Kilfer
Bluelighter
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.
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.
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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.
