Meet the team #7 Thomas

What is your name?

Thomas van Genderen

Can you tell something about yourself?

I was born and raised in Rotterdam before moving to Amsterdam to study Psychobiology at the UvA. I have always been interested in the effect our brains have on our behaviour and perception. During my study I studied a wide variety of topics ranging from biology and anatomy to developmental psychology. I joined the study-association for biologists, Congo and rowing association, Nereus. I enjoy exploring new hobbies and reading in my free time.

What is your role at the NOFA lab?

I’m a third year bachelor student and intern with the Joint Study. Together with the other interns, I assist the researchers where I can with their cross-cultural study into Cannabis Use Disorder (CUD). We mainly occupy ourselves with recruiting, contacting and interviewing participants. When we’re busy with data collection and processing, we work on our theses.

What is your main research interest/topic?

For me, this study is an opportunity to gain more insight into the relation between ADHD symptoms and CUD. Many of the individuals seeking treatment for CUD are diagnosed with ADHD. I believe this is a valuable correlation to explore and potentially relevant for early intervention.

Is there anything else we should know about you?

My favourite movie is the Blues Brothers. I can talk for hours about anything that catches my interest and will probably do so given the chance.

Meet the team #6 Stefanie

What is your name?

Stefanie van den Brink

Can you tell something about yourself?

I am currently in my fourth year of the bachelor psychobiology. I am mostly interested in the psychology side of the study and that is why I am doing an extra year as a trajectory towards the master clinical psychology.

What is your role at the NOFA lab?

I am a bachelor intern on the Joint Study at the NOFA which is cross-cultural and uses neuroimaging. As an intern, my help is required with testing, recruitment, and calling of the participants for the research.

What is your main research interest/topic?

I am mostly interested in the relationship between cannabis use disorder and anxiety. Since anxiety and cannabis disorder have a bidirectional relation in which cannabis is used to relieve anxiety but it can also cause anxiety, I am interested to learn more about this.

Is there anything else we should know about you?

I like to play piano

Meet the team #5 Lana

What is your name?

Lana Hagedoorn

Can you tell something about yourself?

I have recently graduated from the University of Amsterdam with a Bachelor’s degree in Psychobiology. To gain practical experience I have joined the Neuroscience of Addiction Lab. In addition, I am working as a student-assistant: teaching and supporting Psychobiology students.

What is your role at the NOFA lab?

I work as an auxiliary researcher in the Neuroscience of Addiction Lab. My job is to screen potential participants and get in contact with them. If they are eligible I can schedule an appointment. During this appointment, we take some tests and scan the participant in the MRI scanner, this in cooperation with the other researchers.

What is your main research interest/topic?

My interest lies in pathophysiology and medicine: I want to know what exactly defaults in the brain and body when looking into a disorder. Interestingly, we don’t always know what goes wrong: this makes the path to interventions an exciting but challenging one.

Is there anything else we should know about you?

Next school year I will be resuming my studies and apply for a Master.

Meet the team #4 Anne

What is your name?

Anne Tjepkema

Can you tell something about yourself?

I am finishing my last year of the bachelor Psychobiology at the University of Amsterdam. I am in my 4th year right now, as I took extra subjects in my previous year instead of starting an internship.

What is your role at the NOFA lab?

I’m a bachelor intern at the lab, which means I take several tests with subjects in the Cannabis Use Disorder study and also work on recruiting new subjects. Apart from my work in the lab, I work on my bachelor’s thesis.

What is your main research interest/topic?

I am mostly interested in the connection between self-medicating cannabis use behavior and depression and/or anxiety, so I will be writing my thesis on this subject within the study. Psychiatric disorders, addiction and self-medicating behavior or medication in general are within my field of interest.

Is there anything else we should know about you?

I have a 7-year old daughter and 3 cats. I love drawing portraits in my spare time.

Publications: Cannabis & Cognition

Are you interested in the short and long-term effects of cannabis use on cognition? Learn about the evidence for short-term effects of cannabis on learning, memory, attention, and inhibition and the challenges facing research on long-term effects from Emese Kroon (a PhD student in the lab) in her review of recent advances in the field. Click the link to see the open access article.…/pii/S2352250X20301135

NOFA News: ERC starting grant for Janna Cousijn

Great news! Janna Cousijn (the head of the NofA lab) has received an €1.5 million Starting Grant from the European Research Council, which will fund the next 5 years of research on addiction and development in the lab. You can read more about the newly funded project below!

During adolescence, we see a sharp increase in alcohol and cannabis problems, but also remarkable recovery rates, as most adolescents at some point cut down or stop without treatment. Brain development probably plays an important role in this, and in particular the unique social sensitivity and learning flexibility of adolescents. However, we still know too little about this and comparisons between adolescents and adults are largely missing. Janna Cousijn will follow adolescent and adult alcohol and cannabis users for three years. She will focus on both social and cognitive processes and gradually develop new methods to map brain processes and behaviour. By studying similarities and differences between adolescents and adults, she hopes to uncover both common and unique mechanisms of addiction risk and resilience, that can ultimately improve treatment.

Want to ready more? Follow the link to the UvA website:…/eight-uva-researchers-receive-erc…

Publications: Cannabis & Cigarette use

It is very common for cannabis users to smoker cigarettes and vice versa. Despite this, we don’t have a clear understanding of how the effects of cannabis and cigarette might interact in the brain. In our recently published paper, we aimed to study the interactive effect of cannabis and cigarette use on motivational processes towards cannabis in the brain.

The results might surprise you! Click the link to get the article for free and find out more.

Meet the team #3 Lauren

Let’s introduce the team!

In our ‘Meet the team’ posts you will learn more about the NOFA lab members. Always wanted to know more about our projects, research interests, background, or hobbies? Keep reading!

What is your name? Lauren Kuhns

Can you tell something about yourself? I am originally from the UnitedStates, and I received my bachelor’s degree in Psychology at YaleUniversity in 2014. I moved to the Netherlands 5 years ago to do myMasters in psychology at the University of Amsterdam, and havecontinued on because it is a great environment for doing research.

What is your role at the NOFA lab? I am a second year PhD Candidate inthe lab. I spend about half of my time working on the Joint Study which isan ongoing cross-cultural neuroimaging study of Cannabis Use Disorder. Inaddition, I supervise bachelor and master’s student internships and thesisprojects and help teach a psychobiology course on addiction.

What is your main research interest/topic? I am mostly interested in therole of individual differences on the underlying neuromechanisms ofaddiction. In other words, does an addicted brain always look the same?And if not, what does that mean for our theoretical models of addiction?Most of my research centers around how factors such as age(adolescents vs. adults), culture (NL vs US) and co-use of other drugs(e.g. cigarettes/tobacco products) may influence motivational circuits inthe brain in the context of problematic cannabis and alcohol use.

Is there anything else we should know about you? I have a miniaturepoodle named Ralph Ravioli Cucumber.

Food For Thought: Student Edition #3

As the neuroscience of addiction lab is also highly involved in teaching at the University of Amsterdam, we would like to share some of the great output from our recent bachelor course on addiction. In our ‘Food for thought: Student Edition’ series we will share some excellent essays on a variety of addiction related topics. This time you will have the opportunity to read Roos van Oeveren’s essay on ‘Competing models of addiction: two sides of the same coin?’.

About the author: I am a third year Psychobiology bachelor student at the University of Amsterdam. Whilst still deciding on my future specialization, I took the course “addiction” as an elective. I was deeply fascinated by the topic, and I found the neurobiology of addiction especially intriguing.

Competing models of addiction: two sides of the same coin?

Addiction has become a widespread problem. In the United States, 8-10% of people aged 12 years or older are estimated to be addicted to drugs such as alcohol, tobacco and also illicit drugs (Volkow, Koob & McLellan, 2016). With the goal of finding effective treatment, research into the underlying neurobiological mechanisms of addiction increased over the span of the last few decades. A long-accepted theory, that most scientists still admire, is the Brain Disease Model of Addiction (BDMA). This model is suggested by Leshner (1997) and recognizes addiction as a chronic, relapsing disorder characterized by structural brain changes. This model provides structure to the creation of social and health policies, behavioral treatments, and novel medications for addiction. However, some researchers have started questioning the brain disease model recently.

For example, Hall, Carter & Forlini (2015) state that the brain disease model of addiction is only accepted for social implications. Nonetheless, the model has not led to novel effective treatments and it lacks evidence based on animal and neuroimaging studies (Hall et al., 2015). In addition, brain alterations as found in addiction are thought to be an expression of natural brain plasticity, such as learning and development, instead of a disease (Lewis, 2017; Lewis 2018). Finding a comprehensive model to describe addiction is necessary for the development of effective treatments. However, scientists pleading contradicting models drive us only farther from this goal. According to Lewis (2017), the brain disease model of addiction and his proposed ‘developmental-learning model of addiction’ cannot be combined. However, I believe that these two models can be joined together into a novel, comprehensive model explaining addiction.

Firstly, a closer look into the brain disease model of addiction. Addiction has been described in three stages that are associated with different brain areas that indicate that addiction relies on mesolimbic reward systems. These stages are 1) binge/intoxication, mediated by the ventral tegmental area and ventral striatum, 2) withdrawal/negative effect, mediated by the amygdala, and 3) preoccupation/anticipation (craving), mediated by a broad network consisting of areas involving in craving and disturbed inhibitory control (Koob & Volkow, 2010). Throughout these stages, dopamine is an important transmitter that enhances structural changes in synaptic networks, such as in the striatum which mediates the pursuing of rewards (Koob & Volkow, 2010). These brain alterations are in line with the behavioral sensitization towards drugs seen in addiction.

The developmental-learning model of addiction recognizes the neurobiology of the brain disease model. However, it is viewed as a result of natural brain plasticity in the context of learning and development. The idea is that brain alterations should be expected in the presence of an addiction since our brain is supposed to change as a result of new experiences (Lewis, 2017). Addiction is seen as another experience that is strengthened by emotions and social influences. Desire shapes synaptic configuration thereby increasing sensitivity to cues associated with what is desired, resulting in a vicious circle of behavior or drug-taking (Lewis, 2017). The origination of addiction is not different from any other habit; however, it emerges more rapidly and more radical brain changes are observed due to the high motivational value of drugs.

Despite being based on the same neurobiological information, Lewis (2017) claims that the brain disease model and the developmental model of addiction cannot get along. The main statement is that the point of view on the neuroscientific research is very different for both models. Whereas the BDMA draws on the principle of ‘neuronormativity’, the developmental-learning model is based on neuroplasticity. In other words, according to Lewis (2017), the BDMA recognizes only two stages, either ‘normal’ or ‘pathological’, whilst the developmental-learning model acknowledges exclusively ‘normal’ states scattered in the spectrum of radical habit development.

Nonetheless, science nearly never succeeds to draw a harsh line between ‘pathological‘ and ‘normal’, as disorders and diseases go through development and therefore exist gradually in a spectrum. Rather the arbitrary concepts of the Diagnostic and Statistical Manual of Mental Disorders (5th ed.; DSM-5) suggest a harsh lines between ‘pathological’ and ‘normal’ whilst it is acknowledged that disorders develop gradually. For example, in Alzheimer’s disease the distinction between ‘normal’ and ‘pathological’ forgetting is vague. Yet, it is accepted worldwide that Alzheimer’s disease is, in fact, a disease. Regarding this point of view, I propose that the mechanism through which addiction develops is indeed part of the natural, healthy neuroplasticity in habit formation. However, the rapid and radical development that Lewis (2017) states as characteristics of addiction are capable of shifting the addiction into the characteristics of a disease. Additionally, “developmental psychopathology” is an acknowledged term for other disorders that develop in a vague zone between pathology and learning, such as depression and anxiety disorders (Lewis, 2017). Lewis (2017) believes that explaining the etiology of addiction through natural plasticity excludes a disease. However, addiction is the only habit in which we observe such strong and radical habit formation, making the association with normal brain development unfair. We should, contrary to the BDMA, recognize the etiology of addiction through natural brain development mediated by strong motivation. Nonetheless, it is not excluded that this disease can develop through a natural mechanism.

In addition, Lewis (2017) does not distinguish between different types of addiction. However, difference in brain activity for different substance addictions (nicotine, alcohol and cocaine) in the amygdala and anterior cingulate cortex (ACC) have been found (Kühn & Gallinat, 2011). Analyzing brain changes in addiction as a pure expression of normal, standardized brain development fails to explain different effects of different substances. This suggests an effect on the brain activity by the substance itself, alongside the brain alterations due to habit formation. This could be in line with the idea that addiction develops through natural brain mechanisms. I propose that the substance has an extra effect on the neuroplasticity itself, leading to radical, pathological brain development and is in line with what is stated above. An important difference to the BDMA is that the BDMA assumes substance use to be the cause of all observed brain alterations. I believe the substance radicalizes normal habit formation into a pathological habit formation.

Furthermore, addiction is known to be related to genetic vulnerability (Ouzir & Errami, 2016). Yet, Lewis (2017) did not recognize any genetic factors underlying addiction vulnerability. A genetic predisposition for developing an addiction indicates a relationship to a disease. However, the presence of individual differences, such as sensitivity, do not exclude the collaboration between genetic influences and natural mechanisms. Individual differences are the rule and not the exception. Throughout the whole structural and functional development of the brain, individuals differ. The genetic vulnerability could result in a sensitivity for developing radical habit formation, which is in harmony with the aggregation of the BDMA and the developmental-learning model.

Moreover, this genetic predisposition in combination with natural neuroplasticity is in line with research into the social plasticity hypothesis. Briefly, this hypothesis states that vulnerability to social influences (such as peer pressure) increase the chance of excessive substance use when this is used in one’s social environment (Cousijn, Luijten & Feldstein Ewing, 2017). This hypothesis is mainly based on risk and resilience to addiction in adolescence, however, it is also in line with the broad idea that vulnerability to addiction shows high individual differences due to genetic predispositions and that the habit itself (for example excessive drinking use), can also differ between individuals (which is also strictly stated in the developmental-learning model (Lewis, 2017)).

Regarding current scientific knowledge as stated above, the brain disease model of addiction and the developmental-learning model can be combined into a novel, comprehensive model. Harsh distinction lines between pathological and normal habit formation should not be the goal and zones of change should be accepted. It should be highly recognized that I was not able to fully elaborate on all aspects of both models, and further, that more research is needed to expand this novel model. Moreover, combining the BDMA and the developmental-learning model can fulfill the need of a basis for novel treatment. Treatments of addiction based on the BDMA fail to be effective (Hall et al., 2015). Whilst the developmental-learning model fails to explain all symptoms of addiction (as elaborated above), the combination of both models could provide a basis for effective, novel treatments of addiction and new social and psychological policies. Future research should focus on individual treatment as proposed by Lewis (2017) regarding individual development, perspectives, goals and capacities in combination with research into genetic predispositions and the effects of specific substances.


Cousijn, J., Luijten, M. & Feldstein Ewing, S.W. (2018). Adolescent resilience to addiction: a social plasticity hypothesis. The Lancet Child & Adolescent Health, 2(1), 69-78. doi:10.1016/S2352-4642(17)30148-7.

Hall, W., Carter, A. & Forlini, C. (2015). The brain disease model of addiction: is it supported by the evidence and has it delivered on its promises? The Lancet Psychiatry, 2(1), 105-110. doi:10.1016/S2215-0366(14)00126-6.

American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).

Leshner, A.I. (1197). Addiction Is a Brain Disease, and It Matters. Science, 278(45). doi:10.1126/science.278.5335.45

Koob, G., Volkow, N. Neurocircuitry of Addiction. Neuropsychopharmacol, 35, 217–238. doi:10.1038/npp.2009.110

Kühn, S., & Gallinat, J. (2011). Common biology of craving across legal and illegal drugs—A quantitative meta‐analysis of cue‐reactivity brain response. European Journal of Neuroscience, 33(7), 1318–1326.

Lewis, M. (2017). Addiction and the Brain: Development, Not Disease. Neuroethics, 10(1), 7–18. doi:10.1007/s12152-016-9293-4

Lewis, M. (2018). Brain Change in Addiction as Learning, Not Disease. New English Journal of Medicine, 379(16), 1551-1560. doi: 10.1056/NEJMra1602872.

Ouzir, M. & Errami, M. (2016) Etiological theories of addiction: A comprehensive update on neurobiological, genetic and behavioural vulnerability. Pharmacology Biochemistry and Behavior, 148, 59-68. doi:

Volkow, N. D., Koob, G. F., & McLellan, A. T. (2016). Neurobiologic Advances from the Brain Disease Model of Addiction. The New England journal of medicine, 374(4), 363–371. doi:10.1056/NEJMra1511480

Food For Thought: Student Edition #2

As the neuroscience of addiction lab is also highly involved in teaching at the University of Amsterdam, we would like to share some of the great output from our recent bachelor course on addiction. In our ‘Food for thought: Student Edition’ series we will share some excellent essays on a variety of addiction related topics. This time you will have the opportunity to read Maura Fraikin’s essay on the potential of MDMA as a treatment for post traumatic stress disorder.

About the author: I am currently in my third year of the psychobiology bachelor at the University of Amsterdam. I am very intrigued by the intertwining of biology and psychology and how biological processes influence neurological phenomena. Cognition, psychopharmacology and the neurobiological mechanisms underlying psychiatric disorders are some of my main interests.

Is MDMA a safe and effective way to improve treatment for PTSD?

Post-traumatic stress disorder (PTSD) is a devastating mental disorder that is triggered by a traumatic event (American Psychiatric Association, 2013). Approximately 7.4% of the Dutch population develops PTSD at some point in their lives, with women being more likely than men to develop PTSD (De Vries & Olff, 2009). The symptoms of PTSD can be divided into four categories: repeated memories, avoidance, negative alterations in mood and thinking, and changes in arousal and reactivity (American Psychiatric Association, 2013). PTSD quite often co-occurs with other mental illnesses and PTSD has a large impact on quality of life (Brady et al., 2000). PTSD is even associated with an increased risk of attempting suicide (Tull, 2019), emphasising the relevance to expand research on treating the symptoms patients suffer from.

Currently available treatments include Cognitive Behaviour Therapy, Cognitive Processing Therapy, Eye Movement Desensitisation and Reprocessing and/or pharmacotherapy (American Psychiatric Association, 2013; Thal & Lommen, 2019). However, the rate of treatment resistance is high, often causing impairments for life (Rodriguez, Holowka & Marx, 2012). Another problem in PTSD treatment is that psychotherapy methods are trauma-focused, which can be quite overwhelming leading to many patients to drop out of treatment (Zepinic, 2015; Burge, 2018). Moreover, all currently used pharmacotherapies in PTSD are symptomatic treatments that do not get to the heart of the problems (Katzman, 2014; Burge, 2018; Bahji et al., 2020). Therefore, an effective treatment is needed that is capable of reducing the considerable rates of treatment failure related to current PTSD treatments.

MDMA, or 3,4-methylenedioxymethamphetamine, emerges as a promising therapeutic candidate for this. MDMA was invented in 1912 as a potential medicine and used in psychotherapy in the 1960s. At the same time, it ended up in the party scene, after which it ended up on list one of the Dutch Opium Act (Kuypers, 2019). This means that possession, trade, production, import and export of MDMA is illegal (art. 2 & art. 10 Opiumwet, 2019), making it hard to study MDMA in clinical settings. However, the beneficial effects of MDMA are unique and might be useful in PTSD treatment. It temporarily decreases fear while increasing relational trust and could therefore be effective to enhance the effects of psychotherapy (Mithoefer et al., 2011).

This leads to the question: does MDMA treatment in combination with psychotherapy successfully alleviate PTSD symptoms? I will argue why, in my opinion, MDMA has therapeutic potential for treatment of PTSD due to its unique characteristics, unlike other pharmacotherapies, to make psychotherapy effective and explain why people should be less reluctant to use this abused drug for medical purposes.

The effect of MDMA-assisted psychotherapy in treatment-resistant PTSD patients

The first completed clinical trial to indicate that MDMA might serve as a therapeutic adjunct in PTSD was performed by Mithoefer et al. (2011). In their study, 20 treatment resistant PTSD patients were tested in a randomized double-blind placebo controlled design. In the first stage of the study, patients were divided into an inactive placebo or MDMA group, in which participants received a dose of 125 mg MDMA, followed by an optional supplemental dose of 62.5 mg MDMA 2.5 hours later during two psychotherapy sessions. In the second stage, participants in the placebo group were given the option to participate in an open-label crossover part of the study in which they received 125 mg MDMA as well. MDMA significantly reduced the scores on the Clinician-Administered PTSD Scale (CAPS), which is a standard symptom scale used to quantify PTSD symptoms and assess the severity. The clinical response rate, defined as more than 30% reduction in CAPS score from baseline, was 83% in the MDMA group compared to 25% in the placebo group. Interestingly, the clinical response rate of the initial placebo group who transitioned to MDMA-assisted psychotherapy increased to 100% in stage two. Furthermore, no serious adverse effects related to MDMA were found.  However, the double blinded design in their study did not work. The majority of the participants and researchers correctly guessed the condition of the subjects. This is probably because MDMA is a psychoactive substance and it produces some noticeable physical and psychological effects, which might have influenced the results.

To evaluate the durability of the outcomes, the same research group assessed CAPS scores again in a follow-up study 3.5 years later. The statistically and clinically significant reduction in PTSD symptoms was maintained. This is indicative of a persistent effect of MDMA-assisted psychotherapy. None of the subjects reported they felt harmed from participating. Importantly, none of the participants used MDMA recreationally afterwards (Mithoefer et al., 2013).

Oehen et al. (2013), however, did not find a significant reduction of MDMA-assisted psychotherapy in clinical PTSD symptoms, although they did find a positive effect on self-reported PTSD symptoms. They examined the efficacy and safety of MDMA-assisted psychotherapy in 12 treatment-resistant PTSD patients in a randomized double-blind trial. Participants were randomly assigned into either full dose MDMA or placebo groups in stage one. As previously mentioned, MDMA has a psychoactive effect, making it hard to maintain the double blind status in clinical studies. To overcome this methodological challenge, an active placebo control of 25 mg followed by 12.5 mg MDMA 2.5 hours later was used, instead of the inactive placebo used by Mithoefer et al. (2011). The full-dose group received 125 mg MDMA, with a supplemental dose of 62.5 mg 2.5 hours later. This also differs from the study of Mithoefer et al. (2011) in which the supplemental dose of MDMA was optional.

In stage two, subjects in the active placebo condition were given the opportunity to continue in an open-label part of the study, receiving the full active dose of MDMA in conjunction with psychotherapy, similar to the method of Mithoefer et al. (2011). A 23.5% decrease in CAPS scores was found in the full-dose group, although this was not statistically significant. Furthermore, scores on the Posttraumatic Diagnostic Scale (PDS), which serves as a self-reporting measure to assess the presence of PTSD symptoms, significantly improved. Similar to results found in the earlier study (Mithoefer et al., 2011), patients in the active placebo group did not respond to treatment at first, but after receiving the full-dose MDMA in stage 2 they all responded to treatment, with half of the subjects no longer fulfilling PTSD criteria. At the one year follow-up, there was a further reduction in CAPS scores of 35% in the full-dose and 52% in the crossover group, thus indicating clinical response. Regarding the safety, no drug-related serious adverse events occurred, indicating that MDMA can be administered safely in a clinical setting in PTSD patients. Moreover, participants did not report any recreational use of MDMA at 12-month follow-up.


These findings indicate that MDMA-assisted psychotherapy can successfully alleviate PTSD symptoms. There is empirical evidence that MDMA has therapeutic potential to be a successful, long-lasting and overall safe intervention for treatment-resistant PTSD patients. However, there are some limitations to the studies that need to be considered. All studies had small sample sizes and the majority of participants were female and Caucasian. It is possible that both gender and ethnic differences exist in response to psychotherapy in combination with MDMA. Furthermore, both durations of treatments and the extent of treatment before entering the study differed across studies, which makes the results difficult to compare. Moreover, the double-blinding was not effective in one study (Mithoefer et al., 2011), which could have influenced the results due to a bias of participants. These limitations emphasise that the conclusions must be drawn with caution.

Critics argue that the risk of abuse increases when MDMA gets legalised for medical use, since patients might use the drug afterwards to get the same feeling (Parrot, 2014) and as a non-patient it might be easier to gain access to MDMA. However, MDMA will be used in conjunction with psychotherapy in PTSD patients, meaning it will only be available under therapeutic supervision in certified clinics (Burge, 2018). Thus, PTSD patients will not be able to resell MDMA, as is done with Ritalin for example. Moreover, the fact that all studies showed that MDMA was not used for recreational purposes after treatment suggests that MDMA given in the context of psychotherapy has low abuse liability. Although we do need to be very wary about misuse, under appropriate supervision the risk seems small.

Another argument against the use of MDMA in PTSD treatment is that in studies of recreational ecstasy use severe adverse effects did occur. However, we should be careful to compare the morbidity and mortality statistics that are related to recreational ecstasy use with medical MDMA use in a controlled setting (Sessa, 2017). Both dose and content play an important role. Recreational dosages of MDMA in ecstasy vary and have increased over the past years. The mean dosage of MDMA in ecstasy in the Netherlands is 160 mg with outliers above 200 mg of MDMA (Drugs info team, 2018). Considering that recreational users quite often use more than one pill, the dosages of recreational MDMA are often higher than those in medical setting. Also, ecstasy does not always consist of pure MDMA—it may contain other substances. Furthermore, patients will have to be thoroughly screened in advance to minimize risks (Burge, 2018).

Research into the effectiveness of MDMA in alleviation of PTSD symptoms is scarce. The described studies that investigated the effectiveness were more or less the only ones. Thus, more research is needed to confirm the findings and to study long term outcomes. Also, gender and ethnic differences should be taken into consideration in future studies. Furthermore, research into the effective dosage and sessions of MDMA-assisted psychotherapy is useful. If the positive results of MDMA-assisted psychotherapy are replicated in phase three trials, MDMA might be approved by the FDA. Next to the fact that MDMA is on list 1 of the Dutch Opium Act, it will then also be included in the medicines law. If MDMA-assisted psychotherapy can indeed effectively be used in patients with treatment-resistant PTSD, the percentage of patients who commit suicide could decrease, as a result of increased quality of life. Altogether, MDMA is a potential medicine for PTSD and people should be less reluctant to use it for medical purposes, but more research is needed to get to conclusive results.


American Psychiatric Association. (2013) Diagnostic and statistical manual of mental disorders, (5th ed.). Washington, DC: Author

Bahji, A., Forsyth, A., Groll, D., & Hawken, E. R. (2019). Efficacy of 3, 4-methylenedioxymethamphetamine (MDMA)-assisted psychotherapy for posttraumatic stress disorder: A systematic review and meta-analysis. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 109735. DOI:10.1016/j.pnpbp.2019.109735

Burge, B. (2018). MDMA, Psychotherapy, and the Future of PTSD Treatment. Retrieved from:

Brady, K. T., Killeen, T. K., Brewerton, T., & Lucerini, S. (2000). Comorbidity of psychiatric disorders and posttraumatic stress disorder. The Journal of clinical psychiatry

de Vries, G. J., & Olff, M. (2009). The lifetime prevalence of traumatic events and posttraumatic stress disorder in the Netherlands. Journal of Traumatic Stress: Official Publication of The International Society for Traumatic Stress Studies22(4), 259-267. DOI: 10.1002/jts.20429.

Drugs info team. (2018). Xtc feiten. Retrieved from:

Katzman, M. A., Bleau, P., Blier, P., Chokka, P., Kjernisted, K., & Van Ameringen, M. (2014). Canadian clinical practice guidelines for the management of anxiety, posttraumatic stress and obsessive-compulsive disorders. BMC psychiatry, 14(S1), S1. DOI:10.1186/1471-244X-14-S1-S1

Kearney, D., Martinez, M., & Simpson, T. (2018). Posttraumatic Stress Disorder (PTSD). In Integrative Medicine (pp. 86–93.e3). DOI:10.1016/B978-0-323-35868-2.00010-4

Kuypers, K. (2019, 17 oktober). Waarom zeggen alle psychiaters ‘ja’ tegen mdma? AD. Retrieved from:

Mithoefer, M. C., Wagner, M. T., Mithoefer, A. T., Jerome, L., & Doblin, R. (2011). The safety and efficacy of±3, 4-methylenedioxymethamphetamine-assisted psychotherapy in subjects with chronic, treatment-resistant posttraumatic stress disorder: the first randomized controlled pilot study. Journal of Psychopharmacology, 25(4), 439-452. DOI: 10.1177/0269881110378371

Mithoefer, M. C., Wagner, M. T., Mithoefer, A. T., Jerome, L., Martin, S. F., Yazar-Klosinski, B., … Doblin, R. (2013). Durability of improvement in post-traumatic stress disorder symptoms and absence of harmful effects or drug dependency after 3,4-methylenedioxymethamphetamine-assisted psychotherapy: a prospective long-term follow-up study. Journal of psychopharmacology (Oxford, England)27(1), 28–39. DOI:10.1177/0269881112456611

Oehen, P., Traber, R., Widmer, V., & Schnyder, U. (2013). A randomized, controlled pilot study of MDMA (±3,4-Methylenedioxymethamphetamine)-assisted psychotherapy for treatment of resistant, chronic Post-Traumatic Stress Disorder (PTSD). Journal of Psychopharmacology27(1), 40–52. DOI:10.1177/0269881112464827

Opiumwet (2019). Retrieved from:

Parrott, A. (2014). The Potential Dangers of Using MDMA in Psychotherapy. Journal of Psychoactive Drugs46 (1): 37–43. DOI:10.1080/02791072.2014.873690

Rodriguez, P., Holowka, D. W., & Marx, B. P. (2012). Assessment of posttraumatic stress disorder-related functional impairment: A review. J Rehabil Res Dev49(5), 649-65 DOI: 10.1682/JRRD.2011.09.0162

Sessa, B. (2017). MDMA and PTSD treatment:“PTSD: from novel pathophysiology to innovative therapeutics”. Neuroscience letters649, 176-180. DOI: 10.1016/j.neulet.2016.07.004

Thal, S. B., & Lommen, M. J. (2018). Current perspective on MDMA-assisted psychotherapy for posttraumatic stress disorder. Journal of contemporary psychotherapy, 48(2), 99-108. DOI: 10.1007/s10879-017-9379-2

Tull, M. (2019, 23 november). The Connection Between PTSD and Suicide. Retrieved from:

Zepinic, V. (2015). Treatment Resistant Symptoms of Complex PTSD Caused by Torture During War. Canadian Social Science, 11(9), 26-32. DOI:10.3968/7551