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Antioxidants as euphoriants?

2

25-DM-4-LYFE

Greenlighter
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Aug 16, 2009
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27
After a long day of semi-intellectual labor on stimulants I, like many others, try to unwind with some kind of a euphoriant or what the french might call a stupificant. Unfortunately, I find frequent use of cannabis and/or EtOH untenable due to issues they both cause with my sleeping and clarity of thought. I have recently found that a number of drugs sold as a nootropics/neutriceuticals/antioxidants produce (paradoxical) stupefying, euphoriant effects at medium/high doses. Specifically Idebenone and N-Acetylcarnitine produce this effect strongly, and to a lesser extent I get a mood-lifting euphoriant effect from alpha lipoic acid. My question is this: is the euphoria derived from some feature intrinsic to these molecules (e.g. interaction with various NT systems) or is the prevention of oxidative stress, in and of itself, pleasurable?
 
Also as a semi-OT aside, the 2002 paper Role of mitochondria in oxidative stress and aging. states that, "Short-chain coenzyme Q analogues enhance superoxide formation, presumably by mediating electron transfer from N2 to oxygen. The clinically used CoQ analogue idebenone is particularly effective, raising doubts about its safety as a drug." So perhaps my question could also be reversed, can oxidative stress produce euphoria in and of itself?
 
Outta curiosity what for you is a medium-high dose and exactly how noticable is this effect, is this a mild moodlift like an antideppresant or do you consider these things to give you a high
 
stupificants to me mean drugs like anesthetics, stupificants where used in surgury.

I have recently indulged in garlic to qualm me at the end of binging behavior, since its a source of nac.
oh yeah, I was thinking of my friend said organic tobacco was a source of longevity and intelligence boosting, and its benifit was a mechanism of superoxide dimutase, which is similar to rooibor or a similar South american tree(which has use in pain releif)
 
Acetyl-L-carnitine in particular has a structure highly remniscient of the GHB agonist GABOB; it seems possible that if N-demethylation is a major metabolic pathway, it could enter the brain and activate GHB receptors.

Idebenone is kind of a different story -- it prevents neurotoxicity induced by kainate receptor activation but the mechanism for doing so is not mentioned. It does not displace ligands from the kainate/quisqualate receptors.

http://www.sciencedirect.com/scienc...fb9b79aec78bb36b7dd39d3717d30724&searchtype=a
 
atara, you mean GABA ? I cannot find info on GABAB, but seems to lead me to GABA each time i try to get some information. It is either GABA slightly modified or maybe there is some confusion.

on topic about GABA, can it really be neuroprotectant ? if so maybe anything that influences GABA in moderate doses (like alcohol) can play a positive role.
 
holy shit that it starts out about smoking it wtf. Also it just burning the shit out of my mouth and smelling is a NEUTRAL OR BAD EFFECT.
 
sorry to interrupt your teen jokes, but can we stick to topic k tnx.
 
asecin said:
atara, you mean GABA ? I cannot find info on GABAB, but seems to lead me to GABA each time i try to get some information. It is either GABA slightly modified or maybe there is some confusion.

on topic about GABA, can it really be neuroprotectant ? if so maybe anything that influences GABA in moderate doses (like alcohol) can play a positive role.
Click to expand...

You can't find info on GABAB because that is not what Atara typed. GABOB.....gamma-Amino-beta-hydroxybutyric acid. . GABA with an OH group on the beta carbon. Check it out. Used as a medication in some places...and I think maybe it is naturally found in the body as well? I found it very underwhelming , but interesting stuff nonetheless.
 
yeh i did i just dont get whats huge difference if you take GABA vs GABOB.
 
asecin said:
atara, you mean GABA ? I cannot find info on GABAB, but seems to lead me to GABA each time i try to get some information. It is either GABA slightly modified or maybe there is some confusion.

on topic about GABA, can it really be neuroprotectant ? if so maybe anything that influences GABA in moderate doses (like alcohol) can play a positive role.
Click to expand...

GABOB. Gee-Eh?-Bee-Oh!-Bee. Gamma-amino-beta-hydroxy-butyric acid.

The GHB agonist GABOB, and therefore, surely retaining potential as a mild euphoriant.
 
atara help me out here with GABOB vs GABA. it seems one is harder to acquire, GABOB, compared to other but im trying to see how they are different and similar in ways.
 
Oxidative stress plays a complex role in the brain. Exessive reactive oxygen species production has been shown in both animal and human studies to be found during psychological stress or use of rewarding drugs like stimulants and opioids. On the other hand free radicals are thought to be generated in the eyes when exposed to sun light and acting as signalling molecules modify particular proteins resulting in an antidepressant affect. Note this is only the case when free radicals are carefuly controlled by the body, but that in general free radicals are more associated with negative mood states and mental health or neurological problems.
The uforia you feel from antioxidents, may be an indirect affect on mood, in that they eliminate free radicals, prevent oxidative stress and thereby theoreticly reduce or abolish angziogenic and depressive feelings associated with oxidative stress. If there is no down/negative ones, and the reward system is functioning properly, then the only feeling left is pleasure.
In addition, antioxidents protect the reward system, which is very susseptable to oxidation, therefore, possibly amplifying its signalling output.
 
That nootropic antioxidant Emoxypine from Russia has some interesting properties. It raises dopamine levels (okay, in rodents, but still) for example. And when taking it 3-4x daily at 125mg as recommended, it literally erases any rebound / after-effects (and possibly even tolerance development) from dopaminergic stimulants for me ... this is most pronounced with isopropylphenidate because this one is the most selective DRI (it might actually be a DAT inverse agonist, but that's another topic) I know of that's also reasonably safe to use. This combination somewhat takes the IPPD finally out of the 'scheduled' list of psychostimulants and puts it aside modafinil as a very, very clean and really manageable substance that has few urge to redose at all etc.. (but I really prefer the IPPD, it's actually anxiolytic)

Oxidative stress seems to be involved in some major neurological diseases as well as depression / etc. mental disorders especially from chronic stress!

But this thread is a tad old, yet interesting topic! :)
 
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I doubt that oxidative stress is uforic in most cases, although nitric oxide, a free radical and cause of oxidative stress, is involved in the development of reenforcement and addiction to amphetamines and cocaine. However, this may have more to do with memory retention rather than modulation of the hedonic response by nitric oxide.
Also, be aware that superoxide, and peroxinitrite, the product of superoxide and nitric oxide, are key mediaters of pain, depression, and long turm tolerance and loss of pleasureable response to all uforic and addictive drugs. You should never try to increase superoxide levels, particularly in the brain. Superoxide and its breakdown product hydrogen peroxide above the safe and very low levels, are leathal to dopamine neurons, we all relie on for motivation, movement and pleasure.
 
Have you tried that antioxidant with out coadministration of stimulants, it would be interesting to see your response and test my theory.
 
Taken alone I don't feel anything (at regular dosages), I've read some reports that it can become rather sedating especially at higher dosages though. But should try it for a few days to see if it would alleviate things like morning headaches etc. which are more pronounced when using stimulants (and the IPPD doses I use are really low, 5mg is already a decent dose for me and I rarely go above 15mg/d.. can't believe some are taking hundreds of mg's in a single night and then wonder why they are wasted the day after) but I could very well have oxidative stress unrelated to stimulants - I've just came across NADPH oxidase recently which might be a relevant factor in depression, it leads to more free glutamate and is a major source of superoxide (at least that's how I understand it currently) and inhibiting NADPHo even prevents a good deal of the DA neuron loss from that nasty toxin MPTP+. This together with some inflammation-related response resulting in an increased expression of interleukin-6 which is all related in a very complex way (like always when it comes to neurobiology ;)).

I'm running out of the emoxypine, but as it really had better effects than I'd expected, I'll continue researching about it... N-acetyl cysteine maybe also makes an interesting candidate.

Btw, there is one user here on BL (I'll post the link later if I find it) who claimed to have gotten euphoric reactions from emoxypine!
 
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