Caffeine potentiates methamphetamine-induced toxicity both in vitro and in vivo

Sinchai, Theerin; Plasen, Surin; Sanvarinda, Yupin; Jaisin, Yamaratee; Govitrapong, Piyarat; Morales, Noppawan Phumala; Ratanachamnong, Piyanee; Plasen, Duangporn

doi:10.1016/j.neulet.2011.07.026

Cited by 30 publications

(25 citation statements)

References 20 publications

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“…Catecholaminergic and serotonergic nerve signaling may be altered by methamphetamine. Based on the theory, the emphasis is on differences in effects observed between the striatal and nucleus accumbens areas of the brain following acute as well as repeated dosing and withdrawal (19). Caffeine potentiates MA neurotoxicity, possibly via a mechanism involving an increase in dopamine release and excess reactive oxygen species generation (19).…”

Section: Discussionmentioning

confidence: 99%

Comparison of Brain White Matter Hyperintensities in Methamphetamine and Methadone Dependent Patients and Healthy Controls

et al. 2014

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Background:Previous studies have proven the development of white matter hyperintensities (WMH) in methamphetamine and opioid users. Opiates and methamphetamines (MA) are the most common addictive agents in Iran. The adverse effects of drugs on the CNS is of concern to specialists and researchers, and given that the neurotoxicity associated with methamphetamine is greater than opioids, it is hypothesized that the severity of WMH in patients with methamphetamine dependence is more than opioid drug-dependent individuals.Objectives:To our knowledge, this is the first research comparing the effect of methamphetamine and methadone (M) on the brain.Patients and Methods:In a historical cohort study, we compared WMH in the brain MRI of 50 methamphetamine-dependent patients, 50 methadone-dependent patients and 50 healthy volunteers who were matched for age, sex and dominant hand.Results:WMH was detected in 18 methamphetamine users, in 12 methadone users and in seven controls (P = 0.038). The site of brain lesions in MA users was mostly in the frontal lobe in 17 cases, in M users in the frontal lobe in 12 cases and in the control group, it was in the parietal lobe in four cases (P=0.001). The frontal lobes were the predominant locations of WMH in MA and M groups (P = 0.001). The frequency of brain lesions was mostly in the deep WM in 18 cases in MA users, in 12 cases in M users and in two cases in the control group (P=0.007). Hyper-signal foci of deep WM in the MA group were grade I (punctuate) in 12 cases, grade II (beginning confluence) in five cases and grade III (large confluent) in four cases. In the M group, there were six cases in grade I, three cases in grade II and one case in grade III. In the control group, there were three grade I cases, two grade II cases, and no grade III cases. Except for periventricular WMH (P = 0.13), there were statistical significant differences in the deep WMH (P = 0.007) and subcortex WMH (P = 0.01) between the three groups. The history of using other drugs and the duration of MA and M consumption were similar. The prevalence of brain lesions was generally higher in both drug user groups compared with the healthy controls. Increased WMH in the MA group was higher than the M group.Conclusions:A greater number of blood flow defects and ischemic lesions in the brain of MA users compared to opiate users may explain the prevalence of psychiatric disorders in these patients.

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Section: Discussionmentioning

confidence: 99%

Comparison of Brain White Matter Hyperintensities in Methamphetamine and Methadone Dependent Patients and Healthy Controls

et al. 2014

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“…10,11 Besides interest in this interaction with regard to psychostimulant properties, recent studies from our and other groups have indicated that amphetamine-related psychostimulants exert toxic and proinflammatory effects on the brain, and that caffeine may amplify these effects. [12][13][14] This adds to the evidence showing that caffeine exacerbates the noxious effects of amphetaminerelated psychostimulants on peripheral organs, 15 and suggests that combined consumption of caffeine and psychostimulants may pose a health risk, which may even affect the brain.…”

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confidence: 89%

“…Moreover, caffeine may increase locomotor effects, seizures, hyperthermia and death caused by acute amphetamine 2,26 and elevate motility and death induced by METH in rats. 14,33 Of relevance, in relation to the social crowded environment in which amphetamine-related drugs are consumed, MDMA further increases body temperature by 1.5°C-2°C in group-housed rats, 34 and coadministration of caffeine provokes a dose-dependent increase in the peak temperature response and duration of the hyperthermic effect of MDMA. Interestingly, while an elevation in body temperature is observed when rats are housed in groups at standard ambient temperatures, a decrease in body temperature is observed when rats are housed individually or at low ambient temperature.…”

Section: Psychostimulant Effectsmentioning

confidence: 99%

“…12 Administration of METH and MDMA is also known to induce neuroinflammation in rats and mice 13,14,43 and combined use of caffeine and MDMA potentiates the glial activation, which is characterized by increased microglial and astroglial reactivity in different brain areas, 13,43 and by an increased formation of free radical and reactive oxygen species (ROS). 14 In the light of the strict correlation between neuroinflammation and neuronal degeneration, the increase in astroglial and microglial reactivity induced by the interaction between caffeine and MDMA assumes specific importance. 46 In fact, several studies have reported that microglial and astroglial activation represents an early step in amphetamine analog-induced neurotoxicity contributing to neuronal damage by the release of proinflammatory cytokines.…”

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confidence: 99%

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Contribution of Caffeine to the Psychostimulant, Neuroinflammatory and Neurotoxic Effects of Amphetamine-Related Drugs

Frau

Simola

Morelli

2013

Journal of Caffeine Research

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Association of amphetamine-related drugs with beverages containing high levels of caffeine is becoming very popular among adolescents and young adults. This review by examining the psychostimulant properties and the neuroinflammatory and neurotoxic effects of this drug association provides a new vision of the risks correlated to multiple substances consumption. In preclinical studies, caffeine amplifies the effects of amphetamine-related drugs on behavioral parameters, such as locomotor activity, operant behavioral tests, and discriminative stimulus effects, and promotes long-term modifications in the brain. Preclinical data also demonstrate that caffeine contributes to increase the acute toxicity, seizures, hyperthermia, and tachycardia elicited by amphetamine-related drugs in rats. These effects, together with the results showing that caffeine potentiates the loss of central serotonin and dopamine and the induction of neuroinflammation by amphetamine-related drugs, emphasize that, depending on the conditions in which it is consumed, caffeine may amplify the effects of neurotoxic drug

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“…Chronic methamphetamine use leads to the major damage to nearly every system of the body, most notably the lung, liver, heart, kidney and brain 3 . Caffeine, the most widely consumed psychoactive substance in the world, acts as a CNS stimulant but can potentiate the toxic effects of methamphetamine 4 . Thus, methamphetamine and caffeine together is a recipe for disaster and sometimes lethal, without warning.…”

Section: The Truth About Yabamentioning

confidence: 99%