Cocaine addiction and sleep-related problems: the search for genetic culprits
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LETTER TO THE EDITOR
Cocaine addiction and sleep-related problems: the search for genetic culprits Vinícius Dokkedal-Silva 1 & José Carlos Fernandes Galduróz 1 & Sergio Tufik 1 & Monica Levy Andersen 1 Received: 20 February 2020 / Accepted: 5 October 2020 / Published online: 9 October 2020 # Springer-Verlag GmbH Germany, part of Springer Nature 2020
In recent years, there has been a rise in the consumption of cocaine in countries, such as Brazil (Abdalla et al. 2014) and the USA—where a trend of mixing cocaine with synthetic opioids is on the rise (National Institute on Drug Abuse 2019). Cocaine can have a significant impact on different aspects of health, including the impairment of sleep in its users. Sleep deficits may be due to a number of reasons, including the stimulant properties of cocaine per se, but there is strong evidence for sleep impairment related to abstinence (Valladares and Irwin 2007). Sleep is markedly impaired during the first stages of cocaine withdrawal, with results pointing to improvement over time and a possible return to sleep patterns that are similar to control individuals (Angarita et al. 2016a). However, it should be noted that although chronic cocaine users typically have an improvement in self-reported sleep following abstinence, this is not usually supported by objective measures, such as polysomnography, characterizing a phenomenon known as “occult insomnia” and indicating that sleep recovery does not follow a uniform path (Angarita et al. 2016b). Sleep impairment has been seen as a consequence of cocaine use that impacts the functionality of the individual, and these effects have been well studied. However, other studies have assessed a less commonly examined relationship, the possibility that sleep could have a causal impact on the pathology of cocaine use disorder. Evidence from studies that have tackled this issue suggests that this relationship exists, but the studies did not reach a consensus about its nature or the mechanisms behind it. In animal studies, sleep deprivation was shown to alter the time course, but not the magnitude, of locomotor sensitization to cocaine (Bjorness and Greene
* Monica Levy Andersen [email protected] 1
Departamento de Psicobiologia, Universidade Federal de São Paulo (UNIFESP), Rua Napoleão de Barros, 925, São Paulo 04024-002, Brazil
2018). However, other studies have reported that sleep deprivation potentiated the effects of cocaine in rats (Andersen et al. 2005). It also increased the incidence of seizures following cocaine administration, suggesting that sleep deprivation amplifies the toxicity of cocaine (Andersen et al. 2010). In humans, it has been found that sleep-deprived individuals presented an attenuated increase in heart rate following cocaine injection and that reaction time impaired by sleep deprivation was partially reversed by cocaine (Fischman and Schuster 1980). However, the sample for this study was only eight individuals, and more evidence is required from further initiatives, with larger samples exploring the influen
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