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I I I I I I TKe L.iKCET,.t4ARCH 2~1, 1960 WHAT kESEA.RCHERS M.ARE OP WRAT CIGARETTE SMOKERS SAY: FILTERING SMOKEfiS' HOT A,IR LYN.N T. KoZLOWSKt Psychvlog}• Dcpartment. Clinicallr,scicucc,.4ddic:ioa Re:earte Foundation, Torar.to C. PE7ER HERASAN T'sychoiogy Dt,oartMenc, Univcrsiry of Toronto RICHARD C. FRECKER Clinical PrtarmaCOlogy Program, Ciinicallnstitutt, rJd:rctfon Researcit Foundotron, Toronto, Canada GtvE>; the widespread harassment of eigarettc srnokers and the evidence that smoking actually is dan- gerous to health,1-3 it is not surprising that smokers sometimes lie about their smoking. Lying about smoking habits has become so commonplace in smoking-treat- ment clinics that many researchers have used assays for the biological markers of smoking to confirm their pa- ttents' claims to have stopped smoking,'-9 Probably only a few of these "decepdve smo;cers" are indulging in outright self-deception; most no doubt do rea]ise that they arc still smoking. Self-deception and other forms of psychological dis- tortion are alleged to ir3fluence other claims that smokers make about their smoking and related health concerns. Russtli writes: "Of those who profess to be happy about their smoking some are ignorant but the majority use face-saving psychological defence mechan- isms such as 'rationalization' and 'denial' to avoid un- comfortable inconsistency between attitude and behav- iour."i0 Similarly the U.S. Public Health Service report, Adu1t Use of Tobacco--1975, proposes that smokers who claim not to have "persona; knowledge of someone u:hose health has bcen affected by cigarettes" may "sup- press this knowledge in order not to feel too much con- cern or gvilt about their srnoking".' ~ Since researchers have readily challenged the validity of the verbal reports of smokers on the above issues, it is surprising how rarely they have second-guessed the claims of smokers that they want to or have tried to stop smoking.10-l' How better for a smoker to avoid the pes tcrings of a pbysician or other interviewer than to say (whether believing it or not) that he wants to and has even tricd to give up cigarettcs? And, if the questioner asks if the attempts to stop have been serious, who would want to confess to a half-hearted etfor? Yet, answers to questions on "wanting to stop" and "trying to stop" have regularly been used uncritically--as if smokers now must be telling the truth. Mcl:ennell," in discussing the results of an earlier survey of the smoking habits of British males,'s notes that "49 per cent of the adolescents and 45 per cent of the adults would like to quit, and 61 per cent and 52 per cent, respectively, have tried"; and he develops a model for the targeting of anti-smoking appeals, based on a 699 classifieation oF smokers into those who u•ant to give up smoking (dissonant smokers', and those who have no desire to stop (consonant smokers;. This classific2tion is derivcd from the self-repoms of the smoker<; no caution_ arc ofcred lbout their vaiidity. Russell notes that whereas three out of four smokers say they either wish to or n3vc tried to stop smoking, only about 151,~ suc- ceed in stopping permanently before the age of sixty; and from this he concludes that "most peopic smoke not because they w-ish to but b=ause they cannot easily stop"." This last sentence sccros to be presented morc as a statement of fact than as an account of self-reports. Similarly the report, Adult Use of Tuoacco--1975," which concludes that "9 out of 10 smokers have either tricd to quit smoking or would probably do so if there worc an casy way to do it", does not mention psychoiogi- cal pressure:• un smukCrs that might render their state- mcnts suspect, despite a commendable alertness to the influcnce of such pressures on statements of health con- ccrn in genva;. A dramatic example of the imperfect relation between word and deed can be found in a smoking-related survey i:; Philadelphia of 30 796 parents of schoolchildren.'s 70% of the parents responded; 11 709 were current smokers and 4 775 of these said they would be interested in stopping smoking if a smokers' elinic were arranged. 257 ;5tirj attended a preliminary meeting about the clinic, and only 130 (3`,"<.) made use of theclinic. Evcn in groups which are highly motivated to give up smoking, trustworthy reports of successful abstinence can be difftcult to obtain. Almost certainly not every one in these groups has actualh• tried to give up cigarettes, but the quit-rates in such groups should refscct, nonethe- less, the association between trying to stop and success i-, doing so, Patients wit'rh heart-diseasc arc probably highly motivated both to give up smoking and to avoid being chastised by their physicians if they are unable (or unwilling) to do so. In one study of heart patients self- reports indicated that 63 K no longer smoked (even lS months after the heart-attack), but urine assays dis- closed that 16 to 20'/oofthese were still smoking.'E In one survcv 65 % of physicians reported that they had giver, up smoking, compared with 4) ',-( of a control group." In a related study, however, physicians dis- played bchavioural as well as psychological defence mechanisms. Of the S6•7% who respondtd, only 22•6`K confessed to being smokers; but when a special efCort was made to discover the smoking habits of the 13•3 i who had not returned their questionnaires, an estimated 45•5`.i: of them were found to be smokers.'~ (10 phys- icians who had originally rcturncd their questionnaires tried to remain anonymous, and E of these were cigar- ettc smokers.) ule have described some inconsistencies in the appli- cation of critical acumen to the verbal reports o.` smokers and have encouraged caution in what is made of what smokers say about their wish to give up smoking and their attempts to do so. Misleading self-reports (whether self-serving or even sclf-castigating) are not limited to smokers; people who are overwcight or who are guilty of any of the presumably oehaviourally cor- rectable sins of our age" are likely dissemblers. What- ever may cause these lapscs in discernment on the part of investigators, we know of no reliable cure and have ourselves lapsed on exactly the same issues. Both what 9 0 I I I ® 0 ® ® 0 N 0 / ~ ,- W U W F- ^ 0 s 0. ~ n cr~ ~;- :D ~ ~. m

700 smoker5 say lbout their smoking and what researchers "."•3Ke of these staterae,n,ts should be read scepticaliv• \"•'e thank `t. ?ox a-nd K. \Gagner for ,heir :d ice, RKueats for reprints sisould be addrased to L.T. K. REFEREtiCES l. Brody h, °rodv 9. The IeSai nghu oi non smoker.. `!cw Yock: Avon BwR,, 1977. ?. Rov,l CGlty`c o( Phy'siCiOns of London. $mokinS or hea;sh, Izncon: 'itmn-• 19" i. C•J- fkPartmem or 1?echh• L•'au<aucn acW ~/cl(1ce Smokint ]ne health: : repor, oi thc Suryeon Gcn:ral. DF{EW publiention an. ,1'HS) 79-iU066. :.S. C vvcr..m nt Pr,nunj Cjficc, 1979. 1. Eroek-e.• 8S. Chcrns<,1t .•tLdation ot selr-reponed ,.•nok:ng rntes• cenev r'ar•ia:tl; 9, 63S-i5. :. Dclarsc SC, .i aruav in smokina wuhor.w.l.'Iec'tbronto 5mokinR -th. dravnl study cenare-descripuon o( i:tiv,ties. Cj,J P~t! Nlrn 1973; 64: 35-5,4. 6. P:zro1 R. rxarnacea G. :nnary meuttnc :CncM ration as # iunetion ni time uncc tast cqarcltc: in9plieatt<n! rOr JeteCtine Fakjnj ~n smollr.g c:iniG. Be~•n "i'rtr•1ti74;10:5::-=1. '. Rsn:':I MAFI, Ccle I'V. Cannr:nstsur, oi it9:nncnIt iram cnoKing. Br.N;E J l Y7i: ii:' S S-S6. a. Si!le,t Ru', `.t'd5on M8, \tilealm Rp., L,all F:,^. Ik:7nan amoag:mokm 3• N: iJ 197ti:ti: ! I5S-S6, .. Turner :A ltc.\l. Czr•hrm.UCn Ot uxnnMCO itom smokin;. r7r.V,edJ 1975t c 75:. Qccasional Survey CESTROGEN' tMNDOW H'YPOTHESTS OF THE .ETIOLOG'Y OF BREAST CANCER STASLEY G. KOREV.%tA` Depart»ier.r of Medici,ta, UCLRaax Ferna,rdo Vailey Pro;r_m. Vr,zrenr.~dminiscrscron Nospirar, Sepulveda, CJ/;lorr,:2 THERE is considcrable evidence that endocrine fea- tures contribute to the xtiology and pathogenesis ot breast canocr, but despite extensive invt:Stigation t:e hormonal circumstanees that lead to the development of breast caneer have not been elucidated. Evidcncc rclating hormones to the a:tiology of breast cancer includes animal models, epidemiological studies, and hormone measurements in populations at risk. In the dimethvlbenzanthracene-induced mammary car- cinoma the tumour may be induced by a single exposure to the agent in the prescnce of an appropr.ate hormonal cnvironmcnt. The hormones which act as promoters (i.e. increase Susceptibility of mammary ep,thelium to dimzthylbenzanthracene) include unopposed astrogen and a su'ftlciency of anterior pituitary hormoncs, par- ticalarly prolactin. Once the tumours arc expressed they usually require a tavourable cndocrine environment for growth and will often be stimulated 'oy conditions, such as pregnancy, which were not conduave to tumour in- duction. This inducer-promoter model has not been thoroughly explored for human breast cancer. In man, the main indications for an endocrine contri- bution co the a;uology of breast cancer come from cpi- dcmiolo¢ical studics.t The protective effect of an early hrst pregnancy and early castration, and the negative erTcct of early mtnarche, tate monopause, and nulli- parity were demonstrated. The enormous diffcrence in prevalence betu•een populations was emphasised. CCe oostulated :hat normal tzstrogen stimulation and lutesi inadequacy, characteriscd by diminished progesteronc THE LAKCET, AiARCH 29, 1990 10. Ruas:ll uAH. C"gar,ae !n:oang: naiurel h,-tory o! 1^r,r1kx di,prder. 3r1.yelPsy:rrm197:•11:1-tti. -~ 11. Nst~Cnvi t.:c.rmRnou,c !or SmJkin; and Heach. Adult j;~ icbacco--19?>. r.clanca, :xorra: Cancer ior Drscax C:antro6 °_•:reau oC ileulth EJu; ,on. 13e:nes•itt• \taryland: ,%~o,lonal (nstitutc ol Hca;tn, :va,,on.; C:Gnccr 1n,nlwc. 19y5. i2..~'.c.l':nnal AC. Bri:wn r<!:at.n into!moiiny 4hs-tour. In: 2crruta (;F, _•ans RR• ::s. Smoktn; h<tl,h tnd yehtv,or. Chittgo, Ilhnos: AIdme 7uoGshinR Comptny, :969: 140-64, 13. Nauonal Cancer In;titu::. Cigarate irnokin¢ among tccn-agcn and youn; vamen, nlic:C ?ubl,anon no. 'VIH} ''^.l'-0i. CS. Departmcnt oi t';ult1@duesuon snC Weli~rc. t977. ' .=. Au:ic4 LtAH. "he omk,nS .`,aoil anC its ellssiCut,or.. Pre:r«iorter 197:: .'1Z: '91-3tk1. t S• .~Ilen Vi'A, Faekler ICA, An ezplor~un• survey and smohnz:qntrol OreCraa, Conefuaed srr•ong parents oi 1'h,lailct:hie school ehitdren. In: Zagonn $V• n.. Studie•- and ueua in ,moeir•q ecna:ior. 1'uaon. An:ona: t•'mversity C: Ariiona Prus, ;967: 0i-tii. 16. u':Icos: RG, Kugies J, RCland 1. ver,ncation oi :mokin~ :vs:orv is pa~cnts ~1t:r ,nfsxt:on uan¢ unnary :s<otine tnd :ot,nine mctsurcmenas. g. hrel J I979: ii: 1fY.'6-'-i. ,7. °urecn: e4%4, Cxrey D8, Tierr.:y JT• CiYirr•te sr.,dttiny :+y Rhode Islend pnys'a.ns, t9ti3-1973: ampan,on v,th ltwrycrs and oro<r sdult m.la. .;mJP.blHtrA IS73tfS:6i-d:. :d. au.ess AN Jr.'ierney fT. A,as due to nonrqqonsc in a matl surv<y of ithode Is(antl paystc,am' smokm; Itao,u-19oi1. X Enri J,Nec 197U; 252, 40ti. :9. Herman CP, Ko:iawski I.T. Irdulqan.c, eseess and res«atat: ryenyeaivt, o- caruummunr/ oahavior in everyda. lifc. J Dra3 lr.uu 1979; 9: i35-9r„ secre:ion, could explain the main cpidemiological features of the attiology of breast caneer•= A high inci- dence of luteal inadequacy would be expected in,ubj:cts at risK of breast cancer and premenopausal women with thc disease. rlowcver, young women at high _tenctic risk of breast cancer had normal lulxal phases; and despite contrary data' a group oi premenopausal women with brcast cancer also had normal luteal ohases.''° Studics of possible links between hormones and the risk of breast cancer have been revieu'ed thoroughly.''s .1,lany of the flndtngs did not persist in cross{ulture or stngle-culture studi,:s and population bias was a persistent problem. $mail endocrine changes can hardly account for the dvefold differential risk of breast cancer among popula- tions. The incscapable conclusion is that endocrine status merely intlucnces susceptibility to environmental carcinoVn5. CIESTROGfN-wIYDOw' HYPOTHESIS 1. Human breast cancer is induced by cnvironmental carcinogcns in a susceptible mammary gland. 2. Unopposed oatrogen stimulation ;s the most ravourable state for tumour induction. 3. There is a long latent period bctwecn tumour in- duction and clinical expression. 4. The duration of the exposure to cestrogeas deter- mines risk. 5. Susceptibility to induction ("indueibility' ) declines with the establishment of normal-luteal-phase progester- .~ onc s<tretion and becomes c•ery low during pregrlanry. O There would be two main induction periods in women, the first prior to ovulatory menstrual cycles and the second during tne perimenopausal period. The in- itial ¢strogen window opens at aec 8-1.0 yr at Tanner stagc breast-2.10 Both o:stronc and ctstradiol levels hat'e risen by this time and at-_ continuing to rise,' 1 and mam- :nary growth is taking place. The mean time from breast-2 to menses is 2•32 yr but may be as long as 6 FP ~ i t id