RESEARCH AND PRACTICE
Association of Smoking in Adolescence With
Abdominal Obesity in Adulthood: A Follow-Up
Study of 5 Birth Cohorts of Finnish Twins
Suoma E. Saarni, MD, PhD, Kirsi Pietilainen, MD, PhD, Suvi Kantonen, BM, Aila Rissanen, MD, PhD, and Jaakko Kaprio, MD, PhD
Smoking and obesity are major causes of pre-
ventable death in developed countries.1 The
life expectancy of obese smokers is reduced by
as much as 13 years.2 Obesity-related excess
mortality may mainly be caused by abdominal
obesity.3 The association between smoking and
obesity is complex: smoking has been associ-
ated with both low and high body mass index
(BMI; weight in kilograms divided by height in
meters squared) and also with adverse fat distri-
bution. In most cross-sectional studies, adult
smokers were leaner than were nonsmokers but
had a larger waist circumference or smaller
waist-to-hip ratio.48 Also, among smokers, a
greater number of cigarettes smoked per day
was related to waist circumference and BMI.5 In
one large Australian study of women, smokers
were found to be more likely to gain weight
during the follow-up than were women who had
never smoked.9 Age, duration of smoking, and
socioeconomic status have been shown to mod-
ify the effect of smoking on body weight.4,8,10,11
Among adolescents, the results of studies of the
association between smoking and BMI have been
inconsistent. In some studies, the relation between
smoking and lower body weight often observed in
adults was found to be reduced or absent among
youth.12,13 Adolescence is a critical age for the
development of obesity14 and the establishment
of health habits such as smoking, eating behaviors,
and physical activity. Only a few studies dealing
with the association between smoking and later
abdominal obesity have spanned the age period
from adolescence to adulthood. Those studies
were all beset with methodologic problems, how-
ever, and no associations were found.1517
On the basis of previous studies of adults, it
seems reasonable to assume that tobacco smok-
ing is associated with changes in body weight
and shape even though the possible biolog-
ical mechanisms remain unclear. Because
the time span from adolescence to adulthood
is an important period in stabilizing health
348 | Research and Practice | Peer Reviewed | Saarni et al.
Objectives. We studied the association of adolescent smoking with overweight
and abdominal obesity in adulthood.
Methods. We used the FinnTwin16, a prospective, population-based ques-
tionnaire study of 5 consecutive and complete birth cohorts of Finnish twins
born between 1975 and 1979 (N = 4296) and studied at four points between the
ages of 16 and 27 years to analyze the effect of adolescent smoking on abdominal
obesity and overweight in early adulthood.
Results. Smoking at least 10 cigarettes daily when aged 16 to 18 years increased
the risk of adult abdominal obesity (odds ratio [OR]=1.77; 95% confidence interval
[CI] = 1.39, 2.26). After we adjusted for confounders, the OR was 1.44 (95% CI= 1.11,
1.88), and after further adjustment for current body mass index (BMI), the OR was
1.34 (95% CI = 0.95, 1.88). Adolescent smoking significantly increased the risk of
becoming overweight among women even after adjustment for possible con-
founders, including baseline BMI (OR = 1.74; 95% CI = 1.06, 2.88).
Conclusions. Smoking is a risk factor for abdominal obesity among both genders
and for overweight in women. The prevention of smoking during adolescence may
play an important role in promoting healthy weight and in decreasing the morbidity
related to abdominal obesity. (Am J Public Health. 2009;99:348354. doi:10.2105/
AJPH.2007.123851)
habits and in the development of obesity, we the time of the first mailing. The response rates in
examined the effect of smoking during late all surveys were very high (80%90%).
adolescence on overweight and abdominal We excluded respondents with known ill-
obesity in early adulthood. To examine the nesses (i.e., diabetes mellitus, systemic lupus
independent effects of smoking on subsequent erythematosus, inflammatory bowel disease,
measures of obesity, we controlled our analyses celiac disease, hyper- or hypothyroidism, ma-
for several potential confounders. lignancies, mobility disorders, and eating dis-
orders) and those taking medications known
METHODS to affect weight (e.g., insulin, thyroxin, and
antipsychotic medications) from the analyses
Participants (n = 302). We also excluded respondents with
The data for our study originated from the missing data on weight, height, waist circum-
FinnTwin16, a population-based study of 5 ference, or smoking (n =158). Thus, our final
consecutive and complete birth cohorts of data set included 2278 women and 2018 men.
Finnish twins born in 1975 to 1979 and iden- Twins zygosity was determined as described
tified through the Central Population Registry in previous studies by using questions included
of Finland.18 We collected baseline data (wave in the baseline questionnaire.19 Participants in-
T1) through questionnaires mailed within 60 cluded 1326 monozygotic, 1353 same sex dizy-
days of the twins 16th birthdays. Follow-ups gotic, 1478 opposite sex dizygotic, and 139
were at ages 17 and 18.5 years (waves T2 and unknown zygosity twins. Pairwise analyses were
T3, respectively) and in young adulthood (mean conducted when both twins had responded and
age = 24.4 years; range = 2227 years; wave no data were missing. We found 415 pairs
T4). Parents were sent their own questionnaire at discordant for abdominal obesity at wave T4.
American Journal of Public Health | February 2009, Vol 99, No. 2

Measures
Smoking behavior. Adolescent smoking
was categorized as follows: (1) never smokers
(smoked fewer than 50 cigarettes in their
lifetime), (2) former smokers, (3) occasional
smokers (current smokers other than daily
smokers), (4) daily smokers smoking fewer than
10 cigarettes per day, and (5) daily smokers
smoking 10 or more cigarettes per day. We
primarily used the smoking status at age 18
years (wave T3); if this data point was missing,
we used answers from waves T2 and T1. We
had several reasons for this: first, we assumed
the smoking habits to be most stabilized at
wave T3 and therefore to most reliably reflect
the smoking behavior during our follow-up.
Also, at earlier ages, the participants were
probably more ambivalent about their smoking
status than at wave T3. This supposition was
based on our observation that at wave T1, 80%
of those reporting to be former smokers had
smoked fewer than 50 cigarettes in their life-
time. Second, the number of cigarettes smoked
daily (fewer than 10 or 10 or more) was not
asked at wave T1. Third, during data collection,
it became illegal for children and adolescents
younger than 18 years to smoke, which might
have affected how the participants younger than
18 years answered questions concerning to-
bacco use. Also, smoking status remained rea-
sonably stable from waves T1to T3. The j values
comparing all smoking categories across differ-
ent time points were approximately 0.5, and
most of the changes were within categories of
smokers (occasional and daily smokers). The j
value when comparing never versus ever
smokers at waves T1 and T3 was 0.64.
Anthropometric measures. Waist circumfer-
ence was self-reported by the participants by
using a tape measure supplied by mail in the
wave-T4 survey. We used the World Health
Organization20 cutoffs for abdominal obesity of
80 cm for women and 94 cm for men. Height and
weight were self-reported, and body mass index
(BMI; weight in kilograms divided by height in
meters squared) was calculated on the basis of
these values. We categorized the respondents as
being normal weight, overweight, or obese at
waves T1 and T2 by using the International
Obesity Task Force reference for adolescent
obesity, with the cutoffs created by using specific
percentiles linked to adult cutoffs based on UK
data.21,22 The BMI categories for waves T3 and
February 2009, Vol 99, No. 2 | American Journal of Public Health
RESEARCH AND PRACTICE
T4 were defined as less than 25 kg/m2 for normal
weight, 25.00 to 29.99 kg/m2 for overweight,
and 30 kg/m2 or greater for obese.
Confounding Factors
We included selected potential confounding
factors known to be associated with smoking or
the outcome measures (BMI and abdominal
obesity) in the analyses.
To control for dietary behavior, we used
measures assessed at wave T1: the skipping
of breakfast, type of milk and type of spread
on bread, and cola drinking. Skipping breakfast
has been associated with other risk behav-
iors23,24 and with an increased risk of weight
gain.25 Eating breakfast was assessed by using
3 response categories: having breakfast every
morning, having breakfast about 3 to 4 mornings
per week, and having breakfast once per week
or less often. Respondents were asked which type
of milk (no milk, skim milk, 1% low-fat milk,
1.9% low-fat milk, or 3.5% fat whole milk),
and which type of spread (no spread, low-fat,
margarine, butter-margarine, butter, or other)
they used. Type of milk and spread on bread
have been shown to be good indicators of satu-
rated fat intake.26 Cola drinking was assessed as
the number of 12-ounce (0.33 L) bottles con-
sumed per day. Because cola drinking was quite
rare and the distribution was highly skewed, it was
used as a dichotomized variable in the analyses.
The use of sugar-sweetened and possibly even
artificially sweetened27 soft drinks has been
shown to be associated with weight gain and
obesity.28
Physical activity was categorized in 3 classes
on the basis of questions concerning the fre-
quency of physical activity at leisure outside
school repeated in identical form in surveys
from wave T1 to T3. Those who reported
exercising 4 to 5 times per week or more in all
3 questionnaires composed the exerciser
group; the passive group comprised those
reporting exercising 1 to 2 times a month or
fewer in all 3 questionnaires; and the remain-
der composed the intermediate group.29
The age of smoking initiation (experiment-
ing) was asked at wave T1. Parents BMI at age
20 years was calculated by using heights and
weights recalled in the parental survey.
Fathers socioeconomic status was deter-
mined on the basis of questions concerning
occupation, employment, and education.
Saarni et al. | Peer Reviewed | Research and Practice | 349
Socioeconomic status was classified into 6
categories (upper-level employee, lower-level
employee, manual worker, self-employed or
other, farmer, and unclassified) according to the
criteria of the Finnish Classification of Socio-
economic Groups.30 Educational attainment and
employment status at wave T3 were used to
classify the socioeconomic status into 4 cate-
gories (high school/university, vocational school,
employed, and unemployed/other).
Validity Assessment
We assessed the validity of the self-reported
BMI, waist circumference, and height measures
in a subsample of 566 twins. Those partici-
pants had participated in another study on the
consequences of adolescent alcohol use with a
median of 650 days after the self-report.
Height was measured without shoes on a sta-
diometer, and weight was measured in light
clothes on a calibrated beam balance. Waist
circumference was measured while the partic-
ipants were standing, halfway between the
iliac crest and the lowest rib, at the end of a
light expiration. The intraclass correlations
were high. The intraclass correlation for
measured versus self-reported BMI was 0.89,
and the mean difference was 0.93 kg/m2
(95% confidence interval [CI] = 0.79 kg/m2,
1.07 kg/m2). The intraclass correlation for
measured versus self-reported height was 0.99,
and the mean difference was 0.24 cm (95%
CI = 0.14 cm, 0.35 cm). The intraclass cor-
relation for measured versus self-reported
waist circumference was 0.75, and the mean
difference was 2.48 cm (95% CI = 0.96 cm,
3.00 cm).
Statistical Methods
The odds ratios for abdominal obesity and
becoming overweight in adulthood were
obtained from logistic regression models. We
chose the binary outcomes for their relevance
in clinical settings and in identifying high-risk
patients. The potential gender interaction was
tested by using a likelihood-ratio test between
models with and without an interaction term
(gender smoking). A statistically significant
gender interaction was found concerning the
risk of becoming overweight, but this was not
the case for abdominal obesity. Therefore, risk
of becoming overweight was analyzed for men
and women separately, and abdominal obesity
 RESEARCH AND PRACTICE

was examined in gender-adjusted models. All

regression analyses were run in 2 sets: (1) a TABLE 1Background Characteristics of Participants at Age 18.5 Years: Survey Wave T3,
robust model and (2) a model adjusted for FinnTwin16 Study, Finland
confounding factors selected by using the Women Men
stepwise procedure of Stata.31 The dietary var- (n = 2278) (n = 2018)
iables were handled as a cluster in the stepwise
Body mass index, kg/m2, mean (95% CI) 20.9 (20.7, 21.0) 21.8 (21.7, 22.0)
analysis. The risk of abdominal obesity was also
Smoking status, %
adjusted for BMI at wave T4 in addition to the
Never 51.1 48.9
stepwise-selected confounders. Correspondingly,
Former 12.3 11.3
the risk of becoming overweight was also ad-
Occasional 15.3 12.0
justed for baseline BMI.
< 10 cigarettes daily 11.9 12.4
Because socioeconomic status has been
10 cigarettes daily 9.4 15.5
shown to be associated with smoking behavior
Physical activity, %
and to modify the effect of smoking on body
4 times/wk 11.7 18.5
weight,32 we tested for possible interactions
3 times/mo to 3 times/wk 79.2 66.8
between socioeconomic status and smoking on
02 times/mo 5.3 6.2
adult outcomes (BMI, abdominal obesity) by
Data missing 3.8 8.5
comparing models with and without the inter-
Eats breakfast, %
action term (smoking socioeconomic status)
Every morning 68.4 74.9
using a likelihood ratio test. No statistically sig-
34 times/wk 16.7 13.0
nificant interactions were found in the models
Once per week or less 14.9 11.8
mentioned (all P values > .48).
Missing 0.0 0.3
The effect of the twin-sampling design on
Mean age, y, at smoking initiation, by smoking status
standard errors was taken into account in the
Former 13.3 13.0
individual-level analyses by computing robust
Occasional 14.2 13.7
standard errors with use of the cluster option in
< 10 cigarettes daily 13.3 12.9
Stata. All statistical analyses were carried out
10 cigarettes daily 12.7 11.8
by using Stata.31
Type of milk used, %
The analyses were continued by studying
No milk 14.8 8.0
the association between smoking and abdom-
Skimmed milk 34.2 23.9
inal obesity within twin pairs discordant for
Low-fat 1% milk 7.9 6.9
abdominal obesity by using conditional logistic
Low-fat 1.9% milk 36.9 49.7
regression.31 If the association was also found
Whole milk 6.2 11.5
within discordant twin pairs, this suggested that
Type of spread used, %
there was a causal association between smoking
No spread 10.9 4.2
and abdominal obesity or that they were both
Low-fat 18.2 15.2
caused by environmental influences unshared by
Margarine 45.9 53.0
the twins. Thus, if the association between ab-
Butter-margarine 16.7 15.1
dominal obesity and smoking was found only in
Butter 7.8 11.8
individual-level analyses, but not within discor-
Other 0.6 0.7
dant twin pairs, i.e., the smoking twin pair did not
Drinks cola, %
have a higher risk of abdominal obesity than did
Yes 5.9 15.2
the nonsmoking twin pair, this indicated that
No 94.1 84.8
the association was caused by shared familial and
Educational level at T3, %
genetic factors affecting both smoking and weight
High school/university 51.2 38.1
changes.31,33
Vocational school 41.6 50.8
Employed 4.7 6.1
RESULTS
Unemployed or other 2.5 5.0
Mothers BMI at age 20 y, kg/m2, mean (95% CI) 21.0 (20.9, 21.0) 21.1 (21.0, 21.2)
Smoking Behavior
Fathers BMI at age 20 y, kg/m2, mean (95% CI) 22.6 (22.5, 22.6) 22.4 (22.3, 22.5)
About one half of the men and women had
never smoked, and about 12% were former Continued
smokers in adolescence (Table 1). Smoking at

350 | Research and Practice | Peer Reviewed | Saarni et al. American Journal of Public Health | February 2009, Vol 99, No. 2

TABLE 1Continued
Fathers socioeconomic status, %
Upper-level employee
Lower-level employee
Manual worker
Self-employed or other
Farmer
Unclassified
Father nonrespondent
Note. CI = confidence interval; BMI = body mass index.
least 10 cigarettes daily was more prevalent
among men than among women (15.5% versus
9.4%). Among the men, 18.5% were classified
as exercisers, and among the women, 11.7%
were; 5% to 6% of both genders were physically
inactive in adolescence. About 12% of the men
and 15% of the women reported eating break-
fast only once per week or less often. About one
third of the women and one fifth of the men
used fat-free milk, and 15.2% of the men and
5.9% of the women consumed cola drinks.
Overweight and Obesity
The prevalence of overweight remained
low (about 6%) at ages 16 to 18.5 years (waves
T1T3) but rose steeply thereafter; 11.2% of
Note. Overweight and obesity were defined as in reference 21 in adolescents and as a body mass index of 25.0 kg/m2
to 29.9 kg/m2 or 30 kg/m2 or more, respectively, in adults 18 years and older.
FIGURE 1Prevalence of overweight and obesity (%) from ages 16 to 24 years among
2278 female and 2018 male participants: FinnTwin16 cohort, Finland.
February 2009, Vol 99, No. 2 | American Journal of Public Health
RESEARCH AND PRACTICE
smoking had no effect on the risk of becoming
overweight. Overweight in adulthood was thus
most prevalent among girls who smoked 10 or
18.9 20.9 more cigarettes daily, whereas no differences
13.8 13.9 were found among boys (Figure 2). The par-
32.1 31.0 ticipants in all smoking categories gained
9.0 8.1 weight from age 18 to 24 years.
8.0 8.4
0.8 0.8 Abdominal Obesity
17.3 16.9 Girls smoking at least 10 cigarettes daily
during adolescence had an approximately
3.4 cm larger waist circumference as young
adults than did girls who had never smoked.
Adolescent smoking predicted abdominal obe-
sity (i.e., waist circumference 80 cm for
women and 24.3% of men were overweight by
women, 94 cm for men) in adulthood among
wave T4 (Figure1). The proportion of obese men
both men and women. The OR for abdominal
and women at wave T4 (4%) was almost 6 times
obesity was highest among those smoking at
higher than at wave T1 (0.7%).
least 10 cigarettes per day (OR =1.77; 95%
CI =1.39, 2.26) in the model adjusted only for
Smoking and Risk of Becoming
gender (Table 2). Heavy daily smoking (i.e.,
Overweight
10 cigarettes per day) remained a significant
In the unadjusted model, girls who smoked
predictor of an increased risk of subsequent
in adolescence had a higher risk of becoming
abdominal obesity after adjustments for po-
overweight women than did girls who had
tential confounders (Table 2). The risk was
never smoked. The risk was greatest among
partly attributable to overall adiposity, because
girls who smoked at least 10 cigarettes per day
adjustment for current BMI broadened the
(odds ratio [OR] = 2.32; 95% CI =1.51, 3.58).
confidence intervals so that statistical signifi-
Adjustment for possible confounders and
cance was not maintained.
baseline BMI attenuated the effect (OR =1.74;
Comparing those who started daily smoking
95% CI =1.06, 2.88). Among men, adolescent
between T1 and T3 with those who were daily
smokers throughout adolescence did not reveal
any significant differences between groups (data
not shown). In the analyses concerning twin
pairs discordant for abdominal obesity (n= 415),
among all discordant pairs, the abdominally
obese twin was statistically nonsignificantly
more likely to have smoked at least 10 cigarettes
daily (OR =1.60; 95% CI = 0.92, 2.78). Also,
the risk was increased for being a former
smoker during adolescence (OR =1.8; 95%
CI =1.10, 3.02). In the subgroup analyses of
zygosity groups, among the same-sex dizygotic
pairs, the abdominally obese twin was more
likely to have smoked at least 10 cigarettes daily
(OR = 3.2; 95% CI=1.09, 9.42). The number of
monozygotic discordant pairs was small, and no
statistically significant effects were noted.
DISCUSSION
We showed in this population-based cohort
of healthy young adults that smoking predicts
Saarni et al. | Peer Reviewed | Research and Practice | 351
 RESEARCH AND PRACTICE

Note. Overweight was defined as a body mass index of 25 kg/m2 or greater. Abdominal obesity was defined as a waist circumference of 80 cm or greater among women and 94 cm
or greater among men. Never smokers were the comparison group. Results presented in the figure are from regression models without any adjustment for confounding factors.
*P < .05; **P < .01, tested with logistic regression.
FIGURE 2Prevalence of general overweight (a) and abdominal obesity (b) at age 24 years, by smoking status during adolescence: FinnTwin16
cohort, Finland.

abdominal obesity. Smoking at least 10 ciga- importance because of the well-documented those studies used crude measures of smoking
rettes daily during adolescence was associated detrimental metabolic effects of central fat.3 (i.e., weekly smoking versus nonsmoking at
with an increased risk of abdominal obesity and age 1314 years), which may have reflected
overall overweight among women. The risk of Previous Studies smoking habits not yet stabilized. We were
becoming abdominally obese was not fully Our results differ from those of the previ- able to differentiate between occasional and
explained by overall adiposity and other possi- ous studies,1517,34,35 probably as the result of daily smokers, and could further take into ac-
ble factors affecting central fat accumulation, as some methodologic differences. Neither count the number of cigarettes smoked daily.
shown in the models adjusted for current BMI the Amsterdam Growth and Health Study16,17,34 The results of cross-sectional studies of body
and many other possible confounders. The nor the Northern Finland Cohort Study15,35 weight and smoking behavior have been incon-
extra kilograms on the waistline among the found an association between adolescent sistent,36,37 as have the results of longitudinal
heavy smokers are of clinical and public health smoking and later abdominal obesity. However, studies with no inclusion of indicators of abdom-
inal obesity.9,12,36,38,39
In our data, the prevalence of overweight
rose steeply from adolescence into young
adulthood. The determinants of later obesity
TABLE 2Odds Ratios (ORs) for Abdominal Obesity at Age 24 Years, by Smoking Status in
during this important age period are not well
Adolescence: FinnTwin16 Study, Finland
understood. Our results showed that smoking
Model 1 (n = 4296), Model 2 (n = 4296), Model 3 (n = 4269), during adolescence was associated with future
Smoking Status in Adolescence OR (95% CI) OR (95% CI) OR (95% CI) overweight among young women and with
Never (Ref) 1.00 1.00 1.00 abdominal obesity among both women and
Former 1.25 (0.98, 1.61) 1.17 (0.91, 1.52) 1.21 (0.87, 1.67) men. Smoking is known to be associated with
Occasional 1.21 (0.95, 1.54) 1.16 (0.91, 1.49) 1.12 (0.80, 1.57) low education,4042 dietary behavior,23,24 and
Smoked < 10 cigarettes daily 1.28 (1.00, 1.64) 1.11 (0.85, 1.45) 1.25 (0.87, 1.80) physical inactivity,29,43 all of which are docu-
Smoked 10 cigarettes daily 1.77* (1.39, 2.26) 1.44* (1.11, 1.88) 1.34 (0.95, 1.88) mented risk factors for overweight. However,
these confounders explained only a small
Note. CI = confidence interval. Model 1 adjusted for gender. Model 2 further adjusted for physical activity, dietary factors, amount of the association between smoking and
participants own socioeconomic status, fathers socioeconomic status, and parents body mass index. Model 3 further
adjusted for participants body mass index at age 24 years. overweight and later abdominal obesity. This,
*P < .01. together with the dose-dependent effect of
smoking and our findings from twin pairs

352 | Research and Practice | Peer Reviewed | Saarni et al. American Journal of Public Health | February 2009, Vol 99, No. 2

discordant for abdominal obesity, supports the
interpretation that a causal relation may exist
between smoking and the development of
obesity. The pathophysiologic mechanisms be-
hind this possibly causal link remain obscure.
However, one possible explanation may be
that changes in glucocorticoid metabolism
associated with smoking44 and possibly also
with psychosocial stress associated with smok-
ing45,46 are responsible for the central fat
accumulation.47,48
Strengths and Weaknesses
The increase in the risk of abdominal obesity
or overweight among the women was no
longer statistically significant in the fully ad-
justed models. This may have been caused by
insufficient statistical power. Another possible
interpretation of our findings is that adolescent
smoking is a proxy for other factors or is part of a
cluster of factors predisposing to later abdominal
obesity. There are 2 implications of these 2
explanations: first, adolescent smoking should be
seen as a sign of increased metabolic hazards in
clinical work. Second, counteracting smoking
initiation may be a more effective tool against
later metabolic morbidity than previously
thought in both clinical and public health settings.
In this study, we adjusted for selected indi-
cators of dietary behavior, physical exercise,
parental BMI, and fathers and participants
own socioeconomic status as potential con-
founders. Our inability to adjust for dietary
habits in more detail (e.g., in a food-frequency
questionnaire or food diary) can be seen as a
limitation of our study. Even if dietary mea-
sures have several methodologic problems,49
this topic should be addressed in greater detail in
future research. Our validated measurement of
exercise can be seen as reasonably accurate.29
Inclusion of both parents BMI in the analysis is a
special strength of our study because BMI has a
strong genetic component.50
We used self-reported data, and our mea-
surement validation showed good association
with measured values. Self-reports of smoking
status among Finns have previously been
shown to be valid.51 Some underreporting of
body size may occur, which would lead to an
underestimation of the risk of abdominal obesity.
Unfortunately, we had information on waist
circumference only at young adulthood. Given
the low prevalence of obesity and overweight in
February 2009, Vol 99, No. 2 | American Journal of Public Health
RESEARCH AND PRACTICE
adolescence in this and other studies,52 it is
unlikely that abdominal obesity is common at
this young age or that it could have influenced
smoking habits in adolescence.
We used a large population-based sample
with high response rates. Although twins have
slightly lower BMIs than did singletons in
midadolescence,53 this is unlikely to affect the
association between smoking and body compo-
sition. Further, determination of adult body size
takes place from late adolescence to early adult-
hood. Our adolescents were assessed at each
survey in adolescence within a very narrow age
range, thus reducing variation caused by age.
Unlike in previous studies, we adjusted for sev-
eral confounders affecting abdominal obesity
and smoking. We also used a more detailed
measure of smoking behavior than did the earlier
studies and were able to consider the level of
daily cigarette consumption.
Conclusions
Given the greater risk of overweight and
abdominal obesity among girls who smoked
daily and the fact that adolescent smoking is often
associated with preoccupation with weight,54
emphasizing the deleterious effect of smoking on
abdominal fat accumulation could be effective in
smoking prevention among young women.
Counteracting smoking initiation may be a more
effective tool against later morbidity than previ-
ously thought. These results need to be replicated
in other well-conducted epidemiologic studies
with longer follow-ups and possibly more-careful
measurement of the risk factors and the outcome.
Our results show that adolescent smoking
predicts abdominal obesity among young
adults. Both abdominal obesity and smoking
are major risk factors for metabolic dysfunc-
tion55 and cardiovascular disease.56 The pre-
vention of smoking during adolescence could be
a very effective tool for preventing later meta-
bolic morbidity. However, it will be important to
better understand the possible causal pathways
between smoking and later abdominal obesity. j
About the Authors
Suoma E. Saarni, Kirsi Pietilainen, Suvi Kantonen, and
Jaakko Kaprio are with the Department of Public Health,
University of Helsinki, Helsinki, Finland. Aila Rissanen
and Kirsi Pietilainen are with the Obesity Research Unit,
Department of Psychiatry, Helsinki University Central
Hospital, Helsinki. Suoma E. Saarni and Jaakko Kaprio are
also with the Department of Mental Health and Alcohol
Saarni et al. | Peer Reviewed | Research and Practice | 353
Research, National Public Health Institute, Helsinki,
Finland.
Requests for reprints should be sent to Suoma E. Saarni,
Department of Public Health, PO Box 41, 00014
University of Helsinki, Helsinki, Finland (e-mail: suoma.
saarni@helsinki.fi).
This article was accepted June 6, 2008.
Contributors
S. E. Saarni, J. Kaprio, and A. Rissanen were responsible
for the conception and design of this study. All authors
contributed substantially to analysis and interpretation
of data. S. E. Saarni, K. Pietilainen, and S. Kantonen wrote
drafts of the article, and all authors substantially partic-
ipated in revising it critically for important intellectual
content. All authors gave their final approval of the final
version.
Acknowledgments
This study was supported by grants from the Signe and
Ane Gyllenberg Foundation, the National Institute on
Alcohol Abuse and Alcoholism (grants AA-08315,
AA-00145, and AA-12502), the European Union
Fifth Framework Program (QLRT-1999-00916 and
QLG2-CT-2002-01254), the Academy of Finland
(grants 44069, 100499, 118555, and 201461), the
Academy of Finland Centre of Excellence in Complex
Disease Genetics, and Helsinki University Central
Hospital.
We thank Tellervo Korhonen from the Department of
Public Health, University of Helsinki, for valuable com-
ments on the article. We also thank the anonymous
referees for their careful help in improving the quality of
this article.
Note. Funding sources had no involvement in plan-
ning or conducting the study.
Human Participant Protection
This study was approved by the ethical committees of
Helsinki University and Indiana University.
References
1. World Health Report 2002. Geneva, Switzerland:
World Health Organization; 2002.
2. Peeters A, Barendregt JJ, Willekens F, Mackenbach
JP, Al Mamun A, Bonneux L. Obesity in adulthood and its
consequences for life expectancy: a life-table analysis.
Ann Intern Med. 2003;138(1):2432.
3. Bigaard J, Frederiksen K, Tjonneland A, et al.
Waist circumference and body composition in
relation to all-cause mortality in middle-aged
men and women. Int J Obes (Lond). 2005;29(7):
778784.
4. Akbartabartoori M, Lean ME, Hankey CR.
Relationships between cigarette smoking, body
size and body shape. Int J Obes (Lond). 2005;29(2):
236243.
5. Bamia C, Trichopoulou A, Lenas D, Trichopoulos D.
Tobacco smoking in relation to body fat mass and
distribution in a general population sample. Int J Obes
Relat Metab Disord. 2004;28(8):10911096.
6. Barrett-Connor E, Khaw KT. Cigarette smoking and
increased central adiposity. Ann Intern Med. 1989;
111(10):783787.

7. Canoy D, Wareham N, Luben R, et al. Cigarette
smoking and fat distribution in 21,828 British men and
women: a population-based study. Obes Res. 2005;
13(8):14661475.
8. Marti B, Tuomilehto J, Korhonen HJ, et al. Smoking
and leanness: evidence for change in Finland. BMJ.
1989;298(6683):12871290.
9. Ball K, Brown W, Crawford D. Who does not gain
weight? Prevalence and predictors of weight maintenance
in young women. Int J Obes Relat Metab Disord. 2002;
26(12):15701578.
10. Molarius A, Seidell JC, Kuulasmaa K, Dobson AJ,
Sans S. Smoking and relative body weight: an interna-
tional perspective from the WHO MONICA Project.
J Epidemiol Community Health. 1997;51(3):252260.
11. Molarius A, Seidell JC. Differences in the association
between smoking and relative body weight by level of
education. Int J Obes Relat Metab Disord. 1997;21(3):
189196.
12. Klesges RC, Ward KD, Ray JW, Cutter G, Jacobs DR
Jr, Wagenknecht LE. The prospective relationships be-
tween smoking and weight in a young, biracial cohort: the
Coronary Artery Risk Development in Young Adults
Study. J Consult Clin Psychol. 1998;66(6):987993.
13. Klesges RC, Zbikowski SM, Lando HA, Haddock CK,
Talcott GW, Robinson LA. The relationship between
smoking and body weight in a population of young
military personnel. Health Psychol. 1998;17(5):454458.
14. Gordon-Larsen P, Adair LS, Nelson MC, Popkin BM.
Five-year obesity incidence in the transition period
between adolescence and adulthood: the National
Longitudinal Study of Adolescent Health. Am J Clin Nutr.
2004;80(3):569575.
15. Laitinen J, Pietilainen K, Wadsworth M, Sovio U,
Jarvelin MR. Predictors of abdominal obesity among
31-y-old men and women born in Northern Finland in
1966. Eur J Clin Nutr. 2004;58(1):180190.
16. Twisk JW, Kemper HC, van Mechelen W, Post GB,
van Lenthe FJ. Body fatness: longitudinal relationship of
body mass index and the sum of skinfolds with other risk
factors for coronary heart disease. Int J Obes Relat Metab
Disord. 1998;22(9):915922.
17. van Lenthe FJ, van Mechelen W, Kemper HC,
Post GB. Behavioral variables and development of
a central pattern of body fat from adolescence into
adulthood in normal-weight whites: the Amsterdam
Growth and Health Study. Am J Clin Nutr. 1998;
67(5):846852.
18. Kaprio J, Pulkkinen L, Rose RJ. Genetic and envi-
ronmental factors in health-related behaviors: studies on
Finnish twins and twin families. Twin Res. 2002;5(5):
366371.
19. Sarna S, Kaprio J, Sistonen P, Koskenvuo M. Diag-
nosis of twin zygosity by mailed questionnaire. Hum
Hered. 1978;28(4):241254.
20. Han TS, van Leer EM, Seidell JC, Lean ME.
Waist circumference action levels in the identification of
cardiovascular risk factors: prevalence study in a random
sample. BMJ. 1995;311(7017):14011405.
21. Cole TJ, Bellizzi MC, Flegal KM, Dietz WH.
Establishing a standard definition for child overweight
and obesity worldwide: international survey. BMJ.
2000;320(7244):12401243.
22. Vidmar A, Carlin J, Hesketh K, Cole T. Standardiz-
ing anthropometric measures in children and adolescents
354 | Research and Practice | Peer Reviewed | Saarni et al.
RESEARCH AND PRACTICE
with new functions for egen. Stata Journal. 2004;4(1):
5055.
23. Wingard DL, Berkman LF, Brand RJ. A multivariate
analysis of health-related practices: a nine-year mortality
follow-up of the Alameda County Study. Am J Epidemiol.
1982;116(5):765775.
24. Keski-Rahkonen A, Kaprio J, Rissanen A, Virkkunen
M, Rose RJ. Breakfast skipping and health-compromising
behaviors in adolescents and adults. Eur J Clin Nutr.
2003;57(7):842853.
25. Purslow LR, Sandhu MS, Forouhi N, et al. Energy
intake at breakfast and weight change: prospective study
of 6,764 middle-aged men and women. Am J Epidemiol.
2008;167(2):188192.
26. Roos E, Ovaskainen M-L, Pietinen P. Validity and
comparison of three saturated fat indices. Scand J Nutr.
1995;39:5559.
27. Swithers SE, Davidson TL. A role for sweet taste:
calorie predictive relations in energy regulation by rats.
Behav Neurosci. 2008;122(1):161173.
28. Malik VS, Schulze MB, Hu FB. Intake of sugar-
sweetened beverages and weight gain: a systematic
review. Am J Clin Nutr. 2006;84(2):274288.
29. Aarnio M, Winter T, Peltonen J, Kujala UM, Kaprio J.
Stability of leisure-time physical activity during
adolescencea longitudinal study among 16-, 17- and
18-year-old Finnish youth. Scand J Med Sci Sports.
2002;12(3):179185.
30. Classification of Socio-economic Groups 1989.
Helsinki: Helsinki Handbooks, Statistics Finland; 1989.
31. STATA Users Guide Release 9.1. 8. College Station,
TX: Stata Press; 2005.
32. Laaksonen M, Rahkonen O, Karvonen S, Lahelma E.
Socioeconomic status and smoking: analysing inequalities
with multiple indicators. Eur J Public Health. 2005;15(3):
262269.
33. Boomsma D, Busjahn A, Peltonen L. Classical twin
studies and beyond. Nat Rev Genet. 2002;3(11):872882.
34. Bernaards CM, Twisk JW, Snel J, van Mechelen W,
Kemper HC. In a prospective study in young people,
associations between changes in smoking behavior and
risk factors for cardiovascular disease were complex.
J Clin Epidemiol. 2005;58(11):11651171.
35. Laitinen J, Nayha S, Kujala V. Body mass index and
weight change from adolescence into adulthood, waist-to-
hip ratio and perceived work ability among young adults.
Int J Obes (Lond). 2005;29(6):697702.
36. Potter BK, Pederson LL, Chan SS, Aubut JA,
Koval JJ. Does a relationship exist between body
weight, concerns about weight, and smoking among
adolescents? An integration of the literature with
an emphasis on gender. Nicotine Tob Res. 2004;6(3):
397425.
37. Weitzman M, Cook S, Auinger P, et al. Tobacco
smoke exposure is associated with the metabolic syn-
drome in adolescents. Circulation. 2005;112(6):
862869.
38. Cooper TV, Klesges RC, Robinson LA, Zbikowski
SM. A prospective evaluation of the relationships be-
tween smoking dosage and body mass index in an
adolescent, biracial cohort. Addict Behav. 2003;28(3):
501512.
39. Kvaavik E, Tell GS, Klepp KI. Predictors and
tracking of body mass index from adolescence into
American Journal of Public Health | February 2009, Vol 99, No. 2
adulthood: follow-up of 18 to 20 years in the Oslo
Youth Study. Arch Pediatr Adolesc Med. 2003;157(12):
12121218.
40. Pierce JP. International comparisons of trends in
cigarette smoking prevalence. Am J Public Health.
1989;79(2):152157.
41. Saarni SE, Silventoinen K, Rissanen A, Sarlio-
Lahteenkorva S, Kaprio J. Intentional weight loss and
smoking in young adults. Int J Obes Relat Metab Disord.
2004;28(6):796802.
42. Green MP, McCausland KL, Xiao H, Duke JC,
Vallone DM, Healton CG. A closer look at smoking
among young adults: where tobacco control should
focus its attention. Am J Public Health. 2007;97(8):
14271433.
43. Escobedo LG, Marcus SE, Holtzman D, Giovino GA.
Sports participation, age at smoking initiation, and the risk
of smoking among US high school students. JAMA.
1993;269(11):13911395.
44. Rohleder N, Kirschbaum C. The hypothalamic-
pituitary-adrenal (HPA) axis in habitual smokers. Int J
Psychophysiol. 2006;59(3):236243.
45. Cohen S, Doyle WJ, Baum A. Socioeconomic status
is associated with stress hormones. Psychosom Med.
2006;68(3):414420.
46. Lahiri K, Rettig-Ewen V, Bohm M, Laufs U. Per-
ceived psychosocial stress and cardiovascular risk factors
in obese and non-obese patients. Clin Res Cardiol.
2007;96(6):365374.
47. Bjorntorp P, Rosmond R. Obesity and cortisol.
Nutrition. 2000;16(10):924936.
48. Bjorntorp P. Do stress reactions cause abdominal
obesity and comorbidities? Obes Rev. 2001;2(2):7386.
49. Maurer J, Taren DL, Teixeira PJ, et al. The psycho-
social and behavioral characteristics related to energy
misreporting. Nutr Rev. 2006;64(2 Pt 1):5366.
50. Schousboe K, Willemsen G, Kyvik KO, et al. Sex
differences in heritability of BMI: a comparative study of
results from twin studies in eight countries. Twin Res.
2003;6(5):409421.
51. Vartiainen E, Seppala T, Lillsunde P, Puska P.
Validation of self reported smoking by serum cotinine
measurement in a community-based study. J Epidemiol
Community Health. 2002;56(3):167170.
52. Rasmussen F, Johansson M, Hansen HO. Trends in
overweight and obesity among 18-year-old males in
Sweden between 1971 and 1995. Acta Paediatr.
1999;88(4):431437.
53. Pietilainen KH, Kaprio J, Rissanen A, et al. Distri-
bution and heritability of BMI in Finnish adolescents
aged 16y and 17y: a study of 4884 twins and 2509
singletons. Int J Obes Relat Metab Disord. 1999;23(2):
107115.
54. Fulkerson JA, French SA. Cigarette smoking for
weight loss or control among adolescents: gender and
racial/ethnic differences. J Adolesc Health. 2003;32(4):
306313.
55. Manson JE, Ajani UA, Liu S, Nathan DM, Hennekens
CH. A prospective study of cigarette smoking and the
incidence of diabetes mellitus among US male physicians.
Am J Med. 2000;109(7):538542.
56. Mokdad AH, Marks JS, Stroup DF, Gerberding JL.
Actual causes of death in the United States, 2000. JAMA.
2004;291(10):12381245.