Stimulants: Kiss Nasty Vasoconstriction Goodbye

[Kilfer]

I think this belongs in a different forum as it does not truly fit the criteria for this one. Mods feel free to forward where more appropriate if required. Thanks.


Hi all stimulant users. The following is the result of my second experiment conducted extra-field to confirm the first one which I published on my blog earlier. The near-identical results allowed me to retain much of the original text. Those who want further technical details or data PLS PM me or Email me. Now I am extremely exhausted so if I act goofy well, I probably am.

I suggest to those of you looking to get euphoria from those extra-potent RC everlasting stims but end up with tight chest, racing heart and numb lower limbs instead read the following research report and subsequent experiment. It's quite short and not only informative, but from a health POV is a must-read unless you are already versed in the matter, which surprisingly few are to my amazement. Here below is pasted the contents of the blog entry I submitted about this. If you're on a vasoconstriction-laden stim you really want to read this now. And I mean now. The drug I used in the experiment was 3,4-CTMP, one of the most vasoconstrictive stimulants in existence. This is how I transformed the torture device into a pleasure-delivering apparatus. No tools required, just one capsule. A drug, a common Rx drug. Please read:

Base stimulant: 3,4-dichloromethylphenidate 10mg/3h x 18h=60mg tot. at H+0 (had taken 60mg over 18h by H+0)
Base benzodiazepine: Temazepam/15mg/cap/po at H+0 (swallowed this cap at 0H)
Therapeutic effect onset: test: H+16m (felt onset of benzo effects 16 minutes after ingestion)
Full therapeutic effect achieved: H+22m (felt saturation of benzo effect 22 minutes after ingestion on despereately empty stomach)]

Notes: As most among you stimulant users painfully know, vasoconstriction resulting from stimulant use is a party pooper. Be it "panic attack", "fear of imminent death" or "chest crush" the result is the same: it sucks murky lagoon water. It hurts bad and if you have cardiovascular issues, it can kill you. Beta-blockers can't do much for it; neither will niacin. All other exogenous vasodilator agents won't help either, in fact they can be dangerous. All of the medications tested failed to relieve the vascular area from vasoconstriction as they managed to do for peripheral areas. All of them except one class of compounds: Those damned benzodiazepines. Surprised? I certainly was. Up until I, the author of this entry, stumbled upon a "forgotten" snippet buried under several layers of Webfill on "that" site, the one that gets antsy if we try to link to it. Sorry for not being a universal genius, sheesh. So anyway me decides to type the antiquated article by hand and find it so credible I opted to play my own labrat aun my own experiment which, worry not, was still based on solid science. So I'm not here to prove a proven, just to demonstrate it as a reminder that safer is not only better in this case, but a little higher as well. Pharmacology, harm reduction, speed freaks, pill poppers. All together for the cause, it's party time!

"The cause" is the quest for the only drug that can trigger a systematic reverse of the extremely unpleasant and potentially extremely harmful symptoms of the systemic vasoconstriction triggered by various RC stimulants, practically all of them in fact. So far various beta-blockers and even the dietary supplement niacin had been investigated, with mitigated success. The problem was those drugs could not induce a "systematic" vasodilation, one that would release all circulatory areas. They could only achieve peripheral relief, leaving the cardiovascular area untouched and unrelieved. In reality the drugs had flunked miserably. But some people knew of one that worked. Those people wrote a paper about it. And some other people buried that paper. I found it and here it is. Enjoy.


The full statement: (the least biochemically inclined may skip to the last paragraph):


Although controversial over this off-label purpose, benzodiazepines may play a role in lowering blood pressure. They work an agonist of the GABA-a receptors in the brain, thus slowing down neurotransmission and dilating blood vessels. GABA is an abbreviation for gamma-aminobutyric acid. It is an inhibitory neurotransmitter among others (glycine, adenosine, etc.) GABA-a receptors are ion channels that are the primary target for benzodiazepines. When an agonist binds to this receptor site, the protein channel opens, allowing negative chloride ions entering the channel and penetrating the voltage-gated ion site. Thus, giving negative feedback in neurotransmission and easing stress, anxiety and tension in patients that can be associated
with elevated blood pressure. In addition to GABA, benzodiazepines inhibit the rebound elevated blood pressure. In addition to GABA, benzodiazepines inhibit the re-uptake with elevated blood pressure.

In addition to GABA, benzodiazepines inhibit the re-uptake of a nucleoside chemical called Adenosine, which serves as an inhibitory chemical mentioned above. It also serves as a coronary vasodilator, allowing the cardiac muscle to relax and dilating cardiac arteries

There you go. There are no smithereens of a doubt here that among all drugs used during that test only those of the Benzodiazepine class achieved the stated objective of providing complete and sustained results which coincided 100% with the objectives stated. Despite the biochemistry lingo the conclusion leaves little doubt as to what the original author(s) believe(s). First's let's take care of the first sentence. There never was any controversy. Those who doubt it do your own research it's not that hard once pointed in the right direction. I did this from my office and on my own, clues wee all over the place. As for the rest let's get to work. Research involving and RC stimulant and popping benzos can't be that hard.



My setup:
Me. Author is somewhat healthy 50 year-old man, 6-ft tall 153lbs borderline lanky but uses "slim" Auhthor is a very experienced stimulant user and very familiar with a plethora of benzos and associates

at H+0 author had 18mg 3,4-dichloromethylphenidate spread over 18 hours. BCL was not measured but strong vasoconstriction was evident in chest, legs and head (dulled hearing, the feeling of having a headset on when none is present.)
H+0 rapid-onset quick-acting benzo featured: the potent hypnotic temazepam one 15mg/cap/po;
H+16 initial benzo effects felt
H+22 saturation benzo effects felt
H+27 full suppression of vasoconstrictive effects achieved

Systematic vasodilation was achieved within 27 minutes of initial po adm of smallish 15mg dose of temazepam ("smallish" considering the potency of 3,4-CMTP, in reality 15mg of temazepam was heavy'ish). That's 27 minutes from misery to bliss without major interaction between the benzodiazepine used and the positive effects of the stimulant restored. The potent and notoriously vasoconstricting long-acting CNS stimulant 3,4-dichloromethylphenidate which a highly potent derivative of methylphenidate, was chosen for the test, along with the quick-onset hypnotic Temazepam at a modest dosage of 15mg po, to avoid inducing hypnosis. Within 27 minutes of ingestion the benzodiazepine had completely removed any perceptible untoward effect of the stimulants effects on the cardiovascular system, namely tachycardia (from 146 to 77) and perceptible signs of HBP (sorry my cellphone can't measure blood pressure).

Notes: Results published are dose and ratio dependent. Higher stimulant dosage will require ratio recalibration. No other stimulant or benzodiazepine was used but similar results can be projected based on chemical affinities between amphetamine and its congeners, methylphenidate and its congeners, substituted amphetamines and substituted cathinones. Excluded are: psychedelic amphetamine derivatives, methamphetamine, cocaine HCL and its derivatives

The initial job was done. I had demonstrated my point. Now I can proceed to broadcast some stuff I believe ought'a travel around. Plenty older guys doing thsese stims, starting with me. Do you want to risk death over an RC stimulant?

Didn't think so.

 

[lyricabuddy]

Nice report, and I agree, benzos can be a beautiful thing. Unfortunately tolerance and subsequent w/d to a clonazepam script and buying xanax bars on the street was one of the most horrific experiences I've had on any drug. Not that we didn't already know that, just sayin. Currently prescribed 15mg temazepam / night and resisting the urge to ask for the 30's

 

[Kilfer]

Nice report, and I agree, benzos can be a beautiful thing. Unfortunately tolerance and subsequent w/d to a clonazepam script and buying xanax bars on the street was one of the most horrific experiences I've had on any drug. Not that we didn't already know that, just sayin. Currently prescribed 15mg temazepam / night and resisting the urge to ask for the 30's

Since all GABA-a agonists inhibit the re-uptake of Adenosene (the nucleoside responsible for sustaining cardiovascular vasoconstriction when beta-blockers are used to treat peripheral areas only) my hope is that even lo-strength benzos like Diazepam 5mg, sublingual lorazepam 0.5mg or sublingual Bromazepam 3mg, which I consider my best candidate so far due to its lack of noticeable psychoeffects at such a low dose and thus could be used for this purpose without providing any benzo-related reward to the user... provided it's strong enough to keep Adenosine in check. Let's keep in mind that the user's prime objective is to draw pleasure from the "smoothed-out" stimulant effects of the "main" stimulant drug, not from downers. Whether this would be possible to achieve with such a strong stimulant as 3,4-dichloromethylphenidate is doubtful but even there, I admit that the determination to prove that my research and that my suspicions had been conclusive I may have gone somewhat overboard with such a relatively potent benzo as the quick-onset short-acting temazepam 15mg... but it worked! I hated 3,4-CTMP before that, now I like it a little more.

A medium-onset mid to long-acting GABA-a agonist would likely be more suited to my experiments. I had initially opted to use Zopiclone 7's I know I have somewhere in my office but could not get my hands on them, and they are too short-acting (2h) to be practical. As for the Ativan 2mg tabs I keep for my "hippie team" they take 90 minutes to kick in which is too long and too strong. The same problem would affect etizolams and besides those are too strong. I keep seeing Valium 5's pop into my mind but let's not forget that there are two benzos with practically no recreational value out there that could perhaps do away with all the issues: Chlordiapoxide and chlorprozeate (or is it Chlorpromazoid? I'm too tired to loo it up. trade name was Tranxene irc). The user would have to ingest them at least 2 or 3 hours before the "neutering session" though, not very practical.

As far as using Xanax I could see this increasing the enjoyment of short-acting stims like ETH but not near-eternal powerhouses like 3,4-CTMP or Desoxypipradrol, Methioxsomething... I forget, not to mention all the "drone" substitutes that pop up year after year. They all cause vasoconstriction. I keep thinking that fragmented doses of Valium 5 is the way to go for those too, unless... there are many RC GABA-a agonists, one is bound to have universal appeal for this application. Jeez Louise I sound like a hypomaniac... almost 'cause I actually make sense not money. Will get busy on that in the coming days, I am still quite exited by my "discovery" yesterday I must admit. I also have to investigate several non-benzo GABA-a agonists ranging from Z-drugs to powerful downers such as Clomethiazole and the supreme overkill, chloral hydrate. Unlikely candidates but who knows what sort of jet-blast stim is bound to hit the Net sooner or later.

 

[adder]

Benzodiazepines are effective vasodilators. Unfortunately, this is far from the ideal solution. Anyone who was/is addicted to benzodiazepines and tried quitting them knows what I mean. Honestly, benzodiazepine addiction is much worse to quit than amphetamine addiction in my opinion. I didn't dive too deep into the latter, but I was past the border between recreational and compulsive uses. I don't condemn single uses, but if you freak out because of vasoconstriction that your drug of choice is giving you, then something tells me you've overdone it.

Nice report, and I agree, benzos can be a beautiful thing. Unfortunately tolerance and subsequent w/d to a clonazepam script and buying xanax bars on the street was one of the most horrific experiences I've had on any drug. Not that we didn't already know that, just sayin. Currently prescribed 15mg temazepam / night and resisting the urge to ask for the 30's

Which in short means benzodiazepines just like any addictive drugs can bring your self-esteem down to zero. At the very beginning any drug you like may seem beautiful and just what you had always needed before. That's clearly overlooking some very important details and thus missing the big picture.

 

[dopamimetic]

While I am not yet sure in how much it affects or counter-acts the stimulant (maybe this is just that an unreliable kind of effect?), Clonidine does a good job too. It builds tolerance with chronic usage too, must be tapered down and sometimes the postural hypotension is a bit disturbing. But it's not by far comparable to what GABAergics will do.

Just haven't found the right dose regimen yet, but its really kind of agonist-antagonist in that if the one effect gets too strong, take a bit more of the other to balance it out.

 

[Kilfer]

Benzodiazepines are effective vasodilators. Unfortunately, this is far from the ideal solution. Anyone who was/is addicted to benzodiazepines and tried quitting them knows what I mean. Honestly, benzodiazepine addiction is much worse to quit than amphetamine addiction in my opinion. I didn't dive too deep into the latter, but I was past the border between recreational and compulsive uses. I don't condemn single uses, but if you freak out because of vasoconstriction that your drug of choice is giving you, then something tells me you've overdone it.

I was clear that my goal is to determine if benzos can be used for this harm reduction purpose using barely discernible, non-recreational level doses. If one needs to go zonkers on a heavy-duty benzo to obtain a sufficient vasodilator effect, then obviously the objective isn't met. Earlier today I have read that the dosage benzos require to achieve vasodilator effects is very low, as low as 2mg for diazepam on 175 lbs man. Blood plasma concentration is what matters, not the presence of psychoactive effects. You must understand that as a middle aged man I am slightly pissed-off at those who advocate the use of beta-blockers for this purpose, which are clearly not suited for the task.

 

[Kilfer]

While I am not yet sure in how much it affects or counter-acts the stimulant (maybe this is just that an unreliable kind of effect?), Clonidine does a good job too.

I don't think a small dose of clonidine would disturb positive stim effect any more than an equivalent tiny dose of benzo would. But unfortunately clonidine, like beta-blockers, only targets peripheral vascular areas not cardiovascular. Benzos indunce vasodilation in all blood-irrigated areas. Vasodilating cardiovascular area during strong stim use is capital.

In any case I need to procure a milder stim or at least shorter-acting stim in order to pursue my testing with baby-benzos. Anyone who thinks 2mg Valium will have any effect on 3,4-CTMP induced vasoconstriction is likely to be disappointed. My initial experiment was to validate the unearthed article, further testing is required to adjust doses to various stims. So far no other 100% systemic vasodilators have been identified that suit the purpose better than GABA-a agonists which are all hypnotics, sedatives or anxiolytics. It's sorta like in the old days when they gave 1mg or 2mg po morphine to kids for diarrhea. None got stoned off those but they got constipated which was the goal to achieve.

 

[Kilfer]

Which in short means benzodiazepines just like any addictive drugs can bring your self-esteem down to zero. At the very beginning any drug you like may seem beautiful and just what you had always needed before. That's clearly overlooking some very important details and thus missing the big picture.

Methinks you are missing the big picture which is the investigating of a less dangerous way of reducing cardiotoxicity of stimulants strong ad mild via the use of cardiovascular vasodilators (GABA-a agonists) to mitigate those effects and proctect the stim-using patient from being harmed by the untoward effects of the stim's effect on his cardiovascular system. I am not approaching this from a benzo addicted POV but from a stim user/addict's. If you know of a non-GABA-a agonist that can accomplish this please let us know.

 

[ebola?]

But unfortunately clonidine, like beta-blockers, only targets peripheral vascular areas not cardiovascular.

No. Clonidine's primary target, alpha2a adrenergic receptors, is well expressed in neural cardiac tissue and even the CNS (Clonidine also has significant activity at other alpha-receptors). Clonidine should directly reduce vasoconstriction, elevated BP, etc. more effectively than benzos. I suspect that benzos work for you so well because their anxiolytic effect removes your strongly expressed worries about vasoconstriction while high.

ebola

 

[lyricabuddy]

I was clear that my goal is to determine if benzos can be used for this harm reduction purpose using barely discernible, non-recreational level doses. If one needs to go zonkers on a heavy-duty benzo to obtain a sufficient vasodilator effect, then obviously the objective isn't met. Earlier today I have read that the dosage benzos require to achieve vasodilator effects is very low, as low as 2mg for diazepam on 175 lbs man. Blood plasma concentration is what matters, not the presence of psychoactive effects. You must understand that as a middle aged man I am slightly pissed-off at those who advocate the use of beta-blockers for this purpose, which are clearly not suited for the task.

Yeah, I got your point. I used to use .25 - .5mg alprazolam every 3 or 4 hours back when I used to do a lot of cocaine and it was MONEY for the purpose you describe. Although i'm sure other benzos would be even more ideal with stims. Ativan and temazepam come to mind. My point is that if you happen to have them on you while you are doing stims it's great but it takes too much willpower (for me) to have a supply on- hand / prescription solely dedicated to the couple times a month I do stims. Very slippery slope.

 

[adder]

Methinks you are missing the big picture which is the investigating of a less dangerous way of reducing cardiotoxicity of stimulants strong ad mild via the use of cardiovascular vasodilators (GABA-a agonists) to mitigate those effects and proctect the stim-using patient from being harmed by the untoward effects of the stim's effect on his cardiovascular system. I am not approaching this from a benzo addicted POV but from a stim user/addict's. If you know of a non-GABA-a agonist that can accomplish this please let us know.

And I'm approaching this from a perspective of an ex-addict to benzodiazepines and a former (ab)user of stimulants. Like I wrote, I don't condemn single uses, that's a wrong word actually, I don't discourage single uses, but I know quite a few people who first got addicted to amphetamine and then started using benzodiazepines, because at first they thought they were great for comedowns and then they realised they chill them out nicely on their own or on top of amphetamine. I admit I'm over-sensitive having had huge problems with quitting benzodiazepines for years, but trust me few benzodiazepine addicts start off with high doses.

 

[Kilfer]

No. Clonidine's primary target, alpha2a adrenergic receptors, is well expressed in neural cardiac tissue and even the CNS (Clonidine also has significant activity at other alpha-receptors). Clonidine should directly reduce vasoconstriction, elevated BP, etc. more effectively than benzos. I suspect that benzos work for you so well because their anxiolytic effect removes your strongly expressed worries about vasoconstriction while high.

GABA-a agonists effect on adenosine is what results in cardiovascular vasodilator effect from benzos and similar agents but cooling off of my freaking out over untoward effects of stims certainly didn't hurt

But with that being said the ultimate objective is to achieve the desired results with a dosage or formulation carrying only a negligible psychotropic effect, keeping in mind that the prevention of the loss of positive effects from the stimulant is a highly desirable secondary objective. These both require the reduction of GABA-a agents to the absolute minimum required to achieve desired result. Anything that would result in noticeable sedation or even worse, relapse of benzo addiction (although I cannot advise former benzo addicts to abuse stimulants) would be rejected as not meeting the requirement.

 

[Kilfer]

And I'm approaching this from a perspective of an ex-addict to benzodiazepines and a former (ab)user of stimulants. Like I wrote, I don't condemn single uses, that's a wrong word actually, I don't discourage single uses, but I know quite a few people who first got addicted to amphetamine and then started using benzodiazepines, because at first they thought they were great for comedowns and then they realised they chill them out nicely on their own or on top of amphetamine. I admit I'm over-sensitive having had huge problems with quitting benzodiazepines for years, but trust me few benzodiazepine addicts start off with high doses.

You raise an interesting point by indirectly reminding me that this whole project has to be assessed as part of harm reduction strategy applying to stimulant abuse, not as an aid to general health improvement, which can only be viewed as an indirect and unplanned benefit.

 

[sekio]

Are you actually measuring your blood pressure or is this all based upon percieved effects? 15mg of temazepam isn't a super low dose. If you don't use benzos on a regular basis that's more than enough to give you a little buzz... probably quite a bit more than just vasodilation.

My advice is to not take doses of stimulants that jack your blood pressure and/or cause anxiety to the point where it's an issue... benzodiazepines should be drugs used in emergency freakouts, not as part of a cocktail to make your stimulant tolerable. It doesn't help that it's very easy to cause a self-perpetuating loop of anxiety and panic for some people. I think you just have to be at peace with the fact that stimulants will make your body stimulated... and taking a drug that causes release or reuptake inhibition of norepinephrine can, and should indeed, be reasonably expected to boost your blood pressure.

Some people don't like methylphenidate and its friends for this reason... there's no real long term 'harm reduction' in telling them to practice polypharmacy so they can use a drug their body doesn't agree with.

Have you tried using lorazepam sublingually rather than orally? I've never heard of it taking 2 hours to kick in. I would stay away from any N-methylated benzos, so no diazepam, no temazepam, no etizolam or any triazolos, etc. Generally benzos of that family are very prone to abuse compared to the N-demethylated cousins. The idea is to use the lowest potency, least centrally active benzo you can find at the lowest dose. Clonazepam at 0.25mg or something.

Since all GABA-a agonists inhibit the re-uptake of Adenosene

There are a lot of subtypes of GABAa receptors, not all agonists/allosteric modulators will lower bp. For instance zopiclone and the Z-drugs are mostly hypnotics and somewhat anxiolytics but are poor muscle relaxants.

I also question how direct the effect of benzodiazepines on vasodilation is. I was under the impression it was related to their effects as muscle relaxants.

tl;dr: I don't see how encouraging the use of dependency forming drugs to mask the bad effects intrinsic to certain poorly designed RC stimulants is 'harm reduction', but to each his own I guess.

 

[ebola?]

My advice is to not take doses of stimulants that jack your blood pressure and/or cause anxiety to the point where it's an issue...

Precisely: if your chosen dosage of stimulant causes alarming physiological effects, the dosage was too high.

I also question how direct the effect of benzodiazepines on vasodilation is. I was under the impression it was related to their effects as muscle relaxants.

I thought that indirect effects mediated by reducing anxiety (and in turn its physiological correlates) were the greatest factors at play here...

ebola

 

[MeDieViL]

Nice report, and I agree, benzos can be a beautiful thing. Unfortunately tolerance and subsequent w/d to a clonazepam script and buying xanax bars on the street was one of the most horrific experiences I've had on any drug. Not that we didn't already know that, just sayin. Currently prescribed 15mg temazepam / night and resisting the urge to ask for the 30's

Benzo, tolerance and addiction can be prevented with memantine, that said dipyridamole is a non addictive adenosine re-take inhibitor,

 

[MeDieViL]

Also carvedilol, will completely prevent the cardiovascular side effects of stimulants, with far more certainty then Benzos as it directly blocks the receptors that cause stimulants to have this effect while not interfering with the rewarding effects.

 

[MeDieViL]

Are you actually measuring your blood pressure or is this all based upon percieved effects? 15mg of temazepam isn't a super low dose. If you don't use benzos on a regular basis that's more than enough to give you a little buzz... probably quite a bit more than just vasodilation.

My advice is to not take doses of stimulants that jack your blood pressure and/or cause anxiety to the point where it's an issue... benzodiazepines should be drugs used in emergency freakouts, not as part of a cocktail to make your stimulant tolerable. It doesn't help that it's very easy to cause a self-perpetuating loop of anxiety and panic for some people. I think you just have to be at peace with the fact that stimulants will make your body stimulated... and taking a drug that causes release or reuptake inhibition of norepinephrine can, and should indeed, be reasonably expected to boost your blood pressure.

Some people don't like methylphenidate and its friends for this reason... there's no real long term 'harm reduction' in telling them to practice polypharmacy so they can use a drug their body doesn't agree with.

Have you tried using lorazepam sublingually rather than orally? I've never heard of it taking 2 hours to kick in. I would stay away from any N-methylated benzos, so no diazepam, no temazepam, no etizolam or any triazolos, etc. Generally benzos of that family are very prone to abuse compared to the N-demethylated cousins. The idea is to use the lowest potency, least centrally active benzo you can find at the lowest dose. Clonazepam at 0.25mg or something.



There are a lot of subtypes of GABAa receptors, not all agonists/allosteric modulators will lower bp. For instance zopiclone and the Z-drugs are mostly hypnotics and somewhat anxiolytics but are poor muscle relaxants.

I also question how direct the effect of benzodiazepines on vasodilation is. I was under the impression it was related to their effects as muscle relaxants.

tl;dr: I don't see how encouraging the use of dependency forming drugs to mask the bad effects intrinsic to certain poorly designed RC stimulants is 'harm reduction', but to each his own I guess.

Some individuals ALLWAYS get anxiety of any stimulant dose, so in my case I ALLWAYS need a benzo, or phenibut, with them.
sorry for the capitals I made a computer out of a broken tablet with a tv, mouse, keyboard and kitchen table lol but can't turn this autocorrection of Android off

 

[ebola?]

Some individuals ALLWAYS get anxiety of any stimulant dose

Not everyone likes stimulants; it's okay not to take them.

ebola

 

[MeDieViL]

Not everyone likes stimulants; it's okay not to take them.

ebola

I have to its the only thing helping my extreme anhedonia.