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(Circulation. 1997;96:1438-1444.)
© 1997 American Heart Association, Inc.
Articles |
Cigarette Smoking, Weight Gain, and Coronary Mortality
Results From the Chicago Western Electric Study
From The University of Texas–Houston, Health Science Center, School of Public Health.
Correspondence to Janet E. Fulton, PhD, Centers for Disease Control and Prevention, Division of Nutrition and Physical Activity, 4770 Buford Highway Northeast, Mailstop K46, Atlanta, GA 30341-3724.
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Abstract |
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Background Prospective studies of overweight and coronary heart disease (CHD) have presented inconsistent findings. Previous inconsistencies may be explained by the modifying effect of cigarette smoking on the association between weight gain and coronary mortality.
Methods and Results We prospectively studied 1531 men
40 to 59 years of age who were employed at the Hawthorne Works of the
Western Electric Company in Chicago, Ill. Information collected at the
initial examination in 1958 included recalled weight at age 20,
present weight, height, smoking status, and other CHD risk factors.
Vital status was known for all men on the 25th anniversary: 257 CHD
deaths occurred over 31 644 person-years of experience. Cox regression
analysis was used to investigate risk of coronary
mortality associated with change in body mass index (
BMI) and its
modification by smoking status after adjustment for age, major organ
system disease, family history of CHD, and BMI at age 20. Adjustment
was not performed for blood pressure or serum total
cholesterol because these are intervening variables.
BMI was positively associated with risk of coronary
mortality in never-smokers but not in current-smokers (P for
interaction=.088). For never-smokers with BMI classified as stable,
low gain, moderate gain, or high gain, adjusted relative risks of
coronary mortality were 1.00, 1.75, 1.75, and 3.07,
respectively (P for trend=.010). For current-smokers, the
respective adjusted relative risks were 1.00, 0.78, 1.05, and 1.03
(P for trend=.344).
Conclusions These results support the hypothesis that cigarette smoking modifies the association between weight gain and coronary mortality. Future investigations of weight gain and coronary mortality should account for the modifying effect of cigarette smoking.
Key Words: obesity • epidemiology • cardiovascular diseases • exercise
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Introduction |
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Overweight is a major and increasing problem in the United States. The prevalence of overweight has increased from 25% in 1980 to 33% in 1991 such that >34 million Americans are currently considered to be overweight.1 The propensity toward overweight in this country is coupled with the dilemma that weight usually increases while physical activity decreases with age.2 3 It is therefore likely that adult overweight will continue to be an important public health challenge for years to come.
Overweight is clearly associated with the development of coronary heart disease (CHD) risk factors.4 However, prospective studies of overweight and coronary heart disease have reported inconsistent findings.5 6 To date, investigators have reported positive,7 8 9 10 negative,11 and null12 13 14 associations between overweight and weight gain and risk of CHD. Obesity at the extremes appears to increase the risk of all-cause mortality,6 although the magnitude of risk associated with intermediate levels of overweight or weight gain has not been clearly defined. Clarification of previous inconsistent findings is essential to accurately estimate the magnitude of the effect of weight gain on risk of CHD.
The great majority of persons in the United States gain weight during their young adulthood,1 15 but cigarette smokers may gain less weight than nonsmokers due to the metabolic effect of smoking on weight.16 17 18 Effects of nicotine on the resting metabolic rate19 20 or the sympathetic nervous system21 22 23 may account for an increase in energy expenditure and/or a decrease in energy storage, which may explain why smokers tend to weigh less than their nonsmoking counterparts and gain weight on cessation of smoking. Moreover, cigarette smokers may remain lean during their adult years not due to a physically active lifestyle or prudent diet but rather due to their cigarette smoking behavior, making it difficult to assess the true effect of weight gain on coronary disease in cigarette smokers. Examination of the association between weight gain and CHD mortality as being modified by cigarette smoking may help to clarify previous inconsistent findings between overweight and CHD.5 6 We hypothesized that cigarette smoking modifies the association between gain in weight during young adulthood and risk of 25-year CHD mortality in a cohort of 1531 middle-aged, employed men. Specifically, weight gain during young adulthood will be positively associated with 25-year risk of CHD mortality in nonsmokers, but the association will be smaller or absent entirely in cigarette smokers. This report presents a test of this hypothesis.
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Methods |
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Participant Selection
Participants in the Western Electric Study were selected in 1957 from the population of 5397 men whose records indicated that they were 40 to 55 years of age and had been employed for
2 years at the
Hawthorne Works of the Western Electric Company in the Chicago, Ill,
area. Of 3102 randomly selected men, 2080 (67.1%) agreed to
participate. Another 27 men served as a pilot group, bringing to 2107
the total number examined from October 1957 through December 1958. Two
thirds of the men were first-generation or second-generation Americans,
predominantly of German, Polish, or Bohemian ancestry. The remainder
were mostly descendants of earlier emigrants from the British Isles.
The men worked at various occupations associated with the manufacture
of telephones and related products. Selection, examination, and
follow-up procedures have been described elsewhere.24 Of the 2107 men initially examined, 62 did not return for the second examination in 1959 and were excluded from the present study because data from both examinations were required. An additional 74 men (3.6% of 2045) were excluded due to evidence of CHD at either the first or second examination. Of the remaining 1971 men who attended both examinations and did not have evidence of CHD, others were excluded due to missing data on weight (n=36) and cigarette smoking status (n=1). Men reporting being a former cigarette smoker at the baseline examination were excluded from the present analysis (n=242). Individuals who had a decrease in body mass index (BMI) (loss in BMI >0.74 kg/m2) (n=161) were excluded because gain in BMI was the exposure variable of interest for this investigation. Thus, the population at risk for coronary mortality for this investigation comprised 1531 employed men.
Data Collection
The initial examination included a detailed family and medical
history with recall of weight at ages 20, 25, 30, 35, and 40; physical
examination; and measurement of height, weight, and skinfold thickness
(measured at the tip of the scapula and at the triceps). Body mass
index (ie, Quetelet's index) (kg/m2) was used as an
estimate of body fatness due to its correlation with sum of skinfolds
and body density and lack of correlation with height.25
Systolic and diastolic blood pressures were taken
at the beginning of each physical examination with the participant
seated. Serum total cholesterol was measured according to
the method of Abell et al.26 History of using tobacco and
current use of tobacco (cigarettes, pipes, cigars, and other) was
routinely asked each year as part of the medical history. Participants
self-reported their cigarette smoking status (never, former, or current
cigarette smoker) and past use of cigarettes (duration of use, amount
smoked most of adult life, and, for former users, the period of time
since the last use) at the baseline examination.
Major organ system disease was considered present at the initial examination when any one or more of the following conditions were present: history of diabetes mellitus, 2+ urine sugar, cardiomegaly or other clinically significant finding on chest radiograph, hypertensive retinopathy, or a major ECG abnormality. Family history of cardiovascular disease was self-reported at the baseline examination and coded positive for cardiovascular diseases if a parent had died from such causes before age 60 or a sibling had died from such causes at any age past childhood.
Follow-up
Men who continued to participate in the study were reexamined
annually up to 1969. After 1969, vital status was determined
periodically by mailed questionnaire and telephone interview through
the 25th anniversary of the initial examination; at that time vital
status was known for all 2107 men. Underlying cause of death and up to
four additional causes on the death certificate were coded according to
the Eighth Revision of the International Classification of
Diseases adapted for use in the United States.27
Codes 410–412 were coded as CHD deaths.
Analysis
The increase in body fatness from age 20 until baseline was the
primary exposure variable of interest for this investigation as
measured by the change in BMI from age 20 to baseline examination (ie,
during young adulthood and middle age). To reduce the effects of
intraindividual variation, participants were characterized at baseline
by mean values of measurements made at the first and second
examinations in 1958 and 1959 with respect to current BMI, cigarettes
smoked per day, systolic blood pressure, and serum total
cholesterol. BMI at age 20 (kg/m2) was
calculated as recalled weight at age 20 divided by measured height in
1958. BMI at baseline was calculated as the mean of measured weight at
the baseline examination in 1958/1959 divided by measured height in
1958. Change in BMI (BMI) during young adulthood was calculated by
subtracting BMI at age 20 from BMI at baseline. Cigarette smokers were
classified as never-smokers (reported never smoking cigarettes at
baseline) or current-smokers (reported currently smoking cigarettes at
baseline). Subsequent analyses were stratified by never or
current cigarette smoking. Age at baseline was determined as the date
of the second examination minus the date of birth. Time at risk for
coronary mortality was calculated as the number of days from
the date of the second examination to the date of death or the 25th
anniversary, whichever came first.
Proportional hazards regression analysis was used to
investigate the association between BMI and 25-year coronary
mortality separately for never-smokers and current-smokers to test the
hypothesis that cigarette smoking modifies the association between
BMI and coronary mortality. Relative risks (RRs) of
coronary mortality were adjusted for age, family history of
CHD, major organ system disease, BMI at age 20, and number of
cigarettes smoked per day. Relative risks of coronary mortality
were not adjusted in the primary analysis for systolic
blood pressure or total serum cholesterol because these
were believed to be intervening variables. The cross-product of
cigarette smoking and BMI was calculated and added to the
proportional hazards regression model to evaluate the statistical
probability of effect modification.
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Results |
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The prevalence of never-smoking and currently smoking cigarettes at the baseline examination in 1958 was 32.4% (n=575) and 53.9% (n=956), respectively. Former cigarette smokers constituted 13.7% (n=242) of the cohort and were excluded from the present analyses.
Table 1
shows the participant
characteristics by cigarette smoking status at the baseline
examination. Never-smokers and current-smokers were of similar age (49
years) and height (175 cm) at baseline. As expected, mean weight of
current-smokers was significantly lower than that of never-smokers
(77.8 and 80.5 kg, respectively). Mean BMI at age 20 was the same
between never-smokers and current-smokers (22.2
kg/m2), although mean BMI at baseline (middle-age)
was significantly lower for current-smokers than never-smokers (25.5
and 26.5 kg/m2, respectively). Never-smokers gained
significantly more BMI than current-smokers over the course of their
young adulthood (4.3 and 3.3 kg/m2,
respectively).
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BMI was categorized as stable, low gain, moderate gain, or high
gain. Stable was defined as losing or gaining no more than 0.74
kg/m2 (ie, stable=±0.74 kg/m2),
which is equal to 5 lb divided by (1.75 m)2, where
1.75 m is the mean height of the cohort. The low-, moderate-, and
high-gain categories were tertiles of gain in BMI calculated after
excluding the stable category. Low-, moderate-, and high-gain
categories corresponded to changes in BMI of >0.74 and 
2.90,
>2.90 and 4.90, and >4.90 kg/m2,
respectively. The median change in BMI among the stable, low-gain,
moderate-gain, and high-gain categories was 0.05, 1.90, 3.85, and 6.40
kg/m2, respectively.
Fig 1 shows the prevalence of each
category of BMI by cigarette smoking status. Never-smokers compared
with current-smokers had lower prevalence of stability in BMI (7%
versus 15%, respectively). Conversely, the prevalence of high gain in
BMI was somewhat higher in never-smokers than current-smokers (37%
versus 24%, respectively). Prevalence of category of BMI was
significantly different between never-smokers and current-smokers
(
2 [3]=47.8, P<.001).
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Figs 2 and 3 show the mean BMI at ages 20, 25, 30,
35, and 40 by BMI category for never-smokers and current-smokers,
respectively. Gain in BMI occurred linearly from age 20 to 40 among the
low-, moderate-, and high-gain groups for never-smokers and
current-smokers alike. The stable group remained BMI stable from age 20
to 40. Among never-smokers, change in BMI from age 20 to 40 among the
stable and low-, moderate-, and high-gain groups ranged from 23.6 to
24.2, 23.0 to 25.4, 22.2 to 25.8, and 21.3 to 27.3, respectively.
Similarly, among current-smokers, corresponding changes in BMI from age
20 to 40 were 23.1 to 23.9, 22.6 to 24.7, 22.0 to 25.7, and 21.3 to
26.9, respectively. Similar patterns of increase in BMI were observed
among never-smokers and current-smokers. Gain in BMI was inversely
related to BMI at age 20 and thus BMI at age 20 was an important
variable to control for in the multivariate
analysis of BMI and CHD mortality.
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Table 2 shows the mean values of age,
systolic blood pressure, and serum total
cholesterol by BMI category and cigarette smoking
status. Gain in BMI was associated with higher mean systolic
blood pressures at baseline (P<.001), but cigarette smoking
was not (P=.435). Gain in BMI (P=.052) and
cigarette smoking (P<.001) were associated with higher mean
serum total cholesterol values at baseline.
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The association between BMI and risk of CHD mortality separately for
never-smokers and current-smokers was examined as shown in Table 3. For never-smokers in BMI categories
of stable, low gain, moderate gain, and high gain, corresponding
adjusted RRs of CHD mortality were 1.00, 1.75, 1.75, and 3.07
(P for trend=.010).
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To decrease the effect of variability within each category of BMI,
the median value of each BMI category was used to assess the effect
of BMI as a continuous variable. Among never-smokers, the
adjusted relative risk of CHD mortality by BMI was 1.16 (95%
confidence interval, 1.04 to 1.30), indicating for every one unit
change in BMI during young adulthood there was a corresponding 16%
increase in the 25-year risk of CHD mortality.
Among current-smokers in BMI categories of stable, low gain,
moderate gain, and high gain, corresponding adjusted relative risks of
CHD were 1.00, 0.78, 1.05, and 1.03 (P for trend=.344).
Among current-smokers, the adjusted relative risk of CHD mortality for
BMI as a continuous measure was 1.02 (95% confidence interval, 0.96
to 1.09). Thus, among current-smokers, there was no association between
BMI and CHD mortality. Within BMI categories, crude rates of CHD
mortality in current-smokers were greater than crude CHD mortality
rates in never-smokers.
Effect modification by cigarette smoking was evaluated by creating an
interaction term between median values of change in BMI and never or
currently smoking cigarettes (0, never smoking; 1, current smoking).
The interaction term was added to the proportional hazards regression
model containing age, major organ system disease, family history of
CHD, BMI recalled at age 20, number of cigarettes smoked per day at
baseline, median change in BMI, and never- or current-smoking
cigarettes. The adjusted RR of CHD associated with the interaction term
was 0.90 (P=.088).
Alternate explanations for the results were considered and addressed in
post hoc analyses. Misclassification of exposure was evaluated
by examining the risk of CHD in several alternative ways. Among
never-smokers, using alternative groupings of BMI yielded RRs
ranging from 1.0 to 1.8 (P for trend=.027). Inclusion of
individuals with preexisting disease at the baseline examination was
addressed by excluding deaths occurring during the first 5 years of
follow-up and yielded RRs ranging from 1.7 to 2.8 (P for
trend=.025). Exclusion of individuals with diabetes or major organ
system disease or a former alcohol drinker yielded RRs ranging from 1.4
to 3.0 (P for trend=.022), and exclusion of persons with
unusually low or high BMI at age 20 (<18 or >28
kg/m2) yielded RRs ranging from 1.7 to 3.1
(P for trend=.008). Controlling for the intervening
variables, systolic blood pressure, and serum total
cholesterol, low-, moderate-, and high-gain RRs were 2.0,
1.7, and 2.9 (P for trend=.035). Furthermore, when
controlling for baseline triceps and subscapular skinfold measures,
low-, moderate-, and high-gain RRs were 1.8, 1.7, and 3.0 (P
for trend=.015). Confounding by alcohol drinking was explored in
preliminary analyses and yielded corresponding RRs of 1.8, 1.8,
and 3.1 (P for trend=.011). No trend was observed for
current smokers in any of these post hoc analyses.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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These results support the hypothesis that cigarette smoking modifies the association between change in
BMI during young
adulthood and risk of 25-year coronary mortality. Among
never-smokers, men who gained BMI during their young adulthood had 1.8
to 3.1 times the risk of 25-year CHD mortality compared with men with
stable BMI. By contrast, among current-smokers, there was no
association between change in BMI and 25-year coronary
mortality. Furthermore, stable BMI was more common and moderate or high
gain in BMI was less common in current-smokers than in never-smokers.
These results support the idea that there is a blunting effect on the
physiological process of weight gain among
cigarette smokers.17 18 28 This biologic phenomenon may
cause the association between weight gain and CHD death to be obscured
in individuals who are current cigarette smokers. Thus, cigarette
smokers may remain lean through their young adulthood, not due to a
physically active lifestyle or a prudent diet but instead due to their
smoking behavior, making it difficult to estimate the true risk of CHD
death associated with weight gain in populations in whom cigarette
smoking is prevalent. Failure to detect a positive association between
weight or weight gain and CHD in previous investigations may have been
due to inadequate examination of cigarette smoking.
Are These Results Consistent With Other Studies?
Many researchers have investigated the association between obesity
and CHD, but only recently have investigators studied the extent to
which gain in weight or BMI was associated with CHD or all-cause
mortality. In Harvard alumni who reported their weight in 1962 or 1966
and again in 1977, increased risk of CHD mortality (RR, 1.28 to 2.01)
was observed in men who gained weight compared with men with stable
weight.7 The authors did not statistically test for effect
modification by cigarette smoking, although they did point out that a
U-shaped relation between weight change and all-cause mortality was
demonstrated among nonsmokers only. Harvard alumni may not be typical
of many US men because 17% currently smoked cigarettes in 1977 and
only 12% gained >5 kg from 1962 to 1977. In comparison, 54% of men
in the Western Electric study were current smokers, and 76% gained >5
kg from age 20 until the baseline examination in 1958.
Rimm and colleagues9 evaluated weight gain since age 21
and risk of incident CHD among 29 122 men participating in the Health
Professionals Follow-Up Study. Results showed a positive association
between weight gain and risk of 3-year incident CHD such that men
gaining 19 kg were 2.1 times more likely to develop CHD than were men
with stable weight (±2 kg). In a similar study with women, Willett and
colleagues10 investigated the risk of CHD associated with
weight gain since age 18 among 115 818 female nurses in the Nurses'
Health Study. Women gaining 20 kg were 2.7 times more likely to
develop CHD than were women with a stable weight (±4.9 kg). These
results are in agreement with those of the present study as these
populations had many fewer current cigarette smokers than the
present study population. Thus, cigarette smoking in these studies
could not substantially distort the relation between gain in weight and
risk of subsequent CHD.
Could Misclassification of Exposure Have Biased the
Result?
BMI was calculated based on recalled weight at age 20 and
measured weight and height at the baseline examination in 1958/1959. We
did not directly validate recalled weight at age 20 in this study
population, although previous investigators have demonstrated strong
correlations between recalled weight at age 2529 and age
1810 with records of measured weight (r=.80
and .87, respectively). BMI is uncorrelated with height
(r=.00 to .254) and highly correlated with the sum of
skinfolds (r=.61 to .85) and body density from hydrostatic
weighing (r=-.66 to -.85), indicating that it is a good
proxy for body fatness.25 Choice of cut points of strata
of BMI is not a reasonable explanation for the present result in
light of secondary analyses indicating the pattern of
association between BMI and CHD death was similar when the data were
analyzed using alternative groupings of BMI.
Cigarette smoking behavior was believed to be concurrent with gain in BMI from age 20 to baseline. However, cigarette smoking status was collected at the baseline examination in 1958. Misclassification of cigarette smoking status may have occurred during age 20 to baseline, although the mean duration of cigarette smoking among current smokers was 28 years (SD, 6 years), indicating that most current smokers started to smoke cigarettes in their early 20s.
Could Increased CHD Mortality Associated With BMI Be the Result
of Including Individuals With Subclinical or Preexisting Disease at
Baseline Examination? Could Weight Loss Due to Premorbid Conditions Be
a Determinant of CHD Mortality?
These alternative explanations are implausible for several
reasons. First, when deaths occurring during the first 5 years of
follow-up were excluded, the pattern of association between BMI and
CHD death did not change appreciably. Second, when individuals with
diabetes or major organ system disease or a former alcohol drinker were
excluded, the results were minimally affected. Third, exclusion of
persons with unusually low or high BMI at age 20 (<18 or >28
kg/m2) did not appreciably change the results,
indicating that individuals with preclinical disease were likely not
influencing the association between BMI and CHD death in
never-smokers.
Could Misclassification of CHD Mortality or Chance Have Influenced
the Result?
This is highly unlikely because complete 25-year follow-up was
obtained for every member of the cohort. On the 25th anniversary of the
first examination, the vital status of all 2107 participants was
determined. All death certificates were obtained and
coded,27 without knowledge of other information about
participants. Misclassification of CHD mortality was unlikely, although
the inability to examine acute myocardial infarction as a CHD end point
is a limitation of the study. Chance could have been an alternate
explanation for the result as the confidence intervals around the RRs
included unity, although examination of a linear trend in the RRs is
unaffected by the width of the confidence intervals around the
risks.
We hypothesized that blood pressure and serum total
cholesterol were intermediate in the causal pathway between
gain in BMI and CHD death. Therefore, we did not control for their
effect in the primary analysis. In a secondary
analysis, however, the relative risks of CHD death by BMI
strata among never-smokers were slightly lower when the intervening
variables, systolic blood pressure and serum total
cholesterol, were included in the analysis. We
hypothesized that the association between BMI and CHD death would
diminish as at least part of the variance in CHD death could be
explained through the influence of BMI on blood pressure and total
cholesterol.30 This result may suggest that
gain in BMI is directly influencing CHD mortality not through its
influence on blood pressure or cholesterol but via a
different mechanism. Or, perhaps more likely, gain in BMI may be a
surrogate for another factor (eg, body fat patterning) that is
associated with the excess CHD mortality seen among individuals who
gain large amounts of BMI during young adulthood.31 Body
fat patterning or central adiposity may work through other biological
pathways to influence CHD mortality that are only moderately associated
with blood pressure and total cholesterol and not
intermediate in the causal chain. However, when analyses were
controlled for triceps and subscapular skinfold measures at baseline,
the RRs of CHD mortality changed only slightly. Furthermore, a chronic
increase in body fat may affect other biological pathways leading to
CHD mortality. Recently proposed mechanisms such as lipoprotein(a) and
apolipoprotein E or the well-established CHD risk factors, HDL and LDL
cholesterol may be the factors most influenced by weight
gain32 33 that ultimately lead to CHD. These particular
lipoprotein subcomponents were not obtained in the Western Electric
cohort but may explain why total cholesterol does not
appear to be an intermediary variable in this analysis.
The increased mechanization of modern societies as a result of advances in technology to encourage sedentary lifestyles combined with abundant and palatable food sources have resulted in a large proportion of the population being classified as obese or overweight.34 Physical inactivity is an independent risk factor for CHD,35 and evidence is accumulating to suggest that physical inactivity is the most important cause of weight gain in adulthood.36 Weight gain may be due to decreased energy expenditure related to physical inactivity rather than increased energy intake.36 37 38 39 It is proposed that prevention, or a decrease in the rate of progression, of gain in weight during adulthood may be best achieved through promotion of regular, moderately intense physical activity.35 40 41 42 Adult weight gain may be associated with risk of CHD largely as a marker for chronic physical inactivity that can be detected accurately only among nonsmokers due to the interfering effect of cigarette smoking on weight and weight gain. Thus, smokers may remain lean due to their cigarette smoking behavior and not from maintaining a physically active lifestyle or eating a prudent diet.
In conclusion, in this prospective cohort study, we demonstrated that cigarette smoking modifies the association between gain in BMI during young adulthood and 25-year CHD mortality. The evidence presented here may therefore aid in clarifying previous inconsistent results concerning obesity and CHD. Future investigations of weight gain and CHD mortality should account for the modifying effect of cigarette smoking.
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Acknowledgments |
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Dr Fulton is indebted to Drs Darwin R. Labarthe, Ralph F. Frankowski, and James M. Pivarnik for their assistance and contributions to her doctoral dissertation research.
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Footnotes |
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Guest editor was Henry H. Blackburn, MD, University of Minnesota.
Received February 10, 1997; revision received March 25, 1997; accepted April 9, 1997.
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