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Adderall + Selegiline

adderall selegiline

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#1 NeuroGeneration

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Posted 14 July 2014 - 06:07 PM


Does anybody have any thoughts on low dose selegiline (1 mg/day), co-administered with low dose (5-10mg) of Adderall?

 

MAOI's are discouraged while taking Adderall, because of the risk of hypertensive crisis. However, Deprenyl's MAO-B effect is significantly less risky than the MAO-A effect (occurs at higher doses of Deprenyl, >10mg). For that reason, I'm curious if the generalized statement of "avoid MAOIs" while on Adderall would be seen any differently at the low-dose MAO-B levels.
 
I've seen a rodent study that found the dopamine toxicity of Adderall to be reduced when given with Selegiline (first study, below) – though, admittedly, I'm not fluent in biochem and need some help interpreting the below studies.
 
So, realistically speaking, at my 1mg dose, if I titrate up on Adderall (2.5mg, 5mg, 7.5mg, 10mg max), rather than my standard 20mg dosage, am I running a significant risk?
 
Other than watching my blood pressure, what type of damage might take place / what should I be keeping an eye out for?
 
Is it possible that this combo would actually be neuroprotective, due to selegiline's impact on dopamine receptors, and the ability to take lower doses of Adderall?
 

 

STUDIES:

 

http://www.ncbi.nlm....pubmed/17651730

Deprenyl treatment attenuates long-term pre- and post-synaptic changes evoked by chronic methamphetamine.

Abstract

Deprenyl, used clinically in Parkinson's disease, has multiple pharmacological effects which make it a good candidate to treat neurotoxicity. Thus, we investigated deprenyl's ability to attenuate methamphetamine-induced dopamine neurotoxicity. We also examined deprenyl's effect in changing markers associated with psychostimulant sensitization. A potential therapeutic effect on either pathological domain would be a boon in developing novel treatments for methamphetamine abuse. Adult male Sprague-Dawley rats were split into 6 groups. Three groups received a 7-day saline minipump with saline, 0.05 or 0.25 mg/kg SC deprenyl injections given for 10 days before, during and 5 days after the 7-day saline minipump implant. Similarly, 3 groups received methamphetamine pumps (25 mg/kg/day) with escalating daily injections of methamphetamine (0-6 mg/kg) in addition to the minipump treatment. These rats also received saline, 0.05 or 0.25 mg/kg deprenyl injections given before, during and the 7-day minipump treatment. Rats were killed on day 28 of withdrawal and brain samples taken. HPLC analysis for dopamine and 3,4-Dihydroxy-Phenylacetic Acid (DOPAC) revealed a loss of dopamine in the caudate and accumbens which was partially reversed by high dose deprenyl. Tyrosine hydroxylase immunostaining in the midbrain was unaffected by methamphetamine, suggesting that dopamine neurotoxicity was localized to the caudate. Western blot analysis of the caudate after methamphetamine revealed little change in Alpha-Amino-3-Hydroxy-5-Methyl-4-Isoxazole Propionic Acid (AMPA) GluR1 or N-Methyl-d-Aspartate (NMDA) NR2B subunits, or their phosphorylation state. However, methamphetamine increased levels of GluR1 and its phosphorylation state in the prefrontal cortex (PFC), and these increases were attenuated by deprenyl. Methamphetamine also increased levels of PFC NR2B subunit, but these increases were not attenuated by deprenyl. We suggest that deprenyl may be effective in reducing the neurotoxic effects of methamphetamine and may also attenuate changes in prefrontal AMPA receptor function, presumably more associated with addiction rather than neurotoxicity.

 

 

http://www.ncbi.nlm....pubmed/16757017

Amphetamine-induced locomotor activity is reduced in mice following MPTP treatment but not following selegiline/MPTP treatment.

Abstract

MPTP treatment has been used in mice to cause dopaminergic neuronal cell loss and subsequent behavioral abnormalities. As such, this animal model is often used as a method for the characterization of putative novel therapeutics for disease states characterized by dopamine loss, such as Parkinson's disease. Previous reports of behavioral abnormalities in mice following MPTP intoxication, however, have been conflicting. For example, open field spontaneous activity has been reported to increase, decrease or not change in MPTP treated mice. Accordingly, a more robust and direct functional measure of MPTP-induced central dopamine depletion is needed. In the present manuscript, we report on the characterization of amphetamine-induced locomotor activity as a sensitive functional endpoint for dopamine loss following MPTP treatment. We found that the amphetamine-induced locomotor activity of C57BL/6 mice was reduced in a dose-dependent manner following treatment with MPTP. This reduction of activity was associated with decreases in central dopamine levels. Further, the potential for use of this endpoint to evaluate putative therapeutics is exemplified by the amelioration of these effects following pre-treatment with the MAO-B inhibitor selegiline.

 

http://www.ncbi.nlm..../pubmed/9920178

The amphetamine-like reinforcing effect and mechanism of L-deprenyl on conditioned place preference in mice.

Abstract

The present study investigated the reinforcing effect of L-deprenyl on conditioned place preference in mice and its mechanism. Conditioned place preference was induced by 10 and 25 mg/kg L-deprenyl in a dose-dependent fashion during five consecutive conditioning days, and its reinforcing property was about five-fold less potent than that of L-amphetamine. Pretreatment with the dopamine antagonist, haloperidol (1 mg/kg i.p.), effectively blocked the place preference produced by L-deprenyl (10 and 25 mg/kg i.p.) and L-amphetamine (2 and 5 mg/kg i.p.), but haloperidol itself produced no place aversion. The neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), 30 mg/kg did not modify the place preference induced by both L-deprenyl and L-amphetamine, though the dopamine concentration in striata assayed by high performance liquid chromatography with electrochemical detection (HPLC-EC) was significantly reduced. These results suggest that L-deprenyl has amphetamine-like reinforcing properties. The reinforcing effect of L-deprenyl may be mediated by central dopaminergic neuronal systems, while the nigrostriatal dopaminergic pathway is not involved.

 

http://www.ncbi.nlm....pubmed/10193780

Effect of low-dose treatment with selegiline on dopamine transporter (DAT) expression and amphetamine-induced dopamine release in vivo.

Abstract

1. Chronic treatment with low doses of the selective monoamine oxidase (MAO) type B inhibitors selegiline [(-)-deprenyl] and rasagiline, causes elevation in extracellular level of 3,4-dihydroxyphenylethylamine (dopamine) in the rat striatum in vivo (Lamensdorf et al., 1996). The present study was carried out to determine whether this effect of selegiline could be the result of an inhibition of the high-affinity dopamine neuronal transport process. 2. Changes in activity of the dopamine transporter (DAT) in vivo following selegiline treatment were evaluated indirectly by microdialysis technique in the rat, from the change in striatal dopamine extracellular concentration following systemic amphetamine administration (4 mg kg(-1), i.p.). Striatal levels of the DAT molecule were determined by immunoblotting. Uptake of [3H]-dopamine was determined in synaptosomes from selegiline-treated animals. 3. Amphetamine-induced increase in striatal extracellular dopamine level was attenuated by one day and by chronic (21 days) treatment with selegiline (0.25 mg kg(-1), s.c.). 4. Striatal levels of DAT were elevated after 1 and 21 days treatment with selegiline, but were not affected by clorgyline, rasagiline, nomifensine or amphetamine. 5. The increase in DAT expression, and attenuation of amphetamine-induced dopamine release, were not accompanied by a change in [3H]-dopamine uptake in synaptosomes of selegiline-treated animals. 6. The results suggest that a reversible inhibition of dopamine uptake occurs following chronic low dose selegiline treatment in vivo which may be mediated by an increase in endogenous MAO-B substrates such as 2-phenylethylamine, rather than by the inhibitor molecule or its metabolites. Increased DAT expression appears to be a special property of the selegiline molecule, since it occurs after one low dose of selegiline, and is not seen with other inhibitors of MAO-A or MAO-B. The new DAT molecules formed following selegiline treatment appear not to be functionally active.

 

http://link.springer...A:1007632700126

Biphasic Effects of Selegiline on Striatal Dopamine: Lack of Effect on Methamphetamine-Induced Dopamine Depletion
Abstract
We tested the hypothesis that selegiline can attenuate dopamine depletion if administered following high doses of methamphetamine that cause neurotoxicity in the striatum. Methamphetamine produced decreases of 50% or greater in both striatal concentrations of dopamine and combined concentrations of homovanillic acid and DOPAC in mice. For animals not exposed to methamphetamine, chronic treatment with selegiline over 18 days caused biphasic effects on striatal dopamine content, with decreases, no effect, or increases observed for mice receiving treatment with 0.02, 0.2, and 2.0 mg/kg, respectively. Selegiline failed to modify methamphetamine-induced reductions in striatal dopamine content or combined concentrations of homovanillic acid and DOPAC. Significant increases in mortality following the onset of selegiline treatment (24 hours after the initial dose of methamphetamine) occurred in methamphetamine-treated mice that received saline or 2.0 mg/kg of selegiline, but not for mice treated with 0.02 or 0.2 mg/kg of selegiline. These results indicate that selegiline fails to attenuate dopamine depletion when administered chronically following exposure to methamphetamine, but may attenuate methamphetamine-induced mortality. In control animals that did not receive methamphetamine, low doses of selegiline produced decreases the concentration of striatal dopamine, while high dose treatment caused increases in striatal dopamine content.

 

 


Edited by NeuroGeneration, 14 July 2014 - 06:33 PM.

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#2 NeuroGeneration

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Posted 14 July 2014 - 08:13 PM

*Rather than neuroprotective, I should have said, "is it possible that this combination could attenuate the risk / damage caused by Adderall?"



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#3 Valor5

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Posted 15 July 2014 - 01:49 AM

I have had a hypertensive crisis before. It is not fun but it did not kill me but made me very uncomfortable and it could have done a lifelong damage and I had a pain on the side of my neck for like a week after and trouble sleeping for the same. I got to the emergency room and asked for carvedilol (i think that is the name) and told the people i was experiencing pain in my stomach area and having a hypertensive crisis. The physician decided to give me morphine. (ER cost me $10,000. I got it reduced (charity) to like 3 or 4 thousand because I was not making much money.) This caused the pain i was feeling to go away and eventually the blood pressure came down. I think it went up as high as 180 systolic maybe a little higher initially. I was taking parnate (tranylcypromine) at the time, somewhat related to selegiline. This happened very unexpectedly on this drug. I did not combine this with an amphetamine. That probably would have killed me. This drug is very dangerous. I have taken phenelzine before with no problem but this one (parnate) you do not want to play around with. The selegiline is not a complete inhibitor as i understand. I would be very careful. But I don't think it would be a problem if done properly and on a very low dose starting. I am a vegetarian so my arterial health is excellent and I usually have a low blood pressure like 110/70 something like this so I don't know what yours is but because of this I did not have something worse happen to me like a stroke or hemorrhage. But the lethality of the poison is in the dose and in your general health. If you are responsible and have a blood pressure cuff and perhaps some kind of antidote you can probably approach this safely. For the extra edge you are seeking I don't know that it would be worth it. I highly doubt it will somehow really improve you. If you are after cellular protection. There may be safer alternatives, resveratrol, rhodiola, curcummin.



#4 NeuroGeneration

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Posted 15 July 2014 - 02:20 AM

Thanks, Valor5. It's good to hear that you made it out of that situation in good health!

 

Your story is helpful. The more I research, the more I realize that not much is known about this combination. Unless I come across something substantially positive or neutral, I'm going to cycle off of my 1mg selegiline dose.

 

I've read the study that claims that Modafinil can reduce the neurotoxicity of methamphetamine; I think it stands to reason that combining Modafinil with amphetamine (Adderall) would be beneficial via similar mechanisms.

 

These are rough thoughts, but I'm thinking of doing the following stack:

 

Pre-Adderall: CoQ10 or MitoQ, NAC

With Adderall: Modafinil (100mg) + Adderall (10mg)

t+3 hours: B vitamins, TMG, blueberries, grape seed extract & creatine

Evening / Night: Curcumin + Rhodiola + Ashwaganda + Melatonin + Magnesium + Liposomal Vitamin C

Day after: Liposomal Glutathione

 

Adderall / Modafinil combo no more than 3 days per week, with 2 weeks off every 6 weeks.

 

This combination might be a good way to offset the neurotoxicity of the amphetamine stimulant, while also improving overall health. I welcome critiques :-)


Edited by NeuroGeneration, 15 July 2014 - 02:21 AM.


#5 FW900

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Posted 15 July 2014 - 08:55 PM

Please note this following advice is potentially dangerous and risky.

 

There are actually studies indicating that combining selegiline with methamphetamine, reduces the cardiovascular effects of methamphetamine. I would imagine this would ring true for amphetamine but you need to be careful, as dextroamphetamine elevates blood pressure to a greater extent than dextromethampetamine.

 

Reduced cardiovascular effects of methamphetamine following treatment with selegiline.

Selegiline is a specific MAO-B inhibitor. As MAO-B has been shown to be significantly involved in the metabolism of dopamine in certain regions of the primate brain, selegiline has been proposed for use in the treatment of drug addiction. Selegiline is also metabolized in vivo to l-methamphetamine. Therefore, when given in combination with psychostimulants such as d-methamphetamine, there is the potential for adverse effects. To study this possibility, squirrel monkeys were treated with chronic selegiline and tested with two doses of d-methamphetamine (0.1 and 1.0 mg/kg, i.v.). Following at least 7 days of treatment with once daily 0.3 mg/kg i.m. selegiline, the effects of methamphetamine on blood pressure and heart rate were no different than the effects of methamphetamine observed prior to selegiline treatment. However, following at least 10 days of treatment with 1.0 mg/kg i.m. selegiline, the effects of methamphetamine on blood pressure and heart rate were significantly reduced. Both methamphetamine and amphetamine were detected in plasma following chronic selegiline treatment. When monkeys were given an acute selegiline injection prior to methamphetamine, reduced cardiovascular effects were also seen. These results indicate that selegiline can be used safely even in combination with methamphetamine, as the cardiovascular effects of the drug combination were no greater than either drug alone, and were actually reduced at the higher selegiline dose.

→ source (external link)

 

 

The fact that Adderall has the levorotatory isomer of amphetamine in it, which produces parasympathetic nervous system stimulation is the reason I would avoid using it with selegiline. (Even though selegiline only inhibits MAO-B at low dosages, and L-amphetamine's NE release shouldn't matter as it is MAO-A that breaks down NE, it's best to err on the side of caution). If you want to experiment with the combination, you should try to get a prescription for Dexedrine, which only has the dextroratory isomer.

 

 

I've read the study that claims that Modafinil can reduce the neurotoxicity of methamphetamine; I think it stands to reason that combining Modafinil with amphetamine (Adderall) would be beneficial via similar mechanisms.

 

 

The reason why modafinil attenuates the neurotoxicity in that instance is that it acts as a very weak dopamine reuptake inhibitor. There is evidence that other DRIs such as methylphenidate lessen neurotoxicity as well. You might want to reconsider using modafinil though. Both amphetamine and modafinil are known to elevate slightly elevate blood pressure and to a lesser extent heart rate. Both of these substances also reduce to the urge to eat. Both of these require more hydration and more bathroom trips. There are online anecdotes about each of these causing problems like acne and hair thinning. You might be trading neurotoxicity for cardiotoxicity and dehydration.

 

It would probably be more beneficial to you to use cycle between modafinil and Adderall rather than using them both on the same day. Less frequent exposure to amphetamine would be a plus alongside a slower onset of tolerance.

 

NeuroGeneration, you should consider adding an NMDA receptor antagonist, such as memantine, to your neurotoxicity prevention stack. A wide range of NMDAr antagonists have been shown to reduce the neurotoxicity of amphetamine. Even magnesium is a weak NMDAr antagonist and supplementing with it will be better than nothing.

 

Memantine protects against amphetamine derivatives-induced neurotoxic damage in rodents.

Memantine attenuates 3,4-methylenedioxymethamphetamine-induced hyperthermia in rats.

Memantine is a useful drug to prevent the spatial and non-spatial memory deficits induced by methamphetamine in rats.

 

 

Lastly, I have no first hand experiences with any of the substances or combinations mentioned. I've done my fair share of reading on this topic (neurotoxicity) in the event that I need to ever use amphetamine for treatment of my sleepiness.



#6 medievil

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Posted 16 July 2014 - 12:44 PM

Its been reported to blunt stims soo... if your into neuroprotection then its probably the shit for you tough.

 

Why can you die of taking it normal maois, please update me im sure its easy to block the pathway that makes things dangerous.



#7 NeuroGeneration

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Posted 16 July 2014 - 03:08 PM

You're saying that Selegiline is reported to blunt stimulants? If that's the case, why do so many say that reduced dosages of caffeine or Adderall have more pronounced effects? Am I misunderstanding you or them?



#8 medievil

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Posted 16 July 2014 - 03:10 PM

Well it seems to be individual, for those that report blunted effects its because sele increases DATS.

 

Rasagiline doesn't have this problem.



#9 NeuroGeneration

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Posted 17 July 2014 - 09:03 PM

FW900 – thank you for your detailed response. I have a few followup questions, and some stack questions, if you would oblige...

 

1. Modafinil doesn't do much for me, even at 200mg sublingual (if you have any suggestions, I'm all ears!). Since your suggestion of 1 day Adderall, 1 day Modafinil wouldn't be effective for me (since the Modafinil days wouldn't work), would I be better off with combining them to reduce toxicity, as I had originally suggested?

 

2. Would I be better off with a methylphenidate / Adderall combo, as opposed to Modafinil / Adderall, for the sake of blunting some of the toxicity? I can't help but feel that modafinil is less toxic than the methylphenidate stimulant, even if it's less effective as a dopamine reuptake inhibitor than ritalin.

 

3. I already take magnesium every night, and have just ordered magnesium threonate to try to further thwart the NMDA toxicity that you mentioned (since it crosses the BBB better). Re: memantine, are there any risks? Any stronger, natural alternatives than magnesium, or do you think that mag threonate would be sufficient? I also hesitate ordering prescriptions when I may not have to.

 

Here's my revised stack (with questions):

 

30 mins Pre-Adderall:

•Selenium (always w/ iodine)

•NAC

•Liposomal Glutathione

•Ubiquinol or MitoQ

•B's via 2/3 multivitamin (Thorne FX, 2 pills, instead of 3)

 

With Adderall:

•Modafinil or Ritalin

•Grape Seed Extract

•Creatine (for glutamate toxicity)

•Magnesium threonate

•How do you feel about idebenone at this time?

 

End of Day:

•Liposomal Vit C (antioxidants, and to speed up amph clearance from blood)

•Rhodiola / Ashwaganda, for calming effects

•Magnesium Citrate + Zinc

•Melatonin (for neuronal antioxidants, sleep, etc.)

•Trehalose sugar (for autophagy)

•Longvida Curcumin

I'm considering ALCAR, ALA & L-Carnosine. Thoughts? Should it be before, during or after Adderall, if at all?

 

Day After Adderall:

•Liposomal Glutathione (restoring what was used up)

•UMP – restoring dopamine receptors

•Trehalose

•Piracetam (repairing damage)

•Centrophenoxine

•I'm considering adding Jioagulan, CDP choline, inositol on these days, too. Thoughts?

 

 

1x 16-24 hour fast per month for autophagy (without antioxidants), and obviously intend to heavy dose on antioxidants while on Adderall.

 

I exercise regularly, get good sleep, and don't have to worry about eating or drinking adequate water while on Adderall. Do you think that my lifestyle, combined with the above protocol, would have me in a good place for 2-3x/wk with 10-20mg Adderall? I never want to become a vegetable / Alzheimer's / Parkinson's / etc. – if I live until 95 instead of 100, I'm OK with that. But I'm not OK with living until 75 instead of 100, nor living in a wheelchair.



#10 FW900

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Posted 17 July 2014 - 10:52 PM

FW900 – thank you for your detailed response. I have a few followup questions, and some stack questions, if you would oblige...

 

1. Modafinil doesn't do much for me, even at 200mg sublingual (if you have any suggestions, I'm all ears!). Since your suggestion of 1 day Adderall, 1 day Modafinil wouldn't be effective for me (since the Modafinil days wouldn't work), would I be better off with combining them to reduce toxicity, as I had originally suggested?

 

2. Would I be better off with a methylphenidate / Adderall combo, as opposed to Modafinil / Adderall, for the sake of blunting some of the toxicity? I can't help but feel that modafinil is less toxic than the methylphenidate stimulant, even if it's less effective as a dopamine reuptake inhibitor than ritalin.

 

3. I already take magnesium every night, and have just ordered magnesium threonate to try to further thwart the NMDA toxicity that you mentioned (since it crosses the BBB better). Re: memantine, are there any risks? Any stronger, natural alternatives than magnesium, or do you think that mag threonate would be sufficient? I also hesitate ordering prescriptions when I may not have to.

 

I exercise regularly, get good sleep, and don't have to worry about eating or drinking adequate water while on Adderall. Do you think that my lifestyle, combined with the above protocol, would have me in a good place for 2-3x/wk with 10-20mg Adderall? I never want to become a vegetable / Alzheimer's / Parkinson's / etc. – if I live until 95 instead of 100, I'm OK with that. But I'm not OK with living until 75 instead of 100, nor living in a wheelchair.

 

No you are better off with modafinil if you insist on a DRI to mitigate neurotoxicity. I mentioned methylphenidate as an example to illustrate that the DRI properties of modafinil are likely the reason why it attenuates neurotoxicity---I would never recommend taking MPH + amphetamine just to prevent neurotoxicity.

 

In these studies, it is important to keep in mind the dosages used for the rodents. They are typically super high dosages of each substance to observe neurotoxicity. Even amphetamine (more so at higher dosages) acts as a DRI. The real question is would adding it make much of a difference in mitigating neurotoxicity for therapeutic dosages? I still would argue that the side effects from pairing a DRI with amphetamine will exceed the possible gain of neuroprotection. Additionally there is weak evidence that modafinil may elevate core body temperature which is proven to worsen neurotoxicity.

 

http://www.ncbi.nlm....pubmed/12433231

 

I seriously recommend monitoring your heart rate and BP if you decide to proceed with the modafinil and amphetamine combination. The potential for dehydration and increased BP can't possibly be good for life extentsion. Perhaps take modafinil every other time you take amphetamine so less strain will be placed on your body over time.

 

Memantine: As for risks, there are a host of side effects with any drug but memantine seems to be rare. It acts on the Alpha7nAChRs as an antagonist which will dull your cognition, for a few weeks until your brain responds by increasing the density of the receptors. I personally would rather be taking memantine rather than modafinil. You mention that you hate ordering prescriptions (I suppose you mean importing medication that requires a prescription)---- Ceretropic offers memantine domestically as a sublingual solution.

 

As for your last question, it certainly sounds sustainable and healthy, even with the modafinil. I recommend having your doctor switch you to Dexedrine rather than Adderall as there will be less parasympathetic effects, which means a healthier heart in the long run. If you want even less PNS stimulation, you could always ask your doctor for a prescription for Desoxyn (dextromethamphetamine).



#11 NeuroGeneration

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Posted 18 July 2014 - 12:11 AM

If you think that Modafinil produces more complication than protection, I'll eliminate it from the stack.

 

Do any of the supplements in my stack stand out to you (for elimination, or to emphasize as particularly valuable)? Do you think I'm missing anything?

 

Finally, is it reasonable to think that I could maintain this routine for a long time span (say, a few years), at the dosages I mentioned, and while taking these preventative measures, without any significant complications? I know you can't conclude anything, but I'm asking for your best judgment (I realize that I may even be overly paranoid about Adderall's negative effects, but reading longecity & PubMed has got me concerned – am I going over the top?).

 

Thanks so much for your help!



#12 M Lad

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Posted 15 August 2014 - 02:57 AM

Adderall + Selegiline = NO NO NO!!!

sorry, just had to add that!

Took the two together many years ago upon my first (and since very few) Adderall RXs.

Hypertensive to the max. and that was prob. with 2.5 deprenyl and 5mg (or no more than 10mg) Addy.

 

My advice, just try Phenylparacetam with deprenyl instead.

 

 


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#13 FW900

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Posted 15 August 2014 - 03:45 AM

Adderall + Selegiline = NO NO NO!!!

sorry, just had to add that!

Took the two together many years ago upon my first (and since very few) Adderall RXs.

Hypertensive to the max. and that was prob. with 2.5 deprenyl and 5mg (or no more than 10mg) Addy.

 

My advice, just try Phenylparacetam with deprenyl instead.

 

 

Phenylpiracetam is not all that safer either. I had extremely high blood pressure with that paired with large amounts of caffeine. Swollen feet.

 

You're concerns are valid but I would like to point out that others did not experience what you did. Yadyada, medicineman, and plenty of others take Adderall/amphetamines in low dosages alongside selegiline. It probably would be best to take selegiline with either Dexedrine or Desoxyn rather than Adderall, as Adderall produces the most PNS stimulation of the three. 


Edited by FW900, 15 August 2014 - 03:46 AM.


#14 crazepharmacist

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Posted 15 August 2014 - 02:20 PM

Bit of an aside here but is L-Dopa safe to occasionally combine with Selegiline? I'm on 5MG daily, orally.



#15 Ruinmir

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Posted 15 August 2014 - 09:08 PM

L-dopa in isolated pharmaceutical form? Or naturally occurring in Mucuna Pruriens? I've taken mucuna while taking selegiline without issue, but the pharmaceutical form apparently has much higher incidence of undesirable effects.

#16 FW900

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Posted 16 August 2014 - 02:09 PM

L-Dopa + Selegiline is a common combination for PD. You should be fine but I don't see what nootropic effects can come of it. Naturally occurring or pharmaceutical shouldn't matter apart from the dosages.



#17 jerrybusey

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Posted 16 August 2014 - 06:07 PM

I only have anecdotal info to add, so take it for what it's worth. Years ago I did low dose selegiline with low dose methylphenidate while I was between doctors and from what I recall it was the best ADD stimulent solution I've used. This was mainly because the combination allowed me to keep the dosage of the methylphenidate very low (I can't remember specifics but it was slightly below typical therapeutic levels) and I didn't see any tolerance build up over the time I was on it and the side effects of the MPH seemed reduced. Granted that was only like two months or so but I was fairly impressed all the same. I haven't tried this with adderall so I can't say whether or not they would work together. If you do try the combo though make sure to start both drugs at super low dosages and work up gradually.



#18 edshak

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Posted 08 September 2014 - 02:26 AM

hey not sure how much I can contribute but I'm interested what you are using the stack for? 

 

I've taken selegiline at medium dose and messed up drinking the wrong energy drink. I wouldn't use the word crisis but it was very obvious and scary, left work a couple hours early. I know you already got one of these stories, mostly posting it to follow since the rest sounds interesting and i'm the same way on old age outlook.

 

still taking selegiline carefully now.



#19 FrogWarrior

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Posted 08 September 2014 - 09:41 AM

In my experience selegiline has no effect on the potency of dexedrine, but I have only tried selegiline tablets which have absolutely no effect on me on their own. Maybe the patch would be different. It doesn't appear to boost dopamine levels as I would have expected. Although I never used selegiline long term, I know that it has an accumalitive effect by gradually lowering MAO_A levels.

 

And in response to M Lad, I took around 40 mg of dexedrine with 20 mg of selegiline and just felt like I was on 40 mg of dexedrine. I suppose different people respond in different ways. Or maybe I have sugar tablets that don't contain selegiline at all. Its a Spanish brand of 5mg selegiline HCl tablets, called Selegelina Davur. I'd probably get more effects from sugar tablets.


Edited by FrogWarrior, 08 September 2014 - 09:47 AM.


#20 FW900

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Posted 08 September 2014 - 01:47 PM

In my experience selegiline has no effect on the potency of dexedrine, but I have only tried selegiline tablets which have absolutely no effect on me on their own. Maybe the patch would be different. It doesn't appear to boost dopamine levels as I would have expected. Although I never used selegiline long term, I know that it has an accumalitive effect by gradually lowering MAO_A levels.

 

And in response to M Lad, I took around 40 mg of dexedrine with 20 mg of selegiline and just felt like I was on 40 mg of dexedrine. I suppose different people respond in different ways. Or maybe I have sugar tablets that don't contain selegiline at all. Its a Spanish brand of 5mg selegiline HCl tablets, called Selegelina Davur. I'd probably get more effects from sugar tablets.

 

It won't inhibit or lower the production of MAO-A in the range of normal dosages (less than 10mg orally). It acts as irreversible inhibitor to MAO-B, I would not say that it "gradually" lowers them. 90% MAO-B inhibition can be achieved in less than a couple of days.

 

It sounds like they are sugar pills, fortunately for you. 20mg of selegiline +40mg of Dexedrine is much too high of a dose in my opinion.



#21 FrogWarrior

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Posted 08 September 2014 - 07:11 PM

 

In my experience selegiline has no effect on the potency of dexedrine, but I have only tried selegiline tablets which have absolutely no effect on me on their own. Maybe the patch would be different. It doesn't appear to boost dopamine levels as I would have expected. Although I never used selegiline long term, I know that it has an accumalitive effect by gradually lowering MAO_A levels.

 

And in response to M Lad, I took around 40 mg of dexedrine with 20 mg of selegiline and just felt like I was on 40 mg of dexedrine. I suppose different people respond in different ways. Or maybe I have sugar tablets that don't contain selegiline at all. Its a Spanish brand of 5mg selegiline HCl tablets, called Selegelina Davur. I'd probably get more effects from sugar tablets.

 

It won't inhibit or lower the production of MAO-A in the range of normal dosages (less than 10mg orally). It acts as irreversible inhibitor to MAO-B, I would not say that it "gradually" lowers them. 90% MAO-B inhibition can be achieved in less than a couple of days.

 

It sounds like they are sugar pills, fortunately for you. 20mg of selegiline +40mg of Dexedrine is much too high of a dose in my opinion.

 

 

Sorry I meant MAO_B. I've been on dexedrine for years but I expected selegiline to have a strong impact on the effects so yeah these must be duds. I wish they would change the laws (which treat adults like children)  and make these compounds available, I want to try selegiline but have no way of obtaining it. I'm a chemist that makes these compounds for the pharmaceutical companie, its ridiculous thtat I have to go through doctors to obtain them. I generally have to explain the pharmacology to the doctors, and even then they'll only prescribe one drug at a time, as if I'm incapable of comprehending the idea of drug interactions. Its thanks to this system that I've destroyed my health, no doctor will prescribe me memantine along side the dexedrine despite the fact that it enables me to use a much lower dose of dexedrine (without an NMDA antagonist, lower doses make me feel terrible), as well as protects my brain from glutamate excitotoxicity.


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#22 edshak

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Posted 11 September 2014 - 03:30 AM

Neurogen- I've taken alcar while training for a run, usually after with food, seems like a popular supplement and felt like it helped with recovery. hard to say how much thou.

 

frog warrior- I guess I could recommend some real selegiline sources as an alternate to dexedrine since I'm not sure how safe taking both would be. At least scaling up slowly, 20 mg alone is 4 times the daily dose to avoid MAOA side effects. taking a sugar pill/no effect was your reason for upping the dose?  let me know if you want those

 

wondering, how long did you take the dex/ sel ?

 

 

 



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#23 medievil

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Posted 12 September 2014 - 03:22 PM

FW900 – thank you for your detailed response. I have a few followup questions, and some stack questions, if you would oblige...

 

1. Modafinil doesn't do much for me, even at 200mg sublingual (if you have any suggestions, I'm all ears!). Since your suggestion of 1 day Adderall, 1 day Modafinil wouldn't be effective for me (since the Modafinil days wouldn't work), would I be better off with combining them to reduce toxicity, as I had originally suggested?

 

2. Would I be better off with a methylphenidate / Adderall combo, as opposed to Modafinil / Adderall, for the sake of blunting some of the toxicity? I can't help but feel that modafinil is less toxic than the methylphenidate stimulant, even if it's less effective as a dopamine reuptake inhibitor than ritalin.

 

3. I already take magnesium every night, and have just ordered magnesium threonate to try to further thwart the NMDA toxicity that you mentioned (since it crosses the BBB better). Re: memantine, are there any risks? Any stronger, natural alternatives than magnesium, or do you think that mag threonate would be sufficient? I also hesitate ordering prescriptions when I may not have to.

 

Here's my revised stack (with questions):

 

30 mins Pre-Adderall:

•Selenium (always w/ iodine)

•NAC

•Liposomal Glutathione

•Ubiquinol or MitoQ

•B's via 2/3 multivitamin (Thorne FX, 2 pills, instead of 3)

 

With Adderall:

•Modafinil or Ritalin

•Grape Seed Extract

•Creatine (for glutamate toxicity)

•Magnesium threonate

•How do you feel about idebenone at this time?

 

End of Day:

•Liposomal Vit C (antioxidants, and to speed up amph clearance from blood)

•Rhodiola / Ashwaganda, for calming effects

•Magnesium Citrate + Zinc

•Melatonin (for neuronal antioxidants, sleep, etc.)

•Trehalose sugar (for autophagy)

•Longvida Curcumin

I'm considering ALCAR, ALA & L-Carnosine. Thoughts? Should it be before, during or after Adderall, if at all?

 

Day After Adderall:

•Liposomal Glutathione (restoring what was used up)

•UMP – restoring dopamine receptors

•Trehalose

•Piracetam (repairing damage)

•Centrophenoxine

•I'm considering adding Jioagulan, CDP choline, inositol on these days, too. Thoughts?

 

 

1x 16-24 hour fast per month for autophagy (without antioxidants), and obviously intend to heavy dose on antioxidants while on Adderall.

 

I exercise regularly, get good sleep, and don't have to worry about eating or drinking adequate water while on Adderall. Do you think that my lifestyle, combined with the above protocol, would have me in a good place for 2-3x/wk with 10-20mg Adderall? I never want to become a vegetable / Alzheimer's / Parkinson's / etc. – if I live until 95 instead of 100, I'm OK with that. But I'm not OK with living until 75 instead of 100, nor living in a wheelchair.

Jeezes id be concerned of the health effects of all those antioxidants, amphetamine on its own is safe but id be very carefull overdoing it on the antioxidants.

 

Taking dris with amphetamine? What is this paranoia its been in clinical use for such a long time and so far noone provided any evidence for adderall toxiticy, same cant be said for antioxidants overdose.







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