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Comparative effects of MDMA and Psilocybin on Depression and PTSD
Department of Biology
Lake Forest College
Lake Forest, Illinois 60045
Post-traumatic stress disorder (PTSD) and depression, combined, affect about forty-two million people in the United States alone (Carhart-Harris et al. 2016; Oehen et al. 2013).. Current pharmacological therapies have been shown to only be effective for only about 20% . Furthermore, studies on children in war-torn regions have shown that PTSD is comorbid with major depression (Thabet et al. 2004). However, the comorbidity of PTSD and depression has not been extensively studied. The two disorders have been shown to have similar underlying neuronal mechanisms; therefore, it would be worthwhile to compare the effects of similar treatment on the two disorders. 3,4-Methylenedioxymethamphetamine (MDMA) is a hallucinogen that has been shown to be an effectivetreatment for PTSD; however, the effects of MDMA on depression are not well studied. Conversely, the hallucinogen, psilocybin has been shown to be a promising candidate for treatment of depression; however, the effects of psilocybin on PTSD have not been examined closely. et al
Hallucinogens consist of four basic types: serotonin-like, norepinephrine-like, acetylcholine-like, and glutamate-like. Serotonin-like hallucinogens include N, N-Dimethyltryptamine (DMT), psilocybin, and Lysergic acid diethylamide (LSD) (Carhart-Harris et al. 2016). Norepinephrine-like hallucinogens include mescaline and MDMA (Haigler & Aghajanian, 1973). Acetylcholine-like hallucinogens include jimsonweed and deadly nightshade, also known as belladonna (Friedman & Levin, 1989). Lastly, glutamate-like hallucinogens include Phencyclidine (PCP) and ketamine (Moghaddam et al. 1997). Serotonin-like hallucinogens, such as psilocybin, act on the 5-HT serotonin receptor in the brain. Ingesting these serotonin-like hallucinogens can cause users to experience visual and auditory hallucinations. Psilocybin reportedly produces feelings of relaxation and nervousness and elicits spiritual experiences (Carhart-Harris et al. 2016). MDMA, a norepinephrine-like hallucinogen, acts by increasing norepinephrine activity, which is the main neurotransmitter known to heighten arousal. Arousal is a physiological autonomic nervous system response that increases bodily functions, such as blood pressure and heart rate. Furthermore, after taking MDMA people typically report feeling energetic and euphoric and describe experiences of emotional warmth (Oehen et al. 2013). Jimsonweed and other acetylcholine-like hallucinogens are not usually taken for pleasure, due to the large number of negative side effects. The negative side effects of acetylcholine-like hallucinogens include symptoms of bodily rejection, such as nausea, vomiting, and headache (Friedman & Levin, 1989). Glutamate-like hallucinogens, specifically ketamine, act by blocking specific glutamate receptors found in the brain, called NMDA receptors (Moghaddam et al. 1997). In turn, blocking NMDA receptors causes anesthetic and analgesic effects. The effects of blocking NMDA receptors are also why ketamine is commonly used as an anesthetic drug during surgery (Moghaddam et al. 1997). The four basic types of hallucinogens describe the chemical actions and the effects of groups of hallucinogens.
Though hallucinogens may be thought of as modern synthetic drugs, the hallucinogenic actions of plants have been harnessed for centuries. For instance, archeological evidence from Mesoamerica depicting mushroom gods and rituals, indicate that the use of psilocybin mushrooms dates as far back as 7000 years ago Historical records of psilocybin use were largely in the context of religious or ritual purposes. Only much later, in the 1950’s, was recreational use of psilocybin seen in the Western world. Psilocybin was also used for its medicinal properties as a form of treatment among many indigenous people (De Borhegyi, 2012). In 1521, the Europeans began to forbid the use of non-alcohol intoxicants, which included psilocybin mushrooms. In the 1950’s, Richard Evans Schultes supported the idea that the Teonanácatl were in fact referring to mushrooms in their paintings (Hofmann et al., 1959). In 1956, a sample of the mushrooms, taken for the expedition, was given to Albert Hoffman, a chemist who worked at Sandoz Pharmaceuticals. Hoffman was able to isolate the active compounds, psilocybin and psilocin by 1957 (Hofmann et al., 1959). Therefore, modern science was clearly centuries behind in the discovery of psilocybin and psilocin.
Unlike psilocybin mushrooms, MDMA does not have a long history behind it. Firstly, unlike psilocybin mushrooms, MDMA is not natural; it is completely man-made. MDMA was developed in 1912 by Anton Köllisch and German pharmaceutical company, By the 1970’s the recreational use of MDMA appeared in the United States (Shulgin, 1986). MDMA is still used recreationally and is commonly referred to as a party drug.
The structures of psilocybin and MDMA are similar; they are both part of the phenylethylamine class of hallucinogens. MDMA has a methylenedioxy group attached to the 3,4 position of the aromatic ring. This structural characteristic of MDMA allows it to resemble mescaline. The remaining structure of MDMA resembles that of amphetamine. MDMA’s amphetamine-like structure combined with MDMA’s mescaline-like structure lead to the unique effects of MDMA that can be thought of as a blend of both mescaline and amphetamine actions (Pitts et al., 2017). MDMA is absorbed through the intestinal tract and requires about 2 hours to reach peak plasma concentrations. MDMA slowly degrades in the body, taking as long as 40 hours for 95% of the drug to clear from the body (Mas et al., 1999). MDMA works by increasing the synaptic concentration of monoamine neurotransmitters, such as serotonin and norepinephrine. In both cases, MDMA acts by blocking the reuptake of the neurotransmitters, rather than playing a role in their direct release. MDMA blocks the 5-HT2A receptor, inhibiting the reuptake of serotonin (Mas et al., 1999). Blocking serotonin reuptake creates elevated effects of serotonin.
Psilocybin and psilocin are indolealkylamines. Psilocybin is the compound that is ingested from the mushrooms and is converted to psilocin in the body. Psilocybin can be thought of as a prodrug. Only about 50% of the total volume of psilocybin taken orally is absorbed from the digestive tract (Grieshaber et al. 2001). Peak plasma concentrations of psilocin are seen in about 1 hour. Psilocin degraded quickly and 95% of psilocin will be degraded in under 14 hours (Grieshaber et al. 2001). Psilocybin and psilocin are both structurally very similar to serotonin. Psilocybin has a twofold effect. First, it prevents the reuptake of serotonin by blocking the 5-HT2A receptor, which causes serotonin to stay in the synapse longer thus prolonging euphoric effects. Second, as mentioned before, psilocin is similar to serotonin, and therefore, it is able to amplify the effect of serotonin. Both MDMA and psilocybin have a role in increasing the level of serotonin.
Figure 1. The serotonin pathway. Shows all regions of the brain affected by elevated serotonin.
In the United States alone, over 16 million people suffer from depression (Carhart-Harris, et al., 2016). Current treatment options for depression consist of 3 basic types of medication, SSRIs, MAOIs, and TCAs, with SSRIs being the most commonly prescribed. The major issue with these treatments is that they have been found to be useful for only 20% of individuals with depression (Carhart-Harris et al. 2016; Griffiths et al. 2016).
Ries discovered that serotonin and the serotonin 5-HT receptor are acted on by mediations for depression in Drosophila. Furthermore, depression is associated with lower levels of serotonin. After receiving drug treatment, levels of serotonin are typically elevated to normal in depression patients (Ries et al. 2017). These findings show how the level of serotonin is crucial to depression mediation.
Overview of PTSD
Prevalence of PTSD ranges from 8% in the United States to around 1% in European countries (Oehen et al. 2013). The prevalence of PTSD can be higher in certain populations, such as soldiers returning from war (Oehen et al. 2013). The current most effective recognized form of treatment for PTSD is psychotherapy. Cognitive-based therapy that is frequently prescribed for PTSD patients shows efficacy for only some patients, while the majority of people suffering from PTSD are left without effective treatment options (Oehen et al. 2013). Another problem with this type of therapy is that as many as 20% of patients drop-out prematurely. Furthermore, one study showed that 58% of the patients who did complete therapy treatment still showed signs of PTSD (Oehen et al. 2013). Currently, there are two FDA approved treatments of PTSD, sertraline (SSRI) and paroxetine (SSRI), both of which are shown to alleviate some symptoms of PTSD (Oehen et al. 2013). More effective and reliable treatments for PTSD still need to be researched. Both norepinephrine and serotonin levels may play a role in the pathophysiology of PTSD. Moreover, the 5-HT receptor is thought to be involved in PTSD (Mithoefer et al. 2011). Based on the importance of serotonin and 5-HT receptors in PTSD pathology, some research has suggested that hallucinogens, such as MDMA and psilocybin, that target the serotonin pathways may be effective treatment options.
Research into the effectiveness of MDMA for treatment of PTSD has clearly yielded significant results. Currently, MDMA assisted psychotherapy is on track for FDA approval by 2021 (Mithoefer et al. 2011). Furthermore, the FDA has referred to MDMA as a breakthrough therapy for those struggling with PTSD.(Oehen et al. 2013). More research is necessary before the drug can officially be approved, although the current body of research is extremely positive.
Recent research has found evidence that MDMA could be a valuable drug for treating PTSD. Mitoefer et al. (2010) conducted the first clinical trial on the efficacy of MDMA to treat PTSD, and has motivated further research. Mitoefer et al. predicted that MDMA would help treat PTSD because the mechanism of PTSD is linked to the amygdala and the ventral/medial prefrontal cortex. This study found that MDMA was useful in treating PTSD in 20 patients (p<0.05) and also found that the effects of MDMA were not instantly significant (Mithoefer et al. 2011). Ohen et al. (2012) further supported the efficacy of MDMA in treating PTSD by showing that 3 sessions of MDMA therapy were significantly more effective than just 2 sessions (p=0.016). Young et al. (2015) investigated the mechanism through which MDMA influences PTSD by conducting a fear-extinction study in mice. They found that MDMA facilitates fear-extinction learning as well as molecular memory processes (Young et al. 2015). Though these initial findings are not sufficient to conclude that MDMA is a reliable PTSD treatment option, they lay the groundwork for establishing MDMA as a PTSD treatment.
Though Mitoefer et al. (2010), Ohen et al. (2012), and Young et al. (2015) all investigated the efficacy of MDMA as a PTSD treatment, each study had some strengths and some weaknesses. Mitoefer et al. (2010) conducted a randomized double-blind placebo-controlled study, in which the experimental group (12 participants) received two 125 mg therapy treatments of MDMA and the control group (8 participants) received two placebo treatments of lactose. Ohen et al. (2012) also conducted a randomized double-blind study, similar to Mitoefer et al. (2010). However, in order to avoid the inherent problems of blinding in psychedelic studies Ohen et al. (2012) used an active placebo control group. This meant that in Ohen et al. (2012), the experimental group (7 participants) received the same 125 mg therapy treatments of MDMA, as in Mitoefer et al. (2010), but the control group (4 participants) received low-dose 25 mg MDMA placebo treatments. While the active placebo control group improved blinding in Ohen et al. (2012), it may also have contributed to the experimental group not having a significantly greater effect on PTSD symptoms than the control group (p=0.066). The smaller sample size in Ohen et al. (2012) compared to Mitoefer et al. (2010) may also have accounted for Ohen et al. (2012) failing to replicate a significant effect of MDMA treatment on PTSD symptoms. Nevertheless, the findings in Ohen et al. (2012) expanded beyond the finding in Mitoefer et al. (2010) by showing that three treatment sessions were significantly more effective than two treatment sessions (p= 0.016). In contrast, Mitoefer et al. (2010) only studied the effects of two MDMA treatment sessions.
While randomized double blind studies, like Mitoefer et al. (2010) and Ohen et al. (2012), are optimal experimental designs for human research, they still allow for the unavoidable errors due to uncontrollable differences among human participants. Therefore, Young et al. (2015) demonstrated the effects of MDMA on fear extinction in a more controlled experimental design by studying mice. Young et al. (2015) also investigated the mechanism of MDMA’s effects on PTSD that ethically cannot be studied in humans. However, Mitoefer et al. (2010) and Ohen et al. (2012) had a diagnostic baseline that all participants had PTSD diagnoses and were previously resistant to treatment, while Young et al. (2015) could not study the human disorder, PTSD, directly. Young et al. (2015) also did not compare a baseline of fear behaviors prior to fear conditioning or prior to extinction.
Currently MDMA is on the forefront of psychedelic treatment for PTSD; nevertheless, research on psilocybin as a treatment for PTSD is also available and shows significant results. The main goal with PTSD is to find a way to extinguish fear which arises from certain cues. As mentioned before, the amygdala and the fight-or-flight mechanism in the brain are the biggest contributors to PTSD issues. The goal in PTSD research is to find a way in which the brains of PTSD patients can be taught to relearn, so that patients no longer experience unnecessary fear.
A2013 study by Catlow et al. found that psilocybin effects hippocampal neurogenesis and causes extinction of fear. The researchers hypothesized that due to psilocybin altering neurotransmission through the serotonin (5-HT) and specifically the 5-HT2A receptors, which are highly expressed in the hippocampus, it may also play a role in the neurogenesis of the cells in this area. Previous research shows that antidepressant medications such as SSRIs, which also function on the 5-HT receptor, are shown to enhance hippocampal neurogenesis. Therefore, the assumption was made that psilocybin may function in a similar way. Furthermore, the serotonergic system has been implicated in the hippocampal learning (Catlow, Song, Paredes, Kirstein, & Sanchez-Ramos, 2013). Studies show how a knockout mouse model for 5-HT develop heightened contextual fear, and interestingly this fear is reversed with the intracerebroventricular microinjection of 5-HT. Current research has made it clear that the serotonin pathway not only plays a major role in learning and development, but it also plays a large role in fear extinction.
In this study, researchers placed mice in a freezer box for 24 hours after injection of psilocybin. Training the mice consisted of a sequence of 10 trials of conditioned stimulus-unconditioned stimulus presentation (CS-UCS). The trials consisted of a 15 second auditory cue, followed by a silent trace of 30 seconds, and then a brief shock to the feet. After a few trials, animals were conditioned to the stimulus,seen due to the mice freezing after the CS. It was demonstrated that mice that received psilocybin eventually decreased freezing and by trial 10 they no longer exhibited a fear response (Catlow, Song, Paredes, Kirstein, & Sanchez-Ramos, 2013). Furthermore, immunofluorescence was used in order to determine the neurogenesis in the hippocampus. The data showed how the administration of psilocybin produced hippocampal neurogenesis.
The research in this paper is important because it shows how psilocybin acts on the 5-HT2a receptor and is able to produce a response that is beneficial towards fear extinction. Although psilocybin does not act solely on the 5-HT2a receptor, it is the primary receptor on which it acts. This is important because this study shows that psilocybin may be a powerful tool for breaking the cycle of fear conditioned responses due to PTSD. Moreover, psilocybin is also shown to be a tool for repairing parts of the brain associated with that specific fear response. PTSD is usually triggered with a memory or a stimulus that makes the person relive the original trauma over and over again, thus creating a cycle of fear. The ability of psilocybin to break the cycle and reteach the brain to no longer be fearful of such stimuli suggests that psilocybin may be a great treatment for PTSD.
Major depressive disorder is an issue that currently available medications and treatments have failed to address properly. This pervasive problem is evident from the large number of patients who do not receive any alleviation of symptoms from current treatments. Research into psilocybin as a treatment for depression has given hope for a new miracle drug. Interestingly, many of the same researchers who have researched MDMA as a treatment for PTSD are also researching psilocybin and depression. Psilocybin has also been shown to be a valid treatment for other psychological disorders, such as Obsessive-Compulsive Disorder (OCD), alcohol and smoking dependence, as well as anxiety.
Robin Carhart-Harris and his lab are at the forefront of psilocybin research as a treatment for depression. In their 2016 study, Carhart-Harris et al. found that psilocybin may be a safe and effective treatment for depression in lieu of the current treatment. This was one of the first studies conducted on the effectiveness of psilocybin for treating depression. Furthermore, the positive findings from Carhart-Harris et al. (2016) helped increase funding and motivation for further research. Ross et al. (2016) found a robust and immediate improvement of depressive symptoms on all measures of depression used as a result of psilocybin treatment. Furthermore, substantial and sustained treatment benefits from psilocybin were observed for up to 7 weeks post-dosing (Ross et al., 2016). By 7 weeks after the first dose, 83% of patients met criteria for anti-depressant response (Ross et al., 2016). The reduced depression symptoms observed following psilocybin treatment were significantly reduced for up to the 26-week time point. The most promising finding in Ross et al. (2016) was that about 60-80% of patients met the criteria for anti- depressant response in the 6.5-month follow-up. The findings from Carhart-Harris et al. (2016) and Ross et al. (2016) both provide promising evidence that with further research, psilocybin could be established as an effective treatment for depression.
Though both Carhart-Harris et al. (2016) and Ross et al. (2016) supported the effectiveness of psilocybin for depression treatment, Ross et al. (2016) demonstrated these findings with a superior experimental design, and therefore more reliable results. In contrast to the double-blind placebo control-crossover study with 29 participants conducted by Ross et al. (2016), Carhart-Harris et al. (2016) conducted a small within-subjects feasibility study with 12 participants. The validity and reliability of the study conducted by Carhart-Harris et al. (2016) could not be determined because there was no control group to compare to the experimental group. Though a double-blind placebo control-crossover study design, as in Ross et al. (2016), is generally thought to have a strong experimental design, one common weakness of crossover design is that a long-term follow-up is not possible. Carhart-Harris et al. (2016) used a T-test to analyze the effect of psilocybin treatment on depression symptoms at 1 week, 2 months and 3 months after beginning treatment. Depression symptoms were significantly improved at 2 months and 3 months compared to 1 week after beginning treatment (p<0.05) (Carhart-Harris et al., 2016). However, by running multiple T-tests, Carhart-Harris et al. (2016) increased the risk of a type II error. In contrast, Ross et al. (2016) analyzed their results using a mixed effect repeated measures model analysis, which is a much more powerful statistical analysis than a T-test. Overall, while Carhart-Harris et al. (2016) provided preliminary support for further research on psilocybin as a drug for depression, the findings in Ross et al. (2016) establish psilocybin as a potential treatment for depression.
Although MDMA and psilocybin both effect the serotonin pathway, their mechanisms of action are different. MDMA’s ability to increase serotonin in the brain suggests it could make a good candidate for depression treatment; however, research on the abilities of MDMA as a possible form of treatment is severely lacking.
A 2012 study by Majumder et al. found that MDMA has antidepressant-like effects especially in subjects who were predisposed to depression. The study consisted of 40 subjects total, of which 20 took MDMA and 20 did not. Depressive symptoms were measured 60 min after consumption. The study found that patients who were predisposed to depression and did not take MDMA had a greater amount of mood disturbances and depressive symptoms. Furthermore, patients who were predisposed to depression and took MDMA reported a significant decrease in depressive symptoms.Interestingly, current pharmaceutical treatment for depression requires about 6 weeks in order to be effective, MDMA, on the other hand, was shown to be effective in as little as 60 mins (Majumder, White, & Irvine, 2012). This shows that MDMA is a fast-acting drug.
Due to the low efficacy of current depression medications, a fast-acting drug such as MDMA could be very useful. Furthermore, MDMA could be beneficial as a quick acting treatment to help alleviate depression while other forms of therapy are also ongoing. Due to the number of suicides which are linked to depression, a fast-acting drug may be very beneficial to the effective treatment of depression.
PTSD and depression are both global issues that affect millions of people. Current treatment options available for PTSD and for depression are neither reliable nor sufficiently effective for treating either of these issues. As many as 22 veterans commit suicide per day in the US alone. This devastatingly high suicide rate amongst veterans is thought to largely reflect the inadequate treatments available for veterans with PTSD (Mithoefer et al. 2011). Psychedelics, such as psilocybin and MDMA, have given researchers new hope for discovering effective treatments.
The research into MDMA shows its efficacy in treating PTSD. However, research into how MDMA could treat depression is lacking. Furthermore, research shows that psilocybin is a promising candidate for depression treatment. Recent studies suggest that not only MDMA, but also psilocybin, could treat PTSD effectively. Research has demonstrated that both psilocybin and MDMA act on similar brain structures and brain pathways. In particular, both affect serotonin and 5-HT receptors in a similar way. Through the research discussed in this paper, the evidence presented suggests that MDMA may be a good candidate drug for depression treatment, as well as the better studied psilocybin. One key difference between MDMA and psilocybin is that MDMA is shown to deplete serotonin reserves (Mithoefer et al. 2011). As a result, MDMA may relive depression only for a short period of time before then leading to the reappearance of depressive symptoms, due to the depletion of serotonin. The research presented indicates MDMA may not be a good permanent solution to depression treatment. Nevertheless, it may be a good form of short term treatment that could be paired along with other forms of therapy to provide patients with a quick acting, short-term solution to depression while they are getting help.
The studies presented in this paper did not all have good scientific designs, and severe limitations are present in many cases. The study of hallucinogens in general is somewhat limited due to the fact that blinding the experimental condition is not possible due to the patient experiencing a high from them, which clearly shows that the drug is not a placebo. Furthermore, due the schedule 1 restrictions on these drugs, experimentation with them is often hindered. These restrictions also force researchers to have to spend much more in order to comply with schedule 1 guidelines.
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In both cases patients received psychotherapy before and after both sessions. The tests used to measure changes were, Clinician-Administered PTSD Scale (CAPS) and Impact of Events Scale-Revised (IES-R). Initially, no significant results were found.
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