© 2002 Society for the Study of Addiction to Alcohol and Other Drugs Addiction, 97, 915–917

IMPLICATIONS FOR THE NOTION THATMODERATE ALCOHOL USE PROTECTSFROM ISCHAEMIC HEART DISEASE:COMMENT ON GREENFIELD ET AL .

Sir—Can depression and/or social isolation account forthe repeated finding that the risk for all-cause mortalityis reduced in low–moderate consumers of alcohol—usually interpreted as due to protection from alcohol?The question is not taken out of the air. Several studieshave shown not only that depression and social isolationare associated with an increased risk of mortality, butalso that these conditions have different distributionsbetween various categories of alcohol consumers andabstainers (Leifman et al. 1995), and thus that con-founding might exist.

Greenfield, Rehm & Rogers (2002) found no supportfor their question, consistent with the findings by Murray,Rehm & Shatten (1999)

On the face of it the implications seem consider-able, as this report can be perceived as further support forthe contention that certain types of alcohol use protectfrom death; but is all the information really harvested?Analyses with finer categories of the depression andsocial isolation variables than simply dichotomized categories might have given somewhat other results (as of course might other measures of social network,depression and psychosocial working conditions).

External validity is an issue. The interaction betweenalcohol use and social isolation and depression may bedifferent among non-participants. The decision to participate or not can be influenced not only by any of these three ‘factors’ but also by differences in interac-tion. This limits the external validity of the findings.

The markedly increased risk for current (men) and formerly heavy (women, currently abstainers) consumersand depression is interesting and consistent with findingsfrom clinical samples, but the wide confidence intervalsindicate that this is based on few cases. The use of a multi-plicative interaction model with an interaction term canbe questioned. Rothman & Greenland (1998) have, forexample in their standard textbook on epidemiology,launched severe criticism of the usual way of studyinginteraction with ‘an interaction term’, and presented analternative additive model that may be more relevant.

The relevance of the findings to knowledge of the contribution made by various kinds of abstention andvarious kinds of alcohol use to the risk of myocardialinfarction is evidently more limited. The end-point in thestudy is all-cause mortality, not mortality from ischaemicheart disease (IHD) or from myocardial infarction (MI),about which which the authors do not provide infor-mation. Secondly, most identified cases of MI, the mostcommon of the diagnoses in the IHD category needinghospitalization, are non-fatal. There are few studies ofalcohol and the risk of non-fatal MI. There may be dif-ferent risk factors or different importance of risk factorsand interaction for the outcomes of all-cause mortality,mortality from IHD, total MI, fatal and non-fatal MI.Binge drinking is, for example, an established risk factorfor fatal infarction, but not for non-fatal infarction, themuch more common event. Extrapolation of results fromstudies on all-cause mortality or even IHD mortality toevents of MI should be undertaken with caution, and theauthors make no such extrapolation.

It could be mentioned here that analyses exist of theassociation between alcohol use, abstention of differentduration, social isolation, psychosocial working condi-tions, interaction and fatal and non-fatal MI from a largeSwedish case–control study (Romelsjö et al. 2002). Thesestudiesfoundnosupportforaconfoundingimpact of socialisolation or poor psychosocial working conditions, neitheron fatal nor on non-fatal MI, and only limited interaction.

The authors should be acknowledged for their choiceof a theoretically based important research question, and also because they studied interaction. Interactionbetween causes is studied too little, in an era when ‘multiple causation’ is almost a mantra.

ANDERS ROMELSJÖ

Centre for Social Alcohol and Drug ResearchSoRAD

Stockholm UniversityStockholm 10691

SwedenE-mail: anders.romelsjo@sorad.su.se

References

Greenfield, T. K., Rehm, J. & Rogers, J. D. (2002) Effects of depres-sion and social integration on the relationship between

Letters to the Editor

916 Letters to the Editor

© 2002 Society for the Study of Addiction to Alcohol and Other Drugs Addiction, 97, 915–917

alcohol consumption and all-cause mortality. Addiction, 97,29–38.

Leifman, H., Kühlhorn, E., Allebeck, P., Andreasson, S. &Romelsjö, A. (1995) Antecedents and covariates to a soberlifestyle and its consequences. Social Science and Medicine, 41,113–121.

Murray, R. P., Rehm, J. & Shatten, J. (1999) Does social integration confound the relation between alcohol con-sumption and mortality in the multiple risk factor inter-vention trial (MRFIT)? Journal of Studies on Alcohol, 60,740–745.

Romelsjö, A., Branting, M., Hallqvist, J., Reuterwall, C.,Alfredsson, L. & Hammar, N. (2002) Different AssociationsBetween Abstention and Drinking Patterns and MyocardialInfarction in Men and Women—the SHEEP Study. Paper pre-sented at the 26th Annual Epidemiology Symposium of theKettil Bruun Society for Social and Epidemiological Researchon Alcohol, Oslo, 5–9 June 2000.

Rothman, K. J. & Greenland, S. (1998) Modern Epidemiology.Philadelphia, PA: Lippincott-Raven.

CANNABIS, CARROTS AND COMMONEXPERIENCES: A REPLY TO COMMENTSON SMITH

Sir—Firstly, I would like to thank my colleagues for theircomments on my review of cannabis withdrawal symp-toms in human users published in the previous issue ofAddiction ( Smith 2002). Ashton (2002) has provided alucid explanation of the neurological processes that lie behind withdrawal, or discontinuation syndromes,which has been lacking in the cannabis literature.Ashton is correct to emphasize the individual variationthat is seen in response to discontinuing substances asdetermined by individual and genetic factors. I believethis to be a crucial element of this debate in that it may influence the direction of research into treatmentapproaches for individuals experiencing problems withcannabis.

Wayne Hall’s (2002) response wisely refocuses thedebate over withdrawal symptoms onto the issue of theobvious distress that can result from cannabis use anddiscontinuation. However, a central question in thisdebate could be said to be the cause of the distress. Martinretains his belief that cannabis is a drug that directlycauses a physical effect, as backed up by animal studiesand precipitated withdrawal paradigms. Findings in thisdirection emphasize the neurological aspects of the drugeffect, which may lead to more research funding intopharmacological solutions. This can be seen in recentresearch into cannabinoid receptor antagonists (Huestiset al. 2001) and also Bupropion, a drug used in nicotinecessation (Haney et al. 2001).

Martin (2002) rightly points out that the symptomsdescribed by the studies into cannabis withdrawal form areliable pattern, ‘despite the vagaries of the experimental

protocols’. He reads this as evidence that followingcannabis cessation there is an adverse reaction in certainindividuals, which is not in doubt. What is to be queriedis whether it is cannabis itself that is causing these symp-toms. A similar pattern of symptoms is also availablefrom the literature on nicotine cessation, relationshipbreak-ups and bereavement (Gilbert et al. 1998). There iseven a report by researchers in Prague who detail thecases of three individuals abstaining from excessive useof carrots (Cerny & Cerny 1992). These individualsreported symptoms very similar to those seen in thecannabis literature. The paper concludes with a discus-sion of the likely substances within carrots that may becausing these symptoms.

Commonalties observed in adverse reactions in indi-viduals to the withdrawal of substances, people and vegetables suggests that the effect might not be directlycaused by the actual index substance or experience.Certain individuals may be susceptible to becomingdependent to certain experiences, suffering a pronouncedeffect when that experience is removed. Providing people with another substance and expecting this to settle the matter seems a blunt approach at best. Lookingat the reasons why individuals become dependent onthese experiences might improve the outcome of treat-ment. Examining beliefs around the substances or experi-ences may help individuals reduce their need fordependency. The development of psychotherapeutic pro-grammes (Stephens et al. 2000) is as important in theissue of cannabis dependency and abstinence as pharmacological research. A concern is that a preponder-ance of articles providing support for the ‘physical’hypothesis will overshadow the need for continuingresearch into the ‘psychological’ aspects involved in abuseand dependence.

Combining pharmacological and psychological re-search into cannabis dependence and withdrawal wouldlikely advance our understanding of the difficulties indi-viduals experience with cannabis and with other drugs ofabuse. This knowledge could be used to inform individu-als deciding whether to take the drug, to enlighten policymakers involved in legislation issues and to improve theefficacy of the treatments available to clinicians treatingthose experiencing difficulties.

NEIL SMITH

Addictions DirectorateSouth London andMaudsley NHS TrustMarina House63–65 Denmark HillLondon SE5 8RSUKE-mail: spjunts@iop.kcl.ac.uk

Letters to the Editor 917

© 2002 Society for the Study of Addiction to Alcohol and Other Drugs Addiction, 97, 915–917

References

Ashton, H. (2002) Defining the indefinable: comments onSmith. Addiction, 97, 756.

Cerny, L. & Cerny, K. (1992) Can carrots be addictive? An extraordinary form of drug dependence. British Journal ofAddiction, 87, 1195–1197.

Gilbert, D. G., Gilbert, B. O. & Schultz, V. L. (1998) Withdrawalsymptoms: individual differences and similarities acrossaddictive behaviours. Personality and Individual Differences, 24, 351–356.

Hall, W. (2002) Getting the cannabis withdrawal question inproper perspective: comments on Smith. Addiction, 97, 754.

Haney, M., Ward, A. S., Comer, S. D., Hart, C. L., Foltin, R. W. &Fischman, M. W. (2001) Bupropion SR worsens mood during

marijuana withdrawal in humans. Psychopharmacology, 155,171–179.

Huestis, M. A., Gorelick, D. A., Heishman, S. J., Preston, K. L.,Nelson, R. A., Moolchan, E. T. & Frank, R. A. (2001) Blockadeof effects of smoked marijuana by the CB1-selective can-nabinoid receptor antagonist SR141716. Archives of GeneralPsychiatry, 58, 322–328.

Martin, B. R. (2002) Cannabis produces dependence: acomment on Smith. Addiction, 97, 754–755.

Smith, N. T. (2002) A review of the published literature intocannabis withdrawal symptoms in human users. Addiction,97, 621–632.

Stephens, R. S., Roffman, R. A. & Curtin, L. (2000) A compari-son of extended versus brief treatments for marijuana use.Journal of Consulting and Clinical Psychology, 68, 898–908.