Losing Jacque: A Mother on Meth (good read)
- Thread starter Fausto
- Start date
Meth will fvck you if done more than a few times, there's really no point in trying to salvage someone from it. Your brain is literally unrecoverable.
Very true. Even people who can stay clean after becoming addicted (only about 6% AFAIK) are still pretty much worthless as their brains are just fried from the meth (and all the impurities usualy found in it).
Cliff's NotesOriginally posted by: Skoorb
I'll read and get back to you in 5 hours when i"m done
[*]Meth is bad...mmmnkay?
There's a good bit of data to support both claims, actually. Here's a journal article from Neurology regarding brain damage associated with long-term use of meth. I can't link the full text or images since my access to it is an internal CDC thing so here's the full text.
[Neurology]
Copyright © 2000 American Academy of Neurology
Volume 54(6) 28 March 2000 pp 1344-1349
Evidence for long-term neurotoxicity associated with methamphetamine abuse: A 1H MRS study
[Articles]
Ernst, Thomas PhD; Chang, Linda MD; Leonido?Yee, Maria MD; Speck, Oliver PhD
From the Departments of Neurology (Drs. Ernst, Chang, and Leonido?Yee) and Radiology (Drs. Ernst and Speck), Harbor-UCLA Medical Center, Torrance, CA.
Received May 5, 1999.
Accepted in final form December 3, 1999.
Supported by grants from NIH?Scientist Development Award for Clinicians for L.C. (DA00280) and GCRC MO1-RR00425.
Address correspondence and reprint requests to Dr. Thomas Ernst, Department of Radiology, Harbor-UCLA Medical Center, 1124 W. Carson Street, N-11, Torrance, CA 90502; e-mail: Ernst@afp76.humc.edu
Objective: To determine whether proton MRS (1H MRS) can detect long-term metabolite abnormalities in abstinent methamphetamine users.
Background: Methamphetamine is toxic to dopaminergic and serotonergic neurons in rodents; however, little data are available on the toxic effects of methamphetamine on the human brain.
Methods: 1 H MRS was performed in 26 abstinent methamphetamine abusers with a history of methamphetamine dependence (median total cumulative lifetime exposure, 3,640 g; median recency of last methamphetamine use, 4.25 months) and 24 healthy subjects without a history of drug abuse. Cerebral metabolite concentrations on 1H MRS were measured in the frontal cortex, frontal white matter, and basal ganglia.
Results: The concentration of N -acetylaspartate ([NA]), a neuronal marker, was reduced significantly (-5 to -6%) in the basal ganglia and frontal white matter of methamphetamine users compared with control subjects. The frontal white matter [NA] correlated inversely with the logarithm of the lifetime methamphetamine use. The methamphetamine users also showed significantly reduced total creatine in the basal ganglia (-8%), and increased choline-containing compounds ([CHO], +13%) and myo-inositol ([MI], +11%) in the frontal grey matter.
Conclusions: The reduced [NA] on 1H MRS provides evidence for long-term neuronal damage in abstinent methamphetamine users.
Methamphetamine, also known as ?speed,? ?meth,? ?chalk,? ?crank,? ?ice,? ?crystal,? or ?glass,? is being abused at an increasing prevalence. In a 1996 survey, nearly five million Americans have used methamphetamine at some time in their lives?up from approximately 3.8 million in 1994. 1 Similarly, a network covering more than 500 U.S. hospitals reported a sixfold increase in methamphetamine-related emergency department episodes during the past decade. 2 At Harbor-UCLA Medical Center, a Los Angeles County acute care hospital serving a population of approximately 2.5 million people of mixed ethnicity, 15% of the admissions to the psychiatric emergency room in 1995 and 1997 were related to drug abuse. Within this group, the number of admissions related to methamphetamine abuse was comparable with the number of admissions related to cocaine abuse. 3
Methamphetamine is a potent, indirectly acting sympathomimetic that causes a massive release of dopamine in the brain. The marked increase in dopamine level may be related to the subjective ?high,? similar to that observed with cocaine administration, 4 and some of the neurologic complications are likely due to dopamine-mediated vasoconstrictive effects. 5 The drug may be smoked, taken orally, or injected intravenously. After methamphetamine administration, users report experiences of euphoria, increased alertness and confidence, and reduced fatigue and appetite. Because methamphetamine has a plasma half-life of 12 hours, these acute effects may last between 4 and 24 hours. 6 Medical complications associated with methamphetamine abuse include severe neurologic and psychiatric conditions, such as hemorrhagic and ischemic infarcts, subarachnoid hemorrhages, memory loss, and psychosis. 7-12
Clinical and preclinical observations suggest that methamphetamine may cause long-lasting injury to the brain. In humans, some of the psychiatric conditions, such as paranoid psychosis, may occur not only acutely during methamphetamine exposure but may persist for months or even years after cessation of methamphetamine use. 13,14 In rhesus monkeys, the neurotoxic effects of methamphetamine were observed for as long as 4 years after the last drug exposure. 15 Furthermore, several studies in rodents have shown that methamphetamine is toxic to dopaminergic and serotonergic neurons. 16-20 However, in humans, only two recent PET studies demonstrated decreased dopamine transporters, which suggests long-lasting neurotoxicity due to methamphetamine abuse. 21,22 We hypothesized that abstinent methamphetamine users with a history of dependence would show abnormal concentrations of the neuronal marker N -acetylaspartate ([NA]), associated with neuronal damage. Therefore, abstinent methamphetamine users were evaluated for cerebral [NA] using 1H MRS.
Twenty-six subjects with a history of methamphetamine dependence (mean age, 33.4 ± 7.9 years; 13 men, 13 women were recruited from several local drug rehabilitation centers. Twenty-four healthy subjects with no history of drug dependence (mean age, 30.3 ± 4.6 years; 12 men, 12 women were also recruited for comparison. There was no statistically significant difference in age between the two groups. Each subject underwent an extensive screening evaluation, consisting of a physical and neuropsychiatric history and examination, screening blood tests, and urine toxicology screens. Based on the screening evaluation, methamphetamine users were enrolled only if they fulfilled the following criteria:
1. Age, 18 to 50 years
2. History of methamphetamine dependence according to the Diagnostic Statistical Manual, 4th edition, criteria
3. Regular methamphetamine use for at least 12 months, at least 5 days/week, and at least 0.5 g per day
4. Methamphetamine had been their primary drug of choice
5. No present or past alcohol abuse or dependence
6. Last used methamphetamine more than 2 weeks earlier
7. Negative urine toxicology screen for illicit drugs (amphetamines, cocaine, marijuana, benzodiazepine, barbiturates, and opiates)
Subjects in both groups were excluded if they
1. Were seropositive for HIV-1
2. Had a history of head trauma with loss of consciousness for more than 30 minutes
3. Had a history of substance dependence (other than methamphetamine and nicotine), including alcohol
4. Had any chronic medical, neurologic, or psychiatric illnesses (e.g., seizure disorders, depression, schizophrenia, hypertension, or diabetes)
5. Were pregnant
6. Had metallic objects in their body
All healthy control subjects were on no medications and had no history of substance dependence, including alcohol (except for nicotine). Before the study, each subject was informed verbally of the study protocol and signed a consent form approved by our institution.
Magnetic resonance spectroscopy. <http://gateway.ovid.com/rel_live/server1/gifs/ftup.gif>
Subjects were studied with MRI and localized 1 H MRS. MRI was performed on a 1.5-T scanner (General Electric Signa, Milwaukee, WI). Imaging began with the acquisition of a sagittal T1-weighted localizer (echo time/relaxation time [TE/TR], 11/500 msec; slice thickness, 4 mm; gap, 1 mm) followed by an axial fast inversion recovery scan (TE/inversion time/TR, 32/120/4,000 msec; 3.5-mm contiguous slices). Lastly, a coronal fast-spin echo scan (TE/TR, 102/4,000 msec; 5-mm contiguous slices) was performed.
In each subject, three brain regions (voxels) were studied with 1H MRS: the midfrontal gray matter, right frontal white matter, and right basal ganglia (figure 1 ). The voxels were chosen to include only gray matter or only white matter for the two frontal brain regions, and to include the same parts of the caudate, putamen, and globus pallidus in the basal ganglial region. Due to anatomic variations, the resulting voxel sizes were variable, with a range of 3 to 5 mL. The voxel sizes and water line widths were not significantly different between drug users and control subjects. Data were acquired using a double spin echo sequence, or point resolved spectroscopy, which was optimized for acquisition of 1H MR spectra from the frontal lobe. 23,24 The acquisition parameters were TE/TR, 30/3,000 msec; and 64 averages were acquired. To avoid the ambiguities caused by the use of metabolite ratios, metabolite concentrations were determined. 25,26 Briefly, the amplitude of the unsuppressed water signal was measured at 10 different echo times. From these data points, the signal strengths of brain tissue water and CSF, corrected for T2 decay, were estimated by least-squares fitting. 25 The brain tissue water signal (excluding the signal from CSF) was used as a reference to calculate metabolite concentrations. The resulting metabolite concentrations are independent of the partial volumes of CSF in each MRS voxel. The CSF signal strength was used to calculate the percent CSF in each voxel, which represents a quantitative measure of regional cerebral atrophy. The data were processed with a semi-automatic program. 25,26 The program yielded metabolite concentrations in ?institutional units,? which were converted into concentrations with millimoles per kilogram using published normal values. 26 Typical interindividual variations in the metabolite concentrations were approximately 10%, and intrasubject variabilities were 3 to 8%. Because the creatine concentrations ([CR]) were abnormal in the methamphetamine users, we do not report metabolite ratios.
[Graphic]
[Help with image viewing]
Figure 1. Coronal T2-weighted MRI showing the typical locations of the MRS voxels: midfrontal gray matter (left), right frontal white matter (middle), and right basal ganglia region (right).
Statistical analyses were performed using StatView (version 4.51; Abacus Inc., Berkeley, CA). Student?s t -tests were performed to determine the significance of differences in cerebral metabolite concentrations between methamphetamine users and control subjects. To test for possible relationships between drug exposure and cerebral metabolite abnormalities, linear regression analyses were performed using the metabolite concentrations as dependent variables, and the logarithm of the cumulative lifetime drug use in grams and the logarithm of the number of months since last drug use as independent variables. A type I error probability <= 0.05 was used to determine significance.
Results. <http://gateway.ovid.com/rel_live/server1/gifs/ftup.gif>
The drug users had a median total cumulative lifetime exposure to methamphetamine of 3,640 g (range, 550 to 15,300 g) and a median period of abstinence before undergoing MRS of 4.25 months (range, 0.5 to 21 months). The routes of methamphetamine administration were as follows: snorting only (n = 3); smoking only (n = 1); snorting and smoking (n = 17); snorting and IV injection (n = 3); snorting, smoking, and IV injection (n = 1); and snorting, smoking, and oral (n = 1). The methamphetamine users had a median education level of 12.5 years. Their mean annual income, obtained by self-report, after cessation of drug abuse ($17,300) was lower than their income while they were abusing drugs ($27,000;p = 0.008, paired sign test). Eleven subjects had a history of incarceration related to methamphetamine abuse. The lower income after cessation of drug abuse was related to several factors, including the elimination of illegal sources of income, the ability to work longer hours while abusing methamphetamine, and being unemployed during the drug rehabilitation period for some of the subjects.
Methamphetamine users showed metabolite abnormalities in all three brain regions (figure 2 and table). Specifically, there was a significant reduction of the concentration of N-Acetyl compounds, [NA], in the basal ganglia (-6%, p = 0.008), and a trend for reduction in the frontal white matter (-5%, p = 0.1), of methamphetamine users compared to control subjects. In the basal ganglia, the methamphetamine users also showed a reduced concentration of total creatine, [CR] (-8%, p = 0.02). In the frontal gray matter, the concentration of choline-containing compounds ([CHO]) and myo-inositol ([MI]) was increased in the methamphetamine users compared to the control subjects (+13%, p = 0.01; and +11%, p = 0.02, respectively). The percent CSF was slightly, but significantly, higher in the frontal white matter region of the methamphetamine users (2.2% vs. 1.5% in the control subjects;p = 0.04); this may be a result of slight differences in voxel placement.
[Graphic]
[Help with image viewing]
Figure 2. Cerebral metabolite concentrations in the frontal gray matter (GM), frontal white matter (WM), and the basal ganglia of methamphetamine users and control subjects. The error bars represent standard errors. NA =N-acetyl-containing compounds; CR = creatine plus phosphocreatine; CHO = choline-containing compounds; MI = myo-inositol.
[Graphic]
[Help with image viewing]
Table 1. Cerebral metabolite concentrations (mmoles/kg) from 1H MRS in methamphetamine users and control subjects (mean ± SE)[NA] = concentration of N-acetylaspartate; [CR] = concentration of creatine; [CHO] = concentration of choline; [MI] = concentration of myoinositol.
In the linear regression analyses between metabolite concentrations and measures of drug exposure, [NA] in the right frontal white matter region showed a significant decline with the logarithm of cumulative lifetime methamphetamine use (r = -0.61, p = 0.003;figure 3 ). This regression was significant even after applying a Bonferroni correction (i.e., after accounting for the fact that 12 regressions [four metabolites times three regions] were performed). The inverse relationship of [NA] with the lifetime exposure to methamphetamine is also evident from figure 4 . In contrast, there was no relationship between cumulative lifetime exposure or recency of methamphetamine use and [NA] in the frontal cortex or the basal ganglia, or any of the other metabolite concentrations.
[Graphic]
[Help with image viewing]
Figure 3. Dependence of the concentration of N-acetylaspartate ([NA]) in the right frontal white matter region on the logarithm of cumulative lifetime methamphetamine use. The solid line represents the regression line whereas the horizontal dashed line indicates the mean [NA] in the control subjects. The data indicate that there is more severe neuronal injury (i.e., decreased [NA]) in the white matter of subjects with a higher lifetime exposure to methamphetamine. r = -0.61, p = 0.003.
[Graphic]
[Help with image viewing]
Figure 4. Proton MRS spectra from the frontal white matter region of two abstinent subjects with a cumulative lifetime methamphetamine exposure of 1.8 kg and 15 kg, and a control subject. The subject with the high-dose lifetime exposure (15 kg) to methamphetamine shows reduced N -acetylaspartate (NAA) concentration, compared with the subject with the lower exposure (1.8 kg) and with the control subject. MI = myoinositol; Cho = choline; CR = creatine.
Discussion. <http://gateway.ovid.com/rel_live/server1/gifs/ftup.gif>
We found abnormal brain chemistry in abstinent methamphetamine abusers. [NA] is reduced by 6% in the frontal lobe and by 5% in the basal ganglia of methamphetamine users. NA, which comprises 80% of the NA peak, is a marker for mature neurons 27 ; therefore, reduced [NA] indicate reduced neuronal density or neuronal content. Diseases associated with neuronal damage or loss on pathology consistently have shown decreased [NA] on 1H MRS: Examples include dementias, epilepsy, MS, brain tumors, cerebral infarction, HIV brain diseases, and many other neurologic diseases. 28-36 Therefore, the reduced [NA] in all three brain regions, and its dose-dependent decrease in the frontal white matter, in abstinent methamphetamine users suggest neuronal loss or persistent neuronal damage. Furthermore, since our metabolite concentrations are corrected for the percent CSF in each voxel, partial volume effects due to regional brain atrophy cannot account for the decreases in the metabolite concentrations. Except for a very small increase in the percent CSF in the frontal white matter voxel (+0.7%), which may be due to differences in voxel location, the methamphetamine users showed no significant regional brain atrophy, with normal percent CSF in the frontal cortex and the basal ganglia. In contrast, patients with brain atrophy due to degenerative brain diseases, such as Alzheimer?s disease or fronto-temporal dementia, consistently show increased percent CSF within the MRS voxels with our MRS techniques. 33,34
The 1H MRS evidence for neuronal loss or damage in abstinent methamphetamine users is consistent with preclinical data and the results of two recent PET studies in humans. In rodents, methamphetamine has been shown to be toxic to dopaminergic and serotonergic neurons. 16-20 In two rhesus monkeys, the neurotoxic effects of methamphetamine persisted for as long as 4 years. 15 These neurotoxic effects included decreased dopamine and serotonin concentrations and decreased uptake of dopamine and serotonin in the caudate, as well as neuropathologic abnormalities (dystrophic axons and slight fibrillary gliosis in the substantia nigra). Similarly, two recent PET studies in humans found decreased dopamine transporter density in abstinent methamphetamine users. 21,22 It is unclear, however, whether the decreased dopamine transporter density in these abstinent users represents downregulation, occupied transporters, or persistent loss due to neuronal damage. The decreased [NA] measured in our study provides the first in vivo evidence for neuronal injury in the frontal lobes and the basal ganglia of methamphetamine users. The finding that [NA] in the frontal white matter region, but not in the other two regions, was dependent on the cumulative lifetime exposure suggests that white matter may be less susceptible to the toxic effects of methamphetamine than gray matter. The persistence of these 1H MRS abnormalities may be related to persistent abnormal behaviors, such as violence, psychoses, and personality changes, which are observed in some individuals months or even years after their last drug use. 13,14
Other metabolite abnormalities in the methamphetamine users were increased [CHO] and [MI] in the frontal gray matter. MI is present only in glial cell cultures, and thus may be considered a glial marker. 37 Similarly, since increased [CHO] reflects increased cell membrane turnover and since [CHO] is approximately three times higher in glial cells than in neuronal cells, 37 both increased [CHO] and [MI] in the frontal cortex of the drug users may reflect glial proliferation (astrocytosis). Methamphetamine-induced astrocytosis has been observed in several preclinical studies; glial cells in rats showed increased size and staining intensity one day after four low doses (10 or 20 mg/kg) of methamphetamine. 18,19,39 Taken together, the finding of decreased [NA] accompanied by increased [MI], which has been observed in many active brain disorders studied by our group and others, 33,34,36,39 most likely indicate glial proliferation in response to neuronal injury.
Methamphetamine has been used to treat attention deficit hyperactive disorder in children, 40,41 and narcolepsy and idiopathic hypersomnia. 42 The therapeutic doses are much lower (typically 5 to 60 mg per day) than those consumed by our subjects (500 to 3,500 mg per day). At these lower doses, the psychostimulant methamphetamine has a paradoxical calming effect. Recent studies in genetically engineered mice without dopamine transporter demonstrated that the calming effects of several psychostimulants, including amphetamine, at low doses were related to increased serotonergic neurotransmission. 43 Therefore, the dopamine-mediated neurotoxicity of methamphetamine at high doses may not occur with the low-dose treatment regimens used in patients. Lastly, although our study shows cerebral metabolite abnormalities even in subjects with abstinence for as long as 21 months, additional studies are needed to determine whether these abnormalities are reversible with treatment or with longer periods of abstinence.
Acknowledgment
Geekbabe
Moderator Emeritus<br>Elite Member
DainBramaged
Lifer
- Jun 19, 2003
- 23,448
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Originally posted by: Fausto
Cliff's NotesOriginally posted by: Skoorb
I'll read and get back to you in 5 hours when i"m done
[*]Meth is bad...mmmnkay?
Dammit, I knew I shouldn't have ever started. Oh well, guess I am screwed now.
meth is definitely becoming the scourge of our society.
there are no redeemable qualities of that drug, whatsoever.
there are no redeemable qualities of that drug, whatsoever.
Sorry about that. Typical jounal article, but the data is there.Originally posted by: Geekbabe
I dare say that if you can read Fausto's post that you gotta be ok
Is this a lot of meth? Does this qualify for the "more than a few times" caveat? I'm just wondering, because I really know nothing about meth.
This sounds like a fun drug...
I'll find this post and read it later today. Gotta go till 2:00 pm.
I worked as a diesel mechanic on over the road, long haul trucks for 18 yrs.
I came in contact with several drives that had used speed for years.
Most had one oar in the water, never to be whole again.
The brain is a wonderful chemical factory. Don't overclock it.
I am NOT standing on the moral high ground as I post this..:sun:
I worked as a diesel mechanic on over the road, long haul trucks for 18 yrs.
I came in contact with several drives that had used speed for years.
Most had one oar in the water, never to be whole again.
The brain is a wonderful chemical factory. Don't overclock it.
I am NOT standing on the moral high ground as I post this..:sun:
Good article, but depressing as hell. I'm sure there's plenty of other stories just like this one out there....
On a related sidenote: I rented "Spun" yesterday. Good flick, but after seeing that and reading this article, it just reinforced an already firm conviction to never ever touch the stuff. Not to mention, I grew up in Methville (Ramona, California) and knew more than a few people who got hooked on tweek.
On a related sidenote: I rented "Spun" yesterday. Good flick, but after seeing that and reading this article, it just reinforced an already firm conviction to never ever touch the stuff. Not to mention, I grew up in Methville (Ramona, California) and knew more than a few people who got hooked on tweek.
Hang on...still looking. I'm trying to find journal articles rather than stuff from www.drugsarebadmnnnkay.com and such.
Red Dawn
Elite Member
- Jun 4, 2001
- 57,529
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Well that's being buzzed for at least 260 days a year so I would say that was a lot. Also since a dose of Meth lasts longer than a dose of Cocaine that amount taken daily probably would get you pretty much out there. Plus when you take into account that meth causes lack of sleep and lack of appetite and I would say that a person doing that much was living an extremely unhealthy lifestyle. Even if it didn't effect your brain it would take it's toll on the rest of your body.
LMAO....the yahoo/bizrate auto-link-to-whatever-your-search-term-was thingy can be amusing at times.
Oooooo.....any hot deals?
Oooooo.....any hot deals?
i'm not going to read that article because i know it will upset me. meth is the devil.
i had many friends who got addicted to it in highschool and i watched them steal from their parents and friends and litterally waste away until their eyes sunk into their head and their body was little more than just bones. i used to cry when my friends would call me and say things like "i've been awake for 3 days and i still havent eaten" or they'd miss school because they went on a bender and were awake for a week and then needed to sleep for like 4 days when they came down because they hadn't slept or eaten the whole time they were high.
the worst part was they could see that they needed to stop but couldn't.
i had many friends who got addicted to it in highschool and i watched them steal from their parents and friends and litterally waste away until their eyes sunk into their head and their body was little more than just bones. i used to cry when my friends would call me and say things like "i've been awake for 3 days and i still havent eaten" or they'd miss school because they went on a bender and were awake for a week and then needed to sleep for like 4 days when they came down because they hadn't slept or eaten the whole time they were high.
the worst part was they could see that they needed to stop but couldn't.
I couldn't find any definitive data....the recidivism rate is anywhere from 60% to 98% depending who you ask, apparently. I'll keep digging as I was hoping to find peer-reviewed data.
There was a show on HBO. Crank: Made in America. They basically said it was almost impossible to quit and even if you did, your brain would never be right again.
Maybe now, but I can see Meth becoming the larger problem in the long run due to its low cost and ease of manufacture. I couldn't tell you how to get heroin, but any idiot can cook meth if they really want to.
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