This is a guest article by Kamila Wita, who is soon to become an MSc student in Developmental Psychopathology at Durham University. This is a very comprehensive, well-written and up to date account of the cognitive influence of alcohol and MDMA. Note the critical comments throughout; it’s a great example of how to be critical in essays. This is what you need to do in order to get the big marks – just describing the studies is not enough, you must critique them. Thanks Kamila!
Have you ever wondered what effects alcohol and ecstasy have on those people (or perhaps yourself) who do it for fun, treat is as some sort of a sport or perfectly normal part of student life? You know it’s bad for you but just how bad is it? This article is not going to tell you how embarrassing waking up naked next to somebody you don’t remember is, or how confused you can be if you find pictures of yourself wearing a traffic cone. It is serious (I would know, I got a first class mark for this paper) it compares and contrasts the effects of ecstasy and alcohol on mood and cognition in recreational users (note: the below is not exactly what I submitted).
Recreational use of MDMA and alcohol has become increasingly widespread worldwide (Morgan, 2000). However, until recently, little was known about the psychological effects of these drugs. Recent research shows the possible acute and chronic psychological effects of extensive recreational use of these drugs (Boha et al. 2009; Harrison & Fillmore, 2005; Heffernan et al. 2002; Dauman et al. 2003; Morgan, 2000; Gouzoulis-Mayfrank, 2000; Parrot and Lasky, 1998; Davison and Parrot, 1997).
For those of you who know drug actions, just skip this section.
MDMA (3,4-methylenedioxymethamphetamine, ”Ecstasy”) an amphetamine derivative, is a popular recreational drug that has been shown to exhibit a psychoactive profile. It has been assigned to the ‘entactogens’ class as its characteristic psychoactive profile distinguishes it from other hallucinogens and stimulants (Liechti et al. 2000; Morgan, 2000). MDMA is a potent monoaminergic agonist producing both carrier-mediated release and reuptake inhibitor 5-HT and to a lesser extent dopamine (Morgan, 2000; Liechti et al. 2000) and other neurotransmitters (McDowell & Kleber, 1994). Most popular alcohol found in alcoholic beverages is ethanol.
Ethanol is also considered a psychoactive drug. Ethanol acts in the central nervous system by binding to the GABAA receptor, increasing the effects of the inhibitory neurotransmitter GABA. As inhibitory neurotransmitter alcohol reduces signal flow in the brain. This explains how alcohol depresses both a person’s mental and physical activities. Therefore chronic alcohol consumption produces structural and functional alterations of the central nervous system (CNS), which can explain the behavioural impairments associated with chronic alcohol ingestion (Santi et al. 2000).
Humans synthesize GABA from glutamate using the enzyme L-glutamic acid decarboxylase and pyridoxal phosphate as a cofactor. This process converts glutamate, the principal excitatory neurotransmitter, into the principal inhibitory neurotransmitter (Petroff, 2002). In contrast, serotonin is synthesised from the L-tryptophan, found in most of protein-based foods, i.e. meats, dairy products, nuts etc. (Wurtman et al. 1980).
Acute and chronic effects of MDMA and alcohol on mood.
Study of university students by Peroutka et al. (1988) revealed subjective effects of MDMA on mood as reported by the users themselves. The reported acute effects of MDMA were pleasant, with strong feelings of closeness, elevation and intimacy toward other people. However, these were accompanied by negative physical effects, including headaches, jaw clenching and twitches. Followed, 24-hours later, by depression, difficulty concentrating, anxiety, worry and irritability (Peroutka, 1988). The study is disadvantaged by using self-report measures and the fact that the purity of the drugs ingested by the participants cannot be known. Additionally the study failed to control for poly-drug use and to investigate chronic effects of MDMA.
Davison and Parrot (1997) report that MDMA causes feelings of elation, alertness, and happiness. In comparison, acute effects of alcohol also can be pleasant and positive with increased cheerfulness, sociability, and self-confidence. Low doses of alcohol increase total sleep time and reduce awakening during the night. The sleep-promoting benefits of alcohol disappear at moderate and higher doses of alcohol (Stone, 1980). MDMA on the other hand is often ‘accused’ of causing insomnia and sleep distortion.
Given the putative role of serotonin in sleep, it has been hypothesised that one manifestation of serotonin neurotoxicity in humans might be disturbances of sleep (Allen et al., 1993). To determine whether MDMA use has effects on sleep, all-night polysomnograms of 23 MDMA users were compared to those of 22 age- and sex-matched controls. On average, MDMA users had 19 minutes less total sleep and 23.2 minutes less non-REM (NREM) sleep than controls. These statistically significant differences in NREM sleep were due primarily to an average of 37 minutes less stage 2 sleep, with no significant differences noted in stages 1, 3 or 4. Although it is not known whether the alterations in sleep observed in MDMA users are due to serotonin neurotoxicity (Allen et al., 1993).
Curran and Travill (1997) compared results from weekend use of ecstasy or alcohol. The study focused on cognitive function and mood, as deficits in serotonin in humans can be associated with both mood disturbance and detriments in cognition. MDMA users rated elevated mood on day 1 but significantly low mood on day 5, at which point some participants scored within the range for mild or moderate clinical depression, on Beck Depression Inventory. In contrast, the alcohol group showed less pronounced changes, which followed a U-shaped curve over days with the lowest point being day 2 (presumed to be related to hangover effects) (Curran and Travill, 1997).
The researchers linked the low mood of MDMA users with serotonergic depletion which follows the elevation of serotonin levels by MDMA. Curran and Travill (1997) therefore concluded that complete recovery of mood may not occur due to the neurotoxicity of MDMA. The researchers implied that the ‘day after’ effects of both of the drugs are similar in some respects (Curran and Travill, 1997). There is little evidence that light Ecstasy use is associated with long-term depression and lowered mood. However there is some evidence that heavy consumption is associated with persistent depression and psychological disturbances (Morgan 1988). Morgan (2000) reports a plethora of studies in his review that shows that ecstasy use can be associated with depression, dependant on dosage.
There’s logic in there somewhere. Credit: antoinedemorris
In comparison, Ferguson et al. (2009) report that high rates of major depression can occur in heavy drinkers and in those who abuse alcohol. Controversy has previously surrounded whether those who abused alcohol who developed major depressive disorder were self medicating (which may be true in some cases) but recent research has now concluded that chronic excessive alcohol intake itself directly causes the development of major depressive disorder in a number of alcohol abusers (Ferguson et al. 2009). In terms of anxiety, research shows that persistent heavy ecstasy use can cause anxiety elevation, as well as phobic-anxiety, somatisation and obsessionality in MDMA users in comparison to non-drug controls as tested on the Symptom Checklist-90 (SLC-90) (Parrot et al. 2000). However, in this study only heavy users and non-users comparison achieved statistical significance. In comparison, many individuals drink because they are feeling anxious or stressed, and moderate, low-doses help them unwind and relax. Anxiety disorders and alcohol consumption have a complex bi-directional relationship. (Brady et al. 2007; Kushner et al. 2006).
In terms of impulsiveness, research results are somewhat inconclusive, with Parrot et al. (2000) reporting elevated scores of heavy MDMA users compared to non-drug controls, while others report non significant results (Morgan, 1998). In comparison, studies of alcohol intoxication yield mixed results, with some studies claiming that moderate amounts lower impulsivity and make decision-making more cautious under some circumstances (Ortner et al. 2003), while some finding, however partial, support for their claims of alcohol increasing impulsivity (Dougherty, 2008). Finally, Morgan (1998) reported no differences between MDMA users, non-users, and polydrug users who never used MDMA, in levels of hostility. The participants were tested on State/Trait Anger Expression Inventory.
Their findings were supported by Parrot et al. (2000) reporting that light MDMA users and non-drug controls showed no significant differences on SCL-90 in terms of hostility. However, Parrot et al. (2000) further reports that heavy Ecstasy users had significantly higher scores on the hostility trait in comparison to non-drug controls. This notion has been supported by study by Gerra et al. (1998) in which heavy, MDMA-exclusive users scored as aggressive, even after 3 weeks of abstinence; follow up study revealed decreased scores after 12 months. In comparison, findings by White et al. (1993) indicate that early aggressive behaviour leads to increases in alcohol use and alcohol-related aggression, but that levels of alcohol use are not significantly related to later aggressive behaviour.
Therefore they suggest that alcohol-related aggression is engaged in by aggressive people who drink (White et al. 1993). Interestingly, study by Lang et al. (1975) revealed that participants who believed they had consumed an alcoholic beverage were more aggressive than those who actually did but were let to believe they did not. However, the study only assessed males and did not include females at all.
Acute and chronic effects of MDMA and alcohol on cognition.
Previously mentioned study by Curran and Travill (1997) reported that the MDMA group showed significant impairments on an attentional/working memory task, compared with alcohol users. The disadvantage of this study is that it only compared MDMA with alcohol users and did not compare those results with drug-free individuals. However, it has been explained that it was simply due to the lack of drug-free individuals at the club where the testing took place (Curran and Travill, 1997).
A significant flaw of the methodology is the fact that the researchers opted out taking blood samples as they did not want to pose a risk and intimidate potential volunteers. The study only revealed that MDMA users have performed worse than alcohol users. It is of interest to compare drug-users with drugs-free individuals to fully research the observed effects.
One such study has been conducted by Weissenborn and Duka (2003). The study benefited from employing a placebo condition as well as controlling for alcohol, illicit drug and food intake prior to testing. Research revealed the acute alcohol effects on cognitive function on a range of cognitive deficits, for example, deficits in attention, explicit memory paradigms, and executive-type functions (Weissenborn and Duka, 2003). In the planning task, alcohol decreased the number of solutions with the minimum moves. Alcohol also decreased the thinking time before initiating a response, while it increased the subsequent thinking time in the same task. Under alcohol, participants recognised fewer items in the spatial recognition task; however no effect of alcohol was found in a spatial working memory task and in a pattern recognition task. Among the participants with moderate to heavy use of alcohol, those who were ‘bingers’ performed worse in the spatial working memory and in the pattern recognition task than ‘non-bingers’ (Wiessenborn and Duka, 2003).
To compare, regular MDMA users also have been shown to have memory deficits, as tested by word recall tasks (Parrot et al. 1998). Interestingly, even ‘novice’ MDMA users, who used ecstasy less than 10 times have preformed better than drug-free control. Again, the weakness of the study is the unknown drug purity and strength.
Additionally, a study by Heffernan et al. (2002) found that social drinkers who drink over 30 units (on average) a week for minimum of 5 years reported significantly greater number of impairments compared to low-dose/non-user group, in terms of long-term episodic prospective memory impairments. In comparison, ecstasy users, when tested on PMQ showed the same trend for impaired prospective memory (Heffernan et al. 2001).
These deficits in MDMA users have been attributed to the frontal lobe and hippocampus damage associated to ecstasy toxicity. The study however, does not assign the drug users into conditions, and therefore individuals who had taken the drug twice were assigned in the same group as individuals who had taken it 30 times or over. The researchers mention that the participants have been drug-free for period of 24 hours. When previous research on MDMA is considered 24 hours is not long enough, as the participants still would be experiencing the drug effects (Peroutka et al. 1988).
In terms of alcohol, dosage is crucial. Previous studies have shown dosage-dependant effects of alcohol on skills impairment and on cognitive processes such as memory and attention (Little 1999; Kerr et al. 2004; Koob and Moal, 2006). Boha et al. (2009) researched the effects of low-dose alcohol, that is below 0.2g/kg, as well as in other conditions: (control, task, placebo-task, low-dose task [0.2 g/kg alcohol], high-dose task [0.4 g/kg alcohol]). The study used mental arithmetic task, which required addition and working memory effort. EEG spectra with an emphasis on the theta band, error rate and reaction time were analysed (Boha et al. 2009). The study results showed no effect of alcohol on behavioural indices of task performance. However, the ethanol-induced moderate reduction of the task-related frontally dominant theta increase, probably corresponding to working memory demand, this has been considered a modest but clear electrophysiological sign of alcohol effect in this low-dose range (Boha et al. 2009).
The study, however, has only tested male participants and would benefit from testing female data as gender plays a role, and therefore males and females are affected differently by alcoholic beverages. This difference is mainly due to a smaller gastric metabolism in females-because of a significantly lesser activity of glutathione-dependent formaldehyde dehydrogenase (x-ADH) (Baraona et al. 2006).
Critique and methodological problems.
The studies of alcohol and ecstasy users are prone to methodological problems which in turn affect and create interpretative difficulties. These include problems with verifying users histories of drug use and lack of baseline data of cognitive functioning, as well as lack of bodily samples, i.e. blood or urine to test concentration of MDMA or alcohol in participants prior and during testing. Problems arise with representativeness of the samples in particular studies, which vary greatly in amounts of drugs ingested and frequency of use.
A few additional problems arise with the above studies, firstly, the use of self-report measures, especially when testing memory. If it is believed that participants’ memory is impaired it is illogical to ask those participants to self-report their memory function. Therefore validating the data by proxy reports (through significant others and friends) would be beneficial, yet not perfect, due to possible bias (Wagmiller, 2009). Self-reporting amounts of alcohol consumed is also problematic, especially as individuals may simply be ‘giving a wild guess’ rather than actually know how many alcoholic beverages they consumed. This is especially problematic, when no individuals simply had not paid attention to how much they drunk or simply forgot. The issue of defining ‘binge’ also arises. Studies attribute different names to different amounts consumed, i.e. low/high or binge etc. The problem is that there is no clear definition, therefore interpretation poses a difficulty.
Additionally, the phenomena known as ‘stereotype threat’ should be accounted for in all of the studies. Stereotype threat occurs when individuals, believed to be intellectually inferior, perform badly on cognitive tests they perceive to confirm stereotypes about them (Cole et al. 2006). Study by (Cole et al. 2006) tested ecstasy and non-ecstasy using polysubstance misusers on a variety of cognitive tests after they had been exposed to stereotype threat. The participants were given information about the long-term effects of ecstasy which either stated that ecstasy caused memory loss or that it did not. Ecstasy users that had been primed that ecstasy did not cause cognitive deficits performed better than the other three groups. There were no other statistically significant differences between any of the groups on any of the other cognitive tests used. This suggests that stereotype threat exists in ecstasy users and may be influencing their performance in experiments designed to identify cognitive deficits (Cole et al. 2006). In further support, see previously mentioned study by Lang et al. (1975).
Furthermore, as alcohol is considered a legal drug studies involving it can control for the amount and volume ingested by the participants, in turn ecstasy studies are prohibited to do so due to the fact that MDMA is considered a class A drug and giving it to participants would be illegal. Therefore ecstasy studies have to rely on participants’ report of amounts taken, and as previously mentioned the purity and strength may be questionable. Therefore the participants may actually have experienced MDMA related compounds: 3,4-methylenedioxyethamphetamine (MDEA) or 3,4 – methylenedioxyamphetamine (MDA) (Morgan, 2000).
Therefore the effects described in above studies can only by attributed to tablets that were believed by the user to be MDMA (Parrot et al. 1998), Additionally, as previously mentioned the street-available MDMA may in fact be MDEA or MDA, it can also be contaminated with other drugs such as ketamine, LSD, caffeine, ephedrine, seligiline and cocaine (Morgan, 2000). In fact another problem with drug studies, including the ones discussed above, is that often there is no control over what other drugs had been taken other than the drug of interest. Many MDMA and alcohol users also regularly use other illicit drugs including cannabis, amphetamine, cocaine, LSD, psilocybin mushrooms, benzodiazepines, barbiturates and ketamine (Morhan 2000; Morgan, 1999).
Therefore it is not possible to firmly attribute the self-reported affects to MDMA or alcohol itself (Davison and Parrot, 1997). Some studies focused on one gender only, as previously mentioned, it is crucial to test both genders separately due tot he differences smaller gastric metabolism in females-because of a significantly lesser activity of glutathione-dependent formaldehyde dehydrogenase (x-ADH) (Baraona et al. 2006).
Summary and conclusions.
The psychological effects of MDMA and alcohol (in moderate doses) can be seen as similar in that, while on drug both produce positive and relaxing feelings; I.e cheerfulness, increased sociability, and self-confidence. The difference is MDMA users feel elated while alcohol users feel sedated. Both drugs produce negative physiological effects while on drug, i.e. lethargy, respiratory problems, seizures etc. In some cases both drugs can lead to coma and death (Schifano, 2004).
Both drugs cause damage to the human brain, however the areas affected differ. Ecstasy in believed to damage hippocampus and frontal lobe (Puerta et al. 2001; Heffernan et al. 2001; Morgan, 2000). There is some evidence from neuroimaging studies that shows occipito-parietal region of the cortex may be affected by exposure to ecstasy (Reneman et al. 2000). By comparison persistent misuse of alcohol can result in damage to a range of cortical and sub-cortical structures of the brain, can lead to brain shrinkage, neurotransmitter impairments, inhibition of frontal cortex functioning and reduced hippocampal function (Heffernan, 2008).
Additionally, chronic high doses of alcohol can cause damage to vital organs, such as liver (cirrhosis, pancreatitis), pancreas (inflamation), heart (irregularities and weakening of the muscle) and stomach (stomach cancer) (Chao et al. 2003). The main difference is that the more alcohol is consumed the worse effect it has. Therefore an individual can start a night with low doses and have a good time and as the amount of drinks increases, end up confused, vomiting and unconscious at the end of the night. While, taking consecutive doses of MDMA does not prelong the ‘high’ (Downing, 1986).
Alcohol in moderate or low doses is commonly assumed to be beneficial to health. The results of study conducted by Ruitenberg et al. (2002) suggest that light-to-moderate alcohol consumption is associated with a reduced risk of dementia individuals aged 55 years or older. MDMA displays a weak potential for addictiveness and therefore dependence (Davison and Parrot, 1997), while alcohol is highly addictive. Alcohol dependence is a chronic disorder with genetic, psychosocial and environmental factors influencing its development (Parrot et al. 2005).
To summarise MDMA, evidence shows that acute psychological effects of MDMA include feelings of elevation, euphoria, elevated self-awareness, agreeableness, and confidence. The adverse physiological effects of MDMA intoxication include cardiac arrhythmias, hypertension, lethargy, insomnia, hyperthermia, serotonin (5-HT) syndrome, hyponatremia, liver complications, seizures, coma and, in rare cases, death (Schifano, 2004; Davison and Parrot, 1997). Chronic psychological effects in recreational users include depression, lethargy, moodiness, cognitive impairment (mostly memory), insomnia, paranoia, irritability, and other physical and psychological effects (Parrot et al. 2004; Morgan 1998; Davison and Parrot, 1997).
There is an increasing body of research evidence for neurotoxic damage, which in regular MDMA users may cause depression, impulsiveness, phobic anxiety, hostility, reduced appetite, sleep disorder, and selective impairment of episodic memory, working memory, prospective memory and attention (Parrot et al. 2004; Hefferenan et al. 2001; Morgan 2000). Experimental data shows that the cognitive deficits persist for at least 6 months after abstinence, whereas anxiety and hostility diminishes after a year of abstinence (Morgan, 2000). Some of these problems may diminish over time of abstinence, however, the residual neurotoxicity and decline of serotonergic function with age may result in recurrent psychopathology and premature cognitive decline due to damage to hippocampus and frontal lobe (Puerta et al. 2001; Heffernan et al. 2001; Morgan, 2000).
In comparison, evidence shows that acute effects of alcohol depend on the dosage. Low to moderate amounts can, result in pleasant and positive effects with increased cheerfulness, sociability, and self-confidence. As the dosage increases the acute effects worsen and impair (i.e. cause confusion, ataxia etc.). Chronic effects of alcohol involve cognitive deficits and impairments, i.e. in many aspects of memory, judgement, planning, information processing etc. (Boha et al. 2009; Heffernan 2008; Wiessenborn and Duka, 2003; Heffernan et al. 2002; Parrot and Lasky, 1998)
As discusses above, as drug research increases, the understanding of the effects increases. However, as shown above, such research should not be taken for granted, even though published in peer reviewed scientific journal, as research, even though insightful, still may be flawed.
Research into nurtigenomics shows how genetic make up (phenotype) can be influenced by nutrition, it is of interest to find out if ingesting drugs such as alcohol, MDMA and others affect it. Certain polymorphisms affect how individuals react to caffeine, perhaps MDMA and alcohol should also be considered (Trujillo et al. 2006).
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