Drug info - The Great Big Bupropion Thread (Wellbutrin)

[jcyugi]

300mg with 50mg of Adderall XR makes SWIM hallucinate for about 2-3 days

[Orchid_Suspiria]

Originally Posted by jcyugi

300mg with 50mg of Adderall XR makes SWIM hallucinate for about 2-3 days

Is that such a good idea?Using buproprion recreational is bad enough but using it in combination with something as powerful as adderall sounds like a rather unsound plan.

[upperdecker]

Yes snorting was SWIM's desperate way but it was a cocaine like high for about 15 minutes though now SWIM has a sinus infection so no more of that.

[Sitbcknchill]

Aside from the mood swings and not being able to sleep wellbutrin can also cause seizures at a suprisingly low threshold. This is not really something one needs to play with to try and mimic any sort of high. I was prescribed those and still am but i choose not to take them. There is not enough pros and to many cons that come with brupropion. It did not seem to do dick for depression but seemed to make things worse through the mood swings. People have reported having some good effects from it but it is very short lived and not worth the risk.

[hempy666]

Swim and swims friend had some 150mg wellbutrin and first tried soaking then cutting off w a knife the outer coating. Once you smash one you'll be able to see and pick out the little coating pcs. I then add h2o in spoon and heat till bubbly/ clear. draww it up thru a cotton filter(thanx needle exchange) inject it. It sort of gives you a strange bellwringer and sort of happy feeling(dopamine) the ringing is almost like nitrous. I guess they cause seizures this way so don't ever try it!!

[hempy666]

Swim and swims friend had some 150mg wellbutrin and first tried soaking then cutting off w a knife the outer coating. Once you smash one you'll be able to see and pick out the little coating pcs. I then add h2o in spoon and heat till bubbly/ clear. draw it up thru a cotton filter(thanx needle exchange) inject it. It sort of gives you a strange bell ringer and sort of happy feeling(dopamine) the ringing is almost like nitrous. I guess they cause seizures this way so don't ever try it!!

[hempy666]

.oops double

[jazzmetalguitar]

SWIM hunts to find answers and thus returns....and then SWIM thus apologizes that this attempt to provide accurate, detailed info turned into a near psychotic and novel-length rant (but it is still quite informative!):

SWIM will refer to wellbutrin by the name bupropion (it goes under the brand names Wellbutrin, Zyban, Budeprion, and Buproban). As has been previously stated, though bupropion is an anti-depressant it acts much different than the standard anti-depressants pharmacodynamically. Though SWIM is not completely familiar with anti-depressants and the related statistics, he understands that SSRI's are the most commonly prescribed and (now absolute knowledge) those prevent reuptake of serotonin from the involved synapses making serotonin more available. Bupropion, however, works by inhibiting reuptake of dopamine and norepinephrine (at the ratio of 2:1), though also note this process is not selective. It is also noteworthy to point out, given these mechanisms, that bupropion is similar structurally to cathinone (stimulant found in the African shrub Khat), diethylcathinone (marketed as the stimulant/appetite-suppressant Diethylpropion), and most phenethylamines (although technically we are referring to substitutes of phenethylamine which include many drugs, stimulants, hallucinogens, etc). However, it is important to note that bupropion is (to SWIM's understanding) more affected by the liver and thus is not as active as a psychoactive substance [theory here; SWIM is making assumptions due to lack of ability to fully research; obviously].

Now, on to the drugs effects on the CNS. Studies have shown that the frequency of bupropion metabolites on dopamine transporters is somewhere in the range of 6-22% (and thus SWIM makes another logical leap here and believes the freq. for norepinephrine would be roughly 3-11%). Things become interesting here because research has shown that an inhibition of higher than 50% would be required for an x-reuptake inhibition mechanism to be the major means of effect in a drug (this is based on studies of the serotonin system and so, in SWIM's opinion, researchers have no right to make this analogy and should research each independently; however, it is all we have so we must use it). In addition, despite the fact that bupropion has no serotonin inhibition properties it has been noted to cause enhancement of serotonin receptors due to the downstream norepinephrine flow. Furthermore, it acts as an antagonist of the nicotinic receptor alpha-3-beta-4 (sorry, SWIM is too lazy to look up how to type greek alphabet symbols). This specific action allows for its use in quitting smoking. Additionally, reports show that bupropion inhibits an adrenaline and a histamine H1 receptor at the potencies of 14% and 9% respectively as compared to the inhibition of DA receptors. These are the full effects on the CNS that SWIM has discovered. Unfortunately, considering that bupropion is metabolized into several different things once in the body it becomes a problem understanding the actual mechanism of the drug since on studies on each individual piece.

Now, the ranting of SWIM continues further and this paragraph will probably be poorly structured including many random things though I will make quite a few notes about bupropion's pharmacokinetics, he supposes. Bupropion becomes a dangerous issue for one key reason: due to the variability of the liver enzyme CYP2B6 in various people, bupropion is metabolized at highly varying rates in different people. Thus, a dosage (the common starting dosage in fact) of 150mg could be as potent as 400-500mg for others. This is not an issue of tolerance nor is the variance of this enzyme understood really (though history of alcohol use increases rate of metabolization of bupropion due to the fact that alcohol increases presence of the enzyme [and given this enzyme also metabollizes nicotine it makes SWIM wonder the affects alcohol use has on nicotine use]). Due to all of this, this drug is dangerous for recreational use. The statement of that simple fact brings up the issues of the seizures. SWIM has learned the knowledge somewhere, though he is no longer sure of the source, that drug-induced seizures are often related to NMDA receptors, which are stimulated by the excitatory neurotransmitter glutamate (glutamic acid; also an amino acid) and also by the specific agonist NMDA (which mimics the glutamate; NMDA receptors are actually glutamate receptors, however, this specific one was originally discovered by stimulation via NMDA and thus it is oddly named after its agonist not its actual neurotransmitter companion). NMDA, which is an excitotoxin, however is not naturally occuring and was synthesized to study regions of the brain. Pertaining more to seizure-inducing, notably in cases of brain injury glutamate transporters reverse their typical purpose of removing glutamate and excess glumate accumulation (after several unimportant processes; though for the sake of knowledge SWIM will add this at the end) can cause neuronal damage and cell death (a process known as excitotoxicity). In addition, glutamate can be the source for seizures and may be implicated in epilepsy; there have also been studies which link glutamate to amphetamine psychosis, though, again, very difficult studies for SWIM to hunt down currently. Returning to bupropion again, hopefully what SWIY will note from SWIM's ranting is that a lot of jack shit is known about it. It is important to note that is was removed from the market from 1986 to 1989 due to seizure implications and personally, SWIM believes that if the FDA removes a product from the market which has low to no abuse potential there is reason for it.

A few interesting things to point out now. Though bupropion is known to moderately to dramatically decrease alcohol tolerance, studies have shown that 100 mg of bupropion actually negates many of the effects of small doses of alcohol (study declared as 1-2 drinks [by US standards]). Though, in what SWIM believes was the same study, the combination of 100mg bupropion and two alcoholic drinks also increased heart rate by 6 bpm (not a hell of a lot but odd considering the chemicals involved; which reiterates again, we don't know much about bupropion, how its works, why it works, etc. despite its existence for 32 or so years). SWIM supposes he should also point out that he assumes the curiousity about bupropion IV use was piqued by a study that showed rats, when intravenously injected, showed an abuse pattern. However, anyone who read further would also read that the metabolization of bupropion by rats and humans is completely and dramatically different (guinea pigs actually resemble human bupropion metabolization the most, if anyone wished to know).

Conclusion: Sure, bupropion is psychoactive and it will cause some effects, but there are a lot of side effects and we don't even fully understand why it really does what it's prescribed for. Even a search through the erowid experience vaults will render more negatives than positives by far. Maybe another discouraging note to potential users is the fact that though bupropion is sometimes prescribed for ADD, recent studies have shown it has little to no effectiveness (most, or at least SWIM, knows how nice the real ADD drugs can be). Dosage is risky. Neurochemically it's risky. Overall, it's risky. At best, use the 150 mg daily if you smoke and want to stop. After all, it was free pharmaceuticals. Other than that, SWIM wouldn't bother and neither should SWIY, in his opinion. SWIM supplied the info, so SWIY can make SWIY's decision.

AND NOW THE NMDA-RELATED INFO SWIM PROMISED (skip if you don't give two shits):

In humans, glutamate is the most common and abundant excitatory neurotransmitter and it is stored in the pre-synaptic cells in vesicles. When specific nerve impulses arrive at the cell, the glutamate is released into the synapse and in the post-synaptic cell receptors are activated when the glutamate binds to them. The most common purpose of this process is thought to be for learning and memory purposes (hence the possible ties with an Adderall-induced psychosis SWIM believes [though he is also much in line with the dopamine]). The glutamate transporters, which chill out in local membranes, are responsible for clearing the glutamate out of the synapse and the extracelluar space. When certain events occur, the transporters can actually help cause glutamate to accumulate outside the cell which allows Ca2+ to enter the cell via the NMDA receptor. This either causes damage to mitochondria simply due to excess Ca2+ within the cell or causes transcription in the cell DNA which promote apopeosis. Then the cells eventually commit suicide, so to say. Interestingly, the same process occurs in the brain when blood is not sufficient (and thus oxygen; the full process is known as the ischemic cascade) and is the cause of most neuron and cell death, SWIM believes, when a person experiences stroke, brain injury, or heart attack. The understanding of this process has led to a hunt for a new class of drug known as a neuroprotectant, which would shut off this cascade, though has to date been unsuccessful.

EDIT: AN ADDITIONAL NOTE ABOUT BUPROPION: Given this could be of importance to some, bupropion has been shown to cause a false positive on a drug test as amphetamine on some occasions. Though it is rare, it happens, obviously common, cheap, and simple tests cannot always distinguish homologues which are structurally not overwhelmingly different.

Reputation Comments on this post:

Excellent post with many perspectives, theories & ideas. Thanks for sharing.

[~lostgurl~]

Very interesting post, I would love to read more of your thoughts, theories & ideas about this drug, especially on:

* drug interactions
* dosage differences
* it's short & long term effects on dopamine levels
* it's ability to correct dopamine levels depleted due to drug abuse (such as methamphetamine)
* it's ability to help with symptoms that may be related to low dopamine levels such as depression, lack of motivation, inability to concentrate, lethargy, cravings (meth, cigarettes, food) & RLS (Restless Legs Syndrome)
* comparisons with other dopaminergic drugs: dopamine precursors and cofactors, dopamine agonists or DA's, MAOIs and dopamine reuptake inhibitors
* it’s differences to the smoking cessation drug Chantix (which blocks the receptors I think?)

Below is a table showing approved drugs for RLS, and I’m just wondering if any of these drugs could also help other symptoms related to low dopamine levels (as stated in blue above). As bupropion is one of only a few dopaminergic drugs actually prescribed for symptoms of low dopamine levels (other than RLS & Parkinson’s Disease)

Any thoughts, theories, ideas, information, experiences etc are welcomed.

RLS dopamine.jpg



Above table from http://www.bioportfolio.com/reports/...20Approval.htm

[jazzmetalguitar]

SWIM will do his best answering these topics but may have to edit later do to fatigute and near inability to talk about bupropion anymore (lol). Again this turned out much longer than expected:

1) Drug Interactions - Everything SWIM sees here is pretty much straight-forward fact which is not open much to his interpretation. Most of the interactions, as SWIM understands it, are based around that pesky CYP2B6 enzyme. Best source of all of these interactions SWIM could actually find was wikipedia (doh; oh but he loves it). Known CYP2B6 inhibitors, which would slow the body's breakdown of bupropion into hydroxybupropion, are Paxil, Zoloft, Prozac (after it metabolizes to norfluoxetine), Valium, Plavix, and orphenadrine (SWIM was not familiar with this drug and so did not know the most popular brand name; is also a NMDA antagonist so likely not good if SWIM's seizure theory is at all plausible). And then obviously CYP2B6 inducers, which will obviously make the bupropion metabolize more quickly to hydroxybupropion, include carbamazepine (CBZ; anticonvulsant), clotrimazole (anti-fungal medication), rifampicin (antibiotic), ritonavir (part of AIDS cocktail SWIM believes), St Johns Wort, and from here Wikipedia just says "and others," and unfortunately SWIM doesn't have access to the referenced report. SWIM further understands that the recently converted hydroxybupropion also acts itself as an inhibitor of CYP2B6 and so other drugs metabolized by the enzyme as show significant level increases. Such drugs are venlafaxine, desipramine, and DXM. Additionally, since it has been known to lower the seizure threshold, it should be carefully administered in patients who take other drugs which do the same (too many to list). In addition, though not listed, probably due to the fact that they are not legal, SWIM would not recommend taking it with any other DA or NE reuptake inhibitors.

2) SWIM actually knew nothing about dosages and so had to hunt again. It seems it is usually started off at 100mg twice daily and worked up to 100mg thrice daily. It is also recommended to never take a single dose exceeding 150mg. Those all, however, seem to be the doses for the IR tablets, which were originally recommended standard dosage of 400-600mg daily before seizure issues occured. There are also SR and XL versions of the pill. The SR's are used for twice daily dosing and the XL's for once daily. After the removal of the drug from the market in 1986 and the subsequent return in 1989 the maximum recommended dosage was 450mg, no questions asked. SWIM cannot find any information denoting whether the dosage for depression vs. ADD vs. nicotine addiction differ and thus assumes they don't.

3) It is very interesting to look at various drug's effects on the dopamine system overtime, and note that SWIM said the "dopamine system" and not the "dopamine levels." In most everything SWIM's discovered it suggests that not the actual levels of the dopamine are affected but rather the sensitivity of the post-synaptic cell's receptors to their corresponding neurotransmitter, except SWIM has found in the case of meth, to be discussed later. Now, there are two types of drugs used for stimulation of the receptors: agonists and indirect actors. Agonists are compounds which can directly activate receptors because they actually mimic dopamine itself. Such drugs include bromocriptine, cabergoline, Pergolide, Pramipexole, Ropinirole, and apomorphine (despite being a morphine derivative does not bond to opioid receptors). Agonists are often used in cases where the neurons which contain dopamine are lost, such as with Parkinson's and Restless Legs Syndrome. The indirect actors are compounds which control the neurotransmitters which are present. Most of these drugs which SWIM personally knows are reuptake inhibitors but amphetamine, methamphetmaines, cathinones, and methcathinones act somewhat different and have no specific class as far as SWIM understands. Reuptake inhibitors, which include methylphenidate, cocaine (though cocaine technically stimulates more norepinephrine than dopamine SWIM believes dopamine is the focus due to effects and addiction in mesolimbic pathway), and bupropion, act by not allowing the dopamine which is left in excess in the synapse to be returned to the pre-synaptic cell. However, the DA can still be broken down by MAO's and also wander away from the synapse.

Though MAOI's, amps, meth, and cats all act somewhat different although SWIM has also seen them considered as reuptake inhibitors (and technically they do inhibit reuptake but not in the same way) he wants to classify them somewhat differently and explain each. It is easier if SWIM ends with MAOI's so he will start with amphetamines. Amphetamines simply cause a flood of dopamine into the synapse and attach to transporters to not let them reuptake or exit the synaptic area (combined with the flood it is a reuptake inhibitor + more). Speaking of meth is just a slightly different issue. The methyl group makes the compound lipid soluble (amps are not) which allows it to more easily pass through the brain blood barrier (more drugs in the brain). Once there, meth does everything amps do plus one more effect. They inhibit monoamide oxidases from metabolizing dopamine after it has been used. Thus, meth is stronger due to more bioavailibility and longer-lasting do to the monoamide oxidase inhibtor effect. Now note the acronym MAOI. It stands for monoamide oxidase inhibtor and that is exactly what it does, prevents the metabolization of dopamine into homovanillic acid (useless as far as neurochemical stimulation goes). However, when used in addition with other drugs it will potentiate the effects (well known by many; possibly dangerous as well). Cat and Methcat, little are known about, but they are assumed to act like amps and meth respectively.

Now, all these drugs and all these crazy processes. What effect does this all have on the dopamine system? Well, the agonists, reuptake inhibitors, as well as SWIM's "other" class all increase dopamine levels in the synapse, which is why they do what they do. The receptors of the post-synaptic cell become desensitized and no longer react to the same amounts of dopamine (the opposite with happen if dopamine antagonists are excessively used). This is the feeling and effect users get known as tolerance. Contrary to belief, you are not specifically getting tolerant to the drug but rather your body's own dopamine. It is also significant to not that alteration of receptor sensitivity can occur after only one use of a drug. In addition, excessive abuse of a drug can result in an actual, and irreversible, alteration of the reuptake system. This will result in different "natural" levels of neurotransmitters in the brain and at this point your brain has lost much of the ability to recorrect for such things (that is the actual purpose of receptors ability to alter sensitivity; it is a surge protector). Depending on the areas of the brain affected by this extensive damage (i.e. different dopamine receptors with different purposes), various things will happen. On additional irreversible affect of such drugs SWIM has found only occurs with meth. Chronic meth use reportedly can result in a lower dopamine transporter count as well as destroying the typical path of synthesis for dopamine.

So for bupropion, the effects are exactly that of any other reuptake inhibitor, though as noted in SWIM's previous post, it is really not that strong.

4) This topic ties very much in with the last and thus should be quite short. As SWIM stated, alteration of the sensitivity of receptors is a natural process meant to protect the brain. Given that it is a natural process, the process will also naturally reverse itself overtime and this is why tolerance is often lost overtime. Though SWIM cannot feel safe to say that the dopaminergic system will restore 100%, he can say it does restore in most cases and is much more forgiving than the serotoninergic system.

In cases where permanent damage is done, whether it was to the reuptake system, the transporters, or the production of dopamine, the result is sometimes a dopaminergically-linked neurological disorder such as Restless Legs Syndrome or Parkinson's. There is no cure for this, at this point some parts of your brain are literally damaged. Often dopamine agonists can be used to treat these disorders though remember, these agonists (though likely not the drug abuse) are one of the causes of this in the first place. (Note: Mindset of some people who have been on medicine for Parkinson's for quite awhile.)

Now, bupropion would not work well as a drug to treat the effects of the dopamine system since it is a dopamine reuptake inhibitor. You need an agonist of some sort because often the cells can't produce enough dopamine for reuptake inhibitors to even work (hence some people have a "permanent" tolerance).

5) As far as other dopamine related problems go, SWIM can only really say that IS prescribed for depression, ADD (possibly your lack of motivation + inability to concentrate), nicotine addiction (and food as well; as far as meth goes, SWIM has heard of it being used for cocaine addiction so the possibilities are there, but don't make SWIY a guinea pig), sexual dysfunction, and seasonal affective disorder. As far as lethargy and more severe dopamine system issues (such as RLS or Parkinson's) go, bupropion has not shown any significant use, although in treatment of Parkinson's it has been found that it may potentiate carbidopa and levodopa, just as more recent studies are showing MDMA may possibly do (and quite well in fact). Simply put, with that low 6--22% effectiveness in the dopamine system SWIM doesn't expect the bupropion to do a whole lot. A few glances at some studies also seemed to SWIM that bupropion was either no more or less effective than another drug for the given disorder. [NOTE: SWIM is pretty sure that bupropion is only used for ADD when the methylphenidate, amps, and then desoxyn have too many side effects in the patient. In addition, it is usally only prescribed for adults because studies have shown that it has either little or actually the reverse effect in children (note: SWIM is not specifically referring to ADD here; the reversal actually occured in an attempt to stop teenage smoking before it started which actually resulted in twice the control as smokers).]

6) SWIM can't gauge how bioavailable dopamine is a result of specific drugs and seems unable to find such results. The only dopamine precursor SWIM is aware of (other than the prescription L-DOPA which is not the safest anyway) is L-Tyrosine. Apparently, 500-1500mg each day can be helpful in things from ADD to depression to Parkinson's. However, as far as comparing bupropion with other drugs statisically, SWIM cannot do that, but he would probably say it is certainly one of the weaker dopaminergics out there.

7) Previously, SWIM did not actually know the differences between Zyban and Chantix and assumed the two acted much in the same way. SWIM was completely wrong as he is prone to be. Chantix (varenicline) is actually a partial agonist for a specific nicotinic acetylcholine receptor. Thus it attaches to the receptor and makes it think it is receiving nicotine. Thus it will eliminate the craving as well as blocking an actual nicotine molecule from enter the receptor if one does smoke (no positive effects of smoking). Bupropion simply bonds to the receptor and does not allow anything to stimulate the receptor. Therefore there will be nothing gained from smoking (one should say less; there are other nicotinic receptors, and this applies to both drugs) however it will not simulate nictotine like the varenicline; however, despite that it has been shown to cut cravings in half. However, in the long run Chantix was shown to be between 60-90% more effective (by SWIM's quick rough calculations).


*To put forth some ideas regarding SWIY's last question (the chart) SWIM wants to remind that these drugs (dopamine agonists) are the action opposites of a class of drugs called dopamine antagonists (antagonists have been brought up a few times now). The most common dopamine antagonists are anti-psychotics. SWIM would like to put it this way. Anti-psychotics are given often for schizophrenia and possibly more familiarly to some amphetamine psychosis. Given that the agonists are the exact opposite it is fairly easy to predict the side-effects of these drugs (hallucinations, tiredness, compulsion, hypersexuality), everything associated with excess dopamine. That said, the dopamine agonists are too risky to use for basic dopamine issues (this is how SWIM understands it) and so is reserved for conditions where it is the only thing that will work such as Parkinson's.

Any questions just ask.

[TokinIXI]

Swim is not sure if there's necessarily a "high" after taking Wellbutrin, but swim sure feels a lot better if he takes 3 150mg Wellbutrin. Swim's mood seems to be more friendly and more open. Swim thinks that there may be some small potential to Wellbutrin, but swiy would have to consume a couple of them to feel anything.

[Bloodshot]

This is why i love this site, swims dog's block of cheese (don't ask me why i associate with dogs that have cheese for friends) found a bottle of wellbutrin and he was wondering if it had any recreational effects, so i just came here and found out all the answers i needed! I told the cheese everything he needed to know!
thank you!
peace
B