Hester Exam Questions Flashcards
Cognitive neuroscience and related fields are increasingly being applied to reveal the role of the brain in drug addiction, and the impact of drug use upon brain function and human behaviour. Advances in this area have implications for public policy and the treatment of people who use drugs. Please outline two issues and discuss the research findings that have prompted their discussion.
Neurobiology of cognitive neuroscience posits that addiction is genetically predisposed and causes neural and cognitive changes in the brain, suggesting that individuals are not autonomous of their actions. This raises two issues: 1) If genetic tests become available to identify at risk individuals how should it influence drug control policies? 2) How much responsibility and blame should we attribute to addicted individuals for their actions?
Firstly, possession of Taq1A gene has been shown to be a genetic predisposition to dependency, as these individuals are 2-5x more likely to be addicted, respond poorly to treatment and have higher relapse rates (Noble et al., 2003). This is because 2 copies of the Taq1A allele reduces D2 receptor density, creating a hypodopaminergic state. Hence, these individuals benefit from externally direct (cocaine) or indirect (risk-taking) rewarding stimulations that increases their dopamine (DA) levels to optimum. The rewarding association of the DA stimulation and source becomes reinforced and exaggerated, thus increasing desire to seek it. In support of this, Volkow et al. (2002) found that low D2 levels predicted drug dependence while high D2 levels was a protective factor in siblings of drug dependent individuals.
However, a single poly-morphism cannot be predictive of a complex multifactorial disorder like drug dependence. Even a large combination of risk alleles might only contribute to a behaviour that’s intermediary, such as risk-taking, and do so no better than a simple family history. If so, the Taq1A might be associated with higher risk of trying out more drugs and subsequently developing addiction, rather than drug itself. If genetic tests focus on at-risk individuals, this might subdue more effective (and universally applicable) social policies such as: a) reducing drug availability; b) increasing drug prices; c) encouraging peer disapproval.
Secondly, drug use cause long-lasting neural and cognitive changes, suggesting that relapse might be due to uncontrollable biological factors. For example, chronic methamphetamine (MA) users have been found to have significant cognitive impairments (e.g., poor verbal memory, slower processing speed, executive functions; Scott et al., 2007). Moreover, dependent drug users have been found to perform poorly on inhibitory control tasks (e.g., Go/No-go) which requires inhibition of a prepotent response, and this deficit was associated with reduced dorsal anterior cingulate cortex and dorso-lateral prefrontal cortex activity — regions which governs cognitive control (Goldstein & Volkow, 2011). This shows that drug use causes neural and cognitive changes. Further, showing active and abstinent users a 20-minute video of someone doing cocaine was sufficient to activate limbic regions associated with drug effects. This activation level predicted cravings and subsequent relapse, providing evidence that relapse might be due to uncontrollable biological factors.
However, given the cross-sectional nature of most studies, it is unclear whether drug use is caused or causes impairments. Kincaid and Sullivan (2010) noted that a modest correlation between decreased frontal brain activity and self-reported drug craving does not show that drug use is driven by irresistible impulses. Hence, suggesting that their actions are autonomous and individuals are responsible for their actions.
Although thinking of addiction as a genetically predisposed disease might reduce the social stigma and replace imprisonment with more humane policies (e.g., treatments or rehabilitation), it might also promote unethical treatments as a ‘cure’ for dependency. For example, ultra-rapid opioid detoxification has been marketed as a long-lasting cure for opioid addicts but it had in fact caused: a) physical harm, because the treatment reduced tolerance levels and opioid users can run risk of overdose if they relapsed (and most did); and b) economic harm, because the treatment cost AUD $10,000-$15,000 but is largely ineffective (Hall et al., 2000).
