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The relation of smoking to psychological and physiological risk factors for coronary heart disease
0191~8869/91
Person. indicid. Difl Vol. Ii!, No. 5, pp. 487-495. 1991
$3.00 + 0.00
Copyright0 1991PergamonPressplc
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THE RELATION OF SMOKING TO PSYCHOLOGICAL AND PHYSIOLOGICAL RISK FACTORS FOR CORONARY HEART DISEASE SHULAMITH KREITLER,’ KINERET WEISSLER,’ HANS KREITLER’ and DANIEL BRUNNER* ‘Department of Psychology, Tel Aviv University and *Institute for Physiological Hygiene, Sackler School of Medicine, Tel Aviv University, Ramat Aviv, Tel Aviv 69978, Israel (Received
12 April 1990)
Summary-Smoking has been held to be responsible for a great number of diseases. Yet criticism has been raised about the role of smoking as the cause or independent cause of the diseases. This study was motivated by Eysenck’s thesis that smoking and personality affect disease synergistically. The purpose was to examine the relation of smoking to psychological and physiological risk factors for coronary heart disease (CHD). The former were the Type A Behavior Pattern and its constitutents assessed by the Jenkins Activity Survey (JAS), the latter were systolic and diastolic blood pressure, cholesterol, HDL, triglycerides and the Quetelet body mass index. There were 520 randomly selected subjects (302 men, 218 women), 4-5 yr old. The results showed that smoking was related to higher scores on the JAS scales of Type A, Hard Driving, and Speed and Impatience, and lower scores on Job Involvement. Further, smokers had lower HDL, higher body mass index and lower systolic blood pressure. The results indicate that smoking is not an independent risk factor for CHD, and if it affects the risk for CHD then it is only in conjunction with the other psychological and physiological risk factors. Further, in view of deviant findings in different subsamples it is important to study large samples and check results in subsamples of age, gender and education.
INTRODUCTION
A voluminous literature has grown around the claim that cigarette smoking is largely responsible for many different diseases particularly coronary heart disease (CHD) and specific types of cancer, as documented by the Surgeon General of the United States (Richmond, 1981) and the Royal College of Physicians in England (Eysenck, 1980, 1985). On the basis of a large body of research the report of the Surgeon General (Richmond, 1981, p. 116) concludes that smoking is a powerful and independent cause of CHD (see also Gordon, Sorlie & Kannel, 1971; Kannel & Gordon, 1974). There are two separate aspects to this claim. One is that smoking is a cause of the different diseases, the other is that it exerts its noxious impact independently of the other major risk factors for CHD. The numbers of people who supposedly die from smoking are so staggering that anyone who has dared to contest the claim runs the risk of being branded as the “enemy of the people”. Yet, criticism of the claim has been mounting. Most attacks referred to the causal role of smoking in disease and were based on pointing out statistical weaknesses and methodological mistakes in the smoking research (Berkson, 1958; Burch, 1978; Eysenck, 1980, 1985; Fisher, 1959; Guilford, 1968; Katz, 1969; Sterling, 1973; Wakefield, 1988). Other investigators focused their criticism on that aspect of the claim that emphasizes the role of smoking as an independent cause for disease. Grossart-Maticek and others (Grossart-Maticek, 1980; Grossart-Maticek, Eysenck & Vetter, 1988; Grossart-Maticek, Kanazir, Vetter & Jankovic, 1983) showed that smoking can be considered as a risk factor for CHD, apoplexy or lung cancer only in interaction with psychosocial factors. More specifically, they identified rationality and anti-emotionality as the psychosocial factors relevant in regard to CHD, and these two factors as well as life events causing depression and hopelessness as relevant in regard to lung cancer. That is, the risk for the disease in smokers was minimal unless they also scored high on the relevant psychosocial factor. The present study was designed to deal mainly with the claim that smoking is an independent cause for disease. Thus, our first purpose was to provide further support for Eysenck’s (1988) thesis that “smoking and personality form a synergistic relationship” (p. 460) in regard to disease. We chose to concentrate on CHD which is one of the two major diseases linked to smoking. It has been claimed that heavy smokers have a 200% greater risk of dying from CHD than nonsmokers 487
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(U.S. Department of Health and Human Services, 1985; Zeiner-Henriksen & Lund, 1985). Accordingly, the Type A Behavior Pattern (TABP) and its constituents were the psychological factors on which we focused because they are a classical measure of the personality proneness to CHD. This pattern denotes ‘an action-emotion complex’ of features such as competitiveness, aggressiveness, striving for achievement, time pressure and responsibility that have been shown to characterize individuals with CHD or with risk factors for CHD (Brand, 1978; Blumenthal, Williams, Kong, Shanberg & Thompson, 1978; Frank, Heller, Komfeld, Sporn & Weiss, 1978; Rosenman, Brand, Jenkins, Friedman, Straus & Wurm, 1975; Steptoe, 1981; Williams, Haney, Lee, Kong, Blumenthal & Whalen, 1980). In view of the strong evidence linking it to CHD, TABP has been identified by a panel of scientists under the sponsorship of the National Heart, Lung and Blood Institute as an independent risk factor for CHD, roughly equivalent in magnitude to each of the classical risk factors (Cooper, Detre & Weiss, 198 1). Later criticism has been directed mainly against the unitary character of the TABP and against reliance on the content of the interview answers as opposed to the rated interviewee’s behavior (Dembrowski & MacDougall, 1985). However, Type A and especially some of its components have stood the test of multiple studies well and have emerged in meta-analysis as one of the strongest associations between personality and CHD (Booth-Kewley & Friedman, 1987). We expected that smoking would be related to the TABP mainly because of the evidence that extraversion is related both to smoking (Eysenck, 1965, pp. 100-105) and to Type A (Eysenck & Fulker, 1983). Further, since a previous study showed that different components of the Type A measure were related differentially to physiological risk factors for CHD in different subgroups (Kreitler, Weissler, Weissbord & Brunner, 1991), we intended to explore also the relation of smoking to different Type A components and in different subgroups of age, gender and education. A secondary purpose was to explore the relations of smoking to physiological risk factors for CHD. We expected smoking to be related to at least some of these risk factors, especially in specific age, gender and education subgroups. Confirmation of our expectations about the relations of smoking to Type A components and to physiological risk factors could undermine the view that smoking is a major cause of CHD and may help to focus attention on more relevant determinants. METHOD
Subjects
The total number of Ss was 520. They included 302 men and 218 women; 305 of the Ss were 30-45 yr old (called ‘younger’) and 215 Ss were 4665 yr old (called ‘older’); 387 Ss had ‘low’ educational level (the highest level they reached was high school graduation), whereas 133 Ss had ‘high’ educational level (they had been in some institution of higher learning beyond the high school, such as a college or university). Tests atd measures
Information about smoking was obtained in the framework of a questionnaire about demographic variables including age, gender and education. The Ss were asked to state whether they smoked at present and if not whether they had smoked in the past. Since the number of Ss who had smoked and stopped smoking was only 11 (2.1%) they were added to the nonsmokers. The Ss were administered the Jenkins Activity Survey (JAS) Form C (Jenkins, Zyzanski & Rosenman, 1979) scored separately for each of the four scales: Type A scale (Type A), Speed and Impatience scale (scale S), Job Involvement scale (J scale) and Hard Driving and Competitive scale (scale H). The scores of the four scales were used either as continuous variables or were dichotomized with the zero of the scale as the cutting point. The physiological measures obtained were: systolic and diastolic blood pressure: two measurements taken at rest, 5 min apart, and averaged because of their high intercorrelations; total serum cholesterol (mgjdl); high density lipids (HDL; mg/ml); and triglycerides. Further, the information about weight and height was used for constructing the Quetelet body mass index [weight/(height)2] (Garrow & Webster, 1985; Keys, Fidanza, Karvonen, Kimura & Taylor, 1972), which is an indirect measure of adiposity, minimally correlated with height and maximally with body fat (Grunberg, 1982).
Smoking and risk factors for heart disease
489
Procedure
The Ss were selected randomly out of the population lists of the Ministry of the Interior in Israel, in the framework of the first survey of the population in the Israel MONICA area. The total sample comprised 1197 persons, out of whom 520 (43.4%) answered the JAS and thus were included in the sample. RESULTS
Chi-square tests showed that in our sample gender and education were unrelated (chisquare = 0.728, df = 1, n.s.) but gender and age were related (chi-square = 7.318, df = 1, P < 0.01; there were fewer women in the higher age bracket); and so were age and education (chisquare = 68.632, df = 1, P < 0.001; there were fewer individuals with higher education in the older group). Therefore we considered it important to test the major relations of interest in each of the gender, education and age groups separately. The relations of smoking to gender, age and educational level were examined by multi-levelled chi-square analyses. None of these analyses yielded significant results. This indicates that in our sample smoking occurred with about the same frequency in each of the groups of gender, age and eduation. In the total sample, the percentage of smokers was 40%. The relation of smoking to the JAS scales was examined in two ways. One consisted in comparing the frequency of smokers in Ss high and low in each of the JAS scales in the sample as a whole and in the different subgroups of age, gender and education (that is, six subsamples, each defined by one value of the three variables age, gender and education) and their combinations (that is, the eight subsamples, each defined by two values of the three variables age, gender and education). The results are summarized in Table I. The other way consisted of analyzing the data by means of discriminant analyses with the JAS scales as predictors and smoking as the dependent variable. These analyses too were done in the sample as a whole and in the different subsamples of age, gender and education. The results are summarized in Table 2. Both Tables 1 and 2 indicate that the different JAS scales are related to smoking. The results concerning the specific scales are the same according to the two methods except for three cases, in regard to which the discriminant analysis indicated significant results which were not replicated in the comparison of percentages of smokers (i.e. scale J in the subsample of older men, scale A in the subsample of highly educated men, and scale J in the subsample of older highly educated Ss). According to both methods, the scales proved to be related significantly to smoking in 25 cases, which form 41.7% of the total of 60 examined cases (the whole samples and 14 subsamples, four scales in each). The observed percentage deviates significantly from the 5% expected by chance (CR = 4.751, P < O.OOl), and hence cannot be attributed to chance. Each of the four JAS scales was related to smoking. The relation was more frequent in regard to the S and H scales (each in eight cases) than in regard to the A and J scales (each in four cases), but the differences in frequency are not significant (chi-square = 2.67, df = 3, ns.). It is of interest to note that there are differences in the different subsamples in the direction of the relation between the JAS scales and smoking. Thus, in the sample as a whole as well as in the subsamples of the older Ss, the higher educated men and the lower educated older individuals there was a higher percentage of smokers in the high scorers on Type A than in the low scorers on Type A. Only in the subsample of the older men the relation was reversed with more smokers in the low type A Ss. Concerning the J scale, in the whole sample as well as in the subsamples of older Ss, men of lower education and older Ss of lower education there were more smokers in the Ss scoring low on the J scale. This relation was reversed in the two subsamples of men with higher education and older Ss with higher education. Concerning the S scale, the higher scorers included more smokers than the low scorers in the sample as a whole as well as in the subsamples of older Ss, older men, men of lower education, men of higher education, older Ss of low education and older Ss of higher education. The only subsample with a reversed relation was that of the older lowly educated. Finally, in the majority of cases (the whole sample, older men, lowly educated men, lowly educated younger Ss, and lowly educated older Ss) the high scorers on the H scale included more smokers than the low scorers. The relation was reversed only in the subsamples of the highly educated men and of older Ss.
490
SHuLMlmi KRmurt Table
I. Significant comparisons of frequencies the four JAS scales in the-sample JAS scale
Group Whole
sample
A
Whole sample
J
Whole
sample
s
Whole sample
H
Older Ss
A
Older Ss
J
Older Ss
S
Older Ss
H
Men, older
A
Men, older
S
Men, older
H
Men, low educ.
J
Men, low educ.
S
Men, low educ.
H
Men, high educ.
J
Men, high educ.
S
Men, high educ.
H
Younger.
low educ.
S
Younger,
low cduc.
H
Older, low educ.
A
Older, low educ.
J
Older, low educ.
S
Older, low educ.
H
Older, high educ.
S
Older,
H
high educ.
Scores Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High
er al.
of smokers in Ss rot-inn high and low in each of as a whole and differen~subsamples N
No. of smokers
390 130 447 73 360 I60 327 193 173 42 194 21 I89 26 162 53 99 25 89 35 93 31 I87 47 139 95 I52 82 52 16 50 I8 51 I7 I59 83 I64 78 I08 37 II7 28 104 41 90 55 50 20 48 22
133 75 193 I5 I25 83 146 62 43 I8 63 I 50 I4 38 26 44 4 26 22 30 I8 80 IO 32 58 35 55 16 I2 I5 13 26 2 71 20 37 54 39 22 57 4 31 30 I9 42 I2 I4 23 3
No. of nonsmokers 257 55 254 58 238 77 I81 131 130 24 I31 20 139 I2 124 27 55 21 63 I3 63 I3 107 37 107 37 II7 27 36 4 35 5 25 I5 88 63 127 24 69 15 60 24 73 I1 71 I3 38 6 25 I9
Chi-square 21.636*12.465*** 12.871*** 7.419.. 4.540. 5.861
l
7.142.’ 11.647*** 5.661
l
10.609** 5.484* 6.458’ 32.899-• 41.822*** 8.141” 8.076’. 6.557. 8.961** 47.104*** 5.243’ 9.624” 20.944*‘* 40.525*‘* ll.O52*** 6.196’
Only comparisons with significant results are presented. Low and high in each of the JAS scales denote score up to zero and above zero, respectively. lf < 0.05; l*p < 0.01; ***p < 0.001.
The results of the discriminant analyses presented in Table 2 show that the JAS scales enabled a significant prediction of smoking in the sample as a whole as well as in 7 of the 14 examined subsamples. The number of significant results (8 of 15, namely, 53.33%) exceeds significantly the 5% expected by chance (CR = 2.912, P < 0.01). The mean number of JAS scales involved in the predictions was 3.55. The standard discriminant function coefficients indicate that the contributions of the S and H scales to the prediction were relatively larger than those of the A and J scales (the coefficients of the S and H scales were largest, that is, each occurred in either of the first two places in six cases and each occurred in either of the last two places in six cases, whereas for the A and J scales the situation was reversed). It is of interest to note that the improvement in prediction over the chance level of 50% was larger in the subsamples defined more specifically. Thus, in the sample as a whole the improvement in prediction over the chance level was small (6.92%). In the set of six subsamples, each characterized by one value of the dichotomous variables age, gender and education, there was only one significant prediction (in the older group) and the improvement in prediction in that group
Smoking
491
and risk factors for heart disease
Table 2. Significant results of stepwise discriminant analyses with the four JAS scales as independent variables and smoking as the dependent variable Standardiaed discriminant function coefficients
Sample Whole sample Older group Men, older Men, low educ. Men, high educ. Young, low educ. Older, low educ. Older, high educ.
A H S S J H H S
0.675, 0.744. 0.847. 0.660, 0.913, 0.746, 0.779, 0.813,
J A H H s S S H
-0.605. 0.503, 0.496, 0.641, 0.300, -0.733 0.477, -0.545,
s J A J H
0.264, -0.469, -0.224, -0.460 -0.241,
A J
0.463, 0.209
% of correct classif. H s J
0.199 0.125 -0.159
A
0.128
J
The JAS scales are presented in the order of decreasing contribution had no contribution are not presented. CR = critical ratio. lf < 0.05: l*P < 0.01.
56.92 63.26 65.32 12.22 79.41 74.79 79.31 65.71
-0.431
Deviation from chance 6.92% 13.26% 15.32% 22.22% 29.41% 24.79% 29.31% 15.71%
(CR (CR (CR (CR (CR (CR (CR (CR
= = = = = = = =
2.25.) 2.77.) 2.44.) 4.93.O) 3.59**) 5.62**) 5.22**) 1.90’)
to the prediction. Scales which according to the analysis
was almost double that for the whole sample (13.26%). However, in the set of 12 groups, each characterized by two values of the dichotomous variables age, gender and education, the JAS scales were related significantly to smoking in five subsamples and the mean improvement in prediction in these subsamples over the 50% chance level was again almost double that noted earlier (24.21%). The largest improvement was obtained in the more highly educated men (29.41%) or the less educated older men (15.32%). The relation of smoking to the different physiological risk factors for CHD was examined by comparing the means of the latter variables for smokers and nonsmokers. Table 3 shows that as compared to nonsmokers, smokers have lower HDL levels in the whole sample as well as in each of the six subsamples of age, gender and education. They also have lower systolic BP in the whole sample, in women and the lowly educated. Further, the smokers have a higher body mass index in the whole sample, as well as in the subsamples of the younger Ss, those with high education and those with low education. Thus, of the six physiological risk factors, three (namely, 50%) proved to be related to smoking. The relations appeared consistently in the whole sample and in some of the subsamples. Two of the involved factors-HDL and the body mass index-indicated a greater CHD risk for smokers, one (systolic blood pressure) apparently not. Table 3. Mean comparisons of smokers and nonsmokers on the physiological risk factors in the different groups Group
Variable
Whole sample
Systolic BP
Whole sample
HDL
Whole sample
Body mass index
Men
HDL
Women
Systolic BP
Women
HDL
Younger
Systolic BP
Younger
HDL
Younger
Body mass index
Older
HDL
Lowly educated
Systolic BP
Lowly educated
HDL
Lowly educated
Body mass index
Highly educated
HDL
Highly educated
Body mass index
The table presents only the comparisons lP < 0.05; l*P < 0.01; l**p < 0.001.
Smokers
Nonsmokers Smokers Nonsmokers Smokers Nonsmokers Smokers Nonsmokers Smokers Nonsmokers Smokers Nonsmokers Smokers Nonsmokers Smokers Nonsmokers Smokers Nonsmokers Smokers Nonsmokers Smokers Nonsmokers Smokers Nonsmokers Smokers Nonsmokers Smokers Nonsmokers Smokers __ Nonsmokers
N
Mean
SD
r-test
208 312 208 312 208 312 121 I81 81 I31 87 I31 I44 I61 I44 I61 I44 I61 64
126.005 129.805
17.847 19.175 12.190 14.156 36.608 25.567 7.606 12.848 12.801 20.545 12.253 13.060 II.202 13.403 12.176 14.439 39.972 17.234 11.998 13.655 16.251 18.020 11.294 12.835 33.547 21.016 II.513 14.01 I 30.105 4.465
2.31'
I51 I52 235 I52 235 I52 235 56 77 56 77
with significant results.
45.566 49.808 33.439 26.920 39.338 45.210 122.858 129.462 51.981 56.554 119.525 122.532 46.582 51.217 34.174 24.595 43.555 48.240 124.602 128.074 45.500 49.714 31.791 25.817 44.447 49.165 37.237
26.017
3.64*** 2.23' 4.98." 2.92.' 2.63' 2.13. 3.04.. 2.66" 2.51' 1.96. 3.40** 1.96' 2.13. 2.77,.
492
SHULAMITH KREITLER et al.
DISCUSSION
The findings show that smoking is related to both psychological and physiological risk factors for CHD. The psychological risk factors include the different constituents of JAS, primarily H and S, and to a lesser degree A and J. On the average 3.5 of the 4 JAS scales were involved in each prediction of smoking on the basis of discriminant analysis. The means indicate that there are more smokers (a) among high scorers on Type A than among low scorers, (b) among high scorers on scale S than among low scorers, (c) among high scorers on scale H than among low scorers and (d) among low scorers on scale J than among high scorers. Whereas it is evident that scales A, S and H are related to smoking positively, it may seem that scale J is related inversely. Yet, a meta-analysis based on a great number of studies showed that scale J is related to CHD in a negative direction and that the relation is probably small and unreliable (Booth-Kewley & Friedman, 1987). Thus, the result we obtained for scale J shows that in this case too smoking is related to the risk factor, if indeed it is such, but in a positive direction. However this may be, the major thrust of the findings is that at least three of the scales were related to smoking positiviely. These include the elements of the TABP that have been linked most closely to risk for CHD. Major among them is the Type A itself which from the outset was considered as the core of the specific pyschological proneness for CHD (Friedman, Rosenman, Straus, Wurm & Kositchek, 1968). Yet no less important are the Hard Driving (H) and Speed-Impatience (S) scales that were shown to be related to smoking more highly than the A and J scales. It may not be an accident that the H and S scales also fulfill an especially important role in regard to CHD. They have been identified as the main independent components of the JAS (Glass, 1977). Further, in a sample of middle-aged males the H and S scales correlated quite strongly with the JAS global Type A/B scale score but the A and J scales correlated with it only modestly (Byrne, Rosenman, Schiller & Chesney, 1985). Again, by focusing on the H and S scales Lutz, Holmes and Cramer (1987) obtained more specific and significant results than through the global Type A/B score. They showed that only high scorers on the H scale exposed themselves to more challenging and stressful situations. Notably, the H scale is the only one of the JAS scales which was related to recurrence of CHD (Jenkins, Zyzanski, Rosenman & Cleveland, 1971) and in retrospective studies reliably differentiated between CHD and non-CHD patients (Kenigsberg, Zyzanski, Jenkins, Wardwell & Licciardello, 1974). The metaanalysis performed by Booth-Kewley and Friedman (1987, p. 349) confirmed the close relation of the H scale to CHD. Since our findings showed smoking to be related more to H and S than to the J scale, it is of interest to quote Booth-Kewley and Friedman’s (1987) conclusion: “It might be wise to modify the JAS by making it more clearly a measure of hard-driving competitiveness and less a measure of job involvement” (p. 355). In sum, the findings show that smoking is related positively to major psychological risk factors for CHD. Concerning the physiological risk factors for CHD, three of the six risk factors were consistently related to smoking: systolic blood pressure, HDL and the body mass index. The findings for HDL and body mass indicate an increased CHD risk for smokers. These findings correspond to earlier findings about positive associations of smoking with cholesterol level and with overweight (Karvonen, Orma, Keys, Fidanza & Brozek, 1959; Thomas, 1960). The results for systolic blood pressure are ambiguous. The fact that it was lower in smokers could indicate a lower CHD risk for smokers but it could also suggest a certain weakness in the cardiac muscles of the smoking Ss. The finding about an increased body mass index in smokers is of relevance in regard to the often mentioned link between smoking and weight. One of the most frequent claims of smokers against quitting smoking is that it would bring about increase in their weight. Indeed, many smokers, especially women, justify their smoking as a weight control strategy (Meyers & Klesges, 1989). Meyers and Klesges (1989) presented evidence that the smoking/body weight link does not affect initiation, maintenance and cessation of smoking. Our data seem to suggest the possibility that smokers may be particularly sensitive to increase in weight because their body mass index is actually higher than that of nonsmokers. In sum, our data show that all of the four psychological risk factors and two of the six physiological risk factors are related positively to smoking. That is, smokers tend to be high on an impressive set of risk factors for CHD. This conclusion does not however indicate any causal direction. It may be that smoking causes increases in psychological and physiological risk factors.
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For example, perhaps it reduces HDL or, by increasing arousal, enhances the Hard Driving and Speed-Impatience tendencies of the smoking individual (a similiar line of thinking has been presented by Schmidt, Dembrowski & Bluemchen, 1986). There is also some evidence about the higher arousal level of smokers (Brown, 1973; Gilbert, 1988). A second possibility would be that high levels in the psychological and physiological risk factors enhance the tendency to smoke. For example, an individual who is hard driving and hurried (namely, scores high on the H and S scales) tends more to smoke as a means for controlling tension. Finally, one should also consider the possibility that both smoking and the set of psychological and physiological risk factors found by us to be related to smoking are results or manifestations of another set of biological or psychological determinants or both. Yet regardless of the direction of the causal links, what our data imply is that the widely documented higher risk of smokers for CHD may not be due to smoking per se. Rather it could result from the fact that smokers tend to be characterized by other psychological and physiological risk factors which in themselves could account for the higher CHD risk of the smokers. This conclusion implies that smoking is not an independent risk factor for CHD. If it contributes at all to increasing CHD risk then it is only in interaction with and in the background of other risk factors, as has been claimed persistently by Eysenck (1980, 1985, 1988). This implication could contribute to dispersing the theoretical smoke enshrouding the issue of smoking and thus help in focusing the attention of investigators on the more relevant risk factors for CHD. It is possible that the psychological and physiological risk factors related to smoking may also contribute to turning smoking into such a refractory behavior. It is well known that relapse to smoking within 6-12 months after treatment is at least as high as 80% regardless of the treatment technique (Tollison, 1986; Schwartz, 1987). It may be that the sysiphian nature of the attempts to bring about a cessation of smoking is due in no small part to disregard for the psychological and physiological factors characterizing smokers. Thus, if treatment focuses on modifying the personality tendencies of smokers-their extraversion, hard driving competitiveness and speed-we may end up with better rates of long-term quitters of smoking and with the added bonus of a real reduction in their risk for CHD. Finally, it is of importance to note that our findings and the conclusions based on them refer to the whole undifferentiated sample and to the majority of subsamples defined by specific values of age, gender and education. But in regard to most findings there are exceptions in one or another subsample. In regard to the relation of smoking to the psychological risk factors there is a tendency for reversed direction of findings mostly in older men with higher education. Also, the noted relations were not obtained specifically in the subsample of women. Concerning physiological risk factors the reported relations were observed more consistently in the different subsamples and tended to be more pronounced in the more specifically defined subsamples. These observations imply that in studying risk factors for CHD it is important to examine large samples and to check the results in regard to subsamples of gender, age and education (Kreitler et al., 1991). REFERENCES Berkson, J. (1958). Smoking and lung cancer: some observations on two recent reports. Journo/ of the American Smtisticnl Association, 53, 28-38. Blumenthal, J. A.; Williams, R. B., Kong, Y., Shanberg, S. M. & Thompson, L. Y. (1978). Type A behavior pattern and coronary atherosclerosis. Circulation, 58, 634-639. Booth-Kewley, S. & Friedman, H. S. (1987). Psychological predictors of heart disease: a quantitative review. Psychological Bulletin, 101, 343-362. Brand, R. (1978). Coronary-prone behavior as an independent risk factor for coronary heart disease. In Dembrowski, T. M., Weiss, S. M., Shields, J. L. & Feinleib, M. (Eds), Coronary-prone behavior. New York: Springer. Brown, B. (1973). Additional characteristic differences between smokers and nonsmokers. In Dunn, W. L. (Ed.), Smoking behavior: motives and incenrives. Washington, DC: Winston. Burch, P. R. J. (1978). Smoking and lung cancer: the problem of inferring cause. Journal of the Royal Srarisrical Sociery, 141, 437477. Byrne, D. G., Rosenman, R. H., Schiller, E. & Chesney, M. A. (1985). Consistency and variation among instruments purporting to measure the Type A behavior pattern. Psychosomatic Medicine, 47, 242-261. Cooper, T., Detre, T. & Weiss, S. M. (1981). Coronary prone behavior and coronary heart disease: a critical review. Circulation, 63, 1199-1215. Dembrowski, T. M. & MacDougall. J. M. (1985). Beyond global Type A: relationships of paralinguistic attributes. hostility and anger-in to coronary heart disease. In Field, T. M., McCabe, P. M. Kc Shneiderman, N. (Eds), Srress und coping (pp. 223-242). Hillsdale, NJ: Erlbaum.
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Eysenck, H. J. (1965). Smoking, healfh and personality. New York: Basic Books. Eysenck, H. J. (1980). The causes and effects of smoking. London: Maurice Temple Smith. Eysenck, H. J. (1985). Smoking and health. In Tollison, R. (Ed.), Smoking and sociefy (pp. 178-188). Lexington, MA: Heath. Eysenck, H. J. (1988). The respective importance of personality, cigarette smoking and interaction effects for the genesis of cancer and coronary heart disease. Personality and Individual Differences, 9, 453464. Eysenck, H. J. & Fulker, D. (1983). The components of Type A behavior and its genetic determinants. Personaliry and Individual D@erences,
4, 499-505.
Fisher, R. A. (1959). Smoking: the cancer confrocersy. Edinburgh: Oliver & Boyd. Frank, K. A., Heller, S. S., Komfeld, D. S., Spom, A. A. & Weiss, M. B. (1978). Type A behavior pattern and coronary angiographic findings. Journal of fhe American Medical Association, 240, 761-763. Friedman, M., Rosenman, R. H., Straus, R., Wurm, M. & Kositchek, R. (1968). The relationship of behavior pattern A to the state of the coronary vasculature. American Journal of Medicine, 44, 525-537. Garrow, J. S. & Webster, J. (1985). Quetelet’s Index (W/H) as a measure of fatness. Infernarional Journal of Obesiry, 9, 147-153. Gilbert D, G. (1988). EEG and personality differences between smokers and nonsmokers. Personality and Individual DSfferences, 9, 659-665.
Glass, D. C. (1977). Behavior patterns, stress and coronary disease. New York: Wiley. Gordon, T., Sorlie, P. Jr Kannel, W. B. (1971). Section 27. Coronary heart disease, atherothrombotic brain infarction, intermittent claudilication-A multivariate analysis of some factors related to their incidence: Framingham study, 16-year followup. In Kannel, W. B. & Gordon, T. (Eds), The Framingham study: an epidemiological inresfigation of cardiovascular disease. Washington, DC: US. Department of Health, Education and Welfare, Public Health Service, National Institutes of Health. Grossart-Maticek, R. (1980). Synergistic effects of cigarette smoking, systolic blood pressure and psychosocial risk factors for lung cancer, cardiac infarct and apoplexi cerebri. Psychotherapy and Psychosomafics, 34, 267-272. Grossart-Maticek, R., Eysenck, H. J. & Vetter, H. (1988). Personality type, smoking habit and their interaction as predictors of cancer and coronary heart disease. Peronalify and Individual Differences, 9, 479495. Grossart-Maticek, R., Kanazir, D. T., Vetter, H. & Jankovic, M. (1983). Smoking as a risk factor for lung cancer and cardiac infarct as mediated by psychosocial variables. Psychofherapy and Psychosomafics, 39, 49-105. Grunberg, N. E. (1982). Obesity: Etiology, hazards and treatment. In Gatchel, R. J., Baum, A. & Singer. J. E. (Eds). Handbook of psychology and healfh (Vol. 1, pp. 104-l 19). Hillsdale, NJ: Erlbaum. Guilford, J. S. (1968). Smoking and health-revisited. In Borgatta, E. F. & Evans, R. R. (Eds), Smoking, healrh and behavior (pp. 22-40). Chicago, IL: Aldine. Jenkins, C. D., Zyzanski, S. J. & Rosenman, R. H. (1979). Jenkins Acrirify Survey manual. New York: Psychological Corporation. Jenkins, C. D., Zyzanski, S. J., Rosenman, R. H. & Cleveland, G. L. (1971). Association of coronary-prone behavior scores _ with recurrence of CHD. Journal of Chronic Diseases, 24, 601-611. Kannel. W. B. & Gordon. T. (Eds) (1974). Some characteristics related to the incidence of cardiovascular disease and death: 18 year follow-up. In The Pranungham study:an epidemiological invesfigafion of cardiovascular disease. Washington, DC: U.S. Department of Health, Education and Welfare, Public Health Service, National Institutes of Health, DHEW Publication No. (NIH) 74-599. Karvonen, M., Orma, E., Keys, A., Fidanza, F. & Brozek, J. (1959). Cigarette smoking, serum cholesterol, blood pressure, and body fatness. Observations in Finland. Lancer, I, 492. Katz, L. (1969). Hearings on cigarefte labeling and advertising. Part 2. Washington, DC: Committee on Interstate and Foreign Commerce. House of Representatives. Kenigsberg, D., Zyzanski, S. J., Jenkins, C. D., Wardwell, W. I. & Licciardello, T. (1974). The coronary-prone behavior pattern in hospitalized patients with and without coronary heart disease. Psychosomaric .Medicine, 36, 344-351.
Keys, A., Fidanza, F., Karvonen, M. J., Kimura, N. & Taylor, H. L. (1972). Indices of relative weight and obesity. Journal o$ Chronic Diseases, 25, 329-343.
Kreitler, S., Weissler, K., Weissbord, J. & Brunner, D. (1991). The relation of Type A scores to biological coronary risk factors. Cardiovascular Risk Facfors. In press. Lutz, D. J., Holmes, D. S. & Cramer, R. E. (1987). Hard-driving and speed-impatience components of the t!pe A behavior pattern as predictors of physiological arousal, subjective arousal and challenge seeking. Journal of Psychosomatic Research, 31, 7 13-722. Meyers, A. W. & Klesges, R. C. (1989). Behavioral medicine: the smoking/body weight relationship. Infernarional Conference of the Porfugese Association of Psychologisrs, “Psychology and Psychologisrs Today”. Lisbon, Portugal: 23-25 November (Conference Abstracts book, p. 37). Richmond, J. B. (1981). The healfh consequences of smoking: the changing cigarerfe: a reporr of the Surgeon General. Washington, DC: U.S. Department of Health and Human Services, Public Health Service. Office on Smoking and Health. Rosenman, R. H., Brand, R. J., Jenkins, C. D., Friedman, M., Straus, R. & Wurm, M. (1975). Coronary heart disease in the Western Collaborative Group study: final follow-up experience of 85 years. Journal of rhe American .Wedical Association, 233, 872-877.
Schmidt, T. H., Dembrowski, T. M. % Bluemchen, G. (Eds) (1986). Biological and psychological factors in cardiovascular disease. New York: Springer. Schwartz, J. L. (1987). Review and evaluation of smoking cessation methods: rhe Unifed Slates and Canada, 1978-1985. Washington, DC: U.S. Department of Health and Human Services, Public Health Services. National Institutes of Health. Steptoe, A. (1981). Psychological factors in cardiovascular disorders. New York: Academic Press. Sterling, T. D. (1973). The statistician vis-a-vis issues of public health. American Sfarisfician, 27, 212-217. Thomas, C. B. (1960). Characteristics of smokers compared with non-smokers in a population of healthy young adults. Annals of Infernal Medicine, 53, 697-718.
Smoking and risk factors for heart disease
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Tollison, R. (Ed.) (1986). Smoking and society. Lexington, MA: Heath. U.S. Department of Health and Human Services (1985). R decision maker’s guide IO reducing smoking at the workshop. Washington, DC: Office of Disease Prevention and Health Promotion and Office on Smoking and Health. Public Health Service. Wakefield, J. A. (1988). Results and methodological quality of smoking and health studies. Personality and Indicidual Dlflerences, 9, 465-477.
Williams, R. B., Haney, T. L., Lee, K. L., Kong, Y., Blumenthal, J. A. & Whalen, R. E. (1980). Type A behavior, hostility, and atherosclerosis. Psychosomatic Medicine, 42, 539-549. Zeiner-Henriksen, T. & Lund, E. (1985). Roykingog mortalitetsrisiko blant middelaldrende menn i Norge. Tidsskrift for Den Norske Laegeforening,
IOS, 353-357.
Person. indicid. Difl Vol. Ii!, No. 5, pp. 487-495. 1991
$3.00 + 0.00
Copyright0 1991PergamonPressplc
Printedin GreatBritain.All rightsreserved
THE RELATION OF SMOKING TO PSYCHOLOGICAL AND PHYSIOLOGICAL RISK FACTORS FOR CORONARY HEART DISEASE SHULAMITH KREITLER,’ KINERET WEISSLER,’ HANS KREITLER’ and DANIEL BRUNNER* ‘Department of Psychology, Tel Aviv University and *Institute for Physiological Hygiene, Sackler School of Medicine, Tel Aviv University, Ramat Aviv, Tel Aviv 69978, Israel (Received
12 April 1990)
Summary-Smoking has been held to be responsible for a great number of diseases. Yet criticism has been raised about the role of smoking as the cause or independent cause of the diseases. This study was motivated by Eysenck’s thesis that smoking and personality affect disease synergistically. The purpose was to examine the relation of smoking to psychological and physiological risk factors for coronary heart disease (CHD). The former were the Type A Behavior Pattern and its constitutents assessed by the Jenkins Activity Survey (JAS), the latter were systolic and diastolic blood pressure, cholesterol, HDL, triglycerides and the Quetelet body mass index. There were 520 randomly selected subjects (302 men, 218 women), 4-5 yr old. The results showed that smoking was related to higher scores on the JAS scales of Type A, Hard Driving, and Speed and Impatience, and lower scores on Job Involvement. Further, smokers had lower HDL, higher body mass index and lower systolic blood pressure. The results indicate that smoking is not an independent risk factor for CHD, and if it affects the risk for CHD then it is only in conjunction with the other psychological and physiological risk factors. Further, in view of deviant findings in different subsamples it is important to study large samples and check results in subsamples of age, gender and education.
INTRODUCTION
A voluminous literature has grown around the claim that cigarette smoking is largely responsible for many different diseases particularly coronary heart disease (CHD) and specific types of cancer, as documented by the Surgeon General of the United States (Richmond, 1981) and the Royal College of Physicians in England (Eysenck, 1980, 1985). On the basis of a large body of research the report of the Surgeon General (Richmond, 1981, p. 116) concludes that smoking is a powerful and independent cause of CHD (see also Gordon, Sorlie & Kannel, 1971; Kannel & Gordon, 1974). There are two separate aspects to this claim. One is that smoking is a cause of the different diseases, the other is that it exerts its noxious impact independently of the other major risk factors for CHD. The numbers of people who supposedly die from smoking are so staggering that anyone who has dared to contest the claim runs the risk of being branded as the “enemy of the people”. Yet, criticism of the claim has been mounting. Most attacks referred to the causal role of smoking in disease and were based on pointing out statistical weaknesses and methodological mistakes in the smoking research (Berkson, 1958; Burch, 1978; Eysenck, 1980, 1985; Fisher, 1959; Guilford, 1968; Katz, 1969; Sterling, 1973; Wakefield, 1988). Other investigators focused their criticism on that aspect of the claim that emphasizes the role of smoking as an independent cause for disease. Grossart-Maticek and others (Grossart-Maticek, 1980; Grossart-Maticek, Eysenck & Vetter, 1988; Grossart-Maticek, Kanazir, Vetter & Jankovic, 1983) showed that smoking can be considered as a risk factor for CHD, apoplexy or lung cancer only in interaction with psychosocial factors. More specifically, they identified rationality and anti-emotionality as the psychosocial factors relevant in regard to CHD, and these two factors as well as life events causing depression and hopelessness as relevant in regard to lung cancer. That is, the risk for the disease in smokers was minimal unless they also scored high on the relevant psychosocial factor. The present study was designed to deal mainly with the claim that smoking is an independent cause for disease. Thus, our first purpose was to provide further support for Eysenck’s (1988) thesis that “smoking and personality form a synergistic relationship” (p. 460) in regard to disease. We chose to concentrate on CHD which is one of the two major diseases linked to smoking. It has been claimed that heavy smokers have a 200% greater risk of dying from CHD than nonsmokers 487
488
SHUI_AKWI
KREITLER et al.
(U.S. Department of Health and Human Services, 1985; Zeiner-Henriksen & Lund, 1985). Accordingly, the Type A Behavior Pattern (TABP) and its constituents were the psychological factors on which we focused because they are a classical measure of the personality proneness to CHD. This pattern denotes ‘an action-emotion complex’ of features such as competitiveness, aggressiveness, striving for achievement, time pressure and responsibility that have been shown to characterize individuals with CHD or with risk factors for CHD (Brand, 1978; Blumenthal, Williams, Kong, Shanberg & Thompson, 1978; Frank, Heller, Komfeld, Sporn & Weiss, 1978; Rosenman, Brand, Jenkins, Friedman, Straus & Wurm, 1975; Steptoe, 1981; Williams, Haney, Lee, Kong, Blumenthal & Whalen, 1980). In view of the strong evidence linking it to CHD, TABP has been identified by a panel of scientists under the sponsorship of the National Heart, Lung and Blood Institute as an independent risk factor for CHD, roughly equivalent in magnitude to each of the classical risk factors (Cooper, Detre & Weiss, 198 1). Later criticism has been directed mainly against the unitary character of the TABP and against reliance on the content of the interview answers as opposed to the rated interviewee’s behavior (Dembrowski & MacDougall, 1985). However, Type A and especially some of its components have stood the test of multiple studies well and have emerged in meta-analysis as one of the strongest associations between personality and CHD (Booth-Kewley & Friedman, 1987). We expected that smoking would be related to the TABP mainly because of the evidence that extraversion is related both to smoking (Eysenck, 1965, pp. 100-105) and to Type A (Eysenck & Fulker, 1983). Further, since a previous study showed that different components of the Type A measure were related differentially to physiological risk factors for CHD in different subgroups (Kreitler, Weissler, Weissbord & Brunner, 1991), we intended to explore also the relation of smoking to different Type A components and in different subgroups of age, gender and education. A secondary purpose was to explore the relations of smoking to physiological risk factors for CHD. We expected smoking to be related to at least some of these risk factors, especially in specific age, gender and education subgroups. Confirmation of our expectations about the relations of smoking to Type A components and to physiological risk factors could undermine the view that smoking is a major cause of CHD and may help to focus attention on more relevant determinants. METHOD
Subjects
The total number of Ss was 520. They included 302 men and 218 women; 305 of the Ss were 30-45 yr old (called ‘younger’) and 215 Ss were 4665 yr old (called ‘older’); 387 Ss had ‘low’ educational level (the highest level they reached was high school graduation), whereas 133 Ss had ‘high’ educational level (they had been in some institution of higher learning beyond the high school, such as a college or university). Tests atd measures
Information about smoking was obtained in the framework of a questionnaire about demographic variables including age, gender and education. The Ss were asked to state whether they smoked at present and if not whether they had smoked in the past. Since the number of Ss who had smoked and stopped smoking was only 11 (2.1%) they were added to the nonsmokers. The Ss were administered the Jenkins Activity Survey (JAS) Form C (Jenkins, Zyzanski & Rosenman, 1979) scored separately for each of the four scales: Type A scale (Type A), Speed and Impatience scale (scale S), Job Involvement scale (J scale) and Hard Driving and Competitive scale (scale H). The scores of the four scales were used either as continuous variables or were dichotomized with the zero of the scale as the cutting point. The physiological measures obtained were: systolic and diastolic blood pressure: two measurements taken at rest, 5 min apart, and averaged because of their high intercorrelations; total serum cholesterol (mgjdl); high density lipids (HDL; mg/ml); and triglycerides. Further, the information about weight and height was used for constructing the Quetelet body mass index [weight/(height)2] (Garrow & Webster, 1985; Keys, Fidanza, Karvonen, Kimura & Taylor, 1972), which is an indirect measure of adiposity, minimally correlated with height and maximally with body fat (Grunberg, 1982).
Smoking and risk factors for heart disease
489
Procedure
The Ss were selected randomly out of the population lists of the Ministry of the Interior in Israel, in the framework of the first survey of the population in the Israel MONICA area. The total sample comprised 1197 persons, out of whom 520 (43.4%) answered the JAS and thus were included in the sample. RESULTS
Chi-square tests showed that in our sample gender and education were unrelated (chisquare = 0.728, df = 1, n.s.) but gender and age were related (chi-square = 7.318, df = 1, P < 0.01; there were fewer women in the higher age bracket); and so were age and education (chisquare = 68.632, df = 1, P < 0.001; there were fewer individuals with higher education in the older group). Therefore we considered it important to test the major relations of interest in each of the gender, education and age groups separately. The relations of smoking to gender, age and educational level were examined by multi-levelled chi-square analyses. None of these analyses yielded significant results. This indicates that in our sample smoking occurred with about the same frequency in each of the groups of gender, age and eduation. In the total sample, the percentage of smokers was 40%. The relation of smoking to the JAS scales was examined in two ways. One consisted in comparing the frequency of smokers in Ss high and low in each of the JAS scales in the sample as a whole and in the different subgroups of age, gender and education (that is, six subsamples, each defined by one value of the three variables age, gender and education) and their combinations (that is, the eight subsamples, each defined by two values of the three variables age, gender and education). The results are summarized in Table I. The other way consisted of analyzing the data by means of discriminant analyses with the JAS scales as predictors and smoking as the dependent variable. These analyses too were done in the sample as a whole and in the different subsamples of age, gender and education. The results are summarized in Table 2. Both Tables 1 and 2 indicate that the different JAS scales are related to smoking. The results concerning the specific scales are the same according to the two methods except for three cases, in regard to which the discriminant analysis indicated significant results which were not replicated in the comparison of percentages of smokers (i.e. scale J in the subsample of older men, scale A in the subsample of highly educated men, and scale J in the subsample of older highly educated Ss). According to both methods, the scales proved to be related significantly to smoking in 25 cases, which form 41.7% of the total of 60 examined cases (the whole samples and 14 subsamples, four scales in each). The observed percentage deviates significantly from the 5% expected by chance (CR = 4.751, P < O.OOl), and hence cannot be attributed to chance. Each of the four JAS scales was related to smoking. The relation was more frequent in regard to the S and H scales (each in eight cases) than in regard to the A and J scales (each in four cases), but the differences in frequency are not significant (chi-square = 2.67, df = 3, ns.). It is of interest to note that there are differences in the different subsamples in the direction of the relation between the JAS scales and smoking. Thus, in the sample as a whole as well as in the subsamples of the older Ss, the higher educated men and the lower educated older individuals there was a higher percentage of smokers in the high scorers on Type A than in the low scorers on Type A. Only in the subsample of the older men the relation was reversed with more smokers in the low type A Ss. Concerning the J scale, in the whole sample as well as in the subsamples of older Ss, men of lower education and older Ss of lower education there were more smokers in the Ss scoring low on the J scale. This relation was reversed in the two subsamples of men with higher education and older Ss with higher education. Concerning the S scale, the higher scorers included more smokers than the low scorers in the sample as a whole as well as in the subsamples of older Ss, older men, men of lower education, men of higher education, older Ss of low education and older Ss of higher education. The only subsample with a reversed relation was that of the older lowly educated. Finally, in the majority of cases (the whole sample, older men, lowly educated men, lowly educated younger Ss, and lowly educated older Ss) the high scorers on the H scale included more smokers than the low scorers. The relation was reversed only in the subsamples of the highly educated men and of older Ss.
490
SHuLMlmi KRmurt Table
I. Significant comparisons of frequencies the four JAS scales in the-sample JAS scale
Group Whole
sample
A
Whole sample
J
Whole
sample
s
Whole sample
H
Older Ss
A
Older Ss
J
Older Ss
S
Older Ss
H
Men, older
A
Men, older
S
Men, older
H
Men, low educ.
J
Men, low educ.
S
Men, low educ.
H
Men, high educ.
J
Men, high educ.
S
Men, high educ.
H
Younger.
low educ.
S
Younger,
low cduc.
H
Older, low educ.
A
Older, low educ.
J
Older, low educ.
S
Older, low educ.
H
Older, high educ.
S
Older,
H
high educ.
Scores Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High Low High
er al.
of smokers in Ss rot-inn high and low in each of as a whole and differen~subsamples N
No. of smokers
390 130 447 73 360 I60 327 193 173 42 194 21 I89 26 162 53 99 25 89 35 93 31 I87 47 139 95 I52 82 52 16 50 I8 51 I7 I59 83 I64 78 I08 37 II7 28 104 41 90 55 50 20 48 22
133 75 193 I5 I25 83 146 62 43 I8 63 I 50 I4 38 26 44 4 26 22 30 I8 80 IO 32 58 35 55 16 I2 I5 13 26 2 71 20 37 54 39 22 57 4 31 30 I9 42 I2 I4 23 3
No. of nonsmokers 257 55 254 58 238 77 I81 131 130 24 I31 20 139 I2 124 27 55 21 63 I3 63 I3 107 37 107 37 II7 27 36 4 35 5 25 I5 88 63 127 24 69 15 60 24 73 I1 71 I3 38 6 25 I9
Chi-square 21.636*12.465*** 12.871*** 7.419.. 4.540. 5.861
l
7.142.’ 11.647*** 5.661
l
10.609** 5.484* 6.458’ 32.899-• 41.822*** 8.141” 8.076’. 6.557. 8.961** 47.104*** 5.243’ 9.624” 20.944*‘* 40.525*‘* ll.O52*** 6.196’
Only comparisons with significant results are presented. Low and high in each of the JAS scales denote score up to zero and above zero, respectively. lf < 0.05; l*p < 0.01; ***p < 0.001.
The results of the discriminant analyses presented in Table 2 show that the JAS scales enabled a significant prediction of smoking in the sample as a whole as well as in 7 of the 14 examined subsamples. The number of significant results (8 of 15, namely, 53.33%) exceeds significantly the 5% expected by chance (CR = 2.912, P < 0.01). The mean number of JAS scales involved in the predictions was 3.55. The standard discriminant function coefficients indicate that the contributions of the S and H scales to the prediction were relatively larger than those of the A and J scales (the coefficients of the S and H scales were largest, that is, each occurred in either of the first two places in six cases and each occurred in either of the last two places in six cases, whereas for the A and J scales the situation was reversed). It is of interest to note that the improvement in prediction over the chance level of 50% was larger in the subsamples defined more specifically. Thus, in the sample as a whole the improvement in prediction over the chance level was small (6.92%). In the set of six subsamples, each characterized by one value of the dichotomous variables age, gender and education, there was only one significant prediction (in the older group) and the improvement in prediction in that group
Smoking
491
and risk factors for heart disease
Table 2. Significant results of stepwise discriminant analyses with the four JAS scales as independent variables and smoking as the dependent variable Standardiaed discriminant function coefficients
Sample Whole sample Older group Men, older Men, low educ. Men, high educ. Young, low educ. Older, low educ. Older, high educ.
A H S S J H H S
0.675, 0.744. 0.847. 0.660, 0.913, 0.746, 0.779, 0.813,
J A H H s S S H
-0.605. 0.503, 0.496, 0.641, 0.300, -0.733 0.477, -0.545,
s J A J H
0.264, -0.469, -0.224, -0.460 -0.241,
A J
0.463, 0.209
% of correct classif. H s J
0.199 0.125 -0.159
A
0.128
J
The JAS scales are presented in the order of decreasing contribution had no contribution are not presented. CR = critical ratio. lf < 0.05: l*P < 0.01.
56.92 63.26 65.32 12.22 79.41 74.79 79.31 65.71
-0.431
Deviation from chance 6.92% 13.26% 15.32% 22.22% 29.41% 24.79% 29.31% 15.71%
(CR (CR (CR (CR (CR (CR (CR (CR
= = = = = = = =
2.25.) 2.77.) 2.44.) 4.93.O) 3.59**) 5.62**) 5.22**) 1.90’)
to the prediction. Scales which according to the analysis
was almost double that for the whole sample (13.26%). However, in the set of 12 groups, each characterized by two values of the dichotomous variables age, gender and education, the JAS scales were related significantly to smoking in five subsamples and the mean improvement in prediction in these subsamples over the 50% chance level was again almost double that noted earlier (24.21%). The largest improvement was obtained in the more highly educated men (29.41%) or the less educated older men (15.32%). The relation of smoking to the different physiological risk factors for CHD was examined by comparing the means of the latter variables for smokers and nonsmokers. Table 3 shows that as compared to nonsmokers, smokers have lower HDL levels in the whole sample as well as in each of the six subsamples of age, gender and education. They also have lower systolic BP in the whole sample, in women and the lowly educated. Further, the smokers have a higher body mass index in the whole sample, as well as in the subsamples of the younger Ss, those with high education and those with low education. Thus, of the six physiological risk factors, three (namely, 50%) proved to be related to smoking. The relations appeared consistently in the whole sample and in some of the subsamples. Two of the involved factors-HDL and the body mass index-indicated a greater CHD risk for smokers, one (systolic blood pressure) apparently not. Table 3. Mean comparisons of smokers and nonsmokers on the physiological risk factors in the different groups Group
Variable
Whole sample
Systolic BP
Whole sample
HDL
Whole sample
Body mass index
Men
HDL
Women
Systolic BP
Women
HDL
Younger
Systolic BP
Younger
HDL
Younger
Body mass index
Older
HDL
Lowly educated
Systolic BP
Lowly educated
HDL
Lowly educated
Body mass index
Highly educated
HDL
Highly educated
Body mass index
The table presents only the comparisons lP < 0.05; l*P < 0.01; l**p < 0.001.
Smokers
Nonsmokers Smokers Nonsmokers Smokers Nonsmokers Smokers Nonsmokers Smokers Nonsmokers Smokers Nonsmokers Smokers Nonsmokers Smokers Nonsmokers Smokers Nonsmokers Smokers Nonsmokers Smokers Nonsmokers Smokers Nonsmokers Smokers Nonsmokers Smokers Nonsmokers Smokers __ Nonsmokers
N
Mean
SD
r-test
208 312 208 312 208 312 121 I81 81 I31 87 I31 I44 I61 I44 I61 I44 I61 64
126.005 129.805
17.847 19.175 12.190 14.156 36.608 25.567 7.606 12.848 12.801 20.545 12.253 13.060 II.202 13.403 12.176 14.439 39.972 17.234 11.998 13.655 16.251 18.020 11.294 12.835 33.547 21.016 II.513 14.01 I 30.105 4.465
2.31'
I51 I52 235 I52 235 I52 235 56 77 56 77
with significant results.
45.566 49.808 33.439 26.920 39.338 45.210 122.858 129.462 51.981 56.554 119.525 122.532 46.582 51.217 34.174 24.595 43.555 48.240 124.602 128.074 45.500 49.714 31.791 25.817 44.447 49.165 37.237
26.017
3.64*** 2.23' 4.98." 2.92.' 2.63' 2.13. 3.04.. 2.66" 2.51' 1.96. 3.40** 1.96' 2.13. 2.77,.
492
SHULAMITH KREITLER et al.
DISCUSSION
The findings show that smoking is related to both psychological and physiological risk factors for CHD. The psychological risk factors include the different constituents of JAS, primarily H and S, and to a lesser degree A and J. On the average 3.5 of the 4 JAS scales were involved in each prediction of smoking on the basis of discriminant analysis. The means indicate that there are more smokers (a) among high scorers on Type A than among low scorers, (b) among high scorers on scale S than among low scorers, (c) among high scorers on scale H than among low scorers and (d) among low scorers on scale J than among high scorers. Whereas it is evident that scales A, S and H are related to smoking positively, it may seem that scale J is related inversely. Yet, a meta-analysis based on a great number of studies showed that scale J is related to CHD in a negative direction and that the relation is probably small and unreliable (Booth-Kewley & Friedman, 1987). Thus, the result we obtained for scale J shows that in this case too smoking is related to the risk factor, if indeed it is such, but in a positive direction. However this may be, the major thrust of the findings is that at least three of the scales were related to smoking positiviely. These include the elements of the TABP that have been linked most closely to risk for CHD. Major among them is the Type A itself which from the outset was considered as the core of the specific pyschological proneness for CHD (Friedman, Rosenman, Straus, Wurm & Kositchek, 1968). Yet no less important are the Hard Driving (H) and Speed-Impatience (S) scales that were shown to be related to smoking more highly than the A and J scales. It may not be an accident that the H and S scales also fulfill an especially important role in regard to CHD. They have been identified as the main independent components of the JAS (Glass, 1977). Further, in a sample of middle-aged males the H and S scales correlated quite strongly with the JAS global Type A/B scale score but the A and J scales correlated with it only modestly (Byrne, Rosenman, Schiller & Chesney, 1985). Again, by focusing on the H and S scales Lutz, Holmes and Cramer (1987) obtained more specific and significant results than through the global Type A/B score. They showed that only high scorers on the H scale exposed themselves to more challenging and stressful situations. Notably, the H scale is the only one of the JAS scales which was related to recurrence of CHD (Jenkins, Zyzanski, Rosenman & Cleveland, 1971) and in retrospective studies reliably differentiated between CHD and non-CHD patients (Kenigsberg, Zyzanski, Jenkins, Wardwell & Licciardello, 1974). The metaanalysis performed by Booth-Kewley and Friedman (1987, p. 349) confirmed the close relation of the H scale to CHD. Since our findings showed smoking to be related more to H and S than to the J scale, it is of interest to quote Booth-Kewley and Friedman’s (1987) conclusion: “It might be wise to modify the JAS by making it more clearly a measure of hard-driving competitiveness and less a measure of job involvement” (p. 355). In sum, the findings show that smoking is related positively to major psychological risk factors for CHD. Concerning the physiological risk factors for CHD, three of the six risk factors were consistently related to smoking: systolic blood pressure, HDL and the body mass index. The findings for HDL and body mass indicate an increased CHD risk for smokers. These findings correspond to earlier findings about positive associations of smoking with cholesterol level and with overweight (Karvonen, Orma, Keys, Fidanza & Brozek, 1959; Thomas, 1960). The results for systolic blood pressure are ambiguous. The fact that it was lower in smokers could indicate a lower CHD risk for smokers but it could also suggest a certain weakness in the cardiac muscles of the smoking Ss. The finding about an increased body mass index in smokers is of relevance in regard to the often mentioned link between smoking and weight. One of the most frequent claims of smokers against quitting smoking is that it would bring about increase in their weight. Indeed, many smokers, especially women, justify their smoking as a weight control strategy (Meyers & Klesges, 1989). Meyers and Klesges (1989) presented evidence that the smoking/body weight link does not affect initiation, maintenance and cessation of smoking. Our data seem to suggest the possibility that smokers may be particularly sensitive to increase in weight because their body mass index is actually higher than that of nonsmokers. In sum, our data show that all of the four psychological risk factors and two of the six physiological risk factors are related positively to smoking. That is, smokers tend to be high on an impressive set of risk factors for CHD. This conclusion does not however indicate any causal direction. It may be that smoking causes increases in psychological and physiological risk factors.
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For example, perhaps it reduces HDL or, by increasing arousal, enhances the Hard Driving and Speed-Impatience tendencies of the smoking individual (a similiar line of thinking has been presented by Schmidt, Dembrowski & Bluemchen, 1986). There is also some evidence about the higher arousal level of smokers (Brown, 1973; Gilbert, 1988). A second possibility would be that high levels in the psychological and physiological risk factors enhance the tendency to smoke. For example, an individual who is hard driving and hurried (namely, scores high on the H and S scales) tends more to smoke as a means for controlling tension. Finally, one should also consider the possibility that both smoking and the set of psychological and physiological risk factors found by us to be related to smoking are results or manifestations of another set of biological or psychological determinants or both. Yet regardless of the direction of the causal links, what our data imply is that the widely documented higher risk of smokers for CHD may not be due to smoking per se. Rather it could result from the fact that smokers tend to be characterized by other psychological and physiological risk factors which in themselves could account for the higher CHD risk of the smokers. This conclusion implies that smoking is not an independent risk factor for CHD. If it contributes at all to increasing CHD risk then it is only in interaction with and in the background of other risk factors, as has been claimed persistently by Eysenck (1980, 1985, 1988). This implication could contribute to dispersing the theoretical smoke enshrouding the issue of smoking and thus help in focusing the attention of investigators on the more relevant risk factors for CHD. It is possible that the psychological and physiological risk factors related to smoking may also contribute to turning smoking into such a refractory behavior. It is well known that relapse to smoking within 6-12 months after treatment is at least as high as 80% regardless of the treatment technique (Tollison, 1986; Schwartz, 1987). It may be that the sysiphian nature of the attempts to bring about a cessation of smoking is due in no small part to disregard for the psychological and physiological factors characterizing smokers. Thus, if treatment focuses on modifying the personality tendencies of smokers-their extraversion, hard driving competitiveness and speed-we may end up with better rates of long-term quitters of smoking and with the added bonus of a real reduction in their risk for CHD. Finally, it is of importance to note that our findings and the conclusions based on them refer to the whole undifferentiated sample and to the majority of subsamples defined by specific values of age, gender and education. But in regard to most findings there are exceptions in one or another subsample. In regard to the relation of smoking to the psychological risk factors there is a tendency for reversed direction of findings mostly in older men with higher education. Also, the noted relations were not obtained specifically in the subsample of women. Concerning physiological risk factors the reported relations were observed more consistently in the different subsamples and tended to be more pronounced in the more specifically defined subsamples. These observations imply that in studying risk factors for CHD it is important to examine large samples and to check the results in regard to subsamples of gender, age and education (Kreitler et al., 1991). REFERENCES Berkson, J. (1958). Smoking and lung cancer: some observations on two recent reports. Journo/ of the American Smtisticnl Association, 53, 28-38. Blumenthal, J. A.; Williams, R. B., Kong, Y., Shanberg, S. M. & Thompson, L. Y. (1978). Type A behavior pattern and coronary atherosclerosis. Circulation, 58, 634-639. Booth-Kewley, S. & Friedman, H. S. (1987). Psychological predictors of heart disease: a quantitative review. Psychological Bulletin, 101, 343-362. Brand, R. (1978). Coronary-prone behavior as an independent risk factor for coronary heart disease. In Dembrowski, T. M., Weiss, S. M., Shields, J. L. & Feinleib, M. (Eds), Coronary-prone behavior. New York: Springer. Brown, B. (1973). Additional characteristic differences between smokers and nonsmokers. In Dunn, W. L. (Ed.), Smoking behavior: motives and incenrives. Washington, DC: Winston. Burch, P. R. J. (1978). Smoking and lung cancer: the problem of inferring cause. Journal of the Royal Srarisrical Sociery, 141, 437477. Byrne, D. G., Rosenman, R. H., Schiller, E. & Chesney, M. A. (1985). Consistency and variation among instruments purporting to measure the Type A behavior pattern. Psychosomatic Medicine, 47, 242-261. Cooper, T., Detre, T. & Weiss, S. M. (1981). Coronary prone behavior and coronary heart disease: a critical review. Circulation, 63, 1199-1215. Dembrowski, T. M. & MacDougall. J. M. (1985). Beyond global Type A: relationships of paralinguistic attributes. hostility and anger-in to coronary heart disease. In Field, T. M., McCabe, P. M. Kc Shneiderman, N. (Eds), Srress und coping (pp. 223-242). Hillsdale, NJ: Erlbaum.
494
SHULAMITH
KREITLER ef al.
Eysenck, H. J. (1965). Smoking, healfh and personality. New York: Basic Books. Eysenck, H. J. (1980). The causes and effects of smoking. London: Maurice Temple Smith. Eysenck, H. J. (1985). Smoking and health. In Tollison, R. (Ed.), Smoking and sociefy (pp. 178-188). Lexington, MA: Heath. Eysenck, H. J. (1988). The respective importance of personality, cigarette smoking and interaction effects for the genesis of cancer and coronary heart disease. Personality and Individual Differences, 9, 453464. Eysenck, H. J. & Fulker, D. (1983). The components of Type A behavior and its genetic determinants. Personaliry and Individual D@erences,
4, 499-505.
Fisher, R. A. (1959). Smoking: the cancer confrocersy. Edinburgh: Oliver & Boyd. Frank, K. A., Heller, S. S., Komfeld, D. S., Spom, A. A. & Weiss, M. B. (1978). Type A behavior pattern and coronary angiographic findings. Journal of fhe American Medical Association, 240, 761-763. Friedman, M., Rosenman, R. H., Straus, R., Wurm, M. & Kositchek, R. (1968). The relationship of behavior pattern A to the state of the coronary vasculature. American Journal of Medicine, 44, 525-537. Garrow, J. S. & Webster, J. (1985). Quetelet’s Index (W/H) as a measure of fatness. Infernarional Journal of Obesiry, 9, 147-153. Gilbert D, G. (1988). EEG and personality differences between smokers and nonsmokers. Personality and Individual DSfferences, 9, 659-665.
Glass, D. C. (1977). Behavior patterns, stress and coronary disease. New York: Wiley. Gordon, T., Sorlie, P. Jr Kannel, W. B. (1971). Section 27. Coronary heart disease, atherothrombotic brain infarction, intermittent claudilication-A multivariate analysis of some factors related to their incidence: Framingham study, 16-year followup. In Kannel, W. B. & Gordon, T. (Eds), The Framingham study: an epidemiological inresfigation of cardiovascular disease. Washington, DC: US. Department of Health, Education and Welfare, Public Health Service, National Institutes of Health. Grossart-Maticek, R. (1980). Synergistic effects of cigarette smoking, systolic blood pressure and psychosocial risk factors for lung cancer, cardiac infarct and apoplexi cerebri. Psychotherapy and Psychosomafics, 34, 267-272. Grossart-Maticek, R., Eysenck, H. J. & Vetter, H. (1988). Personality type, smoking habit and their interaction as predictors of cancer and coronary heart disease. Peronalify and Individual Differences, 9, 479495. Grossart-Maticek, R., Kanazir, D. T., Vetter, H. & Jankovic, M. (1983). Smoking as a risk factor for lung cancer and cardiac infarct as mediated by psychosocial variables. Psychofherapy and Psychosomafics, 39, 49-105. Grunberg, N. E. (1982). Obesity: Etiology, hazards and treatment. In Gatchel, R. J., Baum, A. & Singer. J. E. (Eds). Handbook of psychology and healfh (Vol. 1, pp. 104-l 19). Hillsdale, NJ: Erlbaum. Guilford, J. S. (1968). Smoking and health-revisited. In Borgatta, E. F. & Evans, R. R. (Eds), Smoking, healrh and behavior (pp. 22-40). Chicago, IL: Aldine. Jenkins, C. D., Zyzanski, S. J. & Rosenman, R. H. (1979). Jenkins Acrirify Survey manual. New York: Psychological Corporation. Jenkins, C. D., Zyzanski, S. J., Rosenman, R. H. & Cleveland, G. L. (1971). Association of coronary-prone behavior scores _ with recurrence of CHD. Journal of Chronic Diseases, 24, 601-611. Kannel. W. B. & Gordon. T. (Eds) (1974). Some characteristics related to the incidence of cardiovascular disease and death: 18 year follow-up. In The Pranungham study:an epidemiological invesfigafion of cardiovascular disease. Washington, DC: U.S. Department of Health, Education and Welfare, Public Health Service, National Institutes of Health, DHEW Publication No. (NIH) 74-599. Karvonen, M., Orma, E., Keys, A., Fidanza, F. & Brozek, J. (1959). Cigarette smoking, serum cholesterol, blood pressure, and body fatness. Observations in Finland. Lancer, I, 492. Katz, L. (1969). Hearings on cigarefte labeling and advertising. Part 2. Washington, DC: Committee on Interstate and Foreign Commerce. House of Representatives. Kenigsberg, D., Zyzanski, S. J., Jenkins, C. D., Wardwell, W. I. & Licciardello, T. (1974). The coronary-prone behavior pattern in hospitalized patients with and without coronary heart disease. Psychosomaric .Medicine, 36, 344-351.
Keys, A., Fidanza, F., Karvonen, M. J., Kimura, N. & Taylor, H. L. (1972). Indices of relative weight and obesity. Journal o$ Chronic Diseases, 25, 329-343.
Kreitler, S., Weissler, K., Weissbord, J. & Brunner, D. (1991). The relation of Type A scores to biological coronary risk factors. Cardiovascular Risk Facfors. In press. Lutz, D. J., Holmes, D. S. & Cramer, R. E. (1987). Hard-driving and speed-impatience components of the t!pe A behavior pattern as predictors of physiological arousal, subjective arousal and challenge seeking. Journal of Psychosomatic Research, 31, 7 13-722. Meyers, A. W. & Klesges, R. C. (1989). Behavioral medicine: the smoking/body weight relationship. Infernarional Conference of the Porfugese Association of Psychologisrs, “Psychology and Psychologisrs Today”. Lisbon, Portugal: 23-25 November (Conference Abstracts book, p. 37). Richmond, J. B. (1981). The healfh consequences of smoking: the changing cigarerfe: a reporr of the Surgeon General. Washington, DC: U.S. Department of Health and Human Services, Public Health Service. Office on Smoking and Health. Rosenman, R. H., Brand, R. J., Jenkins, C. D., Friedman, M., Straus, R. & Wurm, M. (1975). Coronary heart disease in the Western Collaborative Group study: final follow-up experience of 85 years. Journal of rhe American .Wedical Association, 233, 872-877.
Schmidt, T. H., Dembrowski, T. M. % Bluemchen, G. (Eds) (1986). Biological and psychological factors in cardiovascular disease. New York: Springer. Schwartz, J. L. (1987). Review and evaluation of smoking cessation methods: rhe Unifed Slates and Canada, 1978-1985. Washington, DC: U.S. Department of Health and Human Services, Public Health Services. National Institutes of Health. Steptoe, A. (1981). Psychological factors in cardiovascular disorders. New York: Academic Press. Sterling, T. D. (1973). The statistician vis-a-vis issues of public health. American Sfarisfician, 27, 212-217. Thomas, C. B. (1960). Characteristics of smokers compared with non-smokers in a population of healthy young adults. Annals of Infernal Medicine, 53, 697-718.
Smoking and risk factors for heart disease
495
Tollison, R. (Ed.) (1986). Smoking and society. Lexington, MA: Heath. U.S. Department of Health and Human Services (1985). R decision maker’s guide IO reducing smoking at the workshop. Washington, DC: Office of Disease Prevention and Health Promotion and Office on Smoking and Health. Public Health Service. Wakefield, J. A. (1988). Results and methodological quality of smoking and health studies. Personality and Indicidual Dlflerences, 9, 465-477.
Williams, R. B., Haney, T. L., Lee, K. L., Kong, Y., Blumenthal, J. A. & Whalen, R. E. (1980). Type A behavior, hostility, and atherosclerosis. Psychosomatic Medicine, 42, 539-549. Zeiner-Henriksen, T. & Lund, E. (1985). Roykingog mortalitetsrisiko blant middelaldrende menn i Norge. Tidsskrift for Den Norske Laegeforening,
IOS, 353-357.