• Log in with Facebook Log in with Twitter Log In with Google      Sign In    
  • Create Account
  LongeCity
              Advocacy & Research for Unlimited Lifespans

Photo
- - - - -

deprenyl in younger users: safe?


  • Please log in to reply
14 replies to this topic

#1 brain

  • Guest
  • 148 posts
  • 5

Posted 15 September 2009 - 09:08 AM


so i'm considering going and seeing either my doctor or a psychiatrist to get a prescription for deprenyl. if this proves to be difficult (which i'm suspecting it might?) i may decide to order it online. this is partly motivated by the idea that this will dually help with both my add-pi and my moderate depression. the nootropic benefits are a welcomed plus. i've read here in the past that deprenyl is something which is generally taken by people later in life, also that it may be potentially damaging to less aged subjects.

i've noticed that the Emsam patch (transdermal segeline) is now approved for major depression by the FDA and as far as i'm aware there aren't any age limitations mentioned. the Emsam patch is fucking expensive (500+/month) and so i'd rather go with the segeline tablets which don't seem a whole lot less convenient to take once a day than applying a patch. if i did this i would be purchasing the 5 mg tablets, and i would be taking a full 5 mg, for optimum inhibiton of mao-b. i also notice that the Emsam patches have dosages which exceed 10 mg (6 mg, 10mg, 16 mg?)

i don't particularly care about extending my lifespan, though i also don't want to reduce it drastically or cause any problems, neurological or otherwise. i can't really think of why mao-b inhibition would be contradicted in younger users or what harm this may do. it's worth noting that i probably have a deficiency of dopamine. i'm 20 years old, by the way.

i would be taking this in conjunction with piracetam, alpha-GPC, and possibly phenylalanine or other DA precursors.

thanks!

#2 Animal

  • Guest
  • 689 posts
  • 158
  • Location:UK

Posted 16 September 2009 - 01:02 AM

What country do you live in? I'm also interested in getting a prescription for Deprynl for the same reasons you mention and I'm seeing my psychiatrist on Thursday. Do you take any current prescription medication?

sponsored ad

  • Advert
Click HERE to rent this advertising spot for BRAIN HEALTH to support LongeCity (this will replace the google ad above).

#3 acantelopepope

  • Guest
  • 221 posts
  • 21
  • Location:Thailand

Posted 16 September 2009 - 01:27 AM

What country do you live in? I'm also interested in getting a prescription for Deprynl for the same reasons you mention and I'm seeing my psychiatrist on Thursday. Do you take any current prescription medication?


My Jumex deprenyl just got here today from BioGenesis (https://www.biogenesis-antiaging.com). I am 20 and ordered the deprenyl for the same reasons as mentioned. Another member on these forums told me that Deprenyl could actually decrease long term dopamine production: "Be careful with deprenyl. Chronic use lowers tyrosine hydroxylase so you'll have absolutely NO dopamine production. If you do decide to use it, don't go above 1 drop a week. Trust me on this. To raise dopamine, I found that manganese and tyrosine work very, very well. So well, that I don't feel the depression I used to get with choline supplements. You could try that.."

Anyways, I'm putting the deprenyl, hydergine, and pregnenolone that I received today on hold until I get more green lights... or I become desperate.

#4 Animal

  • Guest
  • 689 posts
  • 158
  • Location:UK

Posted 16 September 2009 - 01:53 AM

Well I've got some manganese on order that should be arriving by the end of this week, and I've also just started taking Mucuna pruriens so hopefully that'll rectify my dopamine deficit. I tried pregnenolone, and although it's not indicated at our ages ( I'm 24) it did seem to have some benefit in terms of memory and mood. The problem is that it gave me mild facial acne after only one week of use, so I've put that on hold for the time being.

#5 brain

  • Topic Starter
  • Guest
  • 148 posts
  • 5

Posted 16 September 2009 - 06:48 AM

What country do you live in? I'm also interested in getting a prescription for Deprynl for the same reasons you mention and I'm seeing my psychiatrist on Thursday. Do you take any current prescription medication?


My Jumex deprenyl just got here today from BioGenesis (https://www.biogenesis-antiaging.com). I am 20 and ordered the deprenyl for the same reasons as mentioned. Another member on these forums told me that Deprenyl could actually decrease long term dopamine production: "Be careful with deprenyl. Chronic use lowers tyrosine hydroxylase so you'll have absolutely NO dopamine production. If you do decide to use it, don't go above 1 drop a week. Trust me on this. To raise dopamine, I found that manganese and tyrosine work very, very well. So well, that I don't feel the depression I used to get with choline supplements. You could try that.."

Anyways, I'm putting the deprenyl, hydergine, and pregnenolone that I received today on hold until I get more green lights... or I become desperate.


this is a little scary. i couldn't find the post you were talking about (could you link me?) but i did find some abstracts on the subject. i think that the user quoted above may be misinterpreting the studies a bit.

Reduced striatal tyrosine hydroxylase activity is not accompanied by change in responsiveness of dopaminergic receptors following chronic treatment with deprenyl

Deprenyl is the only selective monoamine oxidase B (MAO-B) inhibitor that is in clinical use for the treatment of Parkinson's disease. Our previous studies showed that chronic treatment of rats with low (MAO-B selective) doses of deprenyl inhibited dopamine (DA) re-uptake and enhanced DA release in the striatum. These changes could affect DA synthesis rate by activation of negative feedback loops. Chronic deprenyl treatment has also been suggested to cause down-regulation of release-modulating DA receptors. The effects of chronic and acute treatment with deprenyl on ex vivo striatal tyrosine hydroxylase activity were therefore studied, by determination of steady-state tissue level of DOPA following administration of NSD-1015 (100 mg/kg i.p.). In addition, we assessed changes in the in vivo sensitivity of dopaminergic receptors from the reduction in DOPA extracellular level after systemic apomorphine administration (2.5 mg/kg s.c.), following elevation of microdialysate DOPA by systemic or local aromatic amino acid decarboxylase inhibition with NSD-1015. Chronic treatment with deprenyl (0.25 mg/kg s.c. daily for 21 days) caused a significant reduction in tyrosine hydroxylase activity to 60% of control, with no change in the apomorphine-induced reduction of microdialysate DOPA and DOP AC. The reduction in tyrosine hydroxylase activity is compatible with our previous results showing an increase in striatal DA extracellular level following chronic treatment with deprenyl. The increased extracellular striatal DA level could reduce tyrosine hydroxylase activity through activation of a negative feedback loop, by activation of either presynaptic or postsynaptic DA receptors.


the stuff here about negative feedback loops isn't making a whole lot of sense to me, but what i'm gathering from this study is that tyrosine hydroxylase is being reduced as a sort of compensatory mechanism. that is, tyrosine hydroxylase production doesn't need to be anywhere near as high since mao-b is inhibited and there is a whole lot of extra dopamine floating around. so when the stock of dopamine is high production (of TH) ceases. what worried me about that quote is that i feel like it might have implied that the drop in tyrosine hydroxylase was permanent or damaging. i don't think there is anything here to suggest this. the creation of TH will probably go right back up once the addition of deprenyl is removed. it's a homeostatic reaction that'll balance out either which way. you're still getting more dopamine despite the counterbalanced TH level. it's possible that i'm getting this study wrong, so anyone please feel free to chime in.

aside from this, i've found a couple of possibly contradictory studies which seem to suggest that deprenyl actually increases TH:

Résumé / Abstract
Chronic treatment of aged rats with deprenyl prevents age-induced protein oxidation in substantia nigra and protects tyrosine hydroxylase (TH) enzyme against inactivation [11]. With these precedents, we treated adult rats with deprenyl for 3 weeks in order to get further insight in the mechanism by which deprenyl exerts such actions. After completing the treatment, dopamine (DA) levels markedly increased in both striatum and substantia nigra while levels of the acid DA metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), decreased in the two brain areas, thus proving MAO-inhibiting properties of the treatment. We then studied the cellular expression of TH mRNA by in situ hybridization. Following treatment with deprenyl, levels of TH mRNA were significantly higher in individual dopaminergic nigral cell bodies than in those of control rats (+74%). Western blotting analysis of TH enzyme amount revealed a positive effect of the treatment in both the terminal field (+44%) and the cell body region (+31%). This correlation between TH mRNA and amount was also extended to TH enzyme activity in the two brain areas studied, which significantly increased in striatum (+57%) and substantia nigra (+35%) following deprenyl treatment. Taken together, our results clearly suggest a TH-inducing effect of deprenyl in the dopaminergic nigrostriatal system, which seems to be independent of its protective action against oxidative stress described previously. These results expand out knowledge about the beneficial effect of deprenyl in the therapy of Parkinson's disease.


We studied the effects of treatment with (-)-deprenyl, a monoamine oxidase B inhibitor, on plasma levels of insulin-like growth factor-I (IGF-I) (as indicator of growth hormone (GH) secretion), levels of monoamines and their metabolites, and the activity and content of tyrosine hydroxylase - the rate-limiting enzyme in the biosynthesis of catecholamines - in the hypothalamus and hypophysis of old male rats. Male Wistar rats (22 months old) were treated with 2 mg deprenyl/kg body weight s.c. three times a week for 2 months. At the end of the treatment period, blood was collected for measurement of plasma IGF-I levels by radioimmunoassay (RIA). The concentrations of dopamine, serotonin (5-HT) and their main metabolites were determined by high performance liquid chromatography (HPLC) with electrochemical detection, and the tyrosine hydroxylase content in hypothalamus and hypophysis was determined by enzyme-linked immunoabsorbent assay (ELISA). (-)-Deprenyl treatment produced a pronounced increase in dopamine and 5-HT in both the hypothalamus and hypophysis (P < 0.01). The main dopaminergic metabolite, 3,4-dihydroxyphenylacetic acid (DOPAC), decreased in hypothalamus but not in hypophysis, and treatment had no effect on the concentration of 5-hydroxyindole-3-acetic acid (5-HIAA). The tyrosine hydroxylase activity and tyrosine hydroxylase content increased in hypothalamus and hypophysis (P < 0.05). In the hypophysis the increase in tyrosine hydroxylase activity was consistent with the increase in tyrosine hydroxylase amount. Moreover, (-)-deprenyl treatment restored the IGF-I plasma levels in old rats to a concentration similar to those found in young animals. Postulated anti-aging effects of (-)-deprenyl could hence be due to restoration of hypothalamic hormones such as GH.


i think we're at least in the clear on this point. would deprenyl be anywhere as close to as prevalent as it is on this forum or at all if that were true? that isn't even an age-dependent argument against it. dude sounds like he probably misinterpreted some stuff. i also find it hard to believe that tyrosine or manganese are going to do a whole lot of good. maybe in certain rare instances tyrosine may be of some help, but everything i've read suggests that if there are any benefits, they're basically short term. neither tyrosine nor manganese are going to come anywhere close to the therapeutic effect that drugs like deprenyl, amphetamines, DA reuptake inhibitors, etc are going to have.

Edited by brain, 16 September 2009 - 07:05 AM.


#6 brain

  • Topic Starter
  • Guest
  • 148 posts
  • 5

Posted 16 September 2009 - 07:42 AM

What country do you live in? I'm also interested in getting a prescription for Deprynl for the same reasons you mention and I'm seeing my psychiatrist on Thursday. Do you take any current prescription medication?


I live in the US. I'm probably just going to order it online so that i can bypass my parents and my GP, saving them for more imperative and less readily accessible pharmacological exigencies. I'm thinking the liquid citrate variety, based on anecdotal responses and despite of the lack of studies backing it. I'll give my mom a call about it and if it flows over well i'll follow though with it. Stuff seems cheap enough that i'd feel better about acquiring it under the radar.

I don't take anything currently, no.

#7 jasonshadow

  • Guest
  • 30 posts
  • 0

Posted 16 September 2009 - 04:37 PM

What country do you live in? I'm also interested in getting a prescription for Deprynl for the same reasons you mention and I'm seeing my psychiatrist on Thursday. Do you take any current prescription medication?


I live in the US. I'm probably just going to order it online so that i can bypass my parents and my GP, saving them for more imperative and less readily accessible pharmacological exigencies. I'm thinking the liquid citrate variety, based on anecdotal responses and despite of the lack of studies backing it. I'll give my mom a call about it and if it flows over well i'll follow though with it. Stuff seems cheap enough that i'd feel better about acquiring it under the radar.

I don't take anything currently, no.


I have 40 pills of Jumex still in the blister pack for sell for anyone who is interested. (I'm in the US)

#8 kevbo

  • Guest
  • 3 posts
  • 1

Posted 17 September 2009 - 07:01 PM

As per selegiline lowering dopamine - I thought this was part of the anti-oxidant mechanism. Doesn't DA metabolize into a free radical?

In other words, selegiline lowers the total amount of DA, thus reducing the amount of harmful oxidants, while allowing it stay in the synapse much longer.

To the OP: I used to take 5mg of selegiline every day. It made me hypermotivated, but only to do the things I wasn't supposed to be doing. I showed symptoms of antisocial personality disorder and mania. Perhaps I am just extremely sensitive.

#9 brain

  • Topic Starter
  • Guest
  • 148 posts
  • 5

Posted 17 September 2009 - 08:29 PM

As per selegiline lowering dopamine - I thought this was part of the anti-oxidant mechanism. Doesn't DA metabolize into a free radical?

In other words, selegiline lowers the total amount of DA, thus reducing the amount of harmful oxidants, while allowing it stay in the synapse much longer.

To the OP: I used to take 5mg of selegiline every day. It made me hypermotivated, but only to do the things I wasn't supposed to be doing. I showed symptoms of antisocial personality disorder and mania. Perhaps I am just extremely sensitive.


has anyone felt motivated by selegiline in a positive way? say, did it help anyone feel more motivated to be 'productive' or to stay on task with school/work assignments? or feel more focused, calm, patient? i keep hearing a lot about people turning into gambling addicts and sexaholics after taking it, and it's a little worrisome.

can i asked if you leaned towards the direction of APD or mania to begin with?

also: do we understand what the neurochemical underpinnings of this might be? is it possible that selegiline doesn't have executive-function enhancing qualities such as some stimulants do? that it doesn't heighten a grasp the frontal lobes have over the rest of one's brain? how does what selegiline is doing qualitatively and biologically differ from what amphetamines and other adhd drugs do, and would it be naive of me to expect anything close to a similar effect?

Edited by brain, 17 September 2009 - 08:37 PM.


#10 brain

  • Topic Starter
  • Guest
  • 148 posts
  • 5

Posted 17 September 2009 - 08:46 PM

if there is theoretically a heightened level of dopamine which is already active in a synapse while on selegiline, why would one go out and seek these very dopamine-rewarding activities - wouldn't that kind of behavior be indicative of a deficiency? why is there not such an effect from adderal, etc?

Edited by brain, 17 September 2009 - 08:48 PM.


#11 FunkOdyssey

  • Guest
  • 3,443 posts
  • 166
  • Location:Manchester, CT USA

Posted 17 September 2009 - 08:54 PM

May be related to differences in areas where MAO-B is distributed vs. areas where dopamine is released by amphetamine.

#12 acantelopepope

  • Guest
  • 221 posts
  • 21
  • Location:Thailand

Posted 22 September 2009 - 04:25 AM

if there is theoretically a heightened level of dopamine which is already active in a synapse while on selegiline, why would one go out and seek these very dopamine-rewarding activities - wouldn't that kind of behavior be indicative of a deficiency? why is there not such an effect from adderal, etc?


Well, I started taking Hydergine 2.5mg x 2 on Saturday, and so far I really like my improvements in memory, insight, and concentration... it's having the side benefit of improving my mood. I've also been taking 1000mg DLPA x 2, with Dopa Mucunus... among many others. I have been taking 75mg Wellbutrin SR for the past week, and tomorrow I'm cutting it out entirely.

The reason I'm posting this is that tomorrow I've decided to dry 5mg deprenyl with my morning stack. As far as I know the effect is pretty immediate... anyways, It can't hurt, right?


edit: that's 75mg wellbutrin down from 150mg, which was also a step down from 300mg I was taking for a couple months before that.

Edited by acantelopepope, 22 September 2009 - 04:26 AM.


#13 shifter

  • Guest
  • 716 posts
  • 5

Posted 22 September 2009 - 04:58 AM

I remember seeing on the news how parkisons disease medication have lead old men being addicted to gambling and hookers. The didn't say what medication it was but I'm pretty sure selegiline would have been in the mix.

I suppose you would have to be already inclined to that sort of behaviour to take up the activity, but I guess it wouldn't only be restricted to gambling and hookers. When I was on it, I was a crazy ebay buyer with a new facination in geology. Maybe it turned me into a shopoholic :p I doubt it but maybe some clicks of the mouse or my new interest were related to the selegiline :p

I was taking the 5mg per day tablets from the doctor (got a presription for it and I'm only 27). However as some doctors weren't happy I was on it and I was using it for a use it was not licenced for, I will get all future orders online.

#14 FunkOdyssey

  • Guest
  • 3,443 posts
  • 166
  • Location:Manchester, CT USA

Posted 22 September 2009 - 03:59 PM

Actually it is usually dopamine agonists (like pramipexole) alone or a combination of dopamine agonists with levodopa that produces the hedonistic addictions. I've never seen deprenyl implicated there.

sponsored ad

  • Advert
Click HERE to rent this advertising spot for BRAIN HEALTH to support LongeCity (this will replace the google ad above).

#15 the_colossus

  • Guest
  • 61 posts
  • -5

Posted 09 December 2009 - 02:45 AM

What country do you live in? I'm also interested in getting a prescription for Deprynl for the same reasons you mention and I'm seeing my psychiatrist on Thursday. Do you take any current prescription medication?


My Jumex deprenyl just got here today from BioGenesis (https://www.biogenesis-antiaging.com). I am 20 and ordered the deprenyl for the same reasons as mentioned. Another member on these forums told me that Deprenyl could actually decrease long term dopamine production: "Be careful with deprenyl. Chronic use lowers tyrosine hydroxylase so you'll have absolutely NO dopamine production. If you do decide to use it, don't go above 1 drop a week. Trust me on this. To raise dopamine, I found that manganese and tyrosine work very, very well. So well, that I don't feel the depression I used to get with choline supplements. You could try that.."

Anyways, I'm putting the deprenyl, hydergine, and pregnenolone that I received today on hold until I get more green lights... or I become desperate.


I started taking 5htp 2 years ago and I've been experiencing a slow but steady decline in motivation, concentration, everything relating to a dopamine reduction. It wasn't until I read that anything boosting 5htp can reduce dopamine over time. Dopamine and Serotonin have a relationship, boosting one can cause the other one to be steadily reduced. This would apply to people taking just dopamine boosters as well.

http://www.chknutrit...emistry.htm#ddd

As that is a site which sells both one always must be very skeptical about the theory it adds. It makes sense and its a possibility for why I have the problems that I do. Im testing it out and hopefully dopamine boosters can fix my problem, otherwise I'd have to cut off 5htp and hope dopamine levels return to normal. I've independently heard many people say you should take tyrosine with 5htp, so its not just one website saying that. I've tried tyrosine, doesn't work for me, strattera did except it gave me insomnia. So Im searching for the right booster. Hopefully deprenyl works, if not I'd go for another ADD med.

Edited by the_colossus, 09 December 2009 - 02:46 AM.





0 user(s) are reading this topic

0 members, 0 guests, 0 anonymous users