A Comparison of Patterns of Methamphetamine and Cocaine Use

Los Angeles Addiction Research Consortium, USA.
Journal of Addictive Diseases (Impact Factor: 1.46). 02/2002; 21(1):35-44. DOI: 10.1300/J069v21n01_04
Source: PubMed


Typical use patterns of methamphetamine (MA) users were examined using self-report measures from 120 MA and 63 cocaine users. Twenty (14 MA and 6 cocaine) of the participants also took part in structured interviews designed to provide more specific descriptions of their drug use. The typical MA user uses more than 20 days a month. Use is evenly spaced throughout the day, and although the amount of drug used per day is not different, MA users use fewer times per day than do cocaine users. Fewer of the cocaine users are continuous users, and they use in the evening rather than the daytime. The cocaine pattern of fewer days of use, evening use, and more frequent doses per day fits a picture of recreational use, whereas the all-day-most-days methamphetamine pattern does not.

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    • "Subjects who are methamphetamine dependent are estimated to selfadminister between 500 and 1400 mg of the drug daily in one to five doses, and more than 20 times per month (Dean et al., 2013; Simon et al., 2002). This becomes a remarkable load on the brain that takes the drug up fast. "
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    ABSTRACT: Administration of amphetamine and methamphetamine can elicit psychiatric adverse effects at acute administration, binge use, withdrawal, and chronic use. Most troublesome of these are psychotic states and aggressive behavior, but a large variety of undesirable changes in cognition and affect can be induced. Adverse effects occur more frequently with higher dosages and long-term use. They can subside over time but some persist long-term. Multiple alterations in the gray and white matter of the brain assessed as changes in tissue volume or metabolism, or at molecular level, have been associated with amphetamine and methamphetamine use and the psychiatric adverse effects, but further studies are required to clarify their causal role, specificity, and relationship with preceding states and traits and comorbidities. The latter include other substance use disorders, mood and anxiety disorders, attention deficit hyperactivity disorder, and antisocial personality disorder. Amphetamine- and methamphetamine-related psychosis is similar to schizophrenia in terms of symptomatology and pathogenesis, and these two disorders share predisposing genetic factors. © 2015 Elsevier Inc. All rights reserved.
    International Review of Neurobiology 12/2015; 120:179-204. DOI:10.1016/bs.irn.2015.02.004 · 1.92 Impact Factor
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    • "Rodents that are allowed to self-administer infusions of MA also approach this range of consumption, with daily intake of MA exceeding 6 mg/kg after only 21 days of access (Parsegian et al, 2011; Reichel et al, 2011; Rogers et al, 2008). As MA-dependent adults typically use the drug between 1 and 5 times a day (McKetin et al, 2008; Simon et al, 2002), we estimate that most doses of MA range between 0.60 to 3.5 mg/kg per dose, although tolerant injecting users can exceed 4 mg/kg per dose, with maximum reported doses exceeding 12 mg/kg per injection (Buffum and Shulgin, 2001; Kramer et al, 1967). As rats and other animals metabolize MA more readily than humans (Caldwell et al, 1972), it is unclear whether equivalent mg/ kg doses are physiologically identical between humans and animals. "
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    ABSTRACT: Methamphetamine (MA) is one of the most commonly abused illicit substances worldwide. Among other problems, abuse of the drug has been associated with reduced cognitive function across several domains. However, much of the literature has not attempted to differentiate cognitive difficulties caused by MA abuse from preexisting cognitive difficulties that are likely caused by other factors. Here, we address this question, evaluating evidence for a priori hypotheses pertaining to six lines of research: (a) animal studies; (b) cross-sectional human studies; (c) a twin study; (d) studies of changes in cognition with abstinence from MA; (e) studies of changes in brain structure and function with abstinence from MA; and (f) studies of the relationship between the severity of MA abuse and the extent of cognitive deficits observed. Overall the findings were mixed, with some support for a causal relationship between MA abuse and cognitive decline, and other findings suggesting that there is no relationship. The preponderance of the data, however, does support the possibility that MA abuse causes cognitive decline, of unknown duration, in at least some users of the drug. When averaged across individuals, this decline is likely to be mild in early-to-middle adulthood. However, moderator variables are likely to contribute to the presence and/or severity of cognitive decline exhibited by a given individual.Neuropsychopharmacology advance online publication, 5 September 2012; doi:10.1038/npp.2012.179.
    Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology 09/2012; 38(2). DOI:10.1038/npp.2012.179 · 7.05 Impact Factor
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    • "Evidence obtained from clinical studies suggests that most human abusers initially use lower doses of METH, administered at relatively long intervals, before progressively increasing the dose, reducing the interval between successive administrations and eventually engaging in multiple daily administrations (Angrist, 1994; Kramer, 1972; Simon et al., 2002). Importantly, the gradually increased levels of METH exposure do not cause the toxic effects that are associated with high acute METH doses in humans (Angrist, 1994; Kramer, 1972; Simon et al., 2002). Thus, to closely approximate METH abuse patterns in humans, we administered METH to mice according to a non-neurotoxic escalating dose treatment. "
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    ABSTRACT: Genetic factors involved in neuroplasticity have been implicated in major psychiatric illnesses such as schizophrenia, depression, and substance abuse. Given its extended interactome, variants in the Disrupted-In-Schizophrenia-1 (DISC1) gene could contribute to drug addiction and psychiatric diseases. Thus, we evaluated how dominant-negative mutant DISC1 influenced the neurobehavioral and molecular effects of methamphetamine (METH). Control and mutant DISC1 mice were studied before or after treatment with non-toxic escalating dose (ED) of METH. In naïve mice, we assessed METH-induced conditioned place preference (CPP), dopamine (DA) D2 receptor density and the basal and METH-induced activity of DISC1 partners, AKT and GSK-3β in the ventral striatum. In ED-treated mice, 4 weeks after METH treatment, we evaluated fear conditioning, depression-like responses in forced swim test, and the basal and METH-induced activity of AKT and GSK-3β in the ventral striatum. We found impairment in METH-induced CPP, decreased DA D2 receptor density and altered METH-induced phosphorylation of AKT and GSK-3β in naïve DISC1 female mice. The ED regimen was not neurotoxic as evidenced by unaltered brain regional monoamine tissue content. Mutant DISC1 significantly delayed METH ED-produced sensitization and affected drug-induced phosphorylation of AKT and GSK-3β in female mice. Our results suggest that perturbations in DISC1 functions in the ventral striatum may impact the molecular mechanisms of reward and sensitization, contributing to comorbidity between drug abuse and major mental diseases.
    Neuropharmacology 02/2011; 62(3):1242-51. DOI:10.1016/j.neuropharm.2011.02.003 · 5.11 Impact Factor
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