mild depression and a weird case of social anxiety (basically, new situations scare the hell out of me so I never try whereas I can dominate a whole class room without any thought to it) and overall overly high anxiety (the effect of which is hard to describe).

While it's too early to say if its Placebo (the immediacy makes me think it is), the effects have been impressive. Base line anxiety totally gone - same for my usually high levels of worry (which rationally is largely unwarranted), giving way to a devil shall care attitude (is that part of beginning hypomania?). Good mood all around (slight smile comes natural, which is totally untypical for me), increasing sex drive and presumably higher energy (that one is bit hard to figure out, see below). Dance music makes me want to dance which is very untypical for me, desire for alcohol has gone down (especially for spirits, the two single malts on my desk have no allure at all, but also for beer to some degree) and the thought of smoking seems pretty weird (but in any case, I only ever smoked socially before). Eye contact - which I am usually pretty bad at - seemingly become easier.


So far mild side effects (slightly dry mouth but nothing gum or bonbons cant fix). Appetite seems to have down some (but the food around here is not too good either way) and I need to remind myself to drink water regularly (usually I drink 3l a day totally unconsciously, I still do that, but needs some conscious choices). My head occasionally feels a bit weird but I hope its more of a weak virus infection as two days in my throat felt sore and I was extremely tired for two days, better again. For that reason, I have been going to bed early and popped 3mg Melatonin to get to sleep quickly.

If things continue like this and maybe my social anxiety gets reduced a little more and I become more pro active with regard to my social life (especially with regards to girls) this is very much worth it.

Edited by nupi, 20 May 2011 - 11:52 AM.

[Iceebear19727]

I've been taking Bupropion for about 6 months now and have noticed the opposite of the effects that I've seen here. I've gained almost 40 pounds and my sex drive has come to a screeching halt, with no change to diet, exercise, lifestyle. The only reason I've been taking it this long is it made it possible to wake up in the morning. Previously, I had to have 2 or 3 alarms going off which worked only half of the time. Even a fire wouldn't have got me up. Then after waking, I was exhausted all day until dusk, when I just started to wake up. It made my life, school, and my future almost unbearable. Now, I wake up even without an alarm and I don't take naps at all. I used to take one every single day and now I am actually unable to. I have actually noticed my memory failing though, which was mentioned here.

I was given this after I requested it from my psychiatrist as an alternative treatment to stimulants. I was diagnosed with ADHD, social anxiety, and also with hypothyroidism by my gp. I have tried Adderall, Dexedrine, and Focalin. Adderall is the only thing that helped. The other two, I swear, had no effect on me. I felt nothing. I've never been able to figure this out because I know Adderall is half Dexedrine. Wellbutrin has done nothing for my social anxiety. Anyway...does anyone have any idea why I responded oppositely of most people? In terms of the wellbutrin and the stimulants? Could it be my low thyroid? and if so, I am on treatment for it and have seen no difference.. I also saw no effect from Piracetam and a range of doses with and without choline..

Edited by Iceebear19727, 16 June 2011 - 05:35 AM.

[Valor5]

I've been taking Bupropion for about 6 months now and have noticed the opposite of the effects that I've seen here. I've gained almost 40 pounds and my sex drive has come to a screeching halt, with no change to diet, exercise, lifestyle. The only reason I've been taking it this long is it made it possible to wake up in the morning. Previously, I had to have 2 or 3 alarms going off which worked only half of the time. Even a fire wouldn't have got me up. Then after waking, I was exhausted all day until dusk, when I just started to wake up. It made my life, school, and my future almost unbearable. Now, I wake up even without an alarm and I don't take naps at all. I used to take one every single day and now I am actually unable to. I have actually noticed my memory failing though, which was mentioned here.

I was given this after I requested it from my psychiatrist as an alternative treatment to stimulants. I was diagnosed with ADHD, social anxiety, and also with hypothyroidism by my gp. I have tried Adderall, Dexedrine, and Focalin. Adderall is the only thing that helped. The other two, I swear, had no effect on me. I felt nothing. I've never been able to figure this out because I know Adderall is half Dexedrine. Wellbutrin has done nothing for my social anxiety. Anyway...does anyone have any idea why I responded oppositely of most people? In terms of the wellbutrin and the stimulants? Could it be my low thyroid? and if so, I am on treatment for it and have seen no difference.. I also saw no effect from Piracetam and a range of doses with and without choline..

I think you may have diabetes but I could be way off

[Iceebear19727]

Wouldn't that be causing more severe symptoms? I mean how could someone have diabetes and not have needed to go to the doctor? I absolutely love sugar tho, I have cravings for it all the time..

[Iceebear19727]

Csn anyone explain to me how Wellbutrin works? And what is different with my brain that would make be "need" it? I would like to find some other substance that can do some of the same functions, if it exists..

[nupi]

https://secure.wikim...anism_of_action

As a primarily dopaminergic ), I guess it could be compared to a whole bunch of amphetamine derivatives and in fact is sometimes tried as ADD treatment as its effects are thought to weaker than those of MPH. The SNRI effects may be emulated with Effexor although that brings a whole host of own issues with it...

[nupi]

https://secure.wikim...anism_of_action

As a primarily dopaminergic substance, I guess it could be compared to a whole bunch of amphetamine derivatives and in fact is sometimes tried as ADD treatment as its effects are thought to weaker than those of MPH. The SNRI effects may be emulated with Effexor although that brings a whole host of own issues with it...

Edited by nupi, 18 June 2011 - 11:11 AM.

[nupi]

Does anyone have any thoughts on supplementing Tyrosine to Wellbutrin? How about 5-HTP (I know that one is kind of risky with SSRIs)?

[longevitynow]

Does anyone have any thoughts on supplementing Tyrosine to Wellbutrin? How about 5-HTP (I know that one is kind of risky with SSRIs)?

I like the idea of taking a bit of tyrosine and/or phenylalanine with Wellbutrin or psychostims. The idea is to give yourself some of the precursors you need to make your own endogenous neurotransmitters. As for 5-HTP, IMO it is dramatically safer and usually as effective as SSRIs, with far fewer side-effects. As Welbutrin mainly increases dopamine, taking 5-HTP with it should keep your serotonin levels adequate while you are raising your relative dopamine levels. I like 5-HTP to help me stay asleep, and Wellbutrin and just about any stimulant or dopaminergic tend to give me sleep problems.

[nupi]

I have trouble staying asleep anyway (falling asleep is usually not a big issue), I dont really feel like Wellbutrin changes much but if 5-HTP could help there, that would be major pro.

[chroncile]

Pretty worrying stuff about bupropion:

Bupropion, an atypical antidepressant, induces endoplasmic reticulum stress and caspase-dependent cytotoxicity in SH-SY5Y cells.

Bupropion is an atypical antidepressant that is currently used as a smoking cessation aid. Bupropion interferes with monoamine reuptake and is potentially neurotoxic, although this is yet to be confirmed. In this study, we evaluated the cytotoxicity of bupropion using SH-SY5Y human catecholaminergic cells as the in vitro model. Exposure of the cells to bupropion for 24h reduced their viability in a concentration-dependent manner. Treatment of the cells with a toxic concentration of bupropion (100μg/mL) induced the phosphorylation of eukaryotic initiation factor alpha (EIF-2α), c-JUN N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) within 1h, which later declined to baseline levels. However, bupropion failed to splice X-box binding protein 1 (XBP1) mRNA. Bupropion caused mitochondrial cytochrome c release and activated caspases 9, 8, and 3 in a time-dependent manner. The reduction in cell viability was significantly inhibited by a caspase 3 inhibitor. Bupropion also induced the mRNA expression of the death receptors DR4 (TRAILR1) and DR5 (TRAILR2). However, bupropion did not increase the level of cellular oxidative stress. Taken together, our data indicate that bupropion activates caspase 3 through the induction of endoplasmic reticulum stress responses and activation of JNK, and consequently induces apoptotic cell death in SH-SY5Y cells.

and a few goodies from the full study:

In a clinical study, the bupropion concentration in human serum after a single oral dose, administered for smoking cessation, was about 0.1–1 μM (27.6–276 ng/mL) (Hsyu et al., 1997), which is lower than the concentration used in this study. However, the brain concentration of bupropion in animals treated with therapeutic doses was about 15–20-fold higher than the serum concentration, with no species differences (Butz et al., 1982). Moreover, the major metabolite of bupropion, hydroxybupropion, has similar activity to bupropion as a dopamine transporter, and can reach a plasma concentration 10–100 times that of bupropion ([Damaj et al., 2004] and [Hsyu et al., 1997]). Therefore, it is likely that the concentration of bupropion used in this study occurs in the brain under certain therapeutic or toxic conditions.

In conclusion, we have reported for the first time that bupropion shows significant cytotoxicity at toxic but clinically relevant concentrations. The cytotoxicity of bupropion may be caused by the combined and interactive mechanisms of the ER stress, mitochondrial stress, and extrinsic apoptotic pathways. The apoptotic systems activated by bupropion converge on the activation of caspase 3, so bupropion-induced cytotoxicity is dependent on caspase 3 activation.

So, how does this affect a person in the long-term? Are the damages done permanent? Also, what do SH-SY5Y cells do?

On another note, I'm worried about the nAChR antagonist part of it. Wikipedia mentions that chronic use of antagonists has been linked to neuronal death.

Because' class='bbc_url' title='External link' rel='nofollow external'>http://en.wikipedia.org/wiki/Receptor_antagonist']Because antagonists often disrupt the normal connectivity between neurons, their long-term, chronic use has been linked to neuronal death and very strong antagonists can be considered to be toxic.

→ source (external link)

This is very troubling for me as I have quit taking Wellbutrin for MDD 3 times now. I started taking it about 2 weeks ago and since yesterday, my motivation has increased. One thing that I do also notice is time dilation. When I was not taking Wellbutrin, time would fly by and a month seemed like a week.

Should I continue taking Wellbutrin or are the damages just too much to justify its benefits?

[Valor5]

I would say stop. It would be good if someone could find a in vivo study to further confirm neurotoxicity or a link to caspase 3 or damage to oligodendrocytes. As far as talking a caspase in hibitor I or others here have never really looked to far into that. But, I think st. Johns wort can offer some protection but that is just me theorizing based on some studies I've seen and an anecdotal report on erowid that says it is good with adderall in terms if lessening the SE's. I think it does affect memory as do most AD's so on that account and many others I don't think it is worth it personally I would try moclobemide or better phenelzine if you are inclined to go the pharmaceutical route or try st johns wort, rhodiola, resveratrol. The latter two are MAOI's that will inhibit both isoenzymes. Good luck.

[Valor5]

In vivo, since the enzymes catalyzing DA metabolism occur intracellularly, blockage of the DA transporter by either application of its selective inhibitors, such as bupropion, or down-regulation using antisense oligonucleotides effectively reduces DA cytotoxicity in bovine chromaffin cells and human neuroblastoma NMB cells, respectively (22, 51). Blockage of DA entry into these cells is assumed to reduce the generation of ROS. We are currently investigating the potential mechanisms of ROS production by DA activation of the JNK pathway and apoptosis.

Bupropion, an atypical antidepressant, induces endoplasmic reticulum stress and caspase-dependent cytotoxicity in SH-SY5Y cells.

Bupropion is an atypical antidepressant that is currently used as a smoking cessation aid. Bupropion interferes with monoamine reuptake and is potentially neurotoxic, although this is yet to be confirmed. In this study, we evaluated the cytotoxicity of bupropion using SH-SY5Y human catecholaminergic cells as the in vitro model. Exposure of the cells to bupropion for 24h reduced their viability in a concentration-dependent manner. Treatment of the cells with a toxic concentration of bupropion (100μg/mL) induced the phosphorylation of eukaryotic initiation factor alpha (EIF-2α), c-JUN N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) within 1h, which later declined to baseline levels. However, bupropion failed to splice X-box binding protein 1 (XBP1) mRNA. Bupropion caused mitochondrial cytochrome c release and activated caspases 9, 8, and 3 in a time-dependent manner. The reduction in cell viability was significantly inhibited by a caspase 3 inhibitor. Bupropion also induced the mRNA expression of the death receptors DR4 (TRAILR1) and DR5 (TRAILR2). However, bupropion did not increase the level of cellular oxidative stress. Taken together, our data indicate that bupropion activates caspase 3 through the induction of endoplasmic reticulum stress responses and activation of JNK, and consequently induces apoptotic cell death in SH-SY5Y cells

Can anyone explain the above discrepancy?
My explanation is it has to do with the transporter by blocking it or inhibiting its protein synthesis it is the route speculated above as protective to the cells. Will this be true however with bupropion???? If the free radical dopamine gets inside the cell the cell is toast because this triggers a genetic predisposition to start building the proteins that will lead to cell death this begs the questions of which cells can dopamine enter and be transformed into the free radical. I would speculate it is the cells with MAO in them.

Another thing about bupropion is that it decreases sperm count but that reversed after discontinuation.

For me it was somewhat motivating but in a confused sort of way and it gave me a terrible nightmare and irritability where little things like a door slamming would greatly agitate me the first time I took it at 150XR. I also have a slight tremor from it along some memory loss but this may be the lexapro I took with it the last couple of days. I also got a strange neck pain in the back of my neck. It did however to me seem to improve my libido where women seemed extraappealing. But I am sure I can do the latter with safer alternatives. Another thing I am noticing is that I have to read things a bunch of times before I "get" it. But I believe this has to do with the lexapro.

Edited by valory5, 21 March 2012 - 04:21 PM.

[Valor5]

For some reason I was not able to edit the above post so here is some more explanation about the discrepancies in the studies noted above.

In this paper, the role of type A MAO (MAO-A) in apoptosis was studied using human neuroblastoma SH-SY5Y cells, where only MAO-A is expressed...To examine the intervention of MAO-B in the apoptotic process, human MAO-B was transfected to SH-SY5Y cells

As you can see the SH-SY5Y cells have only MAO-A unless transfected with MAO-B. And apparently still killed the SH-SY5Y cells whereas in the other cells

[khemix]

Been on this one for a week, 150mg XL. Not a good experience for someone who is anxiety prone because this only exacerbates it, physically and mentally. That leads me to believe it acts much more on norepinephrine than anything else. I can't say there was any increase in focus. It also screwed with my sleep cycle, I'd be getting up 2-3 times a night. And it made be daydream way more than I normally do. I don't know if these effects subside as I was only on it for a week, but I found adderall to be better for cognition - thought that comes with its own set of problems. It really screws with memory. Just the other day it made me re-re-re-re-read a single news paper article for 4+ hours because at that time I had thought it was the greatest things ever written.

Edited by khemix, 21 March 2012 - 07:48 PM.

[Valor5]

For some reason I was not able to edit the above post so here is some more explanation about the discrepancies in the studies noted above.

In this paper, the role of type A MAO (MAO-A) in apoptosis was studied using human neuroblastoma SH-SY5Y cells, where only MAO-A is expressed...To examine the intervention of MAO-B in the apoptotic process, human MAO-B was transfected to SH-SY5Y cells

As you can see the SH-SY5Y cells have only MAO-A unless transfected with MAO-B. And apparently still killed the SH-SY5Y cells (interestingly this cell line is protected from apoptosis by rasagiline where the protection is not mainly because of MAO inhibition) whereas in the other cells one bovine chromaffin cells and human neuroblastoma NMB cells cell death did not occur. WHATS UP WITH THIS????

Abstract

OBJECTIVE:

To evaluate the human neuroblastoma SH-SY5Y cell line as an in vitro model of dopaminergic (DAergic) neurons for Parkinson's disease (PD) research and to determine the effect of differentiation on this cell model.
DATA SOURCES:

The data of this review were selected from the original reports and reviews related to SH-SY5Y cells published in Chinese and foreign journals (Pubmed 1973 to 2009).
STUDY SELECTION:

After searching the literature, 60 articles were selected to address this review.
RESULTS:

The SH-SY5Y cell line has become a popular cell model for PD research because this cell line posses many characteristics of DAergic neurons. For example, these cells express tyrosine hydroxylase and dopamine-beta-hydroxylase, as well as the dopamine transporter. Moreover, this cell line can be differentiated into a functionally mature neuronal phenotype in the presence of various agents. Upon differentiation, SH-SY5Y cells stop proliferating and a constant cell number is subsequently maintained. However, different differentiating agents induce different neuronal phenotypes and biochemical changes. For example, retinoic acid induces differentiation toward a cholinergic neuronal phenotype and increases the susceptibility of SH-SY5Y cells to neurotoxins and neuroprotective agents, whereas treatment with retinoic acid followed by phorbol ester 12-O-tetradecanoylphorbol-13-acetate results in a DAergic neuronal phenotype and decreases the susceptibility of cells to neurotoxins and neuroprotective agents. Some differentiating agents also alter kinetics of 1-methyl-4-phenyl-pyridinium (MPP(+)) uptake, making SH-SY5Y cells more similar to primary mesencephalic neurons.
CONCLUSIONS:

Differentiated and undifferentiated SH-SY5Y cells have been widely used as a cell model of DAergic neurons for PD research. Some differentiating agents afford SH-SY5Y cells with more potential for studying neurotoxicity and neuroprotection and are thus more relevant to experimental PD research.

There are several pathways to apoptosis and different cells lines. So this seems very complicated.

Can someone find this paper?
Dopamine in neurotoxicity and neuroprotection: what do D₂ receptors have to do with it?

• Yuri Bozzi^a,
• Emiliana Borrelli^b,

To add to the confusion a paper I am reading said this, "Thus, oxidative stress as the mechanism of
catecholamine effects observed in our experiments can be ruled out." I think the cells they are using are the neuroblastoma cells expressing the DAT, SK-N-MC.

Another study said this, "This catecholamine-induced cell death appears to be neuronal specific, as demonstrated by their inabilities of triggering apoptosis of A549 lung carcinoma cells and Cos-7 kidney fibroblasts."

Ok so in summary it seems that the death of a cell can be a complicated matter. So would adding rasagiline to bupropion be intelligent? or perhaps to other MAOI's, clorgyline? Here is a link of a case where a doctor prescribed rasagline along side bupropion and ropinirole. Here is the end of that story the guy ended taking both. He had parkinsons.

[Valor5]

Been on this one for a week, 150mg XL. Not a good experience for someone who is anxiety prone because this only exacerbates it, physically and mentally. That leads me to believe it acts much more on norepinephrine than anything else. I can't say there was any increase in focus. It also screwed with my sleep cycle, I'd be getting up 2-3 times a night. And it made be daydream way more than I normally do. I don't know if these effects subside as I was only on it for a week, but I found adderall to be better for cognition - thought that comes with its own set of problems. It really screws with memory. Just the other day it made me re-re-re-re-read a single news paper article for 4+ hours because at that time I had thought it was the greatest things ever written.

As far as effects are concerened. I have a belief that the amount of "substance" be it amphetamine or some other domanigergic will effect which of the the two, dopamine or norepinephrine, is released. With higher doses dopamine is released whereas in lower doses norepinephrine is released. I think this study eludes to that and I have experienced something similar.

[chroncile]

Depression itself is neurotoxic so I have decided to continue taking the Wellbutrin. Also, in the study that showed bupropion to be cytotoxic they used a dosage of 100μg/mL which is quite high.

Still, it is a bit worrying knowing a drug you're taking is potentially harming you. Are there any more studies on bupropion's cytotoxicity?

[Valor5]

I don't know of other studies atm. My main concern for myself was the danger of rhabdomyolysis because I was doing some work and noticed my muscles becoming soar and fatigued earlier than they should I mean it was like a minute into working and I had trouble managing the wand from my preassure washer so that sent up a red flag that morning I took 300 mg xl and 10 mg of lexapro so the point is you have to be very cognizant of SE's. Last point I am speaking to myself on this I don't drink enough water and that is important.

Edited by valory5, 22 March 2012 - 10:13 AM.

[Valor5]

I would say stop. It would be good if someone could find a in vivo study to further confirm neurotoxicity or a link to caspase 3 or damage to oligodendrocytes. As far as talking a caspase in hibitor I or others here have never really looked to far into that. But, I think st. Johns wort can offer some protection but that is just me theorizing based on some studies I've seen and an anecdotal report on erowid that says it is good with adderall in terms if lessening the SE's. I think it does affect memory as do most AD's so on that account and many others I don't think it is worth it personally I would try moclobemide or better phenelzine if you are inclined to go the pharmaceutical route or try st johns wort, rhodiola, resveratrol. The latter two are MAOI's that will inhibit both isoenzymes. Good luck.

BTW PLEASE BE CAREFUL WHEN COMBINING RHODIOLA AND RESVERATROL AS THESE WILL CAUSE A HYPERTENSIVE CRISIS AND/OR SEROTONIN SYNDROM IF COMBINED INCORRECTLY WITH OTHER SUBSTANCES. PEACE.

[Adamzski]

Hi Im taking 150mg wellbutrin and was thinking of trying 300mg per day.

So is it ok? I do know that long term stress is a killer and that failing in life and depression can make people do things like jump off buildings...

I also just started Resveratrol and do take methylene blue, could these interact?

As for its effects

I have been on 150mg Zyban for 45days now. I still smoke like a maniac...

Good,

• Horny
• Orgasm feels way different
• Can concentrate better
• need less sleep
• stops my dwelling on problems too much
• It and time stopped my urges to jump off buildings
• I seem to sometimes be able to drink much more than usual and other times I black out way easier

Bad

• GAS
• Appetite... I really hardly eat now
• The two above points may be connected
• Some say it can make you look older and dry your skin, I have not noticed this but it may

Edited by Adamzski, 23 March 2012 - 06:07 AM.

[Valor5]

Hi Im taking 150mg wellbutrin and was thinking of trying 300mg per day.

So is it ok? I do know that long term stress is a killer and that failing in life and depression can make people do things like jump off buildings...

I also just started Resveratrol and do take methylene blue, could these interact?

As for its effects

I have been on 150mg Zyban for 45days now. I still smoke like a maniac...

Good,

• Horny
• Orgasm feels way different
• Can concentrate better
• need less sleep
• stops my dwelling on problems too much
• It and time stopped my urges to jump off buildings
• I seem to sometimes be able to drink much more than usual and other times I black out way easier

Bad

• GAS
• Appetite... I really hardly eat now
• The two above points may be connected
• Some say it can make you look older and dry your skin, I have not noticed this but it may

Key results:
MB was a potent (tight binding) inhibitor for MAO A. It also inhibited MAO B but at much higher concentration. Interactions of MB with the active site of MAO A were confirmed by its action both as an oxidising substrate and as a one-electron reductant.


Conclusions and implications:
MB is a potent reversible inhibitor of MAO A with implications for gut uptake of amines when administered orally. At concentrations reported in the literature after intravenous administration, MAO B would be partially inhibited but MAO A would be completely inhibited. This inhibition of MAO A would be expected to lead to perturbations of 5-hydroxytryptamine metabolism and hence account for ST occurring when administered to patients on SSRI treatment.

trans-resveratrol dose dependently inhibited MAO-A activity. These findings indicate that the antidepressant-like effect of trans-resveratrol might be related to serotonergic and noradrenergic activation.

This study investigated for the first time the potential effects of cis- and trans-resveratrol (c-RESV and t-RESV) on noradrenaline (NA) and 5-hydroxytryptamine (5-HT) uptake by synaptosomes from rat brain, on 5-HT uptake by human platelets, and on monoamine oxidase (MAO) isoform activity. Both c-RESV and t-RESV (5-200 microM) concentration-dependently inhibited the uptake of [3H]NA and [3H]5-HT by synaptosomes from rat brain and the uptake of [3H]5-HT by human platelets. In both experimental models, t-RESV was slightly more efficient than c-RESV. Furthermore, in synaptosomes from rat brain, the RESV isomers were less selective against [3H]5-HT uptake than the reference drug fluoxetine (0.1-30 microM). On the other hand, both c-RESV and t-RESV (5-200 microM) concentration-dependently inhibited the enzymatic activity of commercial (human recombinant) MAO isoform (MAO-A and MAO-B) activity, c-RESV being slightly less effective than t-RESV. In addition, both RESV isomers were slight but significantly more selective against MAO-A than against MAO-B. Since the principal groups of drugs used in the treatment of depressive disorders are NA/5-HT uptake or MAO inhibitors, under the assumption that the RESV isomers exhibit a similar behaviour in humans in vivo, our results suggest that these natural polyphenols may be of value as structural templates for the design and development of new antidepressant drugs with two important biochemical activities combined in the same chemical structure: NA/5-HT uptake and MAO inhibitory activity.

[Adamzski]

yep, so is it ok?

I have heard of plenty of people on here taking them both

[Valor5]

yep, so is it ok?

I have heard of plenty of people on here taking them both

I think it would be ok but I don't know about the dosing atm.

[Adamzski]

I am just taking 150mg of wellbutrin, 600mg resveratrol, 200mg Modafinil and 1mg MB.

Some times I take heaps of Gabba and 5-HTP to knock me out and get some sleep.

[Valor5]

Would these be good solutions to bupropion cytotoxicity?

Abstract

Endoplasmic reticulum (ER) stress has been implicated in the pathogenesis of neurodegenerative and ischemic disorders. The purpose of this study was to evaluate the effects of Chinese propolis and its constituents [chrysin, galangin, pinocembrin, caffeic acid, and caffeic acid phenethyl ester (CAPE)] against tunicamycin-induced neuronal cell death in SH-SY5Y cells. Both Chinese propolis and chrysin concentration-dependently inhibited such cell death, the tunicamycin-induced activation of caspase-3, and the effects of tunicamycin on mitochondria [release of cytochrome c into the cytosol and disruption of the mitochondrial membrane potential (ΔΨ_m)]. Furthermore, Chinese propolis and chrysin each inhibited staurosporine-induced cell death. These findings indicate that the inhibitory effects of Chinese propolis against neuronal cell death induced by ER stress or staurosporine may be exerted primarily by chrysin. Moreover, the mechanism underlying the protective effects may, at least partly, involve inhibitions of caspase-3 activity and the mitochondrial apoptotic pathway.

Abstract

Reactive oxygen species (ROS) are important mediators in many neurodegenerative diseases including Alzheimer's disease and Parkinson's disease. This study tested the neuroprotective effects of spirafolide, a compound purified from the leaves of Laurus nobilis L. (Lauraceae), against dopamine (DA)-induced apoptosis in human neuroblastoma SH-SY5Y cells. Following a 24-h exposure of cells to DA (final conc., 0.6 mM), we observed a marked increase in apoptosis, increased generation of ROS and decreased cell viability. Pretreatment of the cells for 24 h with spirafolide (0.4, 2, and 10 μM) before exposure to DA notably increased cell survival (p < 0.01) and lowered intracellular ROS levels (p < 0.01). These results indicate that spirafolide has neuroprotective effects against DA toxicity. These effects may contribute to the treatment of neurodegenerative diseases.

Edited by valory5, 26 March 2012 - 02:07 AM.

[Valor5]

I am just taking 150mg of wellbutrin, 600mg resveratrol, 200mg Modafinil and 1mg MB.

Some times I take heaps of Gabba and 5-HTP to knock me out and get some sleep.

Well if you are still alive and doing well that's a good sign.

[Adamzski]

Yeah, alive, close to doing well.

This neurotoxicity, does it creep up on you? would I be experiencing headaches or brain fog or anything out of the ordinary if something was going wrong?

[chroncile]

I'm done with Wellbutrin. I had so many headaches, I felt dizzy from time to time and lightheaded. I thought I was going to faint or even have a stroke.

I'm going to ask my pdoc for selegiline and if he refuses then I'm done with overpriced pharmaceutical crap. I'll try bacopa for depression. I'm hearing a lot of positive things about it.