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Science vs. Moral Panic: An Ecstasy Primer for Defence Counsel

By Lorne Sabsay

As more and more cases involving 3, 4-methylenedioxymethamphetamine (MDMA) wind their way through the court system, there is a very real danger that convicted users and traffickers of this drug (also known as ecstasy) will face inordinately steep sentences owing to ignorance and conjecture. In reviewing materials filed by the Department of Justice in support of higher ecstasy sentences, it is apparent that some judges are having the scientific wool pulled over their eyes.

The unfortunate result of sentencing on the basis of such materials is that an increasing number of judgments incorporate misinformation thus providing "judicial recognition" for unproven allegations and rank speculation. While such speculation may be useful in determining the relative merits or dangers of designer drugs it ought not to be the basis for ever-increasing deprivation of an offender's liberty.

While no one doubts that there is a potential for harm from the ingestion of any illicit substance, there is a big difference between a realistic appraisal of risk and moral panic. "Moral panic" is a term which academics have used for forty years to describe a public debate that revolves around exaggerated fears, rather than around rational discussion of a genuine new problem. Dr. Philip Jenkins, a professor of history and religious studies at Pennsylvania State University, testified about this problem at the inquest into the death of Allen Ho in May of 2000.

As reported in the National Post, Dr. Jenkins testified that moral panics have occurred over drugs in the United States regularly since the 1950s. "They usually concern issues that come out of thin air, he said, and those issues are presented in a way that is far out of proportion to evidence or reliable statistics. Where such panics involve drugs, particular drugs are portrayed as more destructive or addictive than they actually are, and reports tend to use loaded words such as epidemic. Stories about a single high-profile death can also be portrayed as a typical case … The existence of a moral panic doesn't mean that no genuine concerns exist, he explained, but the concept can help cut an issue down to size."

In order to try and reign in the current moral panic over ecstasy, it is important to understand something about what it is and how it works. This leads to a more realistic appraisal of its known risks as opposed to speculative panic and hyperbole.

This article is not an argument for the legalization of MDMA or any other drug. Nor does it purport to represent all current scientific and/or legal information about MDMA or ecstasy. Such articles would be thousands of pages long. Rather, this article is about learning some perspective so that our clients do not pay the price for panic masquerading as science.

How Ecstasy Works

While a full pharmacological lesson is beyond the scope of this article, some fundamental principles are important. I confess at the outset that as complex as some of the following sounds, it is actually extremely simplified.

Brain cells, or neurons, send messages to each other via chemicals known as neurotransmitters. One such neurotransmitter is serotonin. Brain cells that produce serotonin are called serotonin neurons. Serotonin plays an important role in the regulation of such brain functions as mood, heart-rate, pain and many other things. Ecstasy causes serotonin neurons to release large amounts of serotonin from a part of the neuron called the axon terminal. It is this massive release of serotonin that is responsible for the primary subjective effects of MDMA (euphoria, closeness to others, heightened sensation of touch, enjoyment of music, etc.).

The actual neurochemical process involves serotonin molecules being sent into a space between the axon of the serotonin neuron and the receptors of a receiving neuron. This space is known as a synapse and the receiving end of the second neuron is known as a dendrite. When serotonin binds to a receptor on a dendrite, a chemical signal is sent which results in certain mood and other changes. The serotonin is then released from its binding site and is transported back across the synapse and into the axon via reuptake transporters.

If you could chemically block the reuptake transporters, serotonin would remain in the synapse to bind again and again to serotonin receptors causing positive mood effects to continue. That is what anti-depressants such as Prozac do. These are known as SSRIs or specific serotonin reuptake inhibitors. As the name implies, these drugs inhibit the reuptake of serotonin thus leaving more of it in the synapse to bind to receptors and sent positive mood signals to the brain.

While drugs such as Prozac focus on the "reuptake" end, MDMA focuses on the serotonin release end of things. MDMA continues to cause the release of serotonin into the synapse. MDMA also causes the release of another neurotransmitter known as dopamine (more on dopamine in a moment). Some of the serotonin that gets transported back into the axon (the reuptake) is broken down by an enzyme known as monoamine oxidase (or MAO: more on this in a moment as well).

We do not have an inexhaustible supply of serotonin in our brains. The result is that within hours of taking MDMA the subject's serotonin supply begins to diminish. It takes days or even weeks to replenish the body's serotonin supply. This is why taking more ecstasy at this point does not work to keep the feelings going. Ecstasy itself does not create the positive feelings, the subject's own serotonin does that. This is also why ecstasy is not addictive in the sense that cocaine or heroin is. When a cocaine user "comes down" because he has metabolized his dose of cocaine, he needs to take more cocaine to regain the feeling and taking more does have the desired effect. Taking more ecstasy after the serotonin supply is exhausted does nothing to regain the desired effect.

If a person has taken enough ecstasy to deplete their serotonin supply completely, they may experience depression (which may remind the reader about why SSRIs like Prozac are prescribed for depression). As stated above, taking more ecstasy at this point won't work (although some of the "speed" or amphetamine effects may continue to provide more energy). The user would have to remain off the drug for as long as two weeks to allow the natural stores of serotonin to replenish.

Serotonin is replenished in brain cells when an amino acid called 5-HTP is converted into serotonin (also known as 5-HT) via an enzyme called decarboxylase. The amount of 5-HTP (5-Hydroxy-Tryptophan) in a person's body is determined by a person's diet. That is because it is synthesized from another amino acid called tryptophan, which is contained in many foods. 5-HTP is also sold in health food stores. Some researchers believe that serotonin depletion can be ameliorated or decreased by the ecstasy user's taking 5-HTP to rebuild the serotonin supply.

One theory about how MDMA might be neurotoxic may be gleaned from this simplified analysis. Scientists suggest that when MDMA depletes serotonin, the reuptake transporters in the axon are left vacant. Dopamine, which is also released by MDMA enters the axon by mistake and dopamine is toxic to serotonin cells. You will recall that MAO breaks down (oxidases) neurotransmitters re-entering the axon. When MAO oxidases dopamine, hydrogen peroxide is created which is also toxic to the cell.

What scientists have observed in animals injected with MDMA is the probable result of oxidative stress or neurotoxicity caused to the serotonin axon terminal by the process described above. This is the "brain damage" or "nerve damage" we hear about in animal studies conducted by certain MDMA researchers. Whether or not this occurs in humans is a matter of controversy. Even if a number of serotonin axon terminals are degenerated in this way in humans, it is also not certain that this has any appreciable behavioural or psychological effects on the subject. As with all "damage" caused to human beings, the human body has a remarkable ability to repair damage, even at the cellular level. This is probably why even the most damning scientific abstracts concerning MDMA rarely suggest that a single or limited use of MDMA causes any lasting effect.

It also seems possible to avoid this neurotoxicity through the use of Prozac. A number of studies have shown that SSRIs like Prozac prevent MDMA's neurotoxic effect. It is believed that by plugging up the reuptake transporters, dopamine is prevented from getting into the serotonin axon terminal. This prevents the neurotoxic effects of dopamine uptake and the concomitant oxidative stress caused by the breakdown of dopamine by MAO.

Ecstasy Related Deaths

One of the primary justifications for longer sentences in cases involving ecstasy are "ecstasy related deaths". The truth, however, is that like "alcohol related deaths" the ingestion of the intoxicant itself is rarely the real—or only—reason for the tragedy. While there are some very rare and unfortunate souls for whom a peculiar sensitivity makes safe ingestion of ecstasy extremely dangerous, these people are by far in the minority. The vast majority of "ecstasy related deaths" are usually deaths by someone who might have taken ecstasy who:

  1. actually died from heat stroke;
  2. died because they took ecstasy and also took a contraindicated medication;
  3. died because they thought they took ecstasy but actually ingested something else, or
  4. died because of an allergic type reaction to the drug

Considering the very high numbers of people who take ecstasy in the raving and clubbing communities, the often-heard prosecution mantra of "nine ecstasy related deaths last year" does not necessarily reflect a high risk drug. If police estimates that vast majorities of ravers, and a significant proportion of club-goers are taking the drug, then many thousands of people take it every year. Indeed, since thousands of people may attend a single rave, it might be more accurate to say that in any given week in Toronto alone there might be many tens of thousands who took the drug without incident.

The Toronto Star published an article on Tuesday, October 9, 2001, in which it was estimated that some 40,000 people attend the nightclubs on Richmond Street in Toronto every weekend night. This number would not include raves and after-hours clubs that are not on Richmond Street. If only a quarter of these were doing ecstasy (some estimates are even higher) and if a single rave is held on the same weekend, then there might be many weekends in Toronto alone where tens of thousands of people are consuming MDMA without any resulting deaths or hospitalizations. Nine deaths in a year (most, if not all of which are not caused by ecstasy ingestion alone) represents a tiny percentage. It is for this reason that at least one study in England found that the risk of death is much higher amongst tobacco smokers, alcohol drinkers, miners, construction workers and canoeists than it is for ecstasy users.

Where death does occur at a rave or crowded night club, heatstroke is most often the cause of death. Taking MDMA, or any stimulant drug causes an increase in body temperature. Add to this, high temperatures found in crowded venues such as raves and body temperature increases more. When energetic dancing is added to the mix, body temperature rises even more. Such conditions carry a high risk of heat stroke, which can be deadly. Indeed, a considerable number of rave related deaths in England occurred from heat stroke in victims who had not consumed any MDMA at all.

Moreover, when the human body overheats it loses fluid. Some ravers have been known to lose up to 6 pints of fluid in 6 hours. If these fluids are not replaced heatstroke and death may ensue. This is why so many of the recommendations of the jury at the Allen Ho inquest are concerned with ventilation and an adequate supply of water. Dehydration is intensified when the dancer drinks alcohol. Curiously, there have also been some rare cases of people dying from consuming too much water.

These problems are exasperated by the criminal proscription of MDMA. If someone collapses at a rave, ambulance attendants need to know as much as possible about what the victim did or ingested. All too often, friends are afraid to tell medical practitioners the truth for fear of prosecution. This can lead to further complications caused by the administration of contraindicated medications.

Just as severe, even fatal, reactions can result when a patient mixes two or more perfectly legal medications, the same can be said in ecstasy cases.

As indicated above, the enzyme monoamine oxidase plays an important role in neurological serotonin regulation. There is a class of anti-depressants known as MAOIs, or Monoamine Oxidase Inhibitors. They include drugs such as Nardil, Parnate and Marplan. These drugs are very dangerous to combine with MDMA and can result in a potentially fatal condition known as "serotonin syndrome"

Other drugs are dangerous to take with MDMA because they are metabolized through the same liver enzyme as MDMA, known as the CYP2D6. Because both drugs are competing for the same enzyme both will be metabolized more slowly, which is like taking a higher dose of both drugs. One such drug is Ritonivar, which is a protease inhibitor used in the treatment of HIV. At least one person has died from taking MDMA while on Ritonivar.

Other drugs metabolized by CYP2D6 include codeine and other opiate derivatives, as well as DXM (the active ingredient in many over-the-counter cough medications). Obviously, simple education with regard to such facts will save a lot more lives than longer sentences.

As more information has circulated in the rave and club-going communities, harm reduction strategies are employed with increasing frequency, resulting in fewer tragedies. Unfortunately, one thing that is very difficult to manage is the appearance of imposter drugs posing as ecstasy. This is another major cause of what some might call an "ecstasy related death".

In September of 2000 six young people died in Central Florida after consuming fake "ecstasy" tablets that contained paramethoxyamphetamine, or PMA, instead of real ecstasy (MDMA). There have been at least nine confirmed PMA deaths in the United States and in Ontario at least one police service (York Region) warned of finding PMA pills in their jurisdiction. Contrary to what has been suggested in both media and in courtrooms, PMA is not a "new version of ecstasy". PMA is not a recreational drug at all. It is being manufactured and sold as "ecstasy" because the chemicals to make it are easier to obtain than the chemicals to make real ecstasy. Its precursor chemicals are easier to obtain and are not as strictly controlled (at least in the United States) as those used to produce MDMA. It is a scam perpetrated on an unsuspecting population.

At low doses, PMA produces an increase in energy, minor visual hallucinations and mild euphoria. At slightly higher doses it suddenly increases heart rate, blood pressure and body temperature to dangerously high levels that can lead to convulsions, coma and death.

It has been argued that the existence of PMA demonstrates the need for deterrent sentences on possessors and traffickers in MDMA. Somehow, it is thought that by jailing people, who sell real ecstasy, there will be fewer deaths caused by trafficking in PMA. If anything the reverse is the case. Traffickers can place adulterants in ecstasy or sell something else entirely because real MDMA is illegal. The reason people don't regularly die from arsenic sold as aspirin is because aspirin is a legal highly regulated product. The same holds true for cigarettes. It is the "black market" nature of ecstasy that allows for such horror. It is an unregulated industry. So-called deterrent jail sentences in relation to the sale and possession of MDMA obviously do little to deter this pernicious phenomenon.

As noted above, another possible cause of "ecstasy related death" is a particular sensitivity some have to the drug. MDMA is not alone in this area. People with certain sensitivities to peanuts or to drugs like penicillin obviously face grave dangers if they consume the wrong product. Unfortunately, scientists do not presently know why some people will die from ingestion of MDMA (such as Allan Ho) while thousands of others do not.

Certain suspected pre-existing health conditions that might produce complications due to MDMA consumption include heart conditions (as MDMA produces a significant increase in heart rate and blood pressure); liver problems; seizures; and conditions such as Central Core Disease (which make the sufferer more susceptible to heatstroke or malignant hyperthermia).

Legal Lessons learned from the Science

There are many lessons that can be learned from the science. Some of these are alluded to above. But the main intent of this article is to educate counsel so they will be aware of some of the reasons why Crown materials may not be based on scientific data, or on conclusions resulting from the scientific method.

One of the cases which is often cited by the Crown is R. v. Rip (unreported, O.C.J., November 15, 2000) because it contained lengthy testimony by a Deputy Chief Coroner on the topic of ecstasy. Unfortunately, the Deputy Chief Coroner, by her own admission, is not a pharmacologist, or a pathologist, or an epidemiologist, yet she makes all manners of unsubstantiated claims in her testimony.

These include the claims (without any apparent evidence) that raves are attended by children as young as ten and eleven. Or that MDMA causes hallucinations and blurred vision (a number of scientists say the opposite is true because of how MDMA works; that these symptoms would be caused by another drug in the mix). Or that MDMA causes panic attacks and paranoia (which most researchers suggest occur only in overdose). Or that muscle begins to break down.

Many times reports are submitted quoting research performed on laboratory animals or on poorly controlled human tests purporting to prove that ecstasy causes brain damage in humans resulting in memory loss, addiction, or permanent depression. Some of the information provided above demonstrates that some of these claims are unlikely to be true and others certainly have not been proven to be true.

A drug is considered addictive if withdrawal symptoms occur when a regular user stops taking it. MDMA is not addictive at all in this sense. Not only is there not any kind of physical craving for the drug once it wears off, taking more of it will not produce more of the desired effect. Once the serotonin supply is depleted, taking more MDMA will not bring about the desired effect for at least a week or two (although the purely amphetamine side effects will continue).

The truth is that researchers are divided on the effects of MDMA. Moreover, there are difficulties using the available research to make definitive findings with respect to the effects of the drug. In her scientific abstract published in the journal Neuropsychobiology Helen Fox, from the Department of Psychology at the University of East London made the following observation:

The research regarding the neurotoxicity of MDMA remains incongruous due to immense methodological problems. Within the field of animal research, immunostaining data is often unsupported by quantitative data corresponding to 5-HT [serotonin] levels, decreases in 5-HT have (as yet) not been found to relate to corresponding increase in gliosis [the classic marker for neurotoxic brain injury], and doses given to animals often far exceed those of recreational levels. In human studies, control and MDMA user groups are never fully matched, and generally differ in potentially important aspects. While attempts to obtain (pre-ecstasy) baseline data raise difficult ethical and practical issues, these criticisms are not meant to disparage research in general, or to deny the fact that MDMA may well be neurotoxic at certain dosages, but rather to highlight the fact that any conclusions should be interpreted with these factors in mind… [C]aution should also be taken when relating neurotoxicity findings to functional impairments in humans. The functional significance of a single dose (neurotoxic … or not?), is also unclear.

Conclusions

In a sense, there really are no conclusions. That is the main point of this article. The science is unclear and at times prosecutors are making pseudo-scientific claims and defence counsel should do their own homework before accepting such claims as fact.

There IS research that suggests that MDMA, like any drug, should be treated with caution and may very well be harmful. Scientific and even moral debate is a healthy thing in the classroom, the health boards, the legislatures and the laboratory. A debate, however, is not a satisfactory excuse for increasing the period during which a person will be deprived of their liberty.

The Supreme Court of Canada ruled in R. v. Gardiner (1982) 68 C.C.C. (2d) 477, that the Crown must prove all aggravating factors beyond a reasonable doubt in a sentencing hearing. Given the "moral panic" currently enveloping the subjects of ecstasy and raves, it is essential that we don't let pseudo-science and conjecture take the place of such proof.

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