Mortality among cocaine users: A systematic review of cohort studies

Degenhardt, Louisa; Singleton, Jessica; Calabria, Bianca; McLaren, Jennifer; Kerr, Thomas; Mehta, Shruti H.; Kirk, Gregory D.; Hall, Wayne

doi:10.1016/j.drugalcdep.2010.07.026

Cited by 191 publications

(106 citation statements)

References 24 publications

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“…CA treatment consists of psychotherapy and self‐help groups, which do not provide benefits for many patients (Alterman, McKay, Mulvaney, & McLellan, 1996; Carroll et al., 2004; Kampman et al., 2001). Improved treatment for CA is needed as dropout rates in treatment programs are high (Kampman et al., 2002), relapse is common among patients who complete treatment (McKay et al., 2010), and mortality among CA individuals is 4–8 fold greater compared to age and sex‐matched peers (Degenhardt et al., 2011). Despite decades of controlled clinical trials, with some medications showing efficacy in preclinical animal models, no FDA‐approved pharmacotherapy exists for CA.…”

Section: Introductionmentioning

confidence: 99%

Reading LINEs within the cocaine addicted brain

Doyle

Doucet-O’Hare²,

Hammond

et al. 2017

Brain and Behavior

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IntroductionLong interspersed element (LINE)‐1 (L1) is a type of retrotransposon capable of mobilizing into new genomic locations. Often studied in Mendelian diseases or cancer, L1s may also cause somatic mutation in the developing central nervous system. Recent reports showed L1 transcription was activated in brains of cocaine‐treated mice, and L1 retrotransposition was increased in cocaine‐treated neuronal cell cultures. We hypothesized that the predisposition to cocaine addiction may result from inherited L1s or somatic L1 mobilization in the brain.MethodsPostmortem medial prefrontal cortex (mPFC) tissue from 30 CA and 30 control individuals was studied. An Alexafluor488‐labeled NeuN antibody and fluorescence activated nuclei sorting were used to separate neuronal from non‐neuronal cell nuclei. L1s and their 3' flanking sequences were amplified from neuronal and non‐neuronal genomic DNA (gDNA) using L1‐seq. L1 DNA libraries from the neuronal gDNA were sequenced on an Illumina HiSeq2000. Sequences aligned to the hg19 human genome build were analyzed for L1 insertions using custom “L1‐seq” bioinformatics programs.ResultsPreviously uncataloged L1 insertions, some validated by PCR, were detected in neurons from both CA and control brain samples. Steady‐state L1 mRNA levels in CA and control mPFC were also assessed. Gene ontology and pathway analyses were used to assess relationships between genes putatively disrupted by novel L1s in CA and control individuals. L1 insertions in CA samples were enriched in gene ontologies and pathways previously associated with CA.ConclusionsWe conclude that neurons in the mPFC harbor L1 insertions that have the potential to influence predisposition to CA.

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Section: Introductionmentioning

confidence: 99%

Reading LINEs within the cocaine addicted brain

Doyle

Doucet-O’Hare²,

Hammond

et al. 2017

Brain and Behavior

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“…associated with a significant degree of cardiotoxicity, particularly coronary artery disease and ventricular hypertrophy, independent of cocaine concentration [78]. According to Degenhart [79] mortality is four to eight times higher among cocaine users than age and sex peers in the general population.…”

Section: Narcoticsmentioning

confidence: 99%

Doping for Chess Performance

Golf¹

2015

J Sports Med Doping Stud

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During a chess game, the needed energy is first derived instantly from ATP and creatine-phosphate, then within a few seconds later from glycogen stores in brain, glycogen, muscle and liver and finally, 1-2 hours later from adipose tissue. Anaerobic oxidation of glucose-derivative from glycogen delivers energy 6 times faster than aerobic oxidation of glucose and oxidation of fatty acids; correspondingly, mental activity can perform as well 6 times faster as long as glycogen is available.The mental profile of chess players correlates with cerebral processes such as attention, conflict solution, memory, motivation and recognition, which together constitute a specific chess-domain expertise.A chess player may compete best when a) regularly physical exercise is carried out to compete in strenuous chess tournaments and to stimulate mental cognition, b) super compensated glycogen is accumulated in brain, muscle and liver by corresponding nutrition and physical and mental activities, and c. an active mental disposition is available for complex brain tasks during chess by complementary treatment schemes e.g., cogni-tive enhancement (CE) by chess training with chess boards, chess books, building chess images, visual observation of chess games, vocational training with chess, metacognitive training, and additionally regular light physical stress. An illicit improvement of brain performance for chess playing may be achieved by several measures:1.Increase of O 2 supply by therapy with erythropoietin (EPO) for chess tournaments at high altitudes and for chess players with lung diseases 2.Increase of body glycogen by therapy with insulin Regular non-medical use of steroid and proteohormones in elevated concentrations and CE-drugs must also consider numerous side effects ranging from simple metabolic disturbances through cardiac problems to cognitive decline to tumorgenesis and sudden death.

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“…Musto [3] and Behrens et al [4], for example, have argued that the visible adverse effects of a drug epidemic act as a brake on consumption. Five years might seem too short a period for a process such as this to occur, but it is important to remember that we are dealing with non-linear processes.…”

Section: We Know Too Little About Demand: Comments On 'Cocaine's Fall'mentioning

confidence: 99%

“…drug-using) population may diminish rapidly. A third possibility is that the growing purity of cannabis use may have boosted the share of drug 'innovators' trying cannabis rather than cocaine, with the result that ever larger numbers of 'imitators' followed in their wake (for models of this sort see Bass [6] and Behrens [4]). A fourth (and complementary) possibility is that, as the price of cocaine rose and the real price of cannabis fell, heavy users of cocaine switched to cannabis use to moderate the effects of cocaine withdrawal.…”

Section: We Know Too Little About Demand: Comments On 'Cocaine's Fall'mentioning

confidence: 99%

“…Cocaine, and particularly crack cocaine, is no doubt more harmful to the individual and society than marijuana [2]. While some have argued that the scientific basis for such rankings are incomplete, objectively speaking, standardized mortality ratios (SMRs) for heroin (SMR = 15), cocaine and methamphetamines (SMR = 4 to 8) are exceptionally high [3][4][5], whereas marijuana is not associated with an elevated risk of mortality [6].…”

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confidence: 99%

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