It's exam time....Addy vs. Vyvanse

[I have pizza]

Hey guys, so this is my first post. It's exam week for me and obviously some Addy, Vyvanse, Focalin, Ritalin, etc gets sold passed around and such. Just thought I would let you guys know from my experience in the past couple of years and what I have found to work for me. Mostly on Vyvanse and addy because that's what I have found here most commonly.

First, Addy or Adderall. This is what I am most familiar with, lots of people get it and are scripted for this. I used to take this 30 mg every day for like 6 years. I am no longer scripted. I find that 15mg at a time (usually get a 3omg) usually does the trick for me if taken in a line (nasally). If I take a 30 mg orally it usually helps me out quite a bit. I find that if you are trying to get high and have the euphoric effects and just enjoy the rush, I would say to take it nasally because it hits you a lot harder and faster. Orally is the same but depends if it is IR (instant release) or XR (extended release). I find that orally you don't really get high but get the focused effects, but then again I took this stuff for 6 years. I would say to study take like 30 mg or 15 mg IR (depending on tolerance) nasally, that gets the job done the best for me. But it would also work just as well to take and IR or XR to study either works.

Secondly, Vyvanse. I have taken these as well, not as much as Addy but a lot more this year than I have dabbled with Addy this year. I have found that taking this nasally kinda sucks. I don't get a huge rush off of it, I just took a 30 mg capsule, opened it up and took nasally. I don't really find that it did a lot for me but I usually only get them in a 15 mg capsule and take it one at a time, I don't like taking a lot nasally it just boogers me up (yes boogers). I would highly recommend taking this orally rather than nasally, you will feel it a lot harder orally if you are going for a focused effect. If you are going for a high, I think it would work either way that way, but I didn't get that much out of it nasally so I would recommend taking orally. I have taken up to 70 mg orally and that had me sitting behind my computer doing homework for several hours without losing focus.

Last thing, I have mixed both of these while consuming alcohol. I DO NOT recommend doing this AT ALL. When I took Addy and I was drinking it was like getting sobered up in a very short amount of time, lots of fun, I could have out drank anyone. BUT when that wears off and the Addy isn't kicking in anymore, the alcohol you consumed will smash you. Not very smart and not recommended. Thought that Vyvanse would be about the same...WOW. I was very very very VERY wrong. I ended up getting extremely sick, I couldn't even function, I was puking and I was a mess . Highly do not recommend taking Vyvanse if you are intending on consuming any alcohol. Stick with some

if you want to get high while you drink.

Again all of this is based on my own experience with these two dandy scripts. Let me know what you all think.

Thanks for reading my novel. HFF!

 

[Kittycat5]

It makes no difference what route you take Vyvanse, as you seem to have found. Even injecting (which I am not recommending) offers next to no rush due to the nature of lisdexamphetamine.

This probably isnt the correct forum for this topic, btw. Good luck on your tests and dont over do the stimulants.

 

[opanabanana]

Adderall and Vyvanse differ, in that Adderall is a mix of Amphetamine salts, (dex, L), while Vyvanse is lisdexamfetamine, which is essentially is an amphetamine salt with a lysine group attached to its molecular structure. Lysine is an amino acid, and therfore must be ingested in order to be effective. Vyvanse in this sense, is a pro-drug, cannot be snorted or injected effectivley, while Adderall can be consumed in just about every way possible.

3rd year psychopharmacology student checking in

OB

 

[Kittycat5]

Vyvanse can be snorted or injected but there is no benefit. It is not the absorption of lisdexamphetamine that is the rate limiting step, rather cleaving the lysine via RBCs after absorption occurs.

And there are many prodrugs administered by and even designed for routes other than oral. Fosphenytoin and Enalaprilat are prodrugs of phenytoin and enalapril respectively, specifically developed for intravenous administration. Whats your professors number? Im calling him.

 

[opanabanana]

Thanks for the corrections Kitty!
I was merely trying to illustrate that lisdexamfetamine is a prodrug in the sense that it contains a nontoxic
protective group (lysine) used in a transient manner to alter the
properties of the parent molecule. The fact that lisdexamfetamine is only active orally because of this, was not meant to imply that ALL pro-drugs are only active orally. Thanks for the clear up anyway, your clearly more knowledgable on the subject than me.
Live and learn that's what we're here for!

OB

 

[Kittycat5]

I know, I was just joking with you but posting the info for those curious. I assume this is 3rd year of a graduate program? Very fascinating and difficult subject to learn. Good luck to you as well.

 

[I have pizza]

Thanks for the replies. Yeah I noticed low (placebo later realized) when I took the vyvanse nasally. But yeah, exams are over and well stimulants helped me pass those puppies. I took a 30mg orally of vyvanse and I worked out 2x that day and I did well on my exams too. Much better than snorting it. I wont do that anymore that's for sure.

 

[Speed King]

The Vyvanse is my choice for study. I like it due to it's long action. I used to be able to type for eight hours on Adderall. My brain works differently now. Vyvanse or Dexedrine FTW,IMO

 

[Dresden]

Dextromethamphetamine hydrochloride crystals, despite their god awful reputation, kicks all their asses in terms of focus, brain power enhancement (nootropic effects) and length of high time per dose. Street ice methamphetamine when consisting of aforementioned substance also bests Desoxyn (prescription methamphetamine) by what, maybe an order or magnitude or more? And it's a lot easier to source, with no pesky controls on the amount obtained per month. However, if you get caught with it, you will soon come to wish you hadn't, as the legal penalties seem to be rather draconian at the 5 gram or more level.

 

[Epiper888]

Don't tell a collage student to start trying meth...

 

[InterestingFACT]

This doesn't seem suited to NPD.

Anyways. I actually would support a comparison between vyvanse and (oral, d-isomer, reasonably pure) meth.

The two drugs just aren't that different--both rats and humans have trouble discriminating between them. They maintain a similar reinforcement ratio. (actually, regular amphetamine's is stronger, if I remember correctly).

The main take-away is that, while meth causes greater dopamine release at equimolar dosages, its greater serotonin release tends to partially suppress its stimulating and reinforcing effects. Thus, the two are active at around the same dosage (I've heard people claim 1.2:1, 1.5:1... I can't assess that myself because meth purity is obviously more variable. But animal studies assessing potency fail to reach statistical significance), if working with pure material. Differences only become significant when looking at high-dose-stereotypy-inducing models, where rats conditioned with high-dose meth in the presence of a stimulus display greater incidence of stereotypy in response to saline + stimulus than the equivalently conditioned amphetamine-dependent rats.
--As an aside: this is probably a direct result of meth's higher dopaminergic activation at subjectively equipotent dosages... therefore higher transcription of ΔFosB, and resulting higher addiction-related neuroplasticity. This might mean that meth si harder to quit "for good" than regular amphetamine, even if it doesn't promote a higher level of reinforcing behavior.

I think the fact that the hydrochloride salt of meth isn't obscenely hygroscopic--and therefore can be distributed as such on the street, rather than as a sulfate--has more to do with the relative addictive potential of the drugs than anything else.... since the hydrochloride can be vaporized, while the sulfate cannot.

As for its general applicability to ADHD.... I'm not so sure. It depends on the "kind" of ADHD I suppose. Meth (because of its lower NE : DA ratio) does not stimulate dopamine and glutamate release in the PFC the way regular amphetamines do. On the other hand, this naturally sets it up in parallel to the dextro-isomer as a "cleaner" alternative to racemic amphetamine, suited for higher-dose treatment.

Of course there's the other not-totally-insignificant issue of it being a fundamentally more toxic drug, due both to its higher SERT activity and its stronger lipophilicity--it's been implicated in the breakdown of the blood-brain-barrier, and of endothelial glyocalyx.



---

Anyways, studies have shown that adderall (or ritalin) is more effective at treating adhd in mild doses than dexedrine (or focalin). However the spectrum swings the other way as doses increase. Perfectly logical, when you think about it: Dopamine in the PFC is largely regulated by NET. In low doses, the additional NET-affinity of the l-isomer salts helps boost cortical transmission. In higher doses, the dextro-isomer's (lower) NET affinity is sufficient, and the additional excessive activation by the levo salts causes unwanted results.

And as others have stated: vyvanse's bioavailability and onset remains about the same regardless of ROA. Keep in mind, though, what this actually means. Vyvanse has ~100% bioavailability, even orally. So even though, mol for mol, it contains less active drug than for example dexedrine spansules or adderal xr, that drug material will go a lot farther. It also means that there isn't really a 'lock' on vyvanse's potential--it was marketed as less abusable but this is a pretty insubstantial claim, the truth is that oral vyvanse is basically the equivalent of IV dexedrine, except with less rush and an ~1 hour delay before it dumps all that amphetamine into your bloodstream. (lysdexamfetamine has a plasma half life of less than 1 hour).

I've made quite a few claims/references to medical literature here without actually providing those references. This is just off the top of my head for now, but I'll see about finding those references later tonight if I get the chance.

 

[I have pizza]

I know, I was just joking with you but posting the info for those curious. I assume this is 3rd year of a graduate program? Very fascinating and difficult subject to learn. Good luck to you as well.

Haha yeah Kittycat I am indeed a student but my 3rd year undergrad. College is hard as it is, gotta find what you can to give you an edge to help you get the 4 point

 

[Speed King]

This doesn't seem suited to NPD.

Anyways. I actually would support a comparison between vyvanse and (oral, d-isomer, reasonably pure) meth.

The two drugs just aren't that different--both rats and humans have trouble discriminating between them. They maintain a similar reinforcement ratio. (actually, regular amphetamine's is stronger, if I remember correctly).

The main take-away is that, while meth causes greater dopamine release at equimolar dosages, its greater serotonin release tends to partially suppress its stimulating and reinforcing effects. Thus, the two are active at around the same dosage (I've heard people claim 1.2:1, 1.5:1... I can't assess that myself because meth purity is obviously more variable. But animal studies assessing potency fail to reach statistical significance), if working with pure material. Differences only become significant when looking at high-dose-stereotypy-inducing models, where rats conditioned with high-dose meth in the presence of a stimulus display greater incidence of stereotypy in response to saline + stimulus than the equivalently conditioned amphetamine-dependent rats.
--As an aside: this is probably a direct result of meth's higher dopaminergic activation at subjectively equipotent dosages... therefore higher transcription of ΔFosB, and resulting higher addiction-related neuroplasticity. This might mean that meth si harder to quit "for good" than regular amphetamine, even if it doesn't promote a higher level of reinforcing behavior.

I think the fact that the hydrochloride salt of meth isn't obscenely hygroscopic--and therefore can be distributed as such on the street, rather than as a sulfate--has more to do with the relative addictive potential of the drugs than anything else.... since the hydrochloride can be vaporized, while the sulfate cannot.

As for its general applicability to ADHD.... I'm not so sure. It depends on the "kind" of ADHD I suppose. Meth (because of its lower NE : DA ratio) does not stimulate dopamine and glutamate release in the PFC the way regular amphetamines do. On the other hand, this naturally sets it up in parallel to the dextro-isomer as a "cleaner" alternative to racemic amphetamine, suited for higher-dose treatment.

Of course there's the other not-totally-insignificant issue of it being a fundamentally more toxic drug, due both to its higher SERT activity and its stronger lipophilicity--it's been implicated in the breakdown of the blood-brain-barrier, and of endothelial glyocalyx.



---

Anyways, studies have shown that adderall (or ritalin) is more effective at treating adhd in mild doses than dexedrine (or focalin). However the spectrum swings the other way as doses increase. Perfectly logical, when you think about it: Dopamine in the PFC is largely regulated by NET. In low doses, the additional NET-affinity of the l-isomer salts helps boost cortical transmission. In higher doses, the dextro-isomer's (lower) NET affinity is sufficient, and the additional excessive activation by the levo salts causes unwanted results.

And as others have stated: vyvanse's bioavailability and onset remains about the same regardless of ROA. Keep in mind, though, what this actually means. Vyvanse has ~100% bioavailability, even orally. So even though, mol for mol, it contains less active drug than for example dexedrine spansules or adderal xr, that drug material will go a lot farther. It also means that there isn't really a 'lock' on vyvanse's potential--it was marketed as less abusable but this is a pretty insubstantial claim, the truth is that oral vyvanse is basically the equivalent of IV dexedrine, except with less rush and an ~1 hour delay before it dumps all that amphetamine into your bloodstream. (lysdexamfetamine has a plasma half life of less than 1 hour).

I've made quite a few claims/references to medical literature here without actually providing those references. This is just off the top of my head for now, but I'll see about finding those references later tonight if I get the chance.

I am only commenting on the part where it was said Vyvanse isn't far off from meth. I have to call bull on that. The street speed comes on super fast and for whatever reason, direct or indirectly serotonin gets involved. There is a certain happy feeling that comes with meth that my second favorite drug Vyvanse just is not capable of producing atleast because it only gets into your system so fast. Okay now in hindsight I can see if the dosages were compared just right like for example 5mg of meth compared to 70mg of Vyvanse, you might get some similarities.

 

[InterestingFACT]

I am only commenting on the part where it was said Vyvanse isn't far off from meth. I have to call bull on that. The street speed comes on super fast and for whatever reason, direct or indirectly serotonin gets involved. There is a certain happy feeling that comes with meth that my second favorite drug Vyvanse just is not capable of producing atleast because it only gets into your system so fast. Okay now in hindsight I can see if the dosages were compared just right like for example 5mg of meth comparedk to 70mg of Vyvanse, you might get some similarities.

I was speaking strictly in terms of peak effects: obviously there's going to be a delayed and more drawn out onset with Vyvanse, due to the release mechanism. However, 5mg meth is absolutely not comparable to 70mg Vyvanse. 70mg Vyvanse is is ~ 30mg d-amphetamine delivered with 100% bioavailability (and, though there's a delayed onset, the actual time release is relatively minimal: the half life of the parent molecule is less than an hour). 5mg meth--let's say pure for the sake of comparison--will generally only deliver 2.5-4mg of active drug molecule to your bloodstream orally. Even if we assume a 1.5:1 potency ratio (on the higher end of what studies and anecdotes would suggest) that's nearly an order of magnitude difference in activity. If at ~1 hour post-dosing, Vyvanse has metabolized ~50% to produce 15mg amphetamine, that's more than 3x more drug in circulation at its "onset."

There *are* qualitative differences between the two: namely, meths serotonergic activity is large enough to become relevant at higher doses, it's reduced noradrenergic activity might contribute to a calmer "high," and it's unique affinities for VMAT and for α2 receptors likely cause real--though, hard to discriminate--differences in subjective effect. The reality is that in blind trials, users are generally unable to distinguish between d-amphetamine and d-methamphetamine.

And of course, Vyvanse itself isn't merely d-amphetamine: it's mechanism of action precludes it from the same patterns of use common to meth (smoking, IV, even snorting, to increase rate of onset and rush... And the subsequent redosing this tends to promote).

 

[aced126]

This doesn't seem suited to NPD.

Anyways. I actually would support a comparison between vyvanse and (oral, d-isomer, reasonably pure) meth.

The two drugs just aren't that different--both rats and humans have trouble discriminating between them. They maintain a similar reinforcement ratio. (actually, regular amphetamine's is stronger, if I remember correctly).

The main take-away is that, while meth causes greater dopamine release at equimolar dosages, its greater serotonin release tends to partially suppress its stimulating and reinforcing effects. Thus, the two are active at around the same dosage (I've heard people claim 1.2:1, 1.5:1... I can't assess that myself because meth purity is obviously more variable. But animal studies assessing potency fail to reach statistical significance), if working with pure material. Differences only become significant when looking at high-dose-stereotypy-inducing models, where rats conditioned with high-dose meth in the presence of a stimulus display greater incidence of stereotypy in response to saline + stimulus than the equivalently conditioned amphetamine-dependent rats.
--As an aside: this is probably a direct result of meth's higher dopaminergic activation at subjectively equipotent dosages... therefore higher transcription of ΔFosB, and resulting higher addiction-related neuroplasticity. This might mean that meth si harder to quit "for good" than regular amphetamine, even if it doesn't promote a higher level of reinforcing behavior.

I think the fact that the hydrochloride salt of meth isn't obscenely hygroscopic--and therefore can be distributed as such on the street, rather than as a sulfate--has more to do with the relative addictive potential of the drugs than anything else.... since the hydrochloride can be vaporized, while the sulfate cannot.

As for its general applicability to ADHD.... I'm not so sure. It depends on the "kind" of ADHD I suppose. Meth (because of its lower NE : DA ratio) does not stimulate dopamine and glutamate release in the PFC the way regular amphetamines do. On the other hand, this naturally sets it up in parallel to the dextro-isomer as a "cleaner" alternative to racemic amphetamine, suited for higher-dose treatment.

Of course there's the other not-totally-insignificant issue of it being a fundamentally more toxic drug, due both to its higher SERT activity and its stronger lipophilicity--it's been implicated in the breakdown of the blood-brain-barrier, and of endothelial glyocalyx.



---

Anyways, studies have shown that adderall (or ritalin) is more effective at treating adhd in mild doses than dexedrine (or focalin). However the spectrum swings the other way as doses increase. Perfectly logical, when you think about it: Dopamine in the PFC is largely regulated by NET. In low doses, the additional NET-affinity of the l-isomer salts helps boost cortical transmission. In higher doses, the dextro-isomer's (lower) NET affinity is sufficient, and the additional excessive activation by the levo salts causes unwanted results.

And as others have stated: vyvanse's bioavailability and onset remains about the same regardless of ROA. Keep in mind, though, what this actually means. Vyvanse has ~100% bioavailability, even orally. So even though, mol for mol, it contains less active drug than for example dexedrine spansules or adderal xr, that drug material will go a lot farther. It also means that there isn't really a 'lock' on vyvanse's potential--it was marketed as less abusable but this is a pretty insubstantial claim, the truth is that oral vyvanse is basically the equivalent of IV dexedrine, except with less rush and an ~1 hour delay before it dumps all that amphetamine into your bloodstream. (lysdexamfetamine has a plasma half life of less than 1 hour).

I've made quite a few claims/references to medical literature here without actually providing those references. This is just off the top of my head for now, but I'll see about finding those references later tonight if I get the chance.

Methamphetamine does indeed release a fair amount of serotonin, only 10 times less than what it releases of dopamine.

 

[PINKoPANaTHER]

You can claim to prefer methamphetamine to regular amphetamine, but for studying and focusing, especially long-term, the fact that amphetamine doesn't show neurotoxicity at therapeutic doses is a huge +1 in favor of it (Vyvanse, Adderal, Dexedrine) over the neurotoxic methamphetamines (street, Desoxyn). This is also theorized to contribute to the added addiction liability of methamp versus regular amp in that the damage caused contributes to the "low" feeling when coming down/withdrawing further reinforcing the behavior.

This is just my opinion, and from my experience, and the reason I wish regular street amphetamine was more common in my neck of the woods (not very many prescriptions handed out these days). I also enjoy sleeping too much to make a regular habit out of taking these, as even in smaller doses I had a really hard time sleeping after my study binges (sometimes 36 hours later).

 

[aced126]

You can claim to prefer methamphetamine to regular amphetamine, but for studying and focusing, especially long-term, the fact that amphetamine doesn't show neurotoxicity at therapeutic doses is a huge +1 in favor of it (Vyvanse, Adderal, Dexedrine) over the neurotoxic methamphetamines (street, Desoxyn). This is also theorized to contribute to the added addiction liability of methamp versus regular amp in that the damage caused contributes to the "low" feeling when coming down/withdrawing further reinforcing the behavior.

A lot of people say methamphetamine is more neurotoxic than amphetamine, but I don't believe this to be the case. Studies on neurodegeneration are normally done on methamphetamine, but studies on the mechanism of action itself are done on amphetamine. A few reasons why this is so: methamphetamine is easily synthesised and thus more abused. It is consumed in higher quantities as a result so neurotoxicity is observed in methamphetamine but not amphetamine as a result. Also dopaminergic neurotoxicity might be more to do with the S-enantiomer of methamphetamine (which is what it is mainly found as due to the clandestine synthesis using either pseudoephedrine or ephedrine); amphetamine is normally a combination of salts (e.g. adderall) with the R-enantiomers possibly being a lot less neurotoxic to dopaminergic neurons while at the same time being beneficial in providing ADHD relief. Do you have a source expanding on the relative neurotoxicities of methamphetamine and amphetamine?


I also wanted to chime in on the original topic. I'd say Vyvanse is better for studying for exams than amphetamine because it's less abusable (amphetamine slowly released over time so the rate of uptake into the brain and therefore the euphoric effects from fast rate of uptake i.e. the rush are not present). So with Vyvanse you're less likely to fuck around and get down to work whereas with amphetamine you could (taking a generalisation here, but with anyone there is more of a chance this happens) end up going on a binge while trying to chase euphoria; that is never efficient.

 

[Speed King]

^^That is an important, true fact right there. The only reason I am not taking taking Vyvance atm, is I literly got to pick anything(besides meth)!i wanted due to my personal experience with various pharmasutical amphetamines for ADD. I chose Dexedrine/ dextroamphetamine ER, because I never had it and had to see how it compared to the pro drug. I am slightly torn, but for the time being, I'm sticking w/Dextroamphetamine. The fact that Vyvanse has no rush and lasts a solid fully active 8hours, but closer to 10-12hrs, makes it a solid winner. We can split hairs all day long and also we all have our prefrences, but as a harm reduction site, I would have to side with Vyvanse. It's all the things that cannot be done, that make it better . Side note dextroamphetamine has a lot of pluses to it. It feels different from the pro drug and smooth as silk stimulation and comedown. Residual stimulation is IMO the cleanest. The problems are(subjective) the fact that you can snort it and take much higher doses then normal. For the general viewer of this thread, Vyvanse is the winner due to the fact that it is non abisable (very much) and there is really no rush to it. It simply does its job. For those of you who would tell me what is wrong with my post, go easy. I am speaking generally with harm reduction in mind. To each his own.

 

[PINKoPANaTHER]

A lot of people say methamphetamine is more neurotoxic than amphetamine, but I don't believe this to be the case. Studies on neurodegeneration are normally done on methamphetamine, but studies on the mechanism of action itself are done on amphetamine. A few reasons why this is so: methamphetamine is easily synthesised and thus more abused. It is consumed in higher quantities as a result so neurotoxicity is observed in methamphetamine but not amphetamine as a result. Also dopaminergic neurotoxicity might be more to do with the S-enantiomer of methamphetamine (which is what it is mainly found as due to the clandestine synthesis using either pseudoephedrine or ephedrine); amphetamine is normally a combination of salts (e.g. adderall) with the R-enantiomers possibly being a lot less neurotoxic to dopaminergic neurons while at the same time being beneficial in providing ADHD relief. Do you have a source expanding on the relative neurotoxicities of methamphetamine and amphetamine?


I also wanted to chime in on the original topic. I'd say Vyvanse is better for studying for exams than amphetamine because it's less abusable (amphetamine slowly released over time so the rate of uptake into the brain and therefore the euphoric effects from fast rate of uptake i.e. the rush are not present). So with Vyvanse you're less likely to fuck around and get down to work whereas with amphetamine you could (taking a generalisation here, but with anyone there is more of a chance this happens) end up going on a binge while trying to chase euphoria; that is never efficient.

Yes, this is why I tried to qualify by saying "in therapeutic doses". I haven't read the studies on methamphetamine neurotoxicity, but I am very familiar with the studies that demonstrated sustained improvements in function with long term dextroamphetamine use, as I found it rather hard to believe at first (I don't routinely use amphetamines in any form because they cause way too many physical side effects for me). I think it would be very interesting if they actually performed a direct comparison study of groups of patients taking equivalent doses of Dextromethamphetamine and Dextroamphetamine to get a clearer picture of the damage either one can cause (also would be nice if they included high-dose abuse groups, but getting a study like that approved would be difficult).


I just saw the source request: I will look through my article archive and try to get a link posted here

 

[PINKoPANaTHER]

A lot of people say methamphetamine is more neurotoxic than amphetamine, but I don't believe this to be the case. Studies on neurodegeneration are normally done on methamphetamine, but studies on the mechanism of action itself are done on amphetamine. A few reasons why this is so: methamphetamine is easily synthesised and thus more abused. It is consumed in higher quantities as a result so neurotoxicity is observed in methamphetamine but not amphetamine as a result. Also dopaminergic neurotoxicity might be more to do with the S-enantiomer of methamphetamine (which is what it is mainly found as due to the clandestine synthesis using either pseudoephedrine or ephedrine); amphetamine is normally a combination of salts (e.g. adderall) with the R-enantiomers possibly being a lot less neurotoxic to dopaminergic neurons while at the same time being beneficial in providing ADHD relief. Do you have a source expanding on the relative neurotoxicities of methamphetamine and amphetamine?


I also wanted to chime in on the original topic. I'd say Vyvanse is better for studying for exams than amphetamine because it's less abusable (amphetamine slowly released over time so the rate of uptake into the brain and therefore the euphoric effects from fast rate of uptake i.e. the rush are not present). So with Vyvanse you're less likely to fuck around and get down to work whereas with amphetamine you could (taking a generalisation here, but with anyone there is more of a chance this happens) end up going on a binge while trying to chase euphoria; that is never efficient.

I had a whole well written response on the preponderance of evidence for neurotoxicity in either meth or regular amp with multiple sources but it was lost. Anyhow, here are two interesting papers that basically suggest that they are both neurotoxic at high doses, while amp is much less so in therapeutic doses. I didn't have time to check which enantiomers were used, so you may still be right on those mechanisms, however, there are some other interesting mechanisms suggested in paper 2 below based around ubiquitin processing for receptor degradation, and Endoplamic Reticulum errors in processing. Interestingly, that reference in the review suggests (very)low-dose conditioning with meth is neuroprotective when functional doses are administered after

http://www.ncbi.nlm.nih.gov/pubmed/17606768 (abstract only)
http://www.hindawi.com/journals/bn/2015/103969/ (great review on methamphetamine, both acute high dose, and chronic low-dose situations, plus some very interesting stuff on mechanisms and potential treatments, like cannabinoid administration prior to methamp)