Crystal Meth

indeed I have; smoking it in a bulb, I even binged. it was fun, but I dropped it like a failing class, no withdrawals. I've also seen people fall by the wayside, because they didn't have any ambitions.

I don't particularly see how one hit can destroy someone's life (perhaps because it hasn't happened to me), but I don't deny that it can't happen; but I have also seen the widespread abuse of alcohol, and hear about liquor store robberies (imagine that...armed robbery for a legal drug), so tell me that this country doesn't have a worse alcohol problem.

Methamphetamine is C-II regulated, while Ibogaine, a very NON-addictive (it can actually cure addictions) low toxicity substance is C-I, so legislation doesn't necessarily reflect harm potential.

 

You obviously don't live in rural Midwest...here, Meth is the most abused drug...more so than pot or alcohol. I know about six people, myself, that I could get meth from...and only one that I could get pot from. It's an epidemic here...

And as far as liquor store robberies, people don't steal the alcohol, they steal the money LOL.

Either way, meth fucks up your brain...it doesn't allow the neuro-transmitters to fire, it totally blocks them...and it's irreversable.

 

you're right, I don't; I live in South Texas, and have only seen it made in kitchens, and sit as a pound of "glass" in a freezer. I knew of people who ran an interstate drug trade that extended from San Diego, to San Antonio, and these degenerates got too high on their own supply.

media paints it as an "epidemic" everywhere; in the 80's, it was cocaine, in the 90's, crack; and heroin has had it's "epidemic" status in the 70's

plenty of people do both

show me (some abstracts); I don't dispute that it has a degenerative effect, following it's use; but irreversible brain damage after occaisional use, or moderate use, is not really the case; heavy extensive use, probably.

and GABA are the neurotransmitters that block neuronal firing, hence their "inhibitory" action; meth is actually an excitatory drug, not an irreversible inhibitor.

 

look, I'm not trying to say meth is a harmless substance, but there is worse.

and what about the "epidemic" of pharmaceuticals running rampant through pre-grade/grade schools, orchestrated by doctors/HMOs, simply because kids get written off as ADD candidates? scandalous? perhaps...certainly moreso than adults that can make their own decisions.

I'm not comparing seemingly "hopeless addicts" to kids hopped up on methylphenidate, but it sort of reflects irony (methylphenidate is chemically related to methamphetamine)

 

An Abstract from the European Journal of Pharmacology Vol: 439, Issue: 1-3, March 29, 2002 :


A continuing challenge for studies in the neurobiology of drug abuse is to identify and characterize long-lived neuroadaptations that can trigger craving and relapse. We previously reported that rats that had actively self-administered methamphetamine for 5 weeks and were then withdrawn from methamphetamine for 24 h showed marked decreases in somatodendritic dopamine D2 autoreceptor levels in the ventral tegmental area and median and dorsal part of the substantia nigra zona compacta with a corresponding down-regulation of dopamine D1 receptors in the shell of the nucleus accumbens. The purpose of the present study was to determine whether neuroadaptive changes in dopamine receptors or transporters in the brains of rats withdrawn for 24 h from chronic methamphetamine self-administration are persistent changes that can be demonstrated long after withdrawal. A “yoked” procedure was used in which rats were tested simultaneously in groups of three, with only one rat actively self-administering methamphetamine while the other two received yoked injections of either methamphetamine or saline. In vitro quantitative autoradiography was used to determine densities of dopamine uptake sites and dopamine D1 and D2 receptors in different brain regions following 7- and 30-day periods of withdrawal from chronic methamphetamine self-administration. No changes in dopamine transporter and dopamine receptor numbers were detected in any brain region examined in rats self-administering methamphetamine compared with littermates receiving yoked infusions of either methamphetamine or saline. Thus, neuroadaptive changes in densities of dopamine receptors or transporters in certain brain areas may contribute to the reinforcing effects of methamphetamine during the acquisition and maintenance phases of self-administration, but do not appear to contribute to the long-lasting neuroadaptive effects of chronic methamphetamine self-administration, which may trigger craving and relapse.

 

I'm an activist against the use of Methamphetamines because my little sister doesn't have a mom, my grandparents lost their child, and my children and nephew will never meet their grandmother. Because this has happened in my life, I have tried to educate others on what the dangers of meth use really ARE. I don't want anyone else's family go through what my family went through. I believe this has happened in my life for a reason...and I'm trying to do what I can to educate people on the REAL dangers.

 

"rats that had actively self-administered methamphetamine for 5 weeks and were then withdrawn from methamphetamine for 24 h showed marked decreases in somatodendritic dopamine D2 autoreceptor levels in the ventral tegmental area and median and dorsal part of the substantia nigra zona compacta with a corresponding down-regulation of dopamine D1 receptors in the shell of the nucleus accumbens. The purpose of the present study was to determine whether neuroadaptive changes in dopamine receptors or transporters in the brains of rats withdrawn for 24 h from chronic methamphetamine self-administration are persistent changes that can be demonstrated long after withdrawal"

yes, this also occurs from extensive cocaine use, and even chronic MDMA use.


"No changes in dopamine transporter and dopamine receptor numbers were detected in any brain region examined in rats self-administering methamphetamine compared with littermates receiving yoked infusions of either methamphetamine or saline. Thus, neuroadaptive changes in densities of dopamine receptors or transporters in certain brain areas may contribute to the reinforcing effects of methamphetamine during the acquisition and maintenance phases of self-administration, but do not appear to contribute to the long-lasting neuroadaptive effects of chronic methamphetamine self-administration"

this last paragraph doesn't say anything about irreversible receptor damage; given the brain's elasticity to certain stressors, it is able to bring itself to a state of stasis, given a good treatment regimen, such as l-dopa/rasagiline http://www.rasagiline.com/l-dopa.html

mptp is far more damaging to dopamine receptors than meth

 

ah, ok. I don't blame ya, I'd probably do the same.

 

Molecular Brain Research

Vol: 93, Issue: 1, September 10, 2001



Terminal deoxynucleotidyl transferase (TdT)-mediated dNTP nick end labeling (TUNEL) histochemistry is a sensitive method to expose DNA strand breaks in apoptotic cells, but it is difficult to conduct on slide-mounted sections. By using a 80°C/0.5% Triton X-100 pretreatment, we have developed a TUNEL histochemical approach with high specificity and sensitivity using sections from ischemic rat brains. Thereafter, methamphetamine (METH)-induced neuronal death was investigated in mice brains. The results showed that a single injection of 40 mg/kg METH caused neuronal death in several brain areas including the striatum, cortex (frontal, parietal, and piriform), indusium griseum, medial habenular nucleus, and hippocampus. These results further confirmed the presence of METH-induced deleterious effects in nondopaminergic neurons. The significance of these findings is also discussed.

 

This thread is not about any of these drugs...it's about crystal meth.

 

40 mg/kg ?!? jeez...yeah, that'll kill some neurons; that's like a 65kg man doing 2.6 grams of meth, over 50 times a strong dose.

 

i know; just comparatively citing some substances that affect the same receptors.

 

Synapse

Vol: 30, Issue: 3, November 1998




We used Fluoro-Jade, a recently-developed fluorescent indicator of neuronal damage, to identify neurons injured 1–21 days after repeated injections of methamphetamine (m-AMPH) or saline. The m-AMPH-treated rats showed Fluoro-Jade positive neurons in parietal cortex (layers III and IV) and had less striatal tyrosine hydroxylase immunoreactivity than did saline-injected controls. Fluoro-Jade positive neurons were greatest in number 3 days post-treatment; some fluorescent neurons displayed bud-like surface protrusions. These observations support the hypothesis that certain neocortical neurons degenerate after m-AMPH.

AND

Synapse

Vol: 55, Issue: 3, March 2005



Repeated systemic administration of moderate doses of methamphetamine (mAMPH) can result in neuronal damage. In addition to the prominent damage of forebrain dopamine and serotonin terminals, mAMPH also injures certain non-monoaminergic neuronal somata in the cerebral cortex. In previous studies, we have localized the damaged neurons to the “whisker barrels” in primary somatosensory cortex, reported the time course of their appearance, and found that sensory inputs from the mystacial vibrissae appear to play a crucial role in the mechanism of their injury by mAMPH. One common feature of these studies is that they used a single marker for neuronal injury, the fluorochrome dye Fluoro-Jade, which stains neurons injured by disparate mechanisms. Here we compare mAMPH-induced damage to somatosensory cortical neurons as assessed by Fluoro-Jade and immunohistochemical staining for phospho-c-Jun. A neurotoxic regimen of mAMPH induced phospho-c-Jun-positive neurons in both cortical whisker barrels and the substantia nigra. Neurons in the barrel cortex can be sufficiently damaged by mAMPH that they become Fluoro-Jade-positive within 2 hr after the final mAMPH injection. By contrast, phospho-c-Jun immunoreactivity does not appear until 12–24 hr after mAMPH. As reported in an earlier study, unilateral removal of vibrissae prior to mAMPH treatment affords partial protection from injury in the hemisphere contralateral to the vibrissotomy. The vibrissotomized animals show similar decreases in Fluoro-Jade staining and phospho-c-Jun immunoreactivity in the protected hemisphere. Since phospho-c-Jun indicates activation of Jun N-terminal kinase pathways, which have been implicated in apoptosis, we conclude that phospho-c-Jun provides a useful new marker for mAMPH-induced damage to cortical neurons.

 

And just for good measure:

A lot more holes in the Meth abuser's brain.

 

Effect of selegiline on cognitive
functions in Parkinson's disease
by
Dixit SN, Behari M, Ahuja GK
Department of Neurology,
All India Institute of Medical Sciences,
New Delhi.
J Assoc Physicians India 1999 Aug;47(8):784-6

ABSTRACT

BACKGROUND: Selegiline hydrochloride, a selective MAO-B inhibitor is known to improve motor functions in Parkinson's disease (PD). The present study was undertaken to study the effect of selegiline on memory and intelligence of PD patients. MATERIAL AND METHOD: Thirty two patients of PD were divided in two groups: selegiline group (n = 17) received 10 mg selegiline per day and control group (n = 15) did not receive selegiline. Patients receiving trihexyphenidyl and selegiline were excluded. All other treatment remained unchanged. All patients were examined at baseline and after three months for change in UPDRS score, WAIS score, memory test and P300. RESULTS: Patients in selegiline group had less severe disease (UPDRS score 24.11 +/- 14.07) as compared to controls (UPDRS score 40.53 +/- 18.52). There was significant improvement in UPDRS score (p < 0.05), WAIS (p < 0.001) and memory (p < 0.001) in selegiline group. In the control group there was a significant prolongation of P300 latency (p < 0.05). CONCLUSION: The study suggests that selegiline improves memory functions and intelligence in PD patients in addition to motor functions. It also prevents prolongation of P300 latency which is a marker of cognitive function.

(-)Deprenyl (Selegiline): past, present and future
by
Knoll J.
Department of Pharmacology,
Semmelweis University of Medicine,
Budapest, Hungary.
Neurobiology (Bp) 2000;8(2):179-99

ABSTRACT

(-)Deprenyl (Selegiline), the N-propargyl analogue of (-)methamphetamine, is the only drug in clinical case which, by enhancing the impulse propagation mediated release of noradrenaline and dopamine in the brain (catecholaminergic activity enhancer, CAE, effect), keeps in small doses without side-effects the catecholaminergic brain system on a higher activity level. (-)Deprenyl stimulates the catecholaminergic neurons selectively in the brain because, in contrast to PEA and the amphetamines which induce the continuous release of noradrenaline and dopamine from their intraneuronal stores, (-)deprenyl is devoid of this property. It is due to the CAE effect that a) the maintenance of rats on (-)deprenyl during the postdevelopmental phase of their life slows the age-related decline of sexual and learning performances and prolongs life significantly; b) patients with early, untreated Parkinson's disease maintained on (-)deprenyl need levodopa significantly later than their placebo-treated peers, and when on levodopa plus (-)deprenyl, they live significantly longer than patients on levodopa alone; and c) in patients with moderately severe impairment from Alzheimer's disease, treatment with (-)deprenyl slows the progression of the disease. It is reasonable to expect that a prophylactic low dose administration of a safe catecholaminergic activity enhancer substance during the postdevelopmental phase of life will slow the age-related decline of behavioral performances, delay natural death and decrease susceptibility to Parkinson's disease and Alzheimer's disease.

 

Neuroprotection by (-)-deprenyl
and related compounds
by
Maruyama W, Naoi M
Department of Basic Gerontology,
National Institute for Longevity Sciences,
Obu, Japan.
maruyama@nils.go.jp
Mech Ageing Dev 1999 Nov; 111(2-3):189-200

ABSTRACT

There is an increasing number of data by in vitro and in vivo experiments, indicating that (-)-deprenyl is neuroprotective to dopamine neurons, even though detailed mechanism remains to be clarified. In this paper neuroprotection by (-)-deprenyl and structurally related compounds was examined in concern with the suppression of apoptosis induced by a reactive oxygen species, peroxynitrite generated from SIN-1. The apoptotic DNA damage was quantitatively determined using dopaminergic SH-SYSY cells and by a single cell gel electrophoresis (comet) assay. DNA damage induced by peroxynitrite was proved to be apoptotic by prevention of the damage by cycloheximide or actinomycin-D. (-)-Deprenyl and other propargylamines protected the cells from apoptosis in a dose-dependent way. (-)-Deprenyl protected the cells even after it was washed out, suggesting that it may initiate the intracellular process to repress the apoptotic death program. The study on the structure-activity relationship of (-)-deprenyl analogues revealed that a N-propargyl residue with adequate size of hydrophobic structure is essentially required for the anti-apoptotic activity. These results suggest that (-)-deprenyl and related compounds may protect neurons from apoptosis and be applicable to delay the deterioration of neurons during advancing ageing and in neurodegenerative disorders.


my point of posting these: these are viable treatments for chronic meth use;

for moderate use: l-tyrosine, DMAE/choline, and B-complex

 

But it can't reverse what the drug has done to your brain...and they offer their own set of side effects...

 

I didn't think this thread would get junked up by a copy/paste frenzy...

The point is: METH IS BAD, meth kills, and you can be easily addicted. Don't even try it.

 

I'll take your word for it as well as the research cited as a reason not to promote the use of meth, but personally i found it less physically demanding than many other drugs and not addictive at all. This was on several seperate occassions, where I shared a bag with a group of people. I would never buy a bag for myself.

 

Just like any drug (legal or not), it affects everyone differently. Personally, I wouldn't want to chance it, as there have been MANY MANY cases where the person has been addicted after one hit. It also has to do with the history of addiction in your family. Addiction is genetic, so if your parents and grandparents had addictions (nicotine, included), you have a better chance of getting an addiction.