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BDD Moderators: Keif’ Richards | negrogesic
Meth Meth Primer: Post Your Meth Tips Hints & Hacks Here
- Thread starter SecretToke
- Start date
Lovelight123
Greenlighter
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She go anaphylactic? How long did the allergy take to set in?
Scrofula
Bluelight Crew
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No, but she was scary enough they called EMT and ambled her over to the ER, where she stayed a while. Got an EpiPen for a few years.
Anyway, if you had an allergy to meth or one of its contaminants, you wouldn't have reacted on just your lips (and face later)--you took this stuff deep into your lungs. I think that would cause severe asthma pretty quickly, but then, meth is a beta agonist, like albuterol.
It doesn't make any sense to react to the meth or something in it like that. Something on your pipe makes more sense. People get rashes sometimes, more from oily sweat clogged pores I think, but the docs would've said "wash your face".
I'd still blame the shrimp. TBC, that was just the worst out of a few mild ones she probably wouldn't have remembered if it wasn't for the first one. A dose dependent shrimp-shit allergy.
Anyway, if you had an allergy to meth or one of its contaminants, you wouldn't have reacted on just your lips (and face later)--you took this stuff deep into your lungs. I think that would cause severe asthma pretty quickly, but then, meth is a beta agonist, like albuterol.
It doesn't make any sense to react to the meth or something in it like that. Something on your pipe makes more sense. People get rashes sometimes, more from oily sweat clogged pores I think, but the docs would've said "wash your face".
I'd still blame the shrimp. TBC, that was just the worst out of a few mild ones she probably wouldn't have remembered if it wasn't for the first one. A dose dependent shrimp-shit allergy.
zephyr
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http://www.bluelight.org/vb/threads/133903-Hints-and-tips-for-meth-smokers?p=1848465&viewfull=1#post1848465
This is a fucking classic thread, this is what came up on a search for info many many years ago as meth was relatively knew and sold as just the same as speed except smokable.
If only we knew....
This is a fucking classic thread, this is what came up on a search for info many many years ago as meth was relatively knew and sold as just the same as speed except smokable.
If only we knew....
Tubbs
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I'm the one unnaproving all of the comments, if you look his were ua'd as well, this is not the place to stir shit, if you have something of value to add, please do. If not, then keep it out of this thread, I will issue infractions if this continues.
Lorne???
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Anyway, a post comparing amphetamines to methampetamine would interest me
And one study claimed Levo-Methamphetamine produces "liking" responses, not to the extent of Dexmeth, of course, and do not know/remember the doses, however it is interesting, because pretty much Levo-methampetamine should have Almost no practical RC effects.
Other suggestions?
And one study claimed Levo-Methamphetamine produces "liking" responses, not to the extent of Dexmeth, of course, and do not know/remember the doses, however it is interesting, because pretty much Levo-methampetamine should have Almost no practical RC effects.
Other suggestions?
Last edited by a moderator:
Lorne???
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Oh, those are surprising high for a drug with no severe physical wd syndrome
Of course, I am of the crazy mind set that taking anything every day, or abusing it all the time will lead to some adaptations, which at least shall make for an adjustment- If you took >100mg Hydroxyzine per day, with just 7.5 Valium, it oils be an adjustment...
Of course, I am of the crazy mind set that taking anything every day, or abusing it all the time will lead to some adaptations, which at least shall make for an adjustment- If you took >100mg Hydroxyzine per day, with just 7.5 Valium, it oils be an adjustment...
Scrofula
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Here is a massive information dump from our esteemed CFC.
(Mods, feel free to UA the first one, sorry, should have just copied in the first place)
Nevertheless the dominant cardiovascular concern for meth/amp and other stimulant users is more typically the chronic harms - ones that build slowly over time like cardiomyopathies, valvular damage, aortic dilatation and so on. These can increase the risk of premature death, potentially taking years or even decades off a person's normal lifespan, despite not being obviously and directly related to morbidity at the time of death - and so inconveniently not registering in any coroner's report (assuming one's even written - which is rarely the case).
Despite that, and the consequent inadequacy of information we have to hand, even a tip-of-the-iceberg analysis suggests meth use is present in at least 5% of all patients presenting to the ER with heart failure [https://www.ncbi.nlm.nih.gov/pubmed/18940295] and 40% of patients under the age of 45 admitted to hospital with cardiomyopathy [https://www.ncbi.nlm.nih.gov/pubmed/17275458]. Acute coronary syndrome (ie unstable angina and acute myocardial infarction) was diagnosed in 25% of US emergency department patients presenting with chest pain following meth use[https://www.ncbi.nlm.nih.gov/pubmed/12745036]
A selection of reports and studies discussing heart attacks (MI) resulting from meth/amp abuse can be found here:
https://www.ncbi.nlm.nih.gov/pubmed/15011896
https://www.ncbi.nlm.nih.gov/pubmed/12745036
https://www.ncbi.nlm.nih.gov/pubmed/10978660
https://www.ncbi.nlm.nih.gov/pubmed/10097363
https://www.ncbi.nlm.nih.gov/pubmed/17565561
Acute aortic dissection, another well-known complication of meth use, can be read about here:
https://www.ncbi.nlm.nih.gov/pubmed/9987866
https://www.ncbi.nlm.nih.gov/pubmed/10097363
https://www.ncbi.nlm.nih.gov/pubmed/7815027
Meth/amp is also strongly associated with cardiac arrhythmias and sudden cardiac death. You can read more about these cases here:
https://www.ncbi.nlm.nih.gov/pubmed/10344175
https://www.ncbi.nlm.nih.gov/pubmed/7588189
https://www.ncbi.nlm.nih.gov/pubmed/6482074
https://www.ncbi.nlm.nih.gov/pubmed/2979169
https://www.ncbi.nlm.nih.gov/pubmed/7840041
https://www.ncbi.nlm.nih.gov/pubmed/2293467
https://www.ncbi.nlm.nih.gov/pubmed/12877759
https://www.ncbi.nlm.nih.gov/pubmed/6519024
As for the more chronic pathologies, they also include underlying processes and mechanisms that lead to many of the acute outcomes listed above. So for example aortic dissection typically involves prolonged and repeated exposure to elevated BP and heart rate, leading to aortic dilatation, which slowly expands and weakens for years before the aorta finally ruptures in an acute episode. And prolonged tachycardia and catecholamine exposure can modify the behaviour of the heart's pacemaker and its elecrophysiological behaviour (affecting pulse conductivity, for example), leading to atrial fibrillation, which can then lead to clots, thrombus and ultimately MI, sudden death and so on.
However the classic chronic issues are coronary artery disease (CAD) and cardiomyopathy. Minimal to severe CAD is found in around 1-in-5 (20%) of meth users compared to 1-in-20 of the normal population, and occurs at a significantly younger age [https://www.ncbi.nlm.nih.gov/pubmed/17565561].
But as quoted in that paper: "cardiac pathology takes time to develop [and] there may be a long ‘incubation’ period prior to methamphetamine-related death." As already suggested, this implies many of the harms inevitably go unrecorded or get blamed on traditional causes like ageing, poor genetics, a lack of exercise and unhealthy Western diets.
These concerns about the largely under-reported cardiovascular harms aren't just limited to American researchers either:
In a series of 371 Australian coronial cases of methamphetamine-related deaths, cardiovascular complications were the leading direct cause of death after drug toxicity/overdose, responsible for death in 14% of cases. Fifty-four per cent of the cohort exhibited cardiovascular pathology. Notably, this data from 2008 precedes the current rise in methamphetamine use and purity. From 2011/12 - 2012/13, there was an 88% increase in methamphetamine-related ambulance callouts in metropolitan Melbourne and a 109% increase in rural Victoria. Methamphetamines are now the second most common culprit after opioids for drug-related hospital attendances. Methamphetamine-related mortality has also doubled from 2001 to 2009
[https://www.ncbi.nlm.nih.gov/pubmed/26706652]
In Crystal Methamphetamine‐Associated Cardiomyopathy: Tip of the Iceberg? [https://www.ncbi.nlm.nih.gov/pubmed/14705845], the authors summarise the cardiovascular-related harms quite nicely:
The most common cardiovascular manifestations of amphetamine‐related compounds include chest pain, tachycardia, and hypertension. At higher doses tachyarrhythmias may occur. Amphetamines are also linked with coronary artery disease, myocardial ischemia and infarction, acute pulmonary edema, necrotizing vasculitis, endocarditis, pulmonary hypertension, acute aortic dissection, ischemic stroke, cerebrovascular hemmorhage, acute rhabdomyelosis, and sudden cardiac death.
Autopsy studies have demonstrated the occurrence of cardiomyopathy in patients with methamphetamine‐related deaths. Histological analysis of myocardial tissue from methamphetamine users has shown the presence of contraction band necrosis, which usually is an indicator of catecholamine toxicity and a recognized feature in the hearts of cocaine abusers.
Several experimental studies have shown the development of myocyte atrophy, hypertrophy, contraction bands, patchy cellular infiltration, eosinophilic degeneration, cellular edema, myocytolysis, fibrosis, and vacuolization when animals and cultured myocytes are exposed to methamphetamine. The accompanying ultra structural features include sarcolemmal injury, mitochondrial degeneration, myofibrillar hypercontraction, and loss of myofilaments.
The plausible mechanisms for the development of dilated cardiomyopathy in chronic methamphetamine users include recurrent coronary artery spasm, small vessel disease, or diffuse myocardial toxicity due to repeated stimulation of alpha and beta‐adrenergic receptors in the heart. Thus, the adverse pathogenetic role of adrenergic receptor stimulation in this setting is likely similar to that of cocaine and catecholamine‐induced cardiomyopathy.
Evidence for all those harms/claims can be linked directly through the paper (I had to remove the messy hyperlinks unfortunately).
In Cardiovascular Responses Elicited by the “Binge” Administration of Methamphetamine [https://www.ncbi.nlm.nih.gov/pubmed/11907169], the authors have begun to investigate the impact of repeated binge dosing of meth on the cardiovascular system, since this more accurately reflects typical usage patterns, noting that:
The binge administration of METH can produce significant cardiac pathology. In rats subjected to this dosing regimen, we observed myocardial foci of predominantly mononuclear inflammatory infiltrates (primarily monocytes/macrophages) with areas of disrupted architecture and occasional myofibril necrosis. Mast cells, normally present in the rat myocardium (Majeed, 1994), were not increased in rats receiving METH.
One potential mechanism suggests that a METH-induced increase in peripheral catecholamines is responsible for the cardiotoxicity (see Jiang and Downing, 1990). It is known that catecholaminergic stimulation can produce myocardial necrosis and infiltration similar to that observed after administering METH. The mechanisms mediating catecholamine-induced cardiac damage may include ischemia due to catecholamine-mediated coronary vasoconstriction, calcium overload, and the production of oxygen free radicals by either the auto-oxidation of catecholamines or their degradation by monoamine oxygenase. Reactive oxygen species may also be produced by catecholamine degradation, mitochondrial dysfunction, leukocyte activation, and/or xanthine oxidization during the reperfusion of ischemic areas.
METH may produce cardiac damage by direct effects on the myocytes. METH is cytotoxic to myocytes in culture systems devoid of catecholamines. METH may also damage cardiac cells by initiating apoptosis. Apoptotic processes occur in several pathological conditions including myocardial ischemia and reperfusion, infarction, and cardiomyopathy.
The binge administration of METH can produce significant changes in cardiovascular and cardiovascular reflex function and result in significant cardiac pathology. During the binge administration of METH, there was an increase in sensitivity to the pressor actions of the drug and decreases in sensitivity to the depressor actions of NP, Iso, and Ach.
I bring this tendency for binging to aggravate the heart's reaction to meth's pressor effect up as it's of direct concern to OP, who's heart is clearly quite sensitive as it is. Which is a very good reason for OP to further ponder the gravity of his/her addiction to meth, and to try even harder to stop. And all without even needing to consider the escalating risks to the brain, other organs, long-term mental health, intensified addiction and so on.
(Mods, feel free to UA the first one, sorry, should have just copied in the first place)
Nevertheless the dominant cardiovascular concern for meth/amp and other stimulant users is more typically the chronic harms - ones that build slowly over time like cardiomyopathies, valvular damage, aortic dilatation and so on. These can increase the risk of premature death, potentially taking years or even decades off a person's normal lifespan, despite not being obviously and directly related to morbidity at the time of death - and so inconveniently not registering in any coroner's report (assuming one's even written - which is rarely the case).
CFC
Despite that, and the consequent inadequacy of information we have to hand, even a tip-of-the-iceberg analysis suggests meth use is present in at least 5% of all patients presenting to the ER with heart failure [https://www.ncbi.nlm.nih.gov/pubmed/18940295] and 40% of patients under the age of 45 admitted to hospital with cardiomyopathy [https://www.ncbi.nlm.nih.gov/pubmed/17275458]. Acute coronary syndrome (ie unstable angina and acute myocardial infarction) was diagnosed in 25% of US emergency department patients presenting with chest pain following meth use[https://www.ncbi.nlm.nih.gov/pubmed/12745036]
A selection of reports and studies discussing heart attacks (MI) resulting from meth/amp abuse can be found here:
https://www.ncbi.nlm.nih.gov/pubmed/15011896
https://www.ncbi.nlm.nih.gov/pubmed/12745036
https://www.ncbi.nlm.nih.gov/pubmed/10978660
https://www.ncbi.nlm.nih.gov/pubmed/10097363
https://www.ncbi.nlm.nih.gov/pubmed/17565561
Acute aortic dissection, another well-known complication of meth use, can be read about here:
https://www.ncbi.nlm.nih.gov/pubmed/9987866
https://www.ncbi.nlm.nih.gov/pubmed/10097363
https://www.ncbi.nlm.nih.gov/pubmed/7815027
Meth/amp is also strongly associated with cardiac arrhythmias and sudden cardiac death. You can read more about these cases here:
https://www.ncbi.nlm.nih.gov/pubmed/10344175
https://www.ncbi.nlm.nih.gov/pubmed/7588189
https://www.ncbi.nlm.nih.gov/pubmed/6482074
https://www.ncbi.nlm.nih.gov/pubmed/2979169
https://www.ncbi.nlm.nih.gov/pubmed/7840041
https://www.ncbi.nlm.nih.gov/pubmed/2293467
https://www.ncbi.nlm.nih.gov/pubmed/12877759
https://www.ncbi.nlm.nih.gov/pubmed/6519024
As for the more chronic pathologies, they also include underlying processes and mechanisms that lead to many of the acute outcomes listed above. So for example aortic dissection typically involves prolonged and repeated exposure to elevated BP and heart rate, leading to aortic dilatation, which slowly expands and weakens for years before the aorta finally ruptures in an acute episode. And prolonged tachycardia and catecholamine exposure can modify the behaviour of the heart's pacemaker and its elecrophysiological behaviour (affecting pulse conductivity, for example), leading to atrial fibrillation, which can then lead to clots, thrombus and ultimately MI, sudden death and so on.
However the classic chronic issues are coronary artery disease (CAD) and cardiomyopathy. Minimal to severe CAD is found in around 1-in-5 (20%) of meth users compared to 1-in-20 of the normal population, and occurs at a significantly younger age [https://www.ncbi.nlm.nih.gov/pubmed/17565561].
But as quoted in that paper: "cardiac pathology takes time to develop [and] there may be a long ‘incubation’ period prior to methamphetamine-related death." As already suggested, this implies many of the harms inevitably go unrecorded or get blamed on traditional causes like ageing, poor genetics, a lack of exercise and unhealthy Western diets.
These concerns about the largely under-reported cardiovascular harms aren't just limited to American researchers either:
In a series of 371 Australian coronial cases of methamphetamine-related deaths, cardiovascular complications were the leading direct cause of death after drug toxicity/overdose, responsible for death in 14% of cases. Fifty-four per cent of the cohort exhibited cardiovascular pathology. Notably, this data from 2008 precedes the current rise in methamphetamine use and purity. From 2011/12 - 2012/13, there was an 88% increase in methamphetamine-related ambulance callouts in metropolitan Melbourne and a 109% increase in rural Victoria. Methamphetamines are now the second most common culprit after opioids for drug-related hospital attendances. Methamphetamine-related mortality has also doubled from 2001 to 2009
[https://www.ncbi.nlm.nih.gov/pubmed/26706652]
In Crystal Methamphetamine‐Associated Cardiomyopathy: Tip of the Iceberg? [https://www.ncbi.nlm.nih.gov/pubmed/14705845], the authors summarise the cardiovascular-related harms quite nicely:
The most common cardiovascular manifestations of amphetamine‐related compounds include chest pain, tachycardia, and hypertension. At higher doses tachyarrhythmias may occur. Amphetamines are also linked with coronary artery disease, myocardial ischemia and infarction, acute pulmonary edema, necrotizing vasculitis, endocarditis, pulmonary hypertension, acute aortic dissection, ischemic stroke, cerebrovascular hemmorhage, acute rhabdomyelosis, and sudden cardiac death.
Autopsy studies have demonstrated the occurrence of cardiomyopathy in patients with methamphetamine‐related deaths. Histological analysis of myocardial tissue from methamphetamine users has shown the presence of contraction band necrosis, which usually is an indicator of catecholamine toxicity and a recognized feature in the hearts of cocaine abusers.
Several experimental studies have shown the development of myocyte atrophy, hypertrophy, contraction bands, patchy cellular infiltration, eosinophilic degeneration, cellular edema, myocytolysis, fibrosis, and vacuolization when animals and cultured myocytes are exposed to methamphetamine. The accompanying ultra structural features include sarcolemmal injury, mitochondrial degeneration, myofibrillar hypercontraction, and loss of myofilaments.
The plausible mechanisms for the development of dilated cardiomyopathy in chronic methamphetamine users include recurrent coronary artery spasm, small vessel disease, or diffuse myocardial toxicity due to repeated stimulation of alpha and beta‐adrenergic receptors in the heart. Thus, the adverse pathogenetic role of adrenergic receptor stimulation in this setting is likely similar to that of cocaine and catecholamine‐induced cardiomyopathy.
Evidence for all those harms/claims can be linked directly through the paper (I had to remove the messy hyperlinks unfortunately).
In Cardiovascular Responses Elicited by the “Binge” Administration of Methamphetamine [https://www.ncbi.nlm.nih.gov/pubmed/11907169], the authors have begun to investigate the impact of repeated binge dosing of meth on the cardiovascular system, since this more accurately reflects typical usage patterns, noting that:
The binge administration of METH can produce significant cardiac pathology. In rats subjected to this dosing regimen, we observed myocardial foci of predominantly mononuclear inflammatory infiltrates (primarily monocytes/macrophages) with areas of disrupted architecture and occasional myofibril necrosis. Mast cells, normally present in the rat myocardium (Majeed, 1994), were not increased in rats receiving METH.
One potential mechanism suggests that a METH-induced increase in peripheral catecholamines is responsible for the cardiotoxicity (see Jiang and Downing, 1990). It is known that catecholaminergic stimulation can produce myocardial necrosis and infiltration similar to that observed after administering METH. The mechanisms mediating catecholamine-induced cardiac damage may include ischemia due to catecholamine-mediated coronary vasoconstriction, calcium overload, and the production of oxygen free radicals by either the auto-oxidation of catecholamines or their degradation by monoamine oxygenase. Reactive oxygen species may also be produced by catecholamine degradation, mitochondrial dysfunction, leukocyte activation, and/or xanthine oxidization during the reperfusion of ischemic areas.
METH may produce cardiac damage by direct effects on the myocytes. METH is cytotoxic to myocytes in culture systems devoid of catecholamines. METH may also damage cardiac cells by initiating apoptosis. Apoptotic processes occur in several pathological conditions including myocardial ischemia and reperfusion, infarction, and cardiomyopathy.
The binge administration of METH can produce significant changes in cardiovascular and cardiovascular reflex function and result in significant cardiac pathology. During the binge administration of METH, there was an increase in sensitivity to the pressor actions of the drug and decreases in sensitivity to the depressor actions of NP, Iso, and Ach.
I bring this tendency for binging to aggravate the heart's reaction to meth's pressor effect up as it's of direct concern to OP, who's heart is clearly quite sensitive as it is. Which is a very good reason for OP to further ponder the gravity of his/her addiction to meth, and to try even harder to stop. And all without even needing to consider the escalating risks to the brain, other organs, long-term mental health, intensified addiction and so on.
CFC
Scrofula
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And another one from CFC.
Personally, I think these are just general metabolic benefit, not specifically for meth use, and I'm skeptical of more than a few, but the question comes up a lot. I know that vitamin D has been shown to specifically protect brain cells from specifically meth-induced damage.
Personally, I think these are just general metabolic benefit, not specifically for meth use, and I'm skeptical of more than a few, but the question comes up a lot. I know that vitamin D has been shown to specifically protect brain cells from specifically meth-induced damage.
FROM CFC, who was referring to methamphetamine users:
supplements that may or may not (depending on how you interpret a hundred different in vivo, in vitro, rodent, primate, human or cell culture studies) be of benefit, besides vitamin D, in some sort of descending order of usefulness off the top of my head might include:
Taurine (cheap, helps cells everywhere by stabilising their membranes, tenuous potential GABAa agonism)
Vitamin E (the principle lipophilic antioxidant)
Vitamin C (the principle hydrophilic antioxidant, synergises with E somewhat)
Aspirin (COX inhibitor to reduce inflammatory harms including potentially MPTP, lessen risk of clots, strokes and heart attacks; sometimes NSAIDs aggravate heart though)
Selenium (comes up in several studies)
Acetyl-l-carnitine (to aid energy metabolism)
N-acetylcysteine (important glutathione precursor, especially helpful for liver, also potentially stymie development of arterial fibrosis from stimulants)
Creatine monohydrate (energy metabolism/helps myocytes in the heart particularly, but may raise BP/HR in consequence)
Alpha-lipoic acid (also aids energy metabolism)
Coenzyme Q10 (energy metabolism)
Nicotinamide (not niacin, but niacinamide; energy metabolism)
The list could go on, but one of the key points here is about energy metabolism. Ultimately all this oxidative damage from excess catecholamines is harmful because it prevents your mitochondria (the little cellular factories that produce the energy your other cells need to function) producing ATP, and that eventually leads to a cascade of cellular death all across the body.
Therefore getting frequent and sufficient food during any binge is probably more important than any of those supplements. Especially carbohydrates (eg fructose from fruits plus some slower digesting carbs) to deliver a relatively stable blood glucose level and limit the need for what's called beta-oxidation, which is the less efficient burning of fats and ketones for energy that becomes a part of that terminal cascade at the mitochondria.
supplements that may or may not (depending on how you interpret a hundred different in vivo, in vitro, rodent, primate, human or cell culture studies) be of benefit, besides vitamin D, in some sort of descending order of usefulness off the top of my head might include:
Taurine (cheap, helps cells everywhere by stabilising their membranes, tenuous potential GABAa agonism)
Vitamin E (the principle lipophilic antioxidant)
Vitamin C (the principle hydrophilic antioxidant, synergises with E somewhat)
Aspirin (COX inhibitor to reduce inflammatory harms including potentially MPTP, lessen risk of clots, strokes and heart attacks; sometimes NSAIDs aggravate heart though)
Selenium (comes up in several studies)
Acetyl-l-carnitine (to aid energy metabolism)
N-acetylcysteine (important glutathione precursor, especially helpful for liver, also potentially stymie development of arterial fibrosis from stimulants)
Creatine monohydrate (energy metabolism/helps myocytes in the heart particularly, but may raise BP/HR in consequence)
Alpha-lipoic acid (also aids energy metabolism)
Coenzyme Q10 (energy metabolism)
Nicotinamide (not niacin, but niacinamide; energy metabolism)
The list could go on, but one of the key points here is about energy metabolism. Ultimately all this oxidative damage from excess catecholamines is harmful because it prevents your mitochondria (the little cellular factories that produce the energy your other cells need to function) producing ATP, and that eventually leads to a cascade of cellular death all across the body.
Therefore getting frequent and sufficient food during any binge is probably more important than any of those supplements. Especially carbohydrates (eg fructose from fruits plus some slower digesting carbs) to deliver a relatively stable blood glucose level and limit the need for what's called beta-oxidation, which is the less efficient burning of fats and ketones for energy that becomes a part of that terminal cascade at the mitochondria.
Lorne???
Bluelight Crew
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Great Scro- you guys will probably get most of it, though I can help to cull any fun or important facts?
If you need certain links checked(assuming you didn't heck all of them
) Tell me
I'm curious if alternate routes, though meth works fine by the traditional, albeit unhealthy (to some extent) ways-when your doing it properly, it's a bit different, of course
If you need certain links checked(assuming you didn't heck all of them
) Tell me I'm curious if alternate routes, though meth works fine by the traditional, albeit unhealthy (to some extent) ways-when your doing it properly, it's a bit different, of course
Scrofula
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Wait, have I been assigned something? My link is my vast, all-encompassing, multi-faceted one-year experience. That's more than eleven months, you know.
ROA? Every which way and up your butt. All have pros and cons.
I was thinking, which way did he mean is traditional? Then I realized, the whole crystal form is of benefit, ROA-wise, mainly for smokers. Meth-HCl came as a smokable replacement for the unsmokable amphetamine sulfate. I hereby establish that as the traditional way. It's definitely the one I prefer.
EDIT: And mods, anytime you want to like, UA or move or delete that first post of this thread that I fucked up, that'd be great.
ROA? Every which way and up your butt. All have pros and cons.
I was thinking, which way did he mean is traditional? Then I realized, the whole crystal form is of benefit, ROA-wise, mainly for smokers. Meth-HCl came as a smokable replacement for the unsmokable amphetamine sulfate. I hereby establish that as the traditional way. It's definitely the one I prefer.
EDIT: And mods, anytime you want to like, UA or move or delete that first post of this thread that I fucked up, that'd be great.
Last edited:
T. Calderone
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Scrofula, how did you manage to put that post as the first one? If I u/a it, I think that would make the thread private. I could be wrong though. 
Scrofula
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Yeah, I realized that after I posted. Could always just start a new thread and move everything over but the first?, or maybe edit and clear everything in the first post, and make up some witty and wise introduction and attribute it to CFC? Could just edit move the introduction that's there, and stick in the first post? A bunch of medical links is appropriate for the start of a All-About-Meth thread.
Have the time when I merge, I see the usual "which should be the main thread", half it just does it and puts everything chronological.
(PS. Sorry for making messes in your stickies; my impatient tone was meant for those other two.)
ETA: NEVERmind. Except for the sorry, that still goes.
Have the time when I merge, I see the usual "which should be the main thread", half it just does it and puts everything chronological.
(PS. Sorry for making messes in your stickies; my impatient tone was meant for those other two.)
ETA: NEVERmind. Except for the sorry, that still goes.