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#1 mentatpsi

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Posted 20 March 2009 - 06:10 PM


I'm not sure how many people are familiar with the underlying literature of why Deprenyl is believed to have its anti aging properties. I've read one study (of course this was in Smart Drugs II) depicting the ever decreasing amount of dopamine through our life and the reaching of 10% of base levels as a cause.

Now is it not possible that Adderall does the same thing. It just bothers me because Adderall is given really bad press (a lot of it probably the back lash of the Scientology movement on Ritalin). But from what i've heard of both hydergine (+experienced) and deprenyl, the psychological side effects are quite similar. I'm not too aware of the biological side effects of Deprenyl, but i imagine taking a rather potent antioxidant like Idebenone & Alpha Lipoic Acid in conjunction to Adderall, the possible oxidation might not be so bad.

I've also heard of more brain usage (through MRI scans) under the effects of Adderall. The main concern is cardiovascular risks, which seem to be of particular concern after reaching a certain age more so than in youth (if no pre existing deficits are present). At this age it perhaps seems more appropriate to monitor the body, and perhaps switch to Deprenyl.

What do you guys think?
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#2 luv2increase

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Posted 20 March 2009 - 09:12 PM

I'm not sure how many people are familiar with the underlying literature of why Deprenyl is believed to have its anti aging properties. I've read one study (of course this was in Smart Drugs II) depicting the ever decreasing amount of dopamine through our life and the reaching of 10% of base levels as a cause.

Now is it not possible that Adderall does the same thing. It just bothers me because Adderall is given really bad press (a lot of it probably the back lash of the Scientology movement on Ritalin). But from what i've heard of both hydergine (+experienced) and deprenyl, the psychological side effects are quite similar. I'm not too aware of the biological side effects of Deprenyl, but i imagine taking a rather potent antioxidant like Idebenone & Alpha Lipoic Acid in conjunction to Adderall, the possible oxidation might not be so bad.

I've also heard of more brain usage (through MRI scans) under the effects of Adderall. The main concern is cardiovascular risks, which seem to be of particular concern after reaching a certain age more so than in youth (if no pre existing deficits are present). At this age it perhaps seems more appropriate to monitor the body, and perhaps switch to Deprenyl.

What do you guys think?



No, adderall is not anti-aging.

If you are taking it, I suggest halting its use. It will ruin your brain.
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#3 Zosimos

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Posted 20 March 2009 - 09:28 PM

I'm not sure how many people are familiar with the underlying literature of why Deprenyl is believed to have its anti aging properties. I've read one study (of course this was in Smart Drugs II) depicting the ever decreasing amount of dopamine through our life and the reaching of 10% of base levels as a cause.

Now is it not possible that Adderall does the same thing. It just bothers me because Adderall is given really bad press (a lot of it probably the back lash of the Scientology movement on Ritalin). But from what i've heard of both hydergine (+experienced) and deprenyl, the psychological side effects are quite similar. I'm not too aware of the biological side effects of Deprenyl, but i imagine taking a rather potent antioxidant like Idebenone & Alpha Lipoic Acid in conjunction to Adderall, the possible oxidation might not be so bad.

I've also heard of more brain usage (through MRI scans) under the effects of Adderall. The main concern is cardiovascular risks, which seem to be of particular concern after reaching a certain age more so than in youth (if no pre existing deficits are present). At this age it perhaps seems more appropriate to monitor the body, and perhaps switch to Deprenyl.

What do you guys think?



No, adderall is not anti-aging.

If you are taking it, I suggest halting its use. It will ruin your brain.



luv2increase, your timeless wisdom is supremely appreciated. Would you please be so kind as to spoil us infinitismally incompetent human beings as to why adderall (taken in appropriate dosages under the supervision of medical professionals) ruins brains? Of preference are clinically conducted studies of the random sampling sort involving human beings (healthy and non-healthy, studies of both would be informative). It goes without saying that said studies should be conducted by well-respected and well-studied individuals with a high school diploma at the very minimum.

I know that may be asking too much, and I won't be too surprised (I may even be a little understanding, given your level of intelligence) if you return with studies performed on rats by peruvians in coke labs, or even some involving individuals with brains that were "ruined" prior to initial exposure to the drug.

I'm looking forward to learning why governmental agencies approve drugs that could wreak such havoc on our most precious (or second most precious, as Woody Allen would like to say) organ.
Thanks!
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#4 bgwithadd

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Posted 20 March 2009 - 10:48 PM

The antiaging properties of deprenyl are totally separate from its MAO-B/dopamine effects. That's why it's pretty silly to see people who take it weekly expecting antiaging effects.

If anything, adderall is a pro aging drug, in a very real sense. Not so much that it will shorten lifespan but it has bad effects on your skin and that will make you look like the marlboro man with enough use.

As for adderall wrecking your brain goes, I'd say it definitely can in high doses, but amphetamines have been around 70+ years and plenty of famous people have taken high doses of stimulants for 40, even 50 years without 'wrecking their brain'. William F Buckley was a ritalin addict 40+ years, and he seemed sharp enough to me. I used to be more concerned about brain damage, but the damange amphetamines do is mostly to dopamine production...and that is pretty easy to up, using deprenyl, wellbutrin, stims, etc. It's not something to take lightly, but the fact of the matter is virtually everything's neurotoxic, and as you mention your brain simply deteriorates over time anyway.

Even dopamine itself is neurotoxic! Ultimately it comes down to the fact we are dying, and there's nothing (currently) we can due to completely stop that. Many other psych drugs do far more neurologic damage than stimulants. They are actually probably the safest of psych drugs so long as they are used with some semblance of caution...but that does not say much, really. Almost all psych drugs have potentially horrible, permanent or semipermanent negative effects. It really shocks me how antipsychotics get passed around like candy, when just a few weeks on them can be completely liferuining.

If you start taking adderall, you better realize going in it is probably a lifetime commitment, whether you want that or not. But, if you actually NEED it, you have a lifetime problem that can't be fixed in any other way already.

Also, if you do, neuroprotection and neurogenesis becomes much more important for you than other people. Some lithium orotate or other nerve growing agents might be a smart idea.
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#5 k10

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Posted 22 March 2009 - 03:28 AM

And all amphetamines have been shown to cause cancer.

It is wishful thinking on your part to even think that it could be anti-aging.
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#6 Steve_86

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Posted 22 March 2009 - 04:55 AM

And all amphetamines have been shown to cause cancer.

It is wishful thinking on your part to even think that it could be anti-aging.


Do you have any evidence to back up that dextroamphetamine causes cancer?
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#7 mentatpsi

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Posted 22 March 2009 - 05:28 AM

I believe Ritalin has been studied extensively and has not been shown to cause cancer, nor has Adderall. If you want to suggest that, post a link. I hope i don't come off harsh, but remarks like that are usually personal bias.


Thanks bgwithadd, informative reply ;). Do you know primarily how it damages dopamine production? It's an interesting topic to consider.
Now Deprenyl seems to improve an area of the brain associated with dopamine production. So i suppose from a holistic profile Deprenyl is a better choice (in the condition it works adequately).
I also read you're taking both, and from the knowledge represented in your writing i assume it's working nicely?
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#8 bgwithadd

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Posted 22 March 2009 - 05:59 AM

I do ok with both. I maybe get more of the dopamine effects of adderall while taking deprenyl, and I think it lasts slightly longer, but it did not cause dramatic differences.

Basically, the reason that adderall causes neurotoxicity is that it increases dopamine transportation, not that it increases dopamine production. It acts as a neuromodulator in the brain. You get too much in the receptor site and it bursts like a bubble. From what I've read, pretty much any time you experience euphoria, this is what's happening, though not necessarily by the same mechanism. Any time you feel euphoric, it's basically your cells literally bursting with joy and dying off. I guess I should not have said dopamine production, it's more that your brain can't make use of it as easily any more. But, as I said while it's not exactly a pleasant prospect, it's something you can deal with via medication except in the most extreme cases. You can also get serotonergic neurotoxicity at high doses which is really bad, but that should not be an issue at anything approaching therapeutic doses, but only when snorting. Meth neurotoxicity is exactly the same, but meth is about 8 times more powerful so it causes a lot more damage...but even in the most rabid meth users the damage shown was like 5% reduction after several years of use. When you consider you naturally lose 10% per decade, even at the upper reachs of abuse it's probably not as severe as you might think.

Cocaine/ritalin don't change transportation, they work as reuptake inhibitors for dopamine. Like prozac for the dopamine system. They still cause some neurotoxicity in other ways, but they don't have this mechanism...of course, tritalin doesn'tt work for shit for ADD compared to adderall, either.

I guess the moral is that if you use high amounts, you will have big problems, and (hopefully/seemingly) at lower doses few or no problems. I have only ever gotten the slightest hints of euphoria while taking it, but I try to limit my dosing and don't chase the high like many do, but (sadly for people who enjoy it recreationally) the actual euphoria is what's causing the damage, so there's no way to block that out. For me, the physical effects get to be too much too quick to even enjoy snorting if I wanted to, but everyone responds differently.
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#9 yoyo

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Posted 22 March 2009 - 10:33 AM

pros: improved catecholaminergic neuron activity*
much more specific, can be timed to activity one wants to reinforce, as opposed to always-on effect of deprenyl

cons: no propargyl group like deprenyl to upregulate enzyme activity
short, reversable MAO inhibition doesn't give 24/7 protection against MAO-produced toxins


at least in stroke, also evidence in pre-adolescence. not a lot of money to give 'healthy' people amphetamine, at least in moderate dosages. i think most useful for time when trying to instigate behavioral changes.


Enhanced Neocortical Neural Sprouting, Synaptogenesis, and Behavioral Recovery With D-Amphetamine Therapy After Neocortical Infarction in Rats
R. Paul Stroemer, PhD; Thomas A. Kent, MD; Claire E. Hulsebosch, PhD

From the School of Biological Sciences, Division of Neuroscience, University of Manchester, Manchester, England (R.P.S.), and Departments of Neurology (T.A.K.) and Anatomy and Neurosciences and Marine Biomedical Institute (C.E.H.), University of Texas Medical Branch, Galveston.

Correspondence to Dr C.E. Hulsebosch, Department of Anatomy and Neurosciences, 301 University Blvd 1069, University of Texas Medical Branch, Galveston, TX 77555-1069. E-mail CEHulseb@utmb.edu

Background and Purpose—D-Amphetamine administration increases behavioral recovery after various cortical lesions including cortical ablations, contusions, and focal ischemia in animals and after stroke in humans. The purpose of the present study was to test the enhanced behavioral recovery and increased expression of proteins involved in neurite growth and synaptogenesis in D-amphetamine–treated rats compared with vehicle-treated controls after a focal neocortical infarct.

Methods—Unilateral neocortical ischemia was induced in male spontaneously hypertensive Wistar rats (n=8 per time point per group) by permanently occluding the distal middle cerebral artery and ipsilateral common carotid artery in 2 groups of rats: D-amphetamine treated (2 mg/kg IP injections) and vehicle treated (saline IP injections). To determine the spatial and temporal distribution of neurite growth and/or synaptogenesis, growth-associated protein (GAP-43), a protein expressed on axonal growth cones, and synaptophysin, a calcium-binding protein found on synaptic vesicles, were examined by immunohistochemical techniques, and both density and distribution of reaction product were measured. Since the resulting infarction included a portion of the forelimb neocortex, behavioral assessments of forelimb function using the foot-fault test of Hernandez and Schallert were performed on the same rats used for immunohistochemical studies during the period of drug action and 24 hours later. A Morris water maze and other indices of behavioral assays were also measured similarly. Recovery times were 3, 7, 14, 30, and 60 days postoperatively.

Results—Both GAP-43 and synaptophysin proteins demonstrated statistically significant increases in density and distribution of immunoreaction product as determined by optical density measurements in the neocortex of the infarcted group treated with D-amphetamines compared with vehicle-treated infarcted controls. The GAP-43 was elevated to statistically significant levels in forelimb, hindlimb, and parietal neocortical regions ipsilateral to the infarction only at days 3, 7, and 14. By contrast, the synaptophysin demonstrated no statistically significant changes in expression at 3 or 7 days but demonstrated statistically significant increases at 14, 30, and 60 days in the forelimb, hindlimb, and parietal neocortical regions ipsilateral to the infarction as well as increased distribution in the contralateral parietal neocortex. Behavioral assessment of forelimb function indicated that improved recovery of forelimb placement on the side contralateral to the infarction was statistically significant in the D-amphetamine–treated group compared with the vehicle-treated group (P<0.025). Spatial memory, as measured with the Morris water maze, worsened in the vehicle-treated group compared with the D-amphetamine–treated group at 60 days (P<0.025).

Conclusions—These data support the occurrence of neurite growth followed by synaptogenesis in the neocortex in a pattern that corresponds both spatially and temporally with behavioral recovery that is accelerated by D-amphetamine treatment. While the specific mechanisms responsible for D-amphetamine–promoted expression of proteins involved in neurite growth and synaptogenesis and of enhanced behavioral recovery are not known, it is suggested that protein upregulation occurs as a result of functional activation of pathways able to remodel in response to active behavioral performance.

also, this was interesting:

Noradrenaline provides long-term protection to dopaminergic neurons by reducing oxidative stress
Jean-Denis Troadec,* Marc Marien,† Frédéric Darios 1 , Andreas Hartmann,* Merle Ruberg,* Francis Colpaert† and Patrick P. Michel,*,†
*INSERM U289, Experimental Neurology and Therapeutics, Hôpital de la Salpêtrière, Paris, France
†Centre de Recherche Pierre Fabre, Castres, France
Address correspondence and reprint requests to Patrick P. Michel, INSERM U289, Hôpital de la Salpêtrière, 47 boulevard de l'hôpital, 75013, Paris, France. E-mail: ppmichel@ccr.jussieu.fr
Copyright International Society for Neurochemistry
KEYWORDS
catechol • dopamine neurons • neuroprotection • noradrenaline • oxidative stress
ABSTRACT

To better understand the neurotrophic function of the neurotransmitter noradrenaline, we have developed a model of mesencephalic cultures in which we find low concentrations (0.3–10 µm) of noradrenaline to be remarkably effective in promoting long-term survival and function of dopaminergic neurons. This protective action reproduced the effect of caspase inhibition. It was atypical in that it occurred independently of adrenoceptor activation and was mimicked by some antioxidants, redox metal chelators and the hydroxyl radical detoxifying enzyme catalase. Interestingly, intracellular reactive oxygen species (ROS) were drastically reduced by treatment with noradrenaline, indicating that the neurotransmitter itself acted as an antioxidant. Prevention of oxidative stress was, however, independent of the glutathione antioxidant defense system. Chemical analogues of noradrenaline bearing two free hydroxyl groups in the ortho position of the aromatic ring (o-catechols), as well as o-catechol itself, mimicked the survival promoting effects of the neurotransmitter, suggesting that this diphenolic structure was critical for both neuroprotection and reduction of ROS production. Paradoxically, the autoxidation of noradrenaline and the ensuing production of quinone metabolites may be required for both effects, as the neurotransmitter was spontaneously and rapidly degraded over time in the culture medium. These results support the concept that central noradrenergic mechanisms have a neuroprotective role, perhaps in part by reducing oxidative stress.
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#10 k10

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Posted 22 March 2009 - 06:29 PM

And all amphetamines have been shown to cause cancer.

It is wishful thinking on your part to even think that it could be anti-aging.


Do you have any evidence to back up that dextroamphetamine causes cancer?


Amphetamines Cause Cancer:
http://www.imminst.o...showtopic=26930
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#11 mentatpsi

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Posted 22 March 2009 - 10:03 PM

And all amphetamines have been shown to cause cancer.

It is wishful thinking on your part to even think that it could be anti-aging.


Do you have any evidence to back up that dextroamphetamine causes cancer?


Amphetamines Cause Cancer:
http://www.imminst.o...showtopic=26930


nice reply ;). Thanks for the info. Is Ritalin included in these research articles as well because i couldn't find Ritalin? I'm not nitpicking just interested if i missed it. If it's in there let me know.

Also Deprenyl metabolites also include Amphetamine don't they?

It's possible these studies refer primarily to recreational usage of these drugs, but after closer examination of some of the dosages (0.4 mg/kg) ~= 27.2 mg in 68 kg body, i might be mistaken. It is also interesting to note the injection of this compound rather than the oral intake as far as this study goes, but this is a minor argument.

Thanks again for posting your finds.
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#12 k10

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Posted 23 March 2009 - 12:35 AM

I'm unsure if methylphenidate has the same risks. It works in a different way than amphetamines do so I wouldn't come to the same conclusions based on those studies, which only looked at different types of amphetamines, not methylphenidate,

Cancer.
Scientists looking for evidence that methylphenidate causes cancer in rats and humans have instead found lower-than-normal incidence of the disease. In one experiment mice developed liver tumors after receiving many times the therapeutic dose, but the strain of mice used is prone to such tumors, so scientists are uncertain about what the experiment means.


Then there is one study that apparently shows a link between methlphenidate and cancer:
http://thelastpsychi...ses_cancer.html

And here is a comment left by someone on that blog,

The El Zein Study isn't crap, I can assure you. I have a daughter who was on ritalin nearly 8 years. She has aplastic anemia, bad stuff, and often the precursor to leukemia. They'll never do a study lasting that long. I know of others too, some who have died from leukemia related to ritalin exposure, and another who was 19 died of liver cancer just this year, he was on ritalin 10 years. The pyschiatrists don't know what they're doing. God help America's children. Currently there are 5 million Rx's of ritalin filled per day in America.


However, I would think that anything that causes increased amounts of stress would also result in an increase risk of cancer. Stress has been directly linked to cancer. Stimulants stress the body.

Chronic stress promotes tumor growth and angiogenesis in a mouse model of ovarian carcinoma.

Department of Gynecologic Oncology, University of Texas (U.T.) M.D. Anderson Cancer Center, 1155 Herman Pressler, Unit 1362, Houston, Texas 77030, USA.

Stress can alter immunological, neurochemical and endocrinological functions, but its role in cancer progression is not well understood. Here, we show that chronic behavioral stress results in higher levels of tissue catecholamines, greater tumor burden and more invasive growth of ovarian carcinoma cells in an orthotopic mouse model. These effects are mediated primarily through activation of the tumor cell cyclic AMP (cAMP)-protein kinase A (PKA) signaling pathway by the beta(2) adrenergic receptor (encoded by ADRB2). Tumors in stressed animals showed markedly increased vascularization and enhanced expression of VEGF, MMP2 and MMP9, and we found that angiogenic processes mediated the effects of stress on tumor growth in vivo. These data identify beta-adrenergic activation of the cAMP-PKA signaling pathway as a major mechanism by which behavioral stress can enhance tumor angiogenesis in vivo and thereby promote malignant cell growth. These data also suggest that blocking ADRB-mediated angiogenesis could have therapeutic implications for the management of ovarian cancer.

http://www.ncbi.nlm....l=pubmed_docsum
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#13 bgwithadd

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Posted 23 March 2009 - 03:09 AM

If you need them, they reduce your stress a great deal. That's a lot of (most of?) how they work, to simplify things dramatically.
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#14 mentatpsi

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Posted 26 March 2009 - 07:43 AM

The more i think about it, the more it seems if Deprenyl works, it would be a more appropriate decision. Adderall may be safe, even though the evidence k10 had posted states the opposite, but given the dependency it creates. It seems foolish to rely on it for a good portion of one's life given later possibilities of cardiovascular impairments which would prevent the intake of the substance.

I'm still a bit confused though, isn't one of the metabolites of Deprenyl l-amphetamine?

Lastly, sorry for posting it with the subtopic chosen. It was misleading, as if i had evidence for it. It was just a thought I was playing around with.

Edited by mysticpsi, 26 March 2009 - 07:45 AM.

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#15 bgwithadd

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Posted 26 March 2009 - 08:12 AM

Unless you have serious attentional problems, there's no good reason to ever take adderall, and every reason not to. Even as a recreational drug I'd say take cocaine over amphetamine any day of the week, if you enjoy having a functional brain.

It's true that deprenyl metabolizes to l-amp and l-methamp. So, it might well have some neurotoxicity, but I believe that the issue with neurotoxicity could be compared to working your brain cells to death. At low doses I am guessing there's no danger at all, and at very high doses that the damage is not just linear but exponential.
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