MDMA NEUROTOXICITY..RECENT STUDIES &. NEW PERSPECTIVESBy EARTH EROWID - 11 DECEMBER 1998

'r he drug Ecstasy causes brain damage in people who take

Tit frequently, scientists have proved .... The capacity forthought, memory and emotion is impaired," or so The

Times of London reported the results of a recent studyinto the long term effects of MDMAon the structure and chemistry ofthe brain.la] The study. published in The Lancet medical journal atthe end of October, was conducted by Dr. U.D. McCann, GeorgeRicaurte, and colleagues, and is another in a series of studiesindicating that MDMAmay cause semi-permanent changes in thefunctioning of serotonin neurons. It involved some of the mostsensitive brain imaging techniques to date, using PET(PositronEmissions Tomography) scans to studvthebratns-cj-rs-controlindividuals and 14men and women who had ingested MDMAbetween70 and 400 times, from I to 16 times per month, at dosages estimatedby the researchers to be between 150 and 1250 mg.

Aspart of the study, each subject was injected with a radioactivemarker that selectively binds to S-HT transporters (serotonin re-uptake sites) on the axons of S-HTneurons. Transporters are proteinstructures embedded in the membranes of nerve endings that arepart of the inter-neuron communication system. The test showedthat the marked chemical bound to an average of 22% fewer S-HTtransporter sites in measured areas of the brains of MDMAusers thannon-users. Theresearchers believe that this reduced binding indicatesthat the transporters have been destroyed and the serotonin neuronsare damaged. Some dispute this interpretation and point out thatreduced binding could also indicate neuroregulation similar to that

12

produced by Prozac or other SSRls.[b] While this study shows themost direct evidence so far that heavy MDMAusers may have lowerserotonin levels than non-users, it does not demonstrate that MDMAcauses reductions in serotonin transporters.

Unfortunately, the study, its press release, and the media reportssurrounding it do not stop at reporting the measured data. Theyassert that not only is there a measurable difference in the amount ofbinding to S-HT transporter sites, but they conclude that thisdifference is caused by the use of MDMA,that increased use causesfurther decreases in serotonin levels, that reduced S-HT bindingconstitutes "brain damage", and that this "damage" may havenegative consequences including "depression, anxiety, memorydisturbance, and other neuropsychiatric disorders".[c]

Critics of the study point out several possible weaknesses in theassumption that MDMAis the cause of the differences in S-HTtransporter binding. First, with only 14 MDMA-using participants inthe study, the sample is extremely small. Second, McCann-Ricaurteassume that other drugs played no role in whatever changes occurred,yet they did not attempt to control for exposure to drugs other thanMDMA,MDA,and MDE.[d]TheMDMA-using subjects may have takenlarge amounts of many other drugs and it is very likely that theyunwittingly took MDMAmixed with an unknown assortment ofadulterants.le] Third, the researchers mistakenly assume they canknow that the differences between study subjects did not predatetheir ingestion of MDMA.From this type of study, there is no way ofknowing that the MDMA-using subjects did not have naturally lower

TRP 4

-

Whether one refers to

changes in neurochernistry

as "brain damage" or not

appears to be mostly a

S-HTtransporter binding levels before their MDMAuse. McCann etal. argue that "since none of the MDMAusers had a neuropsychiatricdisorder in which s-HT has been implicated, [the possibility that thelower levels preexisted] is unlikely." But this logic is flawed. Neitherthe MDMAnor control subjects were found to have any disorders,and their binding levels were different, so lack of disorder cannot beused as an indicator of S-HT levels. Also, since even the heaviestusers had levels within the range of levels found in non-users, thedifferences between the two groups could be accounted for byimproperly matched subjectgroups. Some researchers pointout that the criteria for selectingsubjects from the pool ofavailable MDMA users is notincluded in the published study.[fJ It is quite possible that theseheavy MDMAusers belong to agroup with naturally lower S-HTbinding levels and that lowerlevels may even correspond to anincreased likelihood to use

neuropsychiatric disorders in which brain S-HT has beenimplicated. "[e] All too frequently, negative speculations byresearchers are misread as scientific "proof" when it comes torecreationally used psychoactives.[j]

Proponents of MDMAtherapy and critics of the designation "braindamage" point out that there is little to no evidence that heavy MDMAusers experience any functional problems. Optimists suggest that itis even possible that MDMA-precipitated neurochemical changes arepositive. Administration of SSRIantidepressants such as Prozac cause

similar reductions in S-HTtransporterslb] and one studyfound that MDMAusers were"less impulsive, more harm-avoidant, and had decreasedhostility, "lkl a finding which isat odds with what researchersexpect to see in people withabnormally low serotoninlevels. As mentioned earlier,the subjects in the study weretested for" axis I psychiatricdisorders". Only subjects whowere both heavy MDMAusers

and free of psychiatric problems were chosen for the study. If theresearchers are right that the lower levels of 5-HT transporters canlead to "neuropsychiatric disorders", why do none of the heavy MDMAusers studied have any of these problems?

One explanation given by reporters is the "Time Bomb" theory,which suggests that as users age, their past use will come back tohaunt them: "Users of the drug would be likely to have a higherincidence of depression in later life."[I] But there is no evidence tosupport this theory. While other neurotransmitter systems have beenshown to decline with age (dopamine, for example), serotonin hasnot been shown to decline over time. While caution is prudent, thisspeculation is refuted by current knowledge about serotonin.

. An additional criticism is that the study's findings do not pointout that the level of MDMAuse exhibited by the subjects is extremelyhigh, well above the levels used in therapeutic contexts or by mostrecreational users. The reported average dose is 386 milligrams withmaximum doses estimated at 1250mg, where the normal dose ofMDMAis between 100 and 200 mgs. Animal studies suggest thateven a single very high dose of MDMAcan cause long term changes(and damage) to the S-HT system, while Ricaurte himself showedthat in non-human primates lower doses (2.5 mg per kg)administered every two weeks for four months had no measurableeffect. Byfailing to point this out where the study mentions potentiallong term health consequences, the non-expert reader is left toincorrectly assume that even carefully controlled therapeutic use ufMDMAcauses "brain damage".

Considering that there are few long time users of MDMAwho report

MDMA. question of perspective.McCann-Ricaurte also assert

that they demonstrate a "strong" correlation between increasedMDMAuse and increasingly lower levels of the s-HT transporter."Scans tended to [show lower levels) in those who had taken the drugmore often. "Ig) Thiscorrelation has been questioned by several criticsof the paper because it is based on controversial readings of the data.Specifically, the calculation of the "strong correlation" includes boththe controls and the MDMAusers which improperly weights theanalysis by exaggerating the influence of the control group. Theremoval of the controls and a single MDMAuser from the equationcauses the apparent correlation to dlsappear.lh.i] Both groups ofsubjects showed substantial variation between individual S-HTtransporter binding levels and all but one of the MDMAusers fellwithin the same overall range as the non-users. The most that canbe said is that the MDMAusers tended to cluster near the lower endof the overall range. Even Ricaurte reportedly does not consider thecorrelation between increased use and further decreased levels to bea primary finding of the paper because the small size of the studymay make extrapolations from the data inaccurate or misleading.

The published study and its press release refer to the differencesin 5-HT transporter levels as "brain damage". Whether one callsthese differences in neurochemistry "brain damage" or not appearsto be mostly a question of perspective. Opponents of MDMA'stherapeutic and recreational use argue that any reduction in availableserotonin (or in this case transporters) should be considered "neuralinjury" and that "potential functional consequences of MDMA-induced brain S-HT neurotoxic lesions are not yet clear, but mayinclude depression, anxiety, memory disturbance, and other

!.1-·

13

~

;IIiI

permanent negative health consequences, that preliminary researchhas failed to detect serious clinical problems!c. m.nl, and that MDMA

has been used therapeutically and recreationally for over 15 years,the practical negative health consequences of moderate MDMA useare likely to be subtle and may even be non-existent. For most users,the dangers associated with ingesting "street E" of unknown qualityare far more concrete.

But neither should the research be ignored. Prospective users ofMDMA should weigh carefully the collected data before swallowingtheir next dose. Individuals who choose to take the risk of long termchanges to their neurophysiology make themselves research subjectsin an uncontrolled investigation of the long term effects of theirchosen psychoactives. Will we live to regret our decisions? Will those

users who choose to use more heavily be prone to problems later inlife?

In choosing how to live, we assume known and unknown risksevery day. We weigh benefits against risks and choose a path basedon our own unique situation. Learning a sense of appropriate risk ispart of maturing into ourselves as fragile living creatures. Yet inmost of the world, political and social organizations have tried totake the freedom to decide whether to ingest a psychoactive away

from the individual, under the auspices of protecting citizens frompsychological and physical harm. Any risk is considered too great arisk: "Any non-medical use is abuse. "[01 This extreme position failsto minimize physical and mental harms because it offeh no practicalknowledge of how to make intelligent choices in real situations.Instead, our communities and governments should encourage peopleto become aware of the risks and help them relate to psychoactivesmore responsibly.

For millions of MDMA users there is little trust in the dire "scientific"

claims of brain decay. Unless verified individual dysfunctions surface,or at least reliable anecdotal reports of problems, users will remainjaded and unconvinced, hardened by warning after hyperbolicwarning of immanent "Murder! Insanity! oeathl'Tp] Despite claimsby popular news media and medical "experts" that we now have

"direct evidence" that MDMA is harmful to manlql, the question ofhow much risk is still far from answered.

Comments and rebuttals welcomed: earthiVerowid.org.More information on this study can be found at:http://www. erowid. orglmdmalricaurtel

COMMENTARY: MDMA NEUROTOXICITYBY LAMONT GRANQUIST

MDMACAUSES A SHORT-TERM RElfASE of S-HT from the neuron. MDMAblocks both the reuptake pump from the synapse into the neuron,

and the pump into the synaptic vesicles. It also causes the release of s-HTfrom the synaptic vesicles and a release of S-HT out of the neuron.Because of this action, it tends to flood the synapse with serotonin inthe short-term. In the long-term, the S-HT which is outside of thevesicles can be broken down by metabolic enzymes like MAO, andfollowing treatment with MDMA there will be a downswing in theavailability of S-HT. That's why tryptophan-containlT19.io.o~sJikemilk and bananas are a good idea after MDMA in order to help toreplenish S-HT.

The McCann-Ricaurte study actually wasn't looking at S-HT levels,but the binding of a radioactive tracer chemical to the S-HT reuptakesites in the brain. If, as the authors would like to theorize, there is anarrowly defined range of number of s- HT reuptake sites per neuron,then a reduction in S-HTreuptake sites should correspond to a reductionin S-HT neurons. Unfortunately, they entirely ignored the researchshowing that proven non-neurotoxic drugs like SSRls, imipramine andtianeptine (a serotonin-specific reuptake stimulanting drug) all causedecreases in S-HT reuptake densities and in gene expression of s-HTreuptake pump mRNA - suggesting that there are regulatorymechanisms operating at the gene level. Therefore, one pretty muchexpects that MDMAwould similar/ycause regulation of S-HT sites in theabsence of any neurotoxicity, and pretty much eliminates this wholeapproach to assessing MDMAneurotoxicity as being flawed.

Furthermore, the study found that the highest dosing MDMA usersstill had S-HT transporter levels that were the same as the low end of thecontrol non-MDMA using subjects. The fact that there were control

subjects with S-HT transporter levels which were as low as the MDMAsubjects suggests that there might be selection effects at work -particularly as these were subjects that had taken some 200· doses ofMDMAat an average does of over 300m9 at a time. It's possible that lowtransporter levels lead to this pattern of MDMA use and not the otherway around.

Other studies have shown that MDMA users have lower levels of s-HIAA, which is a S-HT metabolite (and low levels of s-HIAA and S-HThave been correlated in monkeys). However, this ignores evidence inmonkeys that MDMAcan cause transient and substantial decreases in s-HTand S-HIAA in the absence of any decreases in binding to the S-HTtransporter (and hence, in the absence of any neurotoxicity).Furthermore, the effect on MDMAusers' sleep and psychology has beenshown to be generally the opposite of what one would expect as a resultof lesioning the S-HT system. Of course the fact that a statisticallysignificant effect was found to occur in the sleep of MDMA users (andone which probably increased sleep quality overall, nothing which couldbe interpreted as damage) was claimed to be evidence of possible"damage" by the study's authors-never mind that the results were 180

degrees away from what was predicted.I think that MDMA definitely knocks your serotonin system around

and therefore it's not a good idea to do it a lot. Personally, I feel after-effects for about a week. This is not, however, evidence of neurotoxicity.Similar after-effects have been described for cocaine, which isneurochemically very similar to MDMA, only it preferentially does todopamine neurons what MDMApreferentially does to serotonin neurons(although there's overlap and effects of MDMAon dopamine, and effectsof cocaine on serotonin). Cocaine is also not a neurotoxin.

MDMA NOTES AND REFERENCES

a. 'The End of Ecstasy," The Times (of London), 31 October 1998. Internet

edition: http://www.the-times.co.Uk/

b. Granquist, Lamont. - http://www.eroWid.orgientheogens/x/ricaurte/

ricaurte_comment5.shtml, referring to: Hoffman BJ, Hansson SR, Mezey

E, Palkovits M. "Localization and dynamic regulation of biogenic amine

transporters in the mammalian central nervous system." Front

Neuroendocrinol 1998; 19: 187-231 and Lesch KP, Aulakh CS, Wolozin

BL, Tolliver T], Hill JL, Murphey, DL. "Regional brain expression of

serotonin transporter mRNA and its regulation by reuptake inhibiting

antidepressants." Braln Res Mol Braln Res 1993; 17:31-35.

c. McCann, U.D., et al. "Positron emission tomographic evidence of

toxic effect of MDMA (Ecstasy') on braln serotonin neurons in human

beings." The Lancet, Volume 352, Number 9138, 31 October 1998.

Internet edition: www.thelancet.com

d. H (anonymous contributor). "A Prospective Guinea Pig." The Vaults

of Erowid, 1998. http://www.erowid.org/mdma/ricaurte/

ricaurte_ comment3 .shtml.

e. Numerous studies of "street E" have round that they are unreliable

sources of MDMA and often contain other substances. See http://

www.ecstasy.orgitestingTOC.

f. EroWid, Earth. "A Summary of Karl Jansen's Comments." The Vaults of

E rowi d. http://www . erowid. or g/md mal ri cau t t e ]ricaurte_comment6.shtml

g. Press Release for McCann study: http://www.eroWid.orglmdma/

ricaurte/ricaurte_press_release.shtml

h. Erowid, Earth. "Questioning the Correlation between Increased

MDMA Use and Decreased Binding - an Analysis of Figure 4 of the

McCann-Rlcaurte MDMA Study Results." The Vaults of Erowid, 1998.

http://www.erowid.orglmdma/ricaurte/ricaurte_statistics.shtml

i. Doblin, Rick. "More Comments on the Rlcaurte Data." 11 November

1998, emall to the MAPS list.

j. Murray, Ian (Medical Correspondent)." Proof that Ecstasy damages

brain," The Times (of London), 3D October 1998. Internet ed. avallable

at: http://www.erowid.orglmdma/ricaurte/ricaurte_artide3.shtml

k. Saunders, Nicholas. £cstasy- Dance, Trance &. Transformation. Quick

American Archives, 1996. He is missed: \

I. Henry, Dr. John. Professor at St. Mary's Hospital in London, as quoted

in SenJose Mercury, 29 October 1998. His 'TIme Bomb" theory makes

it into "Study Says Ecstasy Causes Brain Damage" in The HoustonChronide, October 3D 1998.

m. Granquist, Lamont. "Yet Another MDMA FAQ." 1998. http://

www.hyperreal.org/drugs/mdma/FAQ-YAMF.html. The Neurotoxicity

section is the best, most up to date overview of the issue that Iknow of.

n. McCann, UD, Ridenour, A, Shaham, Y, Rlcaurte, GA. "Serotonin

neurotoxicity after (+ / -) 3,4-methylenedioxy-methamphetamine

(MDMA, Ecstasy): a controlled study in humans,"

Neuropsychopharmaco/ogy, Vol 10(2), P 129-138, 1994.

o. 1997 Annual Report of the International Narcotics Control Board, the

policy writing wing of the United Nation's Drug Control Program and

other INCB publications.

p. Text from an anti-marijuana leaflet from the 1940's, produced under

Harry Anslinger, Commissioner of the newly formed U.S, Narcotics

Bureau.

q .. "Study Says Ecstasy Causes Braln Damage," The Houston Chronide,3D'October, 1998. Internet edition: http://www.chron.com/. [-I

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