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  • N&PD Moderators: Skorpio | someguyontheinternet

Cleanest stims for chronic use?

Ya my amp tolerance is kind of high atm.

I don't really like pramiracetam on it's own. I first combined DMAE with it, then added picatertam, and already took a booster of aniracetam.
I'd much rather take 2-FMA orally myself now too, but my supply was running low.

I pop fish oil with both pramiracetam and aniracetam, because they're fat soluble. I'm not sure this even helps, but I just take them when I take my fish oil anyways.
 
I wouldn't advise taking *any* methamphetamine derivative with regularity due to the well known neurotoxic effects.

I think the "nicest" stimulants are probably caffeine (and related xanthines, yerba mate is esp. good) or plain old dextroamphetamine in reasonably small doses. (<15mg)
Methylphenidate actually has a pretty tolerable side effect profile when used in moderation as well.
 
Modafinil, MPH, and caffeine probably win this contest, but it seems like a love it or hate it situation with DRI's and caffeine in general. However, there are some VERY interesting modafinil analogs in the pipeline right now.
 
In my personal experience, caffeine is the worst for me. Being bi-polar, xanthines trigger mania. Great if it only goes to hypomania, horrible if it goes to hypermania.

I've tried adderall and it honestly is too jittery for me and gives me bad body odor, and most I ever did was 60mg in one day.

The best I've found at -therapeutic- dosages (15 to 30mg at most twice a day) is unfortunately one with a very bad reputation. When I found out that people recreationally do meth orally at 200mg... I was shocked. I can't imagine what that's like. Before I ever did it, I looked up the dosage strengths of Desoxyn (prescription methamphetamine) and accounted for likely impurities so instead of taking 5 or 10mg (hard to measure anyways at that small of dose), decided on 15 to 30.

15 to 30mg of meth is about the equivalent of a 15 to 30mg adderall to me, feels far cleaner, no body odor, and no jitteriness.

I only use it maybe a 5 days a month, and like any other drug I take, if it ever stops working I don't up the dose, I find something else.

At one point when work was busy as hell I was on a bi-weekly rotating schedule of caffeine then coke then meth. But once work slowed down I stopped altogether my stim usage except occasional bump of coke when I need to stay awake for another hour for some reason.

Though I know there is such a heavy stigma attached to it, responsible/therapeutic use is possible. Whether or not you have the ability to refrain from upping doses or seeking a "high" from it is a personal question though.
 
Dextromethylphenidate wins this contest in regards to prescription stimulants. Subjective toxicity is significantly less than dextroamphetamine. Fewer psychiatric ADR's than d-amphetamine. Fewer drug interactions.

I will be quite frank here. I myself have been using d-MPH with some regularity for quite a number of years now. I have an 'off and on' relationship with the drug, meaning that I will either take the drug regularly in rather significant doses (30-50mg/day) or I will not take it at all for long periods of time. The risk of MPH in particular is the logical allure to administer the drug via insufflation given the very tangible reward over oral administration. With d-amphetamine sulfate preparations, this route is not nearly as enticing. Mixed salt amphetamine preparations have some insufflation allure, but this is largely a function of high dose formulations. In other words, 5 mg d-amphetamine tablets are logistically harder to abuse than a 20mg amp mixed salt preparation.

And quite honestly, I am generally suspicious of adult patients prescribed large doses of mixed salt amphetamines (large doses being 40-80mg/day). By reflex I tend to see these patients as drug seekers/abusers.

The use of dextromethylphenidate is quite common among physicians, particularly middle age to 'older' physicians. Younger physicians are actually somewhat 'drug' adverse and abuse naive, and if necessary will resort to modafinil.

Somewhat off topic, it is worth noting that (in a very general sense) a rapidly aging generation of seemingly tight-scripted, opiophobic physican is being replaced by a younger physician, who unlike their older counterpart, grew up in a time when experimental drug use was not socially acceptable and high stigmatized. Instead, of these young physicians (some having never smoked marijuana - let alone a cigarette) are a breed of alarmingly 'drug-naive' practitioners who are quite unknowingly the unfortunate product of highly sensationalized anti-drug campaigns and modern anti-drug hysteria.

'Writers-block' is even common in the very few who like myself, have had a had a 'hushed' history of drug abuse.

Disclaimer: The above is the product of sleep deprivation, stress, transbuccal racemic methylphenidate and the better part of 100ml/tanqueray gin. Discount appropriately.
 
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Sekio how do you feel on modafinil? I find myself hypersensitive to comedowns (even caffeine produces bad depression for me) and modafinil I've found to produce weakest comedown compared to everything else.

Edit: also I'll say bupropion has made me feel worse than any other drug I've used.

sekio said:
I wouldn't advise taking *any* methamphetamine derivative with regularity due to the well known neurotoxic effects.

I think the "nicest" stimulants are probably caffeine (and related xanthines, yerba mate is esp. good) or plain old dextroamphetamine in reasonably small doses. (<15mg)
Methylphenidate actually has a pretty tolerable side effect profile when used in moderation as well.
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sekio said:
I wouldn't advise taking *any* methamphetamine derivative with regularity due to the well known neurotoxic effects.
Click to expand...

Why is that?

You used 15mg as an example for d-amp. In vivo if I remember correctly d-meth is about twice as potent? Would chronic 7.5mg d-meth pose a greater risk?
 
Mtahmaphetamine is notably much more potent as a monoamine releaser than D-amphetamine & also induces release of serotonin
 
sekio said:
Mtahmaphetamine is notably much more potent as a monoamine releaser than D-amphetamine & also induces release of serotonin
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Since I don't know enough about the effects of serotonin (other than specific receptors), and have never heard of monoamines, can you explain simply by chance what the differences are associated with these compared to D-amphetamine?

Never did quite understand the actual differences between the two.
 
The gist of it, from what I understand -

Monoamines are the lovable molecules that so many of us think control "happiness" and "pleasure" and all that junk. In reality they are no more than a set of chemical messengers with (at least) one (mono-) nitrogen (-amine) in their structure. These are: (in descending order of "popularity") dopamine, serotonin, norepinephrine/noradrenaline, epinephrine/adrenaline, histamine, tyramine, phenethylamine, and the iodothyronamines. Dopamine/Norepinephrine/Serotonin are the "big three" because they are often implicated in mood, memory, cognition, and the "human" aspects of our beings.

The cellular synapse is a wild west of chemicals kept in check by various systems like autoreceptors (which I am only going to touch on temporarily) and monoamine oxidase/MAO enzymes. When a nerve cell recieves an electrical signal (or enough cumulative electrical signals in a short time) it can cause the release of neurotransmitters - in many cases these are the monoamines mentioned above. Some cell types have "preference" for one ore more monoamines though - i.e. cells in the motor pathways like to use dopamine as a transmitter. Breaking down monoamines every time they were released would be very wasteful, so your cells also have protiens called "transporters" that suck the monoamines back into the cell to be used again.

There are basically four major transporters most recreational drug users are concerned with.
Amphetamine at low doses binds mainly to NET (norepinephrine transporter) & blocks its effect. Despite the name, norepinephrine and dopamine share enough similarities that this transporter also transports dopamine (but not as effectively as...)
At higher doses it also binds & blocks the DAT, or Dopamine Transporter. In higher doses still it reverses the effects of these transporters (so they cause the cell to be firing constantly). The threshold for "releasing" versus "reuptake inhibition" is much smaller with methamphetamine.

Methamphetamine (and MDMA) also bind, block, and cause release from the serotonin transporter SERT. This means more monoamines, and more stimulation for your body to deal with.

But wait, there's more. That's only 3 of 4 transporters. In addition there is a "master transporter" called the VMAT, or vesicular monoamine transporter. Methamphetamine blocks/reverses this too - amphetamine does not.

So in summary, amphetamine is already known to cause your brain stress via flooding its "communication circuitry" with messages. Constant electrical activity in the brain is not healthy - it's stressful for your brain cells and will eventually cause cell death. Amphetamine has been proven to be neurotoxic if abused - and if meth is more potent and even more stressful on cells, I think it should be avoided except in desperate cases.
 
Does this overexcitation leading to neurotoxic effects happen at therapeutic dosage ranges used occasionally (at most 5 times a month)?

By therapeutic dose ranges, I mean ones that prescriptions are actually written for, and not more than that.

Desoxyn I know has prescription dose ranges of 5 and 10mg (though 10mg was discontinued). So would taking 15 to 30mg of obviously less pure street version, say 10 times a month (two doses each of those 5 times a month) pass that threshold for neurotoxicity?

And, on the assumption that everything I've read about chelated magnesium being neuroprotective for amphetamine usage would taking that daily even when not using prevent neurotoxicity at that level of usage?

Thanks for your reply, some of that information I was already familiar with, but some of it I definitely was not. I really appreciate you taking the time to respond.
 
Does this overexcitation leading to neurotoxic effects happen at therapeutic dosage ranges used occasionally (at most 5 times a month)?
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Does it really matter? D-N-methamphetamine is toxic in cell culture and there's very little way around that.

I think the problem is, it's hard to extrapolate from "Chemical X is toxic to mouse neurons at a concentration of 3 mmol" to "15mg of this compound produces a reduction in brain cell density of 40%". There's too many factors to consider - the compound's distribution pattern, how fast it is absorbed and metabolised, and of course personal genetics and sensitivity.

Methamphetamine is a real loser on the neurotoxicity front simply because it's way too effective. It's fat soluble (moreso than amphetamine) which means it wants to stick around in bodily tissues a lot more, and the methyl group also helps protect it from being broken down. Since cell membranes are made out of fatty acids, meth can also diffuse around the body, and blood brain barrier really rapidly. So unless you can account perfectly for individual variances in the compound's absorbtion, distribution, and excretion, you essentially have to put a fucking pump in your brain to suck the compound out and measure it's concentration if you want to say for sure "has this passed a toxic level?"

Of course you can also do the fire-and-forget thing of taking progressively escalating doses punctuated with FMRI scans and just see where your brain activity begins dropping, but that's not nice.

There is especially not safe usage of street methamphetamine of unknown purity. It's way too easy to take a humongous 100mg bolus dose of ice - not so easy if you have to eat 20 pills.
 
sekio said:
The gist of it, from what I understand -

But wait, there's more. That's only 3 of 4 transporters. In addition there is a "master transporter" called the VMAT, or vesicular monoamine transporter. Methamphetamine blocks/reverses this too - amphetamine does not.

So in summary, amphetamine is already known to cause your brain stress via flooding its "communication circuitry" with messages. Constant electrical activity in the brain is not healthy - it's stressful for your brain cells and will eventually cause cell death. Amphetamine has been proven to be neurotoxic if abused - and if meth is more potent and even more stressful on cells, I think it should be avoided except in desperate cases.
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Any refs for methamphetamine causing more VMAT2 reversal than regular amphetamine?
 
g0to said:
There is no 'safe' use of d-methamphetamine, it lends itself to abuse - for how many months will you be taking 15-30 mg? I can say with some confidence that after a few months of that dosage regimen, tolerance will occur and you will feel the need to increase your dose to achieve the same subjective stimulating/euphoric effects.
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I've been using it for about 6 months now at this point with no increase in usage levels or dosage. Usage is very sporadic. Haven't even used more than a gram so far. Only taken ~25mg once in the past 2 weeks.

I don't even have to feel it for it to work. It seems almost subconscious. I can tell it's working due to changes in thought patterns, but there is no noticeable stimulant or euphoric feeling unless I've gone 2 or 3 weeks without taking a dose.

Usually my usage tends to stick to depression phase of bipolar when I can't just wait it out due to work deadlines or when 80/90 hour work weeks hit since I can't use caffeine.

The math works out at my dose level that it's much cheaper than adderall at the levels I use it, the noticeable side effects are negligible or non-existent, and it doesn't kick me into mania like caffeine does which is very harmful to me due to anger issues when I hit hypermanic.

So I'm still risking neurotoxicity no matter how little or sporadic my usage is, but the question is whether or not it'd ever reach noticeable or non-trivial amounts. Compared to the cost/side effects of adderall, the cardiotoxicity of cocaine, and the socio-toxicity (yeah I made that up) of caffeine... I guess it's still my best option. And all of those are preferable to me than the side effects of prescribed medication I quit taking 6 years ago, which include massive weight gain, emotional numbness, and loss of mental productivity.

I'd estimate I'm going to have heart/lung issues from smoking cigarettes long before I have neurotoxicity issues from the usage of this.

If y'all have any recommendations, suggestions or advice for harm reduction with my experience/current choice please let me know. Thanks!
 
LuxEtVeritas said:
Wanted to get some opinions on cleanest stim for non-rec chronic use (chronic fatigue, insomniacs, et al)
i guess ultimate criteria is a clean feel for focus, mood, least potential sides, least tolerance, ability to not interfere with sleep et al)

was thinking offhand modafinil and analogues and sulbutiamine
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come on dude ya couldnt even get away scott free drinking coffee all day
let alone taking uppers
 
^ caffeine and bipolar is a strange beast. Amphetamine is a better alternative for a small population.
Also, neurotoxicity/cognitive issues due to amphetamine use in humans doesn't seem to have as strong of an effect as was widely believed before according to a recent meta analysis. IIRC the amphetamine addicts scored in the lower side of the normal range.
 
Anyone know of any evidence that d-amp is less likely to produce mania in bipolar patients than mph? Not sure why that would be, but personally I've found it to be the case.
 
greenberryhaze said:
Anyone know of any evidence that d-amp is less likely to produce mania in bipolar patients than mph? Not sure why that would be, but personally I've found it to be the case.
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Well it seems stimulants and psychotic mania at least are hit and miss
http://ajp.psychiatryonline.org/article.aspx?articleID=96782

This study seems to have what you want, but I'm hitting a pay wall.
http://www.medscape.org/viewarticle/583510_1

A pet theory of mine is that since amphetamine leads to a more rapid down regulation of D2 it is less likely to produce mania after longer course of treatment. Caffeine increases D2 receptor sensitivity which may cause its weird effects in bipolar, and modafinil is a D2 partial agonist which may prevent over activation of the D2 receptor.

This of course is on the assumption that D2 is the largest factor in mania,.
 
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