ArticlePDF Available

Alcohol, ecstasy, Aldous Huxley's 'soma'

Authors:
http://jop.sagepub.com
Journal of Psychopharmacology
DOI: 10.1177/0269881106075426
2007; 21; 8 J Psychopharmacol
A. C. Parrott
Alcohol, ecstasy, Aldous Huxley’s ‘soma’
http://jop.sagepub.com
The online version of this article can be found at:
Published by:
http://www.sagepublications.com
On behalf of:
British Association for Psychopharmacology
can be found at:Journal of Psychopharmacology Additional services and information for
http://jop.sagepub.com/cgi/alerts Email Alerts:
http://jop.sagepub.com/subscriptions Subscriptions:
http://www.sagepub.com/journalsReprints.navReprints:
http://www.sagepub.com/journalsPermissions.navPermissions:
http://jop.sagepub.com#BIBL
SAGE Journals Online and HighWire Press platforms):
(this article cites 2 articles hosted on the Citations
© 2007 British Association for Psychopharmacology. All rights reserved. Not for commercial use or unauthorized distribution.
at University of Bristol Information Services on February 8, 2007 http://jop.sagepub.comDownloaded from
Alcohol, ecstasy, Aldous Huxley’s
‘soma’
Comment
J
Psychopharm
Journal of Psychopharmacology
21(1) (2007) 8–9
©
2007 British Association
for Psychopharmacology
ISSN 0269-8811
SAGE Publications Ltd,
London, Thousand Oaks,
CA and New Delhi
10.1177/0269881106075426
David and I have broadly similar views on alcohol, since we are
both aware of its damaging social and psychobiological effects
(Nutt, 2006). In a recent summary chapter I wrote: ‘In global terms,
alcohol is one of the most damaging drugs known to mankind’
(Chapter 15 in Parrott et al., 2004). Hence I agree with David that
all governments need to take the problems of alcohol drinking, and
indeed tobacco and cannabis smoking, far more seriously. However,
we seem to have very different views on two other topics. First, the
relative costs and dangers of using ecstasy/MDMA versus alcohol.
Second, on whether it might be possible to develop a psychophar-
macologically safe recreational drug.
On the first question, I suspect that most people might agree
with David that alcohol is more dangerous than ecstasy/MDMA.
Alcohol is widely used, many individuals have personal experi-
ences of its deleterious effects, and its adverse consequences are
manifest every day in our towns and cities. In contrast, few adults
have any direct knowledge or experience about ecstasy/MDMA,
its use is quite rare even amongst young people, so that fortunately
there are comparatively few people with ecstasy-related problems.
This may help to explain why on the scale of socially constructed
dangers, MDMA would be far lower than alcohol. However in
many ways MDMA is more damaging than alcohol. The acute
physical effects of MDMA are extremely powerful and wide-
ranging (see initial reply), so that neural overstimulation is an
intrinsic part of the drug experience (Parrott, 2002). Hence the
positive mood effects of MDMA can only be achieved at psy-
chophysiological costs. The chronic problems of MDMA are also
subtle and insidious. The first psychobiological deficits to be
recognized were in memory and depression; these have been fol-
lowed by more recently demonstrated deficits in cognitive plan-
ning, impulsivity, emotional intelligence, social awareness and
other functions (Parrott, 2006). MDMA is also a powerful meta-
bolic stressor, and it has basic (cellular) effects which may eventu-
ally prove even more troublesome; hence the increase in markers
for oxidative stress, reduced immunocompetence, and the cardiac,
hepatic and other changes noted in my initial reply. At the risk of
repeating myself, let me note that MDMA is a far more powerful
psychoactive drug than alcohol, its acute effects are more pro-
found, the post-drug recovery problems are more pervasive and
prolonged, and chronically it can have a range of adverse effects
after a far shorter period of usage (Parrott, 2006). Hence on a
direct drug-for-drug comparison, MDMA is potentially far more
damaging than alcohol.
Turning to the broader question, I do not believe that it is pos-
sible to design a neurochemically safe drug of pleasure. There are
many psychoactive drugs with acute mood enhancing properties;
not only alcohol and MDMA, but also cannabis, amphetamine,
cocaine and the opiates. The main problem is that they all have
many adverse effects: acute, subacute and chronic. Furthermore
these deleterious aspects are an intrinsic part of the overall equa-
tion; they reflect a number of basic psychopharmacological
processes, with neuroadaptation being a core element. Hence the
paradox for all drugs of pleasure is that their positive effects are
countermanded by numerous negative sequelae (again see Chapter
15 in Parrott et al. 2004 for a fuller discussion). Since this pattern
is true for opiates, cocaine, nicotine, amphetamine, cannabis and
alcohol, I see no reason why any new drug would not display a
similar adverse cost–benefit ratio. Even ‘soma’, which Aldous
Huxley (1932) invented for his novel Brave New World, was not
problem free. In Huxley’s idealistic, yet ultimately dystopic view
of the future, soma was used as a universal drug of pleasure:
‘Delicious soma, half a gram for a half-holiday, a gram for a
week-end, two grams for a trip to the gorgeous East, three for a
dark eternity on the moon.’ Its acute pharmacodynamic profile
was surprisingly similar to MDMA: ‘By this time the soma had
begun to work. Eyes shone, cheeks were flushed, the inner light of
universal benevolence broke out on every face’ … The warm,
richly coloured, infinitely friendly world of soma-holiday. How
kind, how good-looking, how delightfully amusing every one was’
(Huxley, 1932). However soma also caused psychobiological
problems, including rebound negative moods, tolerance and
dependence: ‘If the morning after was disagreeable, it was … only
by comparison with the joys of the holiday. The remedy was to
make the holiday continuous. Greedily she clamoured for ever
larger, ever more frequent doses’ (Huxley, 1932). To summarize,
it is probably impossible to design a safe and effective drug of
pleasure without untoward side effects. Alcohol clearly fits the
picture, the modern ‘designer’ drug MDMA illustrates the same
pattern, while even Aldous Huxley’s mythical soma is consistent
with this general principle.
Professor A.C. Parrott,
Department of Psychology,
Swansea University,
Swansea SA2 8PP,
UK
Corresponding author: Professor A.C. Parrott, Department of Psychology, Swansea University, Swansea SA2 8PP, UK. Email: a.c.parrott@swansea.ac.uk
© 2007 British Association for Psychopharmacology. All rights reserved. Not for commercial use or unauthorized distribution.
at University of Bristol Information Services on February 8, 2007 http://jop.sagepub.comDownloaded from
Alcohol, ecstasy, and the inherent problems of ‘soma’ 9
References
Huxley A (1932) Brave New World. Chatto and Windus, London (also
Penguin)
Nutt D (2006) A tale of two Es. Jour Psychopharmacol 20: 318–320
Parrott A C (2002) Recreational Ecstasy/MDMA, the serotonin syndrome,
and serotonergic neurotoxicity. Pharmacol Biochem Behav 71:
837–844
Parrott A C (2006) MDMA in humans: factors which affect the neuropsy-
chobiological profiles of recreational Ecstasy users, the integrative role
of bio-energetic stress. J Psychopharmacol 20: 147–163
Parrott A C, Morinan A, Moss M, Scholey AB (2004) Understanding
Drugs and Behaviour. Wiley, Chichester
© 2007 British Association for Psychopharmacology. All rights reserved. Not for commercial use or unauthorized distribution.
at University of Bristol Information Services on February 8, 2007 http://jop.sagepub.comDownloaded from
Article
Full-text available
AIMS AND RATIONALE: The purpose of this study was to review whether methylenedioxymethamphetamine (MDMA) has the appropriate pharmacodynamic profile to be a therapeutic agent. Empirical descriptions of MDMA's subjective effects in humans will be reviewed to evaluate the proposal that MDMA has psychotherapeutic properties. The focus will be published evidence on its functional effects in therapeutic, medical, and other situations. MDMA is a powerful central nervous system (CNS) stimulant which affects several neurotransmitter systems and intensifies a range of psychobiological functions. Its acute mood effects can be very positive and life enhancing, and the affirmative cognitions engendered during MDMA therapy may well endure afterwards. However, MDMA also has a number of potential anti-therapeutic characteristics. Acutely, it can also intensify negative cognitions, and these may similarly endure over time. Psychotherapists have found that setting, intention, and expectancy are crucial for a positive outcome, but these factors cannot be guaranteed. Post-MDMA, there is a period of neurotransmitter recovery when low moods predominate, and these may exacerbate psychiatric distress. The explanations proposed for MDMA-assisted therapy are all psychodynamic, and a neurochemical model needs to be outlined. It has been suggested that enduring therapeutic gains can follow a single session, but again, this lacks a clear psychopharmacological rationale. Finally, diathesis-stress models suggest that psychiatric individuals are more prone to acute and chronic abreactions to CNS stimulants such as MDMA. There are a number of issues which need to be addressed before it can be argued that MDMA might be clinically useful for psychotherapy.
Article
Full-text available
Many recreational ecstasy/MDMA users display neuropsychobiological deficits, whereas others remain problem free. This review will investigate some of the drug and non-drug factors which influence the occurrence of these deficits. Acute and chronic MDMA usage are both important. Intensive use within a session is often associated with more problems. In term of lifetime usage, novice users generally remain unimpaired, whereas most heavy users report memory or other psychobiological problems which they attribute to ecstasy. These complaints are confirmed by objective deficits in working memory, attention, frontal-executive, and episodic memory tasks. Psychobiological deficits include disturbed sleep, sexual dysfunction, reduced immuno-competence, and increased oxidative stress. Further MDMA-related factors which may contribute to these changes, include acute and chronic tolerance, and drug dependence. Around 90ñ95% of ecstasy/MDMA users also take cannabis, and this can independently contribute to the adverse neuropsychobiological pro.les; although in some situations the acute co-use of these two drugs may be interactive rather than additive, since cannabis has relaxant and hypothermic properties. Alcohol, nicotine, amphetamine, and other drugs, can also affect the psychobiological pro.les of ecstasy polydrug users in complex ways. Pure MDMA users are rare but they have been shown to display significant neurocognitive deficits. Psychiatric aspects are debated in the context of the diathesis-stress model. Here the stressor of ecstasy polydrug drug use, interacts with various predisposition factors (genetic, neurochemical, personality), to determine the psychiatric outcome. Recreational MDMA is typically taken in hot and crowded dances/raves. Prolonged dancing, feeling hot, and raised body temperature, can also be associated with more psychobiological problems. This is consistent with the animal literature, where high ambient temperature and other metabolic stimulants boost the acute effects of MDMA, and cause greater serotonergic neurotoxicity. In conclusion, the neuropsychobiological effects of MDMA are modulated by a wide range of drug and non-drug factors. These multiple influences are integrated within a bioenergetic stress model, where factors which heighten acute metabolic distress lead to more neuropsychobiological problems.
Article
Full-text available
Article
Many recreational ecstasy/MDMA users display neuropsychobiological deficits, whereas others remain problem free. This review will investigate some of the drug and non-drug factors which influence the occurrence of these deficits, Acute and chronic MDMA usage are both important. Intensive use within a session is often associated with more problems. In term of lifetime usage, novice users generally remain unimpaired, whereas most heavy users report memory or other psychobiological problems which they attribute to ecstasy. These complaints are confirmed by objective deficits in working memory, attention, frontal-executive, and episodic memory tasks. Psychobiological deficits include disturbed sleep, sexual dysfunction, reduced immuno-competence, and increased oxidative stress. Further MDMA-retated factors which may contribute to these changes, include acute and chronic tolerance, and drug dependence. Around 90-95% of ecstasy/MDMA users also take cannabis, and this can independently contribute to the adverse neuropsychobiological profiles; although in some situations the acute co-use of these two drugs may be interactive rather than additive, since cannabis has relaxant and hypothermic properties. Alcohol, nicotine, amphetamine, and other drugs, can also affect the psychobiological profiles of ecstasy polydrug users in complex ways. Pure MDMA users are rare but they have been shown to display significant neurocognitive deficits. Psychiatric aspects are debated in the context of the diathesisstress model. Here the stressor of ecstasy polydrug drug use, interacts with various predisposition factors (genetic, neurochemical, personality), to determine the psychiatric outcome. Recreational MDMA is typically taken in hot and crowded dances/raves. Prolonged dancing, feeling hot, and raised body temperature, can also be associated with more psychobiological problems. This is consistent with the animal literature, where high ambient temperature and other metabolic stimulants boost the acute effects of MDMA, and cause greater serotonergic neurotoxicity. In conclusion, the neuropsychobiological effects of MDMA are modulated by a wide range of drug and non-drug factors. These multiple influences are integrated within a bioenergetic stress model, where factors which heighten acute metabolic distress lead to more neuropsychobiological problems.
Article
Brave New World
Article
The ring-substituted amphetamine derivative 3,4-methylenedioxymethamphetamine (MDMA) or "Ecstasy" is widely used a recreational drug. It stimulates the release and inhibits the reuptake of serotonin (5-HT) and other neurotransmitters such as dopamine to a lesser extent. The acute boost in monoamine activity can generate feelings of elation, emotional closeness, and sensory pleasure. In the hot and crowded conditions of raves/dances, mild versions of the serotonin syndrome often develop, when hyperthermia, mental confusion, and hyperkinesia predominate. Rest in a cooler environment generally reverses these problems, although they can develop into medical emergencies, which occasionally prove fatal. This acute serotonergic overactivity is exacerbated by the high ambient temperatures, overcrowding (aggregate toxicity), and use of other stimulant drugs. The on-drug experience is generally followed by negative moods, with 80--90% of weekend Ecstasy users reporting 'midweek blues', due probably to monoaminergic depletion. Single doses of MDMA can cause serotonergic nerve damage in laboratory animals, with repeated doses causing extensive loss of distal axon terminals. Huether's explanatory model for this 5-HT neurotoxicity will be briefly described. There is an increasing body of evidence for equivalent neuropsychobiological damage in humans. Abstinent regular Ecstasy users often show: reduced cerebrospinal 5-HIAA, reduced density of 5-HT transporters, blunted response to a fenfluramine challenge, memory problems, higher cognitive deficits, various psychiatric disorders, altered appetite, and loss of sexual interest. Functional deficits may remain long after drug use has ceased and are consistent with serotonergic axonal loss in higher brain regions.
Understanding Drugs and Behaviour
  • A C Parrott
  • A Morinan
  • M Moss
  • A B Scholey
Parrott A C, Morinan A, Moss M, Scholey AB (2004) Understanding Drugs and Behaviour. Wiley, Chichester