Energy drink use frequency among an international sample of people who use drugs: Associations with other substance use and well-being

Peacock, Amy; Bruno, Raimondo; Ferris, Jason; Winstock, Adam

doi:10.1016/j.drugalcdep.2017.01.010

Cited by 17 publications

(23 citation statements)

References 37 publications

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“…Toxic and inflammatory effects of MDMA are exacerbated by its co-administration with other psychoactive substances (Khairnar et al 2010 , 2014 ). Caffeine is commonly consumed with MDMA in energy drinks to reduce drowsiness and fatigue, or it is present in illicit drug preparations, e.g., in ecstasy pills (Peacock et al 2017 ). Molecular mechanism of caffeine action in the brain is based on adenosine receptor antagonism.…”

Section: Introductionmentioning

confidence: 99%

Neurochemical and Neurotoxic Effects of MDMA (Ecstasy) and Caffeine After Chronic Combined Administration in Mice

et al. 2017

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MDMA (3,4-methylenedioxymethamphetamine) is a psychostimulant popular as a recreational drug because of its effect on mood and social interactions. MDMA acts at dopamine (DA) transporter (DAT) and serotonin (5-HT) transporter (SERT) and is known to induce damage of dopamine and serotonin neurons. MDMA is often ingested with caffeine. Caffeine as a non-selective adenosine A1/A2A receptor antagonist affects dopaminergic and serotonergic transmissions. The aim of the present study was to determine the changes in DA and 5-HT release in the mouse striatum induced by MDMA and caffeine after their chronic administration. To find out whether caffeine aggravates MDMA neurotoxicity, the content of DA and 5-HT, density of brain DAT and SERT, and oxidative damage of nuclear DNA were determined. Furthermore, the effect of caffeine on MDMA-induced changes in striatal dynorphin and enkephalin and on behavior was assessed. The DA and 5-HT release was determined with in vivo microdialysis, and the monoamine contents were measured by HPLC with electrochemical detection. DNA damage was assayed with the alkaline comet assay. DAT and SERT densities were determined by immunohistochemistry, while prodynorphin (PDYN) and proenkephalin were determined by quantitative PCR reactions. The behavioral changes were measured by the open-field (OF) test and novel object recognition (NOR) test. Caffeine potentiated MDMA-induced DA release while inhibiting 5-HT release in the mouse striatum. Caffeine also exacerbated the oxidative damage of nuclear DNA induced by MDMA but diminished DAT decrease in the striatum and worsened a decrease in SERT density produced by MDMA in the frontal cortex. Neither the striatal PDYN expression, increased by MDMA, nor exploratory and locomotor activities of mice, decreased by MDMA, were affected by caffeine. The exploration of novel object in the NOR test was diminished by MDMA and caffeine. Our data provide evidence that long-term caffeine administration has a powerful influence on functions of dopaminergic and serotonergic neurons in the mouse brain and on neurotoxic effects evoked by MDMA.

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Section: Introductionmentioning

confidence: 99%

Neurochemical and Neurotoxic Effects of MDMA (Ecstasy) and Caffeine After Chronic Combined Administration in Mice

et al. 2017

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“…18 However, the remaining sociodemographic and alcohol use differences between AmED and alcohol-only consumers were largely consistent between the online and street surveys and confirm what is reflected in international research -AmED consumers are younger, more likely to be male, more likely to have only secondary school education but also be currently studying, consume more alcohol in general, and report greater use of tobacco and other drugs. 10,[17][18][19][20][21][22] Although AmED users generally consume more alcohol than alcohol-only consumers, the role AmED plays in driving risky consumption remains unclear. 17,23 It may be that AmED consumers are attracted to EDs because they are prone to riskier consumption practices and risktaking behaviour.…”

Section: Discussionmentioning

confidence: 99%

“…One representative population study (n = 2000) in 2013 reported that only 5% of Australian adults had consumed AmED in the past 3 months; a higher rate of use (20%) was observed among people aged 18-24. 10 The other two studies targeted the younger ED consumer demographic: 42% of a community sample (n = 403) aged [18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35] reported AmED use in the past 6 months in 2011 11 , and 21% of adults interviewed in five Australian city entertainment precincts on weekend nights (n = 4227) reported AmED use in the past 12 hours in 2011-2012. 12 The lack of prevalence data and inconsistency in estimates across study designs points to the need to replicate these approaches to obtain further estimates of use.…”

Section: Introductionmentioning

confidence: 99%

What do we know about alcohol mixed with energy drink (AmED) use in Australia? Expanding local evidence

Pennay¹,

Peacock²,

Droste³

et al. 2018

Public Health Res Pract

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Objectives: Despite continued health concerns associated with the practice of consuming alcohol mixed with energy drinks (AmED), few Australian studies have examined the popularity of this combination or attempted to characterise AmED consumers. The purpose of this paper is to replicate two previously used survey approaches to consolidate a national picture of AmED consumption in Australia. Methods:The survey approaches used were: an online survey with a convenience sample of New South Wales (NSW), Australia, residents (n = 1931; 63.7% female; median age 23.0 years); and street intercept surveys in regional and metropolitan entertainment precincts in NSW (n = 1265; 58.2% male; median age 21.0 years). Analyses explored the rates and frequency of AmED use across both samples, and the sociodemographic and substance use predictors of AmED consumption in the past 12 months.Results: More than 90% of participants in both samples reported alcohol consumption in the past 12 months, with approximately 40% of current drinkers also reporting AmED use in the past 12 months. Three-quarters of participants interviewed in entertainment precincts reported alcohol consumption in the previous 12 hours, with one in six of these also reporting AmED consumption in the past 12 hours. AmED users across both samples were more likely than alcohol-only consumers to be younger and male, and to report riskier substance use practices.

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“…Alcohol (ethyl alcohol; ethanol) and caffeine are the two most widely used psychoactive substances in the world (Ferreira & Willoughby, 2008; Cappelletti et al, 2015; Peacock et al, 2017). Episodic, moderate-to-heavy alcohol intake, such as during “binging,” constitutes the primary form of excessive alcohol consumption in the US.…”

Section: Introductionmentioning

confidence: 99%

Extra-endothelial TRPV1 channels participate in alcohol and caffeine actions on cerebral artery diameter

Chang

Bukiya

Dopico

2018

Alcohol

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Alcohol (ethyl alcohol; ethanol) and caffeine are the two most widely used psychoactive substances in the world. Caffeine and ethanol have both been reported to constrict cerebral arteries in several species, including humans. We have recently shown that application of 10 μM caffeine mixed with 50 mM ethanol to in vitro pressurized cerebral arteries of rat reduced ethanol-induced constriction. This effect was dependent on the presence of nitric oxide (NO•) and could be observed in de-endothelialized arteries supplied with the NO• donor sodium nitroprusside (SNP). The molecular target(s) of ethanol-caffeine interaction in cerebral arteries has remained unknown. In the present work, we used rat and mouse middle cerebral arteries (MCA) to identify the extra-endothelial effectors of NO•-mediated, caffeine-induced protection against ethanol-evoked arterial constriction. Constriction of intact MCA of rat by either 50 mM ethanol or 10 μM caffeine was ablated in the presence of a selective TRPV1 pharmacological blocker. TRPV1 pharmacological block, but not block of TRPA1, PKG or BK channels, removed caffeine-induced protection against ethanol-evoked rat MCA constriction, whether evaluated in arteries with intact endothelium or in SNP-supplemented, de-endothelialized arteries. In mouse arteries, caffeine-induced protection against ethanol-induced MCA constriction was significantly amplified, resulting into actual vasodilation, upon pharmacological block of TRPV1, and in TRPV1 knock-out arteries. Despite some species-specific differences, our study unequivocally demonstrates the presence of functional, extra-endothelial TRPV1 that participates in both endothelium-independent MCA constriction by separate exposure to ethanol or caffeine and caffeine-induced protection against ethanol-evoked MCA constriction.

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Energy drink use frequency among an international sample of people who use drugs: Associations with other substance use and well-being

Cited by 17 publications

References 37 publications

Neurochemical and Neurotoxic Effects of MDMA (Ecstasy) and Caffeine After Chronic Combined Administration in Mice

Neurochemical and Neurotoxic Effects of MDMA (Ecstasy) and Caffeine After Chronic Combined Administration in Mice

What do we know about alcohol mixed with energy drink (AmED) use in Australia? Expanding local evidence

Extra-endothelial TRPV1 channels participate in alcohol and caffeine actions on cerebral artery diameter

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