Instant gratification as a way out of addiction?

Impulsivity is often seen as a hallmark of addiction — acting without thinking about the consequences of your actions and valuing the immediate reward of a drug-induced high over the future long-term payout of a healthy lifestyle. This type of delay discounting has been linked to a greater risk for drug addiction, but new research suggests that this type of “myopia for the future” may also improve someone’s chances of staying sober when they’re trying to get clean.

My latest piece for The Fix investigates the research behind this paradox, which suggests that those who are the most impulsive have the most to gain from effective treatment, cognitive training successfully improving their self-control. But is this effect a result of the treatment program itself or just a regression to the mean? Check out the article here to find out.

Cannabis and memory loss: dude, where’s my CBD?

I’ve got a new piece in The Guardian today on memory deficits in heavy cannabis users, and how the type of weed you’re smoking can actually impact your risk for impairment. Dedicated Brain Study readers might recognize it as a revamped, beefed-up version of the infamous “Weed be better off smoking our parents’ pot” post from last year. Now, I’ve incorporated some new research into the piece on cognitive problems in heavy smokers, as well as the relevant policy news from Colorado, Washington and Uruguay regarding legalization. I also talk about how these developments could result in more than one type of harm reduction, which is an exciting prospect for improving the safety of the drug with government regulation.

Check out the full piece here, and as always, let me know what you think.

If I can’t remember it, it didn’t happen: A susceptibility for alcohol-induced blackouts

As anyone who’s ever taken an Alcohol Edu course (or been 21 in the last decade) knows, consuming too much alcohol can cause memory loss, colloquially known as a “blackout”. This anterograde amnesia stems from an inability of the brain to form new long-term memories and is caused by a disruption in the GABA and NMDA receptors in the prefrontal cortex (PFC) and medial temporal lobes when drinking.

First, for those of you who skipped (or drank) your way through your alcohol education, a brief reminder on the effects of alcohol on the brain. GABA is a primary inhibitory neurotransmitter, acting to decrease the likelihood of a cell’s firing. Alcohol acts as a GABA agonist, elevating levels throughout the brain and therefore diminishing the rates of firing in normal cellular processes. At high levels, alcohol also acts upon glutamate NMDA receptors, one of the main excitatory neurotransmitter systems. Alcohol works as an NMDA antagonist, blocking the NMDA receptors and preventing glutamatergic activation, further inhibiting neuronal functioning. This inhibition particularly occurs in the PFC, medial temporal cortex and the parietal lobe, primary targets of alcohol in the brain. In the hippocampus in particular, an area in the medial temporal cortex crucial to memory formation, this inhibition can result in a disruption of long-term potentiation, a cellular process involved in the consolidation of short-term to long-term memories.

Alcohol’s effect on the PFC also impacts memory ability, as short-term memories are maintained there while they are being worked on or rehearsed. However, when attention shifts to a new stimulus this memory must be consolidated into a more stable long-term version via cellular activity in the hippocampus, or else it will be discarded and forgotten. Alcohol’s inhibition of the PFC via its effects on GABA and glutamate can disrupt the maintenance of these short-term memories, decreasing the likelihood of consolidation and preservation. The dampening of firing in the PFC is also attributed to the behavioral disinhibition that so commonly succeeds alcohol consumption, as the PFC can no longer inhibit or control impulses as well.

Now, on to the exciting bit! In individuals who regularly experience alcohol-induced memory loss, or a blackout, it is the contextual memory that seems to be most impaired. This refers to the details surrounding an experience, such as where, when and with whom the event occurred. However, blackouts seem to affect some drinkers more than others, and are not necessarily determined by the amount of alcohol that an individual consumes. Simply put, you either blackout when drinking large amounts of alcohol or you do not.

Published online this week in Alcoholism: Clinical and Experimental Research, psychologists from the University of California, San Diego and the University of Texas, Austin have recently confirmed this urban drinking legend by testing 24 regular binge drinkers, 12 of whom admitted to blacking out on a regular basis, reporting on average two blackouts per month, and 12 who drank comparable amounts of alcohol but declared no memory problems when drinking. Both groups were matched on their typical alcohol consumption, averaging 3 drinking days per week and consuming 4-5 drinks at a time on a typical day when drinking. Both groups also had comparable binge tendencies, consuming 10 or more drinks on occasion over the previous 3 months.

Participants were tested on a contextual memory task using functional magnetic resonance imaging (fMRI) both when sober and after drinking to a blood alcohol content of .08, the legal limit in the United States, typically 3 drinks for a male and 2 for females. During both the sober and intoxicated trials, participants performed equally well in their behavioral scores, recalling similar amounts of information regardless of their blackout group status. Groups also did not differ in their response times on the task during either condition, however both groups recalled significantly fewer trials when intoxicated and were significantly slower than when sober.

In the imaging analysis, there were no differences in activation levels between the groups during either encoding or retrieval for the sober condition of the task. However, when intoxicated, both groups demonstrated significantly less activation in the right frontopolar PFC during retrieval. The blackout group also had significantly less activation during both the encoding and recall portions of the experiment after consuming moderate amounts of alcohol as compared to the non-blackout group. Specifically, participants with a history of blacking out showed less activation in the left frontopolar PFC during encoding, and decreased activity in the right posterior parietal cortex and the bilateral dorsolateral PFC during retrieval as compared to their non-blackout contemporaries. This fronto-parietal network is implicated in attentional maintenance and inhibition, as well as working memory and executive control, suggesting that there could be greater difficulties in these skills in the blackout group when drinking.

The researchers speculate that the decrease in activity in the frontal pole during intoxication is indicative of an alcohol-induced impairment in executive functioning in both groups, particularly in regards to working memory and cognitive maintenance. The additional decrease in activation in the fronto-parietal network seen in the blackout group also suggests a greater disability in executive functioning and memory maintenance in these individuals when drinking. However, it is notable that there were not any significant behavioral differences between the two groups in total memory recall, particularly during the intoxication condition.

While it is reassuring that there were no impairments in either group during the sober condition, the drinking results do seem to suggest that there may be underlying problems with memory and executive functioning in those individuals with a proclivity for forgetting, which could emerge after more chronic drinking behaviors. Why some people are predisposed towards these additional memory impairments is still unclear, but there does seem to be something different in the brains of those who blackout regularly that is not just dependent on the amount of alcohol they drink.

(Insert poor taste joke about drinking away your memory problems here.)

Did I do that? Reality monitoring in the brain

Most of us have no problem telling the real from the imagined. Or so we think.

Reality monitoring, the incorporation and distinction of internal thoughts and imaginings from external experiences and memories, typically happens seamlessly for most individuals. However, there are times when we cannot recall if someone else told us about that interesting article or whether we read it ourselves, or if we remembered to lock the door before leaving the house or not. Did we actually do or hear these things, or did we only imagine them? This is a common problem in patients with schizophrenia, who at times cannot distinguish between what they think they remember or believe to be true, and what actually occurred.

A new study on reality monitoring published last week in the Journal of Neuroscience reveals that many of us are not as good at making this distinction as we might think. Additionally, the ability to discern between perceived and imagined events may be rooted in one very specific region of the brain, which nearly 30% of the population is missing. Led by Marie Buda and Dr. Jon Simons at the University of Cambridge*, researchers administered a very particular type of memory test to healthy participants who had been pre-selected based on the prominence of the paracingulate sulcus (PCS) in their brains. Running rostral-caudal (front to back) and located in the anteriomedial (middle-frontal) prefrontal cortex, this region is involved in higher level cognitive functioning and is one of the last parts of the brain to mature. Consequently, it can be relatively underdeveloped or even seemingly absent in many people. This is particularly the case in individuals with schizophrenia, where as many as 44% of patients lack this particular region.

Participants for the current study were chosen from a database of individuals who had previously undergone an MRI scan and clearly showed a presence or absence of the PCS in either one or both of the neural hemispheres. The memory task in question involved a list of common word pairs such as “yin and yang” or “bacon and eggs”. These words were either presented together (perceive condition), or only one word was presented and the participant was to fill in the complimenting phrase (imagine condition). The second portion of the experiment involved the source of this information, i.e. whether the subject or the experimenter was the one to read off or verbally complete the pair. After the task, the subject was asked to report whether the pair was fully perceived or imagined, and whether this information was attributed to themselves or the experimenter. They were also asked to rate their confidence in both of these responses.

Participants with a complete absence of the PCS in both hemispheres performed significantly worse on the reality monitoring task than individuals who exhibited a definite presence of the sulcus. This difference was based on their source attribution memory (themselves vs. the experimenter); performance on the perceive or imagine condition did not differ between the groups. Interestingly, the two groups also did not differ in their confidence in their responses. Thus, even though the PCS-absent group performed significantly worse on attributing the source of the information, they were still just as confident in their answers as individuals who responded correctly, indicating a lack of interospective awareness in the absent group in regards to their memory abilities.

It should be noted that there was also a correlation between overall gray matter volume in the prefrontal and motor cortices and scores on the reality monitoring task. This is important as it may indicate that there are other regions involved in this process outside of the PCS, and the authors caution that this enhanced ability may stem from an increase in gray matter and connectivity in the medial prefrontal cortex, rather than from the PCS itself.

These findings could have useful applications in clinical psychiatry. As stated above, an impairment in reality monitoring is often associated with schizophrenia, and the absence of the PCS could serve as a potential biomarker for this disorder. Additionally, although not commonly discussed in terms of reality monitoring, another psychiatric diagnosis that could potentially benefit from this type of research is obsessive compulsive disorder (OCD). OCD often consists of obsessions and the urge for frequent compulsive checking of things, such as whether one remembered to turn off the stove. This ruminating and checking behavior could be indicative of a breakdown in reality monitoring where patients can not determine whether a target action actually occurred or not. While this problem is not encompassing of all OCD patients, reality monitoring disability could be a potential area to investigate in those patients for whom checking is a significant problem.

*Disclaimer: Marie Buda and Jon Simons are fellow members of the Department of Experimental Psychology at the University of Cambridge with me.