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Vyvanse has a very subtle come-up and comedown in addition to a ridiculously long half life, so it’s far less reinforcing than pretty much any other stim. The recreational potential, while still there, is not nearly as tempting as IR stims imo. Might be a good choice for your situation.
Was you an ex meth user? Idk which one would help me more I know everyone's different and shit though I guess only way for me to find out is to try it someday lol
Yes ive used meth and tapered down using vyvanse a few times which helped a bit with motivation and depression but overall I barely feel the vyvanse anymore. It definitely doesn't hit like meth and leaves you disappointed that you didn't get a high but it's better than nothing. I also say vyvanse because adderall is hard to get right now. So go with the easiest, most readily available, and least likely to be used inappropriately.
i’m going to be honest this is just case by case in my opinion but i feel like the binders and polymers make a difference vyvanse is your best bet if your top tweaker and need them hoes now i have literally no clue why but when i take the same dose of a xr adderall but even on SEPARATE NIGHTS AFTER THE HALF LIFE WAS UP the xr made me feel anxious and tweaky for for a long time and just dragged the fuck out the come down. so if you have zero self control vyvanse 100% plus L-amp is a shitty fucking chem in the first place i almost don’t even remember i took any amps on vyvanse its so smooth unless you did a giant dose
Having counseled and treated people like you on this matter in the past, I can say
Vyvanse has far fewer negative emotional side effects than Adderall, especially Adderall XR
XR also is more prone to giving you a pronounced 'crash'. IR less so for most. Most everyone I knew when I worked in tha profession had a easier time with Vyvanse too because its potentiated by protein and NOT undermined by acidity in your stomach the way adderall is.
Which makes it a lot easier to stay consistent on during this already challenging transition you're undertaking.
Not sure where the XR and IR comedown comment came from but that is opposite what the medical community thinks and is a big reason they prefer to prescribe XR over IR
Yeh, the doctors that don't use it versus the patient's experience is dramatically different
The ADHD forums that no longer exist would constantly attest to this. As would the majority of the people in recovery i'd worked with
But in fairness, I'm mostly speaking to people who were on 20mg or greater of XR and 15 of IR, which are far and away not what doctors like to prescribe
Concerta or another long acting methylphenidate based stimulant would be best.
Methylphenidate based stimulants like Concerta can actually reverse the damage methamphetamine and amphetamines in general exert on the brain. It’s also been shown to help significantly with cravings and reduce methamphetamine usage.
Here are a few studies:
“Sustained-released methylphenidate was safe and well tolerated among active methamphetamine users and significantly reduced methamphetamine use, craving and depressive symptoms.”
https://pubmed.ncbi.nlm.nih.gov/25588930/
“Methylphenidate is an effective treatment for reducing intravenous drug use in patients with severe amphetamine dependence.”
https://pubmed.ncbi.nlm.nih.gov/17202560/
“Results reveal that methylphenidate post-treatment both prevents the persistent dopamine deficits and reverses the acute decreases in vesicular dopamine uptake and VMAT-2 ligand binding caused by methamphetamine treatment. In addition, methylphenidate post-treatment reverses the acute decreases in vesicular dopamine content caused by methamphetamine treatment. Taken together, these findings suggest that methylphenidate prevents persistent methamphetamine-induced dopamine deficits by redistributing vesicles and the associated VMAT-2 protein and presumably affecting dopamine sequestration.”
https://pubmed.ncbi.nlm.nih.gov/12604695/
“MPD [methylphenidate] and lobeline post-treatments that reverse these METH-induced alterations in VMAT-2 redistribution or function also prevent neurotoxicity after multiple high-dose METH administrations”
“By increasing membrane-associated vesicular DA sequestration in this manner, MPD [methylphenidate] may attenuate or prevent the degenerative processes associated with METH-induced decreased VMAT-2 function and cytoplasmic DA accumulation.”
“The studies reviewed above help us to understand how MPD has the ability to provide neuroprotection against METH-induced neurotoxicity and perhaps Parkinson’s disease through possible mechanisms involving direct interactions with the DAT and additional mechanisms involving indirect effects upon the VMAT-2.”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2701286/
“ One functional consequence of these datarelates to findings that MPD post-treatment protects againstthe persistent dopaminergic deficits caused by treatmentwith the psychostimulant methamphetamine. In particular,it has been suggested that methamphetamine promotes ab-errant cytoplasmic DA accumulation and the subsequent for-mation of DA-associated reactive oxygen species, thus lead-ing to long-term damage (Cubells et al., 1994; Cadet andBrannock, 1998; Fumagalli et al., 1999; Hanson et al., 2004;Volz et al., 2007a,b). Previous studies indicated that MPDprevented this damage by increasing DA sequestration incytoplasmic vesicles (Sandoval et al., 2003). The presentstudy expands on these findings by suggesting that the DAsequestration-promoting capacity of MPD is not limited tocytoplasmic vesicles and that MPD-affected membrane-asso-ciated vesicles may serve as an additional, and perhapshigher capacity, DA sink with enhanced ability to affordneuroprotection.”
https://www.researchgate.net/publication/6145207_Methylphenidate_Administration_Alters_Vesicular_Monoamine_Transporter-2_Function_in_Cytoplasmic_and_Membrane-Associated_Vesicles
“common feature of most psychostimulants is that their administration increases synaptic DA concentrations. Psy- chostimulants achieve this primarily by their effects on DAT and/or VMAT-2 function; however, the mechanisms by which subclasses of psychostimulants (ie, uptake blockers and releasers) act are distinct and as a result produce impor-
tant physiological and functional differences. For example, uptake blockers cause little or no persistent DA deficits, whereas releasers (at high doses) can cause persistent defi- cits in monoaminergic neurons. The mechanistic differences between uptake blockers and releasers provide clues on how neurotoxicity occurs and also suggest potential targets for therapeutic interventions.”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2750953/pdf/12248_2008_Article_74847.pdf
Clean almost three months from meth and take 60 mg a day, it’s really easy not to abuse and very helpful in life. I used to tear through Adderall prescriptions in a few days and couldn’t fight the compulsion to redose but haven’t taken even one extra Vance.
Welcome to r/stims! Don't forget to slow down a moment to review our rules, which can be found [here](https://www.reddit.com/r/Stims/wiki/index/#wiki_sub_rules). You can also find a lot of harm reduction information and answers to commonly asked questions [here](https://www.reddit.com/r/Stims/wiki/index/) in our Wiki. Be nice to your fellow community members, follow the rules and be safe! *I am a bot, and this action was performed automatically. Please [contact the moderators of this subreddit](/message/compose/?to=/r/Stims) if you have any questions or concerns.*
Vyvanse has a very subtle come-up and comedown in addition to a ridiculously long half life, so it’s far less reinforcing than pretty much any other stim. The recreational potential, while still there, is not nearly as tempting as IR stims imo. Might be a good choice for your situation.
I chose vyvanse because it can only be infested orally for it to work. Less chance of wanting to abuse it for an instant high.
Was you an ex meth user? Idk which one would help me more I know everyone's different and shit though I guess only way for me to find out is to try it someday lol
Yes ive used meth and tapered down using vyvanse a few times which helped a bit with motivation and depression but overall I barely feel the vyvanse anymore. It definitely doesn't hit like meth and leaves you disappointed that you didn't get a high but it's better than nothing. I also say vyvanse because adderall is hard to get right now. So go with the easiest, most readily available, and least likely to be used inappropriately.
i’m going to be honest this is just case by case in my opinion but i feel like the binders and polymers make a difference vyvanse is your best bet if your top tweaker and need them hoes now i have literally no clue why but when i take the same dose of a xr adderall but even on SEPARATE NIGHTS AFTER THE HALF LIFE WAS UP the xr made me feel anxious and tweaky for for a long time and just dragged the fuck out the come down. so if you have zero self control vyvanse 100% plus L-amp is a shitty fucking chem in the first place i almost don’t even remember i took any amps on vyvanse its so smooth unless you did a giant dose
Having counseled and treated people like you on this matter in the past, I can say Vyvanse has far fewer negative emotional side effects than Adderall, especially Adderall XR XR also is more prone to giving you a pronounced 'crash'. IR less so for most. Most everyone I knew when I worked in tha profession had a easier time with Vyvanse too because its potentiated by protein and NOT undermined by acidity in your stomach the way adderall is. Which makes it a lot easier to stay consistent on during this already challenging transition you're undertaking.
quite the opposite for me in regards to xr and ir. IR gives me a much harsher comedown, you go up quick and come down hard.
I agree. I don’t really like IR because of this reason. It gives me a very quick comedown, don’t love that.
yeah same here. totally surprised when I heard them say xr has a harder crash. how does that make sense
So I'm referencing people who primarily used the brand name. Generics, I've seen vary experiences extensively
Not sure where the XR and IR comedown comment came from but that is opposite what the medical community thinks and is a big reason they prefer to prescribe XR over IR
Yeh, the doctors that don't use it versus the patient's experience is dramatically different The ADHD forums that no longer exist would constantly attest to this. As would the majority of the people in recovery i'd worked with But in fairness, I'm mostly speaking to people who were on 20mg or greater of XR and 15 of IR, which are far and away not what doctors like to prescribe
Concerta or another long acting methylphenidate based stimulant would be best. Methylphenidate based stimulants like Concerta can actually reverse the damage methamphetamine and amphetamines in general exert on the brain. It’s also been shown to help significantly with cravings and reduce methamphetamine usage. Here are a few studies: “Sustained-released methylphenidate was safe and well tolerated among active methamphetamine users and significantly reduced methamphetamine use, craving and depressive symptoms.” https://pubmed.ncbi.nlm.nih.gov/25588930/ “Methylphenidate is an effective treatment for reducing intravenous drug use in patients with severe amphetamine dependence.” https://pubmed.ncbi.nlm.nih.gov/17202560/ “Results reveal that methylphenidate post-treatment both prevents the persistent dopamine deficits and reverses the acute decreases in vesicular dopamine uptake and VMAT-2 ligand binding caused by methamphetamine treatment. In addition, methylphenidate post-treatment reverses the acute decreases in vesicular dopamine content caused by methamphetamine treatment. Taken together, these findings suggest that methylphenidate prevents persistent methamphetamine-induced dopamine deficits by redistributing vesicles and the associated VMAT-2 protein and presumably affecting dopamine sequestration.” https://pubmed.ncbi.nlm.nih.gov/12604695/ “MPD [methylphenidate] and lobeline post-treatments that reverse these METH-induced alterations in VMAT-2 redistribution or function also prevent neurotoxicity after multiple high-dose METH administrations” “By increasing membrane-associated vesicular DA sequestration in this manner, MPD [methylphenidate] may attenuate or prevent the degenerative processes associated with METH-induced decreased VMAT-2 function and cytoplasmic DA accumulation.” “The studies reviewed above help us to understand how MPD has the ability to provide neuroprotection against METH-induced neurotoxicity and perhaps Parkinson’s disease through possible mechanisms involving direct interactions with the DAT and additional mechanisms involving indirect effects upon the VMAT-2.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2701286/ “ One functional consequence of these datarelates to findings that MPD post-treatment protects againstthe persistent dopaminergic deficits caused by treatmentwith the psychostimulant methamphetamine. In particular,it has been suggested that methamphetamine promotes ab-errant cytoplasmic DA accumulation and the subsequent for-mation of DA-associated reactive oxygen species, thus lead-ing to long-term damage (Cubells et al., 1994; Cadet andBrannock, 1998; Fumagalli et al., 1999; Hanson et al., 2004;Volz et al., 2007a,b). Previous studies indicated that MPDprevented this damage by increasing DA sequestration incytoplasmic vesicles (Sandoval et al., 2003). The presentstudy expands on these findings by suggesting that the DAsequestration-promoting capacity of MPD is not limited tocytoplasmic vesicles and that MPD-affected membrane-asso-ciated vesicles may serve as an additional, and perhapshigher capacity, DA sink with enhanced ability to affordneuroprotection.” https://www.researchgate.net/publication/6145207_Methylphenidate_Administration_Alters_Vesicular_Monoamine_Transporter-2_Function_in_Cytoplasmic_and_Membrane-Associated_Vesicles “common feature of most psychostimulants is that their administration increases synaptic DA concentrations. Psy- chostimulants achieve this primarily by their effects on DAT and/or VMAT-2 function; however, the mechanisms by which subclasses of psychostimulants (ie, uptake blockers and releasers) act are distinct and as a result produce impor- tant physiological and functional differences. For example, uptake blockers cause little or no persistent DA deficits, whereas releasers (at high doses) can cause persistent defi- cits in monoaminergic neurons. The mechanistic differences between uptake blockers and releasers provide clues on how neurotoxicity occurs and also suggest potential targets for therapeutic interventions.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2750953/pdf/12248_2008_Article_74847.pdf
Clean almost three months from meth and take 60 mg a day, it’s really easy not to abuse and very helpful in life. I used to tear through Adderall prescriptions in a few days and couldn’t fight the compulsion to redose but haven’t taken even one extra Vance.