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Both overweight or obesity and cigarette smoking are relevant risk factors for public health. Cigarette smoking is associated with lower body weight while smoking cessation is associated with weight gain. Most smokers who quit experience a weight gain, particularly within one year, and it may persist up to 8 years after smoking cessation. However, only a minority of quitters gain excessive weight. Some individual characteristics have been found to be associated with excessive weight gain after smoking cessation while methodological problems may affect estimates of weight gain observed in different studies. Main mechanisms to explain weight gain after smoking cessation include increased energy intake, decreased resting metabolic rate, and decreased physical activity. The health benefits of smoking cessation far exceed any health risks that may result from smoking cessation-induced body weight gain. As weight gain may be a barrier against quitting smoking or a reason to restart smoking, behavioural and pharmacological methods have been evaluated to control weight gain after smoking cessation. Physicians should apply efficient strategies to promote smoking cessation on their weight-concerned smoking patient. This review briefly addresses some issues on the relationship between smoking cessation and weight gain, with regard to the size of the problem, mechanisms, health risks and control strategies.
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Monaldi Arch Chest Dis
2009; 71: 2, 81-87 TOBACCO POUCH
Weight Gain after Smoking Cessation
F. Pistelli1,2, F. Aquilini1, L. Carrozzi1,2
Introduction
Both overweight or obesity and cigarette smok-
ing are relevant risk factors for public health, being
associated with an increased risk of death [1, 2].
Epidemiological data indicates that the prevalence
of overweight and obesity has doubled or tripled in
the past few decades in the US, in Europe, and even
in many developing countries [3]. According to es-
timates from the National Health and Nutrition Ex-
amination Survey (NHANES), a nationally repre-
sentative sample of the US population, in 2003-
2004 the prevalence of overweight or obesity
(Body Mass Index (BMI) 25 kg/m2) in adults
aged 20 years or older was 66.3% [4].
Cigarette smoking is associated with lower
body weight while smoking cessation is associated
with weight gain [5-8]. Weight gain may be a bar-
rier against quitting smoking, a reason to restart
smoking or a risk for health problems. This review
briefly addresses some issues on the relationship
between smoking cessation and weight gain, with
regard to the size of the problem, mechanisms,
health risks and control strategies.
The size of the problem
Amount of weight gain and likelihood of gaining
weight after smoking cessation
In 1990, the US Surgeon General published a
landmark report on The Health Benefits of Smok-
ing Cessation, which included a chapter on smok-
ing cessation and body weight change [6]. Based
on 15 longitudinal studies conducted between
1970-1990, with a median follow-up of 2 years
and an average sample size of 1348 subjects, the
average weight gain after smoking cessation was
about 2.3 kg, ranging between 0.74 and 5.15 kg.
Overall, in five reviewed studies, the risk of
weight gain after cessation was 45% (mean l.45,
range 1.31-1.75) greater for quitter than for con-
tinuing smokers. The report concluded that ap-
proximately 80% of smokers who quit gain weight
after cessation, but only about 3.5% of those who
quit smoking gain more than 9 kg [6].
Data from the third NHANES study [7], con-
ducted from 1988 through 1991, has shown that
the weight gain among smokers who quit that was
in excess of the gain among continuing smokers
was 4.4 kg for men and 5.0 kg for women over a
10-year period. 16% of the men and 21% of the
women who had quit smoking within the past 10
years gained 15 kg or more. Quitters were signifi-
cantly more likely to become overweight than
those who had never smoked (OR 2.42, 95% C.I.
1.02–5.775 for men, and OR 2.02, 95% C.I. 1.04-
3.94 for women).
Among participants in the Lung Health Study
[8], a randomised clinical trial of smoking cessa-
tion on middle-aged volunteers with asymptomatic
airway obstruction, men who achieved sustained
quitting for 5 years gained a mean of 4.9 kg in the
first year and a mean of 2.6 kg over the 5-year fol-
Key words: Smoking cessation, Weight gain, Body mass index, Nicotine withdrawal symptoms, Gender-related differences.
1UO Pneumologia e Fisiopatologia Respiratoria 1 Universitaria, Dipartimento Cardiotoracico, Azienda Ospedaliero-
Universitaria Pisana, Pisa,
2Unità di Epidemiologia Ambientale Polmonare, Istituto di Fisiologia Clinica CNR, Pisa, Italy.
Correspondence: Francesco Pistelli, Unità di Epidemiologia Ambientale Polmonare, Istituto di Fisiologia Clinica CNR, Via
Trieste 41, 56126 Pisa, Italy; e-mail francesco.pistelli@ifc.cnr.it
ABSTRACT: Weight Gain after Smoking Cessation. F. Pistelli,
F. Aquilini, L. Carrozzi.
Both overweight or obesity and cigarette smoking are
relevant risk factors for public health. Cigarette smoking is
associated with lower body weight while smoking cessation
is associated with weight gain. Most smokers who quit ex-
perience a weight gain, particularly within one year, and it
may persist up to 8 years after smoking cessation. Howev-
er, only a minority of quitters gain excessive weight. Some
individual characteristics have been found to be associated
with excessive weight gain after smoking cessation while
methodological problems may affect estimates of weight
gain observed in different studies. Main mechanisms to ex-
plain weight gain after smoking cessation include increased
energy intake, decreased resting metabolic rate, and de-
creased physical activity. The health benefits of smoking
cessation far exceed any health risks that may result from
smoking cessation-induced body weight gain. As weight
gain may be a barrier against quitting smoking or a reason
to restart smoking, behavioural and pharmacological
methods have been evaluated to control weight gain after
smoking cessation. Physicians should apply efficient strate-
gies to promote smoking cessation on their weight-con-
cerned smoking patient. This review briefly addresses
some issues on the relationship between smoking cessation
and weight gain, with regard to the size of the problem,
mechanisms, health risks and control strategies.
Monaldi Arch Chest Dis 2009; 71: 2, 81-87.
82
F. PISTELLI ET AL.
low-up, while corresponding figures for women
were 5.2 kg and 3.4 kg, respectively. Also, among
sustained quitters, 7.6% of men and 19.1% of
women gained 20% of baseline weight; 60% of
the gain occurred in year 1, although significant
weight gains continued through year 5. Over one
third of those who sustained smoking cessation for
5 years gained > 10 kg.
In a sample of 7124 residents of Germany aged
18-79 years from a national health examination
survey [5], adjusted OR of the risk for former
(> 12 months) smokers of 20 cigarettes per day to
become overweight (BMI 25 kg/m2) or obese
(BMI 30 kg/m2) was 1.7 and 2.3 in males, and
1.4 and 1.1 in females, respectively, as compared
to never smokers. The proportions of overweight
or obesity ranged from 78.7 to 91.1% and from
51.9 to 64.3% among male and female former
smokers, respectively, depending on the number of
cigarettes smoked per day.
The mean increase in waist circumference after
smoking cessation has been reported in a popula-
tion-based study in Copenhagen: an increase 5 cm
was observed in 42% of the quitters, and it was 3.88
cm (± 5.4 cm) higher in females than in males [9].
With regard to the trend over time, evidence
suggests that weight gain is greater within one year
[8] and even in the 1-2 months following cessation
[10]. In the long term, population-based data from
the third NHANES study showed that quitters
within the past 10 years prior the examination
were significantly more likely than never smokers
to remain overweight (OR 1.50, 95% C.I. 0.47-
4.85 for men, and OR 1.45, 95% C.I. 0.54-3.92 for
women) [7]. In a cohort (n = 1532) of treatment-
seeking heavy smokers (15 cigarettes per day)
participating in a double-blind randomised place-
bo-controlled trial with nicotine transdermal patch,
an increase in BMI (2.5 kg/m2more on average vs.
baseline) persisted up to 8 years after smoking ces-
sation [11]. In a cross-sectional study, it was ob-
served that heavy smokers (25 cigarettes per
day), after experiencing large weight gain in the
few years after smoking cessation, thereafter lose
weight to the never smoker level, while light and
moderate smokers gain weight up to the never-
smoker level without any excess after smoking
cessation [12].
Methodological issues
We selected relevant references on weight gain
after smoking cessation by using the PubMed
searching engine of the United States National Li-
brary of Medicine and the National Institutes of
Health (URL: www.pubmed.org). A manual
search starting from selected references was also
performed. No systematic selection procedure was
applied. Those large, population-based, longitudi-
nal studies or large clinical trials from United
States and Europe were preferably selected.
In order to correctly interpret data on weight
gain after smoking cessation, some general
methodological issues should be taken into ac-
count. The magnitude of the weight gain varies ac-
cording to the study population, while it could al-
so be related to the increase of weight observed in
the general population. There are few studies de-
signed specifically to assess the effect of smoking
cessation on weight gain prospectively. Existing
studies may have methodological problems, in-
cluding limited follow-up periods, the use of self-
reported height and weight, failure to biochemical-
ly validate smoking status, and a tendency to re-
port point prevalence instead of continuous absti-
nence.
Characteristics associated with excessive weight
gain after smoking cessation
Smokers gaining excessive weight after smok-
ing cessation may differ from those who do not
gain weight. Several individual characteristics
should be considered, including gender, age, race,
number of cigarettes smoked per day before cessa-
tion, weight history, comorbidity, life styles such
as eating patterns and physical activity, or con-
cerns about post-cessation weight gain.
Subjects younger than 55 years old, smokers of
25 cigarettes per day, and those with low socio-
economic status has been associated to higher
weight gain [10, 13, 14]. Most studies report that
women tend to gain more weight than men [7-9,
14], but in other studies an opposite figure has
been found [5, 15]. Longitudinal data from the Na-
tional Academy of Sciences-National Research
Council Twin Registry [14] has shown that weight
change was significantly greater in monozygotic
than dizygotic pairs in which both twins quit
smoking, suggesting that underlying genetic fac-
tors may influence weight changes. In this study,
super-gainers were significantly younger, with a
lower socio-economic status, and differed on a
number of health habits before quitting, including
physical activity, alcohol consumption and other
diet habit.
Mechanisms
Although there is convincing evidence for the
association between smoking and lower body
weight, underlying mechanisms are not clear.
Nicotine may be involved in feeding behaviour by
influencing the levels and expression of many pep-
tide hormones and neurotransmitters, including
leptin (negative regulator of food intake and a pos-
itive regulator of energy expenditure), neuropep-
tide Y (stimulator of feeding), orexins (positive
regulators of food intake), noradrenaline (stimula-
tor of food ingestion), dopamine and serotonin (in-
hibitors of food ingestion) [16].
Effects of cigarette smoking on adipose tissue
metabolism have also been evaluated. It has been
observed that fat oxidation increases with increas-
ing nicotine uptake [17] and smoking cessation is
associated with increases in lipoprotein lipase ac-
tivity in adipose tissue, which contribute to weight
gain after smoking cessation [18]. On the other
hand, it has been shown that cigarette smoking
stimulates lipolysis without increasing oxidation
83
WEIGHT GAIN AFTER SMOKING
of fat and that smoking cessation does not result in
a rebound tendency to synthesis or storage of fat,
both under controlled eucaloric dietary conditions
[19] and even in the presence of positive short-
term energy balance [20].
Main mechanisms that have been evaluated to
explain weight gain after smoking cessation in-
clude increased energy intake, decreased resting
metabolic rate, and decreased physical activity.
However, it has been also observed that lower
BMI of smokers compared to non-smokers re-
flects the personality characteristics of those who
choose to smoke and that the tendency to gain
weight after smoking cessation may have behav-
ioural rather than tobacco-related pharmacologi-
cal explanations [21]. Further research is needed
in this field.
Increases in food intake and decreases in rest-
ing energy expenditure are largely responsible for
weight gain after smoking cessation, while change
in physical activity does not play a role in either
differences in body weight between smokers and
nonsmokers or the weight gain associated with
smoking cessation [6]. Among studies reviewed in
the 1990 Surgeon General report, large individual
differences in subjects’ dietary and metabolic
changes after smoking cessation were demonstrat-
ed. Most short-term evaluations (e.g. 3 days or
less) found that food intake, particularly the con-
sumption of sweet foods and simple carbohy-
drates, increases after smoking cessation. Prospec-
tive investigations found that both self-reported
and quantified food intake changes over time in-
creased among subjects after quitting. In a quoted
comprehensive evaluation of change in energy bal-
ance, analysing changes in food intake, physical
activity, and resting metabolic rate in 13 sedentary
females who quit smoking for 48 days, mean daily
food intake increased by 177 kcal and explained
69% of the variance in changes in weight (1.84
kg), while no changes in physical activity or rest-
ing metabolic rate were observed [22].
Even in subsequently published studies, con-
trasting results have been reported on decreased
resting metabolic rate as mechanisms partly ex-
plaining weight gain after smoking cessation, with
the mean resting metabolic rate reduction ranging
between 4% and 16% and accounting for less than
40% of the weight gain [16]. In a clinical trial that
monitored dietary intake and had biochemically
validated smoking status over 5 years (Multiple
Risk Factor Intervention Trial), weight gain con-
tinued after quitting smoking despite decreases in
caloric intake [23].
Changes in weight-related health risks
after smoking cessation
The health benefits of smoking cessation far
exceed any health risks that may result from smok-
ing cessation-induced body weight gain. This af-
firmation has been initially supported by studies
demonstrating that individuals who quit smoking
and gain weight experienced relatively small
changes in health-related risk factors such as blood
pressure, serum cholesterol and blood glucose [6].
Indeed, some of the potentially adverse effects of
weight gain on health risks are mitigated by the re-
duction of the risk of cardiovascular problems. For
example, according to reviewed evidence [16], in
spite of the weight gain, smoking cessation seems
to improve insulin sensitivity and is associated
with an increase in high density lipoprotein cho-
lesterol, while it is associated with a gradual nor-
malisation of blood and plasma viscocities,
haematocrit, blood cell filter ability, plasma fib-
rinogen levels as well as total white cell count.
Only those smokers who have large weight gain
after smoking cessation would experience impor-
tant changes in weight related risk factors, and the
proportion of ex-smokers who gain large amounts
of weight (e.g. more than 10 kg) is small [6]. It
should be noted that these figures might be revisit-
ed over time, if it is taken into account that mean
BMI tends to increase in the general population.
Consistently with other longitudinal studies, in
an Italian general population sample, we showed
that weight gain over time affects lung function in-
dependently of age, occupational exposure and al-
so smoking habit reported at baseline [24, 25].
Those longitudinal studies that have assessed the
relation of change in lung function to smoking ces-
sation and change in BMI have shown that the
beneficial effect of smoking cessation outweighs
the adverse effect of weight gain [26-28]. For ex-
ample, according to estimates based on data from
the Lung Health Study, a person who quit smoking
would have to gain about 60 kg or 38 kg of weight
to have the same effect of 5 years changes in
forced expiratory volume in one second (FEV1) or
in forced vital capacity, respectively, as continuing
to smoke.
The net effect of both smoking cessation and
weight gain on lung function in a population-based
study has been evaluated among participants in the
European Community Respiratory Health Study
[29]. The authors found a similar net effect of
smoking cessation in men and women, but a
greater decline in lung function due to weight gain
in men: the FEV1changed by -11.5 mL (-13.3 to -
9.6) per kg of weight gained in men, and by -3.7
mL per kg (-5.0 to -2.5) in women, which dimin-
ished the benefit of quitting by 38% in men, and by
17% in women.
Control strategies
Smoking may be used as a means of weight
control, especially by younger adults [30], and
weight gain after smoking cessation is of concern
to many cigarette smokers, particularly women
[31, 32]. Even in the context of poor health and
limited physical functioning, smokers have been
found to be concerned about weight gain after
quitting [33]. There are several weight-related
smoking variables that characterise weight-con-
cerned smokers, including: importance of weight
as a factor in smoking initiation; smoking as a
weight control strategy; increased appetite and
weight gain as withdrawal symptoms; willingness
84
F. PISTELLI ET AL.
to quit to gain weight; self-efficacy about relapse
in the face of weight gain; readiness to quit smok-
ing; preoccupation with body image - rather than
weight gain [32, 34]. Also pregnant women who
are more concerned about post-cessation weight
gain may be less likely to quit smoking during
pregnancy or remain abstinent in the postpartum
period [35]. It has been also hypothesised that
weight gain and weight concerns are independent
factors, as daily smokers were found to be signif-
icantly less concerned about their weight than
never-smokers, and neither weight concerns nor
eating patterns were predictive of point abstinence
at 1-year follow-up, in a Danish general popula-
tion sample of more than 6000 adults aged 30-60
years [36].
Strategies that successfully moderate weight
gain after smoking cessation may encourage
weight-conscious smokers to attempt cessation
and may facilitate the efforts of successful quitters
to remain abstinent. Behavioural and pharmaco-
logical methods have been evaluated to reduce
weight gain after smoking cessation.
There is no convincing evidence that coun-
selling interventions specifically designed to miti-
gate weight gain during a quit attempt result in re-
duced weight gain [37, 38], and smoking cessation
programmes that include a weight control compo-
nent have not successfully increased smoking ces-
sation [6]. Also, simultaneously dieting and quit-
ting has been observed to undermine attempts to
quit smoking [39, 40]. A different approach, i.e. to
combat the weight concerns themselves rather than
the weight gain, has been shown to be efficient. In
a group of weight-concerned women, cognitive-be-
havioural therapy to reduce weight concern while
discouraging dieting improved smoking cessation
outcome compared to a behavioural weight control
programme to prevent weight gain [41]. In obser-
vational studies [42] and randomised trials [43] it
has been observed that physical activity at the time
of smoking cessation can lessen the weight gain as-
sociated with quitting. Evidence suggests that rela-
tively small doses of exercise should be recom-
mended also as an aid to managing cigarette crav-
ings and withdrawal symptoms [44].
With regard to the pharmacological methods,
according to 2008 update of US Guidelines on
Treating Tobacco Use and Dependence, for smok-
ers who are greatly concerned about weight gain, it
may be most appropriate to prescribe or recom-
mend bupropion SR or nicotine replacement ther-
apy (NRT) (in particular, nicotine gum 4 mg and
nicotine lozenge 4 mg), which have been shown to
delay weight gain after quitting (strength of evi-
dence B) [45].
A number of other pharmacological approach-
es have been evaluated. In three studies satisfying
criteria for a Cochrane systematic review was
found that Rimonabant 20 mg, a selective type 1
cannabinoid receptor antagonist, may increase the
odds of quitting approximately 1(1/2)-fold and
moderate weight gain in the long term [46]. Pre-
liminary results suggest that combining naltrexone
and bupropion may help minimise post-cessation
weight gain [47]. Some evidence has shown that
weight gain can be minimised to some degree by
serotoninergic drugs such as fluoxetine [48, 49].
From a clinical viewpoint, the physician
should neither deny the likelihood of weight gain
nor minimise its significance to the patient. Rather,
the physician should inform the patient about the
likelihood of weight gain and prepare the patient
for its occurrence. Clinician statements to help a
patient prepare for and cope with weight gain after
quitting recommended in the 2008 update Guide-
lines on Treating Tobacco Use and Dependence
are reported in table 1 [45].
The experience of the Smoking Cessation
Clinic of the University Hospital of Pisa (Italy)
As an example of what can be observed in the
real life of a clinical routine, we present some da-
ta on weight gain observed in smokers following a
physician-assisted smoking cessation programme
within the Smoking Cessation Centre of the Uni-
versity Hospital of Pisa (Italy). This is a clinic op-
Table 1. - Clinician statements to help a patient prepare for and cope with weight gain after smoking cessation.
From 2008 update Guidelines on Treating Tobacco Use and Dependence [45]
The great majority of smokers gain weight once they quit smoking. However, even without special attempts at dieting or
exercise, weight gain is usually 4.5 kg or less.
Some medications, including bupropion SR and nicotine replacement medicines, may delay weight gain.
There is evidence that smokers often gain weight once they quit smoking, even if they do not eat more. However, there are
medications that will help you quit smoking and limit or delay weight gain. I can recommend one for you.
The amount of weight you will likely gain from quitting will be a minor health risk compared with the risks of continued
smoking.
I know that you don’t want to gain a lot of weight. However, let’s focus on strategies to get you healthy rather than on weight.
Think about eating plenty of fruits and vegetables, getting regular exercise, getting enough sleep, and avoiding high-calorie
foods and beverages. Right now, this is probably the best thing you can do for both your weight and your health.
Although you may gain some weight after quitting smoking, compare the importance of this with the added years of healthy
living you will gain, your better appearance (less wrinkled skin, whiter teeth, fresher breath), and good feelings about quitting.
85
WEIGHT GAIN AFTER SMOKING
erating in a Respiratory Unit since 1994, where
controlled clinical trials, interventions on specific
groups of smokers (e.g. participants in a lung can-
cer screening project, pregnant women, etc.), and
routine interventions are carried out [50-57].
Briefly, pneumologists conduct a programme
based on individual counselling and prescription
of pharmacotherapy (NRT - in the form transder-
mal patches, lozenges, inhalers or gums - Vareni-
cline or Bupropion, separately or in various asso-
ciations). Five visits are scheduled in the first three
months after a baseline evaluation, and follow-up
visits are planned at 6 and 12 months.
We analysed data provided by 1765 smokers
(1025 males and 740 females) who underwent to a
smoking cessation programme between January
2001 and May 2007. Figure 1 shows the percent-
age change of BMI from baseline observed at var-
ious follow-up visits over 12 months in smokers
continuously abstinent from their target quit day.
Both in males and females a higher change in BMI
was observed starting from one-month follow-up
visit and continued up to 12 months. The distinc-
tion between males and female were not statisti-
cally different. Even those smokers who had been
abstinent for a certain period showed a change in
BMI significantly higher than those who had been
never abstinent. For example, at the fourth control
visit (70-140 days from baseline), the percentage
change in BMI was 2.93% in those male smokers
who had been continuously abstinent up to the
control visit while it was 1.55% in those who had
been continuously abstinent less than 70 days; the
corresponding figures for female smokers were
3.73 and 1.58%. Gaining weight after smoking
cessation was significantly related to the duration
of continuous abstinence (about 90 gr per each
week of abstinence, p< 0.001) and the number of
cigarettes smoked per day at baseline (about 37 gr
per each cigarette smoked per day, p= 0.002) but
not to the age of the smoker. The mean absolute
gain in weight observed in this study population of
smokers was 0.42, 1.43, 3.66, and 4.08 kg at 1
week, 1 month, 6 month and 12 months control
visit, respectively, ranging from to a minimum of
–6.20 to a maximum of 17.0 kg. Only 6% of smok-
ers continuously abstinent over 12 months gained
more than 10 kg.
Conclusions
Weight gain after smoking cessation is expect-
ed, but only a minority of quitters experience ex-
cessive weight gain. In our experience, the mean
absolute weight gain was 4 kg after 12 months of
continuous abstinence from smoking. Altogether,
the health benefits of smoking cessation far exceed
any health risk that may result from weight gain.
Physicians should intervene on their weight-con-
cerned smoking patients to promote smoking ces-
sation by offering both behavioural and pharmaco-
logical support. Thus, avoiding weight gain would
not only remove a barrier to cessation, but also al-
low for greater health benefits.
References
1. Adams KF, Schatzkin A, Harris TB, et al. Overweight,
obesity, and mortality in a large prospective cohort of
persons 50 to 71 years old. N Engl J Med 2006; 355:
763-778.
2. U.S. Department of Health and Human Services. The
Health Consequences of Smoking: A Report of the Sur-
geon General. Atlanta, GA: U.S. Department of Health
and Human Services, Centers for Disease Control and
Fig. 1. - Percentage change of BMI from baseline observed at various follow-up visits over 12 months in male and female smokers continuously
abstinent from their target quit day. Data from the Smoking Cessation Centre of the University Hospital of Pisa (Italy).
BMI = body mass index (kg/m2). BMI % change from baseline was computed as follows: (BMI at follow-up – BMI at baseline) / BMI at baseline
x 100. The control visits were performed in the following follow-up periods: 1 week = between 7-12 days from baseline; 2 weeks = 13-19 days; 1
month = 20-69 days; 3 months = 70-140 days; 6 months = 141-299 days; 12 months = >300 days.
86
F. PISTELLI ET AL.
Prevention, National Center for Chronic Disease Pre-
vention and Health Promotion, Office on Smoking and
Health, 2004.
3. International Association for the Study of Obesity.
www.iotf.org. Accessed: January 2009.
4. Ogden CL, Carroll MD, Curtin LR, McDowell MA,
Tabak CJ and Flegal KM. Prevalence of overweight and
obesity in the United States, 1999-2004. JAMA 2006;
295: 1549-1555.
5. John U, Hanke M, Rumpf HJ and Thyrian JR. Smoking
status, cigarettes per day, and their relationship to over-
weight and obesity among former and current smokers
in a national adult general population sample. Int J
Obes (Lond) 2005; 29: 1289-1294.
6. U.S. Department of Health and Human Services. The
Health Benefits of Smoking Cessation. U.S. Depart-
ment of Health and Human Services. Public Health Ser-
vice. Centers for Disease Control. Center for Chronic
Disease Prevention and Health Promotion. Office on
Smoking and Health. DHHS Publication No. (CDC)
90-8416, 1990.
7. Flegal KM, Troiano RP, Pamuk ER, Kuczmarski RJ
and Campbell SM. The influence of smoking cessation
on the prevalence of overweight in the United States. N
Engl J Med 1995; 333: 1165-1170.
8. O’Hara P, Connett JE, Lee WW, Nides M, Murray R
and Wise R. Early and late weight gain following smok-
ing cessation in the Lung Health Study. Am J Epidemi-
ol 1998; 148: 821-830.
9. Pisinger C and Jorgensen T. Waist circumference and
weight following smoking cessation in a general popu-
lation: the Inter99 study. Prev Med 2007; 44: 290-295.
10. Klesges RC, Winders SE, Meyers AW, et al. How
much weight gain occurs following smoking cessation?
A comparison of weight gain using both continuous and
point prevalence abstinence. J Consult Clin Psychol
1997; 65: 286-291.
11. Munafo MR, Murphy MF and Johnstone EC. Smoking
cessation, weight gain, and DRD4 -521 genotype. Am J
Med Genet B Neuropsychiatr Genet 2006; 141B: 398-
402.
12. Mizoue T, Ueda R, Tokui N, Hino Y and Yoshimura T.
Body mass decrease after initial gain following smok-
ing cessation. Int J Epidemiol 1998; 27: 984-988.
13. Williamson DF, Madans J, Anda RF, Kleinman JC,
Giovino GA and Byers T. Smoking cessation and
severity of weight gain in a national cohort. N Engl J
Med 1991; 324: 739-745.
14. Swan GE and Carmelli D. Characteristics associated
with excessive weight gain after smoking cessation in
men. Am J Public Health 1995; 85: 73-77.
15. Bartholomew HC and Knuiman MW. Longitudinal
analysis of the effect of smoking cessation on cardio-
vascular risk factors in a community sample: the Bus-
selton Study. J Cardiovasc Risk 1998; 5: 263-271.
16. Filozof C, Fernandez Pinilla MC and Fernandez-Cruz
A. Smoking cessation and weight gain. Obes Rev 2004;
5: 95-103.
17. Jensen EX, Fusch C, Jaeger P, Peheim E and Horber
FF. Impact of chronic cigarette smoking on body com-
position and fuel metabolism. J Clin Endocrinol Metab
1995; 80: 2181-2185.
18. Ferrara CM, Kumar M, Nicklas B, McCrone S and
Goldberg AP. Weight gain and adipose tissue metabo-
lism after smoking cessation in women. Int J Obes Re-
lat Metab Disord 2001; 25: 1322-1326.
19. Hellerstein MK, Benowitz NL, Neese RA, et al. Effects
of cigarette smoking and its cessation on lipid metabo-
lism and energy expenditure in heavy smokers. J Clin
Invest 1994; 93: 265-272.
20. Neese RA, Benowitz NL, Hoh R, et al. Metabolic in-
teractions between surplus dietary energy intake and
cigarette smoking or its cessation. Am J Physiol 1994;
267: E1023-1034.
21. Bamia C, Trichopoulou A, Lenas D and 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: 1091-1096.
22. Stamford BA, Matter S, Fell RD and Papanek P. Effects
of smoking cessation on weight gain, metabolic rate,
caloric consumption, and blood lipids. Am J Clin Nutr
1986; 43: 486-494.
23. Stamler J, Rains-Clearman D, Lenz-Litzow K, Tillot-
son JL and Grandits GA. Relation of smoking at base-
line and during trial years 1-6 to food and nutrient in-
takes and weight in the special intervention and usual
care groups in the Multiple Risk Factor Intervention
Trial. Am J Clin Nutr 1997; 65: 374S-402S.
24. Bottai M, Pistelli F, Di Pede F, et al. Longitudinal
changes of body mass index, spirometry and diffusion in
a general population. Eur Respir J 2002; 20: 665-673.
25. Pistelli F, Bottai M, Carrozzi L, et al. Changes in obe-
sity status and lung function decline in a general popu-
lation sample. Respir Med 2008; 102: 674-680.
26. Carey IM, Cook DG and Strachan DP. The effects of
adiposity and weight change on forced expiratory vol-
ume decline in a longitudinal study of adults. Int J Obes
Relat Metab Disord 1999; 23: 979-985.
27. Wang ML, McCabe L, Hankinson JL, et al. Longitudi-
nal and cross-sectional analyses of lung function in
steelworkers. Am J Respir Crit Care Med 1996; 153:
1907-1913.
28. Wise RA, Enright PL, Connett JE, et al. Effect of
weight gain on pulmonary function after smoking ces-
sation in the Lung Health Study. Am J Respir Crit Care
Med 1998; 157: 866-872.
29. Chinn S, Jarvis D, Melotti R, et al. Smoking cessation,
lung function, and weight gain: a follow-up study.
Lancet 2005; 365: 1629-1635; discussion 1600-1621.
30. Wee CC, Rigotti NA, Davis RB and Phillips RS. Rela-
tionship Between Smoking and Weight Control Efforts
Among Adults in the United States. Arch Intern Med
2001; 161: 546-550.
31. Borrelli B, Spring B, Niaura R, Hitsman B and Papan-
donatos G. Influences of gender and weight gain on
short-term relapse to smoking in a cessation trial. J
Consult Clin Psychol 2001; 69: 511-515.
32. Pomerleau CS and Saules K. Body image, body satis-
faction, and eating patterns in normal-weight and over-
weight/obese women current smokers and never-smok-
ers. Addict Behav 2007; 32: 2329-2334.
33. Sepinwall D and Borrelli B. Older, medically ill smok-
ers are concerned about weight gain after quitting
smoking. Addict Behav 2004; 29: 1809-1819.
34. Pomerleau CS, Zucker AN and Stewart AJ. Character-
izing concerns about post-cessation weight gain: results
from a national survey of women smokers. Nicotine
Tob Res 2001; 3: 51-60.
35. Berg CJ, Park ER, Chang Y and Rigotti NA. Is concern
about post-cessation weight gain a barrier to smoking
cessation among pregnant women? Nicotine Tob Res
2008; 10: 1159-1163.
36. Pisinger C and Jorgensen T. Weight concerns and
smoking in a general population: the Inter99 study.
Prev Med 2007; 44: 283-289.
37. Copeland AL, Martin PD, Geiselman PJ, Rash CJ and
Kendzor DE. Smoking cessation for weight-concerned
women: group vs. individually tailored, dietary, and
weight-control follow-up sessions. Addict Behav 2006;
31: 115-127.
38. Alberg AJ, Carter CL and Carpenter MJ. Weight gain
as an impediment to cigarette smoking cessation: a lin-
gering problem in need of solutions. Prev Med 2007;
44: 296-297.
87
WEIGHT GAIN AFTER SMOKING
39. Perkins K. Issues in the prevention of weight gain after
smoking cessation. Ann Behav Med 1994; 16: 46-52.
40. Hall S, Tunstall C, Vila K and Duffy J. Weight gain
prevention and smoking cessation: cautionary findings.
Am J Public Health 1992; 82: 799-803.
41. Perkins KA, Marcus MD, Levine MD, et al. Cognitive-
behavioral therapy to reduce weight concerns improves
smoking cessation outcome in weight-concerned
women. J Consult Clin Psychol 2001; 69: 604-613.
42. Kawachi I, Troisi RJ, Rotnitzky AG, Coakley EH and
Colditz GA. Can physical activity minimize weight
gain in women after smoking cessation? Am J Public
Health 1996; 86: 999-1004.
43. Marcus BH, Albrecht AE, King TK, et al. The efficacy
of exercise as an aid for smoking cessation in women: a
randomized controlled trial. Arch Intern Med 1999;
159: 1229-1234.
44. Taylor AH, Ussher MH and Faulkner G. The acute ef-
fects of exercise on cigarette cravings, withdrawal
symptoms, affect and smoking behaviour: a systematic
review. Addiction 2007; 102: 534-543.
45. Fiore MC, Jaén CR, Baker TB and et al. Treating To-
bacco Use and Dependence: 2008 Update. Clinical
Practice Guideline. Rockville, MD: U.S. Department of
Health and Human Services. Public Health Service.
May 2008, 2008.
46. Cahill K and Ussher M. Cannabinoid type 1 receptor
antagonists (rimonabant) for smoking cessation.
Cochrane Database Syst Rev 2007: CD005353.
47. Toll BA, Leary V, Wu R, Salovey P, Meandzija B and
O’Malley SS. A preliminary investigation of naltrexone
augmentation of bupropion to stop smoking with less
weight gain. Addict Behav 2008; 33: 173-179.
48. Spring B, Wurtman J, Wurtman R, et al. Efficacies of
dexfenfluramine and fluoxetine in preventing weight
gain after smoking cessation. Am J Clin Nutr 1995; 62:
1181-1187.
49. Borrelli B, Spring B, Niaura R, Kristeller J, Ockene JK
and Keuthen NJ. Weight suppression and weight re-
bound in ex-smokers treated with fluoxetine. J Consult
Clin Psychol 1999; 67: 124-131.
50. Paoletti P, Tonnesen P and Rodriguez-Roisin R.
CEASE (Collaborative European Anti-Smoking Evalu-
ation). A challenging multicenter trial organized by the
European Respiratory Society. Chest 1993; 103: 1317-
1319.
51. Paoletti P, Fornai E, Maggiorelli F, et al. Importance of
baseline cotinine plasma values in smoking cessation:
results from a double-blind study with nicotine patch.
Eur Respir J 1996; 9: 643-651.
52. Tonnesen P, Paoletti P, Gustavsson G, et al. Higher
dosage nicotine patches increase one-year smoking ces-
sation rates: results from the European CEASE trial.
Collaborative European Anti-Smoking Evaluation. Eu-
ropean Respiratory Society. Eur Respir J 1999; 13:
238-246.
53. Carrozzi L, Pistelli F, Fornai E, Desideri M, Viegi G
and Giuntini C. Smoking cessation clinic: an Italian ex-
perience. Monaldi Arch Chest Dis 2000; 55: 502-505.
54. Carrozzi L, Pistelli F and Viegi G. Pharmacotherapy for
smoking cessation. Ther Adv Respir Dis 2008; 2: 301-
317.
55. Pistelli F, Aquilini F, Tavanti L, et al. Smoking cessa-
tion over the first year of follow-up in a lung cancer
screening with spiral chest CT scan (Italung_CT study).
Eur Respir J 2007; 30 (suppl. 51).
56. Cosci F, Corlando A, Fornai E, Pistelli F, Paoletti P and
Carrozzi L. Nicotine dependence, psychological dis-
tress and personality traits as possible predictors of
smoking cessation. Results of a double-blind study with
nicotine patch. Addict Behav 2008.
57. Cosci F, Schruers KR, Pistelli F and Griez EJ. Negative
affectivity in smokers applying to smoking cessation clin-
ics: a case-control study. Depress Anxiety 2008; 0: 1-7.
Pavia - Almo Collegio Borromeo
... Smoking is related to obesity, and various association analyses between smoking and obesity-related traits have been conducted. Typically, smoking is associated with weight loss [13,14,[20][21][22]. Previous studies have reported that nicotine causes weight loss by increasing energy expenditure and insulin resistance, as well as reducing appetite and insulin sensitivity [13,20]. ...
... However, smoking increases the waist circumference, WHR, and abdominal and visceral fat [15,23,24]. Moreover, former smokers tend to increase in body weight and subcutaneous fat for 1-8 years after smoking cessation; however, most of them do not gain excessive weight, and their average BMIs tend to be similar to those of nonsmokers [14,20,21,25,26]. Thus, smoking is a complex environmental factor affecting obesity and obesity-related traits, and more accurate information can be obtained about its effects by identifying genes and pathways that interact with smoking. ...
... Waist circumference and WHR were analyzed with adjustment for BMI using residuals from linear regression. We defined the smoking status as current smoker and current nonsmoker [30] because former smokers and never smokers tend to have a similar trend of obesity [21,26]. ...
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Introduction: Although many studies have investigated the association between smoking and obesity, very few have analyzed how obesity traits are affected by interactions between genetic factors and smoking. Here, we aimed to identify the loci that affect obesity traits via smoking status-related interactions in European samples. Methods: We performed stratified analysis based on the smoking status using both the UK Biobank (UKB) data (N = 334,808) and the Genetic Investigation of ANthropometric Traits (GIANT) data (N = 210,323) to identify gene-smoking interaction for obesity traits. We divided the UKB subjects into two groups, current smokers and nonsmokers, based on the smoking status, and performed genome-wide association study (GWAS) for body mass index (BMI), waist circumference adjusted for BMI (WCadjBMI), and waist-hip ratio adjusted for BMI (WHRadjBMI) in each group. And then we carried out the meta-analysis using both GWAS summary statistics of UKB and GIANT for BMI, WCadjBMI, and WHRadjBMI, and computed the stratified P-values (Pstratified) based on the differences between meta-analyzed estimated beta coefficients with standard errors in each group. Results: We identified four genome-wide significant loci in interactions with the smoking status (Pstratified < 5×10-8); rs336396 (INPP4B) and rs12899135 (near CHRNB4) for BMI, and rs998584 (near VEGFA) and rs6916318 (near RSPO3) for WHRadjBMI. Moreover, we annotated the biological functions of the SNPs using expression quantitative trait loci (eQTL) and GWAS databases, along with publications, which revealed possible mechanisms underlying the association between the smoking status-related genetic variants and obesity. Conclusions: Our findings suggest that obesity traits can be modified by the smoking status via interactions with genetic variants through various biological pathways.
... Diferentes estudios han referido la ganancia de peso como una objeción frecuente para dejar de fumar (27)(28)(29)(30)(31), al igual que ha ocurrido en nuestro estudio. Muchos pacientes expresaron su temor a ganar peso al dejar de fumar, especialmente los que habían tenido intentos previos. ...
... No obstante, no se pudo establecer una relación estadísticamente significativa entre la ganancia de peso y la dependencia al tabaco. Algunos estudios han intentado esclarecer la relación entre la ganancia de peso y el éxito en la cesación tabáquica, obteniendo resultados discrepantes (28,31). En nuestro caso, no hemos podido establecer esta relación, pero nuestra muestra de pacientes es pequeña y serían necesarios más estudios con mayores muestras de pacientes para encontrar resultados concluyentes. ...
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Objetivo: evaluar los resultados de la implementación de un programa multidisciplinar médico-farmacéutico de cesación tabáquica combinando vareniclina y terapia conductual. Métodos: el médico de atención primaria valoró la dependencia y motivación del paciente para dejar de fumar mediante los test de Fagerström y Richmond, respectivamente. Los pacientes candidatos a entrar en el programa recibían la prescripción de vareniclina, si era necesaria, y se incorporaban a un programa de terapia conductual de tres meses de seguimiento en la farmacia comunitaria. Para el abordaje de la terapia conductual, el farmacéutico comunitario desarrolló una guía estructurada en 8 visitas y materiales de soporte para el paciente. El seguimiento de los pacientes se realizó en la farmacia comunitaria y el farmacéutico solo derivó a los pacientes a la consulta de atención primaria cuando aparecieron efectos adversos graves. Se recogió el historial de tabaquismo de los pacientes y sus comorbilidades, el tratamiento farmacológico recibido y sus efectos secundarios. Resultados: se incluyeron 26 pacientes. La puntuación media del test de Richmond fue de 8,31 (DE 1,54). La puntuación media del test de Fagerström fue de 5,73 (DE 2,10). La salud fue el principal motivo para dejar de fumar. Los pacientes recibieron vareniclina como tratamiento farmacológico para dejar de fumar, 21 pacientes (80,8 %) completaron las 12 semanas de tratamiento. Del total de la muestra, 18 pacientes (69,2 %) se mantuvieron sin fumar durante 3 meses. Los efectos secundarios observados más frecuentes fueron insomnio y diarrea. La terapia conductual llevada a cabo por el farmacéutico ayudó a mantener la adherencia al tratamiento farmacológico y la motivación durante el proceso de cesación tabáquica. Conclusión: el programa de cesación tabáquica basado en la colaboración médico - farmacéutico, con la combinación de terapia farmacológica y conductual y con la ayuda de una guía desarrollada específica-mente se mostró eficaz para dejar de fumar.
... Interestingly, the majority of participants who were smokers (75.8% (n = 25/33)) did not want to quit smoking, as they believed that they would gain weight. This agrees with various studies that state that most smokers gain weight when quitting smoking, which can interfere with cessation efforts [46]. Although cessation-related weight gain is modest [46], many smokers report gaining more than 10 kg, placing them at high risk of obesity-related chronic diseases. ...
... This agrees with various studies that state that most smokers gain weight when quitting smoking, which can interfere with cessation efforts [46]. Although cessation-related weight gain is modest [46], many smokers report gaining more than 10 kg, placing them at high risk of obesity-related chronic diseases. ...
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Aims The primary aim of the programme was a minimum of a 5% weight reduction of the initial weight, while the secondary outcomes were a reduction in participants’ body mass index (BMI), waist circumference (WC), blood pressure (BP), AUDIT-C score and an increase in the Mediterranean diet (MD) score and an improvement in physical activity levels. Methods This 'before and after' study was a 10-week weight management (WM) programme and it was developed and delivered in community pharmacies in Patras chosen for convenience, thus consisting the first service of its type in Greece. The sample size was calculated ( n = 96) based on the mean BMI for a Greek male and female individual, and the standard deviation (SD) of weight at baseline of 14 kg. Results Nearly every participant enrolled in the 20 participating pharmacies, 97.4% ( n = 114/117), achieved the programme’s aim, losing at least 5% of their initial weight. The mean percentage of total weight loss of the 117 participants at the 10th week was 8.97% (SD 2.65), and the t -test showed statistically significant results ( P -value < 0.001; 95% CI [8.48, 9.45]). A significant reduction in the waist-to-height ratio (WHtR) was observed in both male ( P -value = 0.004) and female ( P -value < 0.001) participants. The participants’ BP and AUDIT-C score and physical activity levels significantly improved ( P -value < 0.001), as well as their MD score. Conclusion This study provides the first evidence that Greek pharmacists have the potential to play an important role within primary healthcare and that after training they are able to provide public health services for both the public’s benefit and their clinical role enhancement.
... They also found that smoking cessation was associated with weight gain [5]. Numerous cohort studies have shown that people who stop smoking gain weight [6][7][8][9][10][11][12]. ...
... Although smoking cessation results in considerable health improvements, it is often accompanied by weight gain, with patients who are trying to quit smoking more likely to put on 3-5 kg of weight in the first three months to a year [3]. Although weight gain does not offset the health benefits of smoking cessation, which far exceed any health risks that may result from smoking cessation-induced weight gain, it is frequently a source of concern for smokers planning to quit [7]. This substantial effect may inhibit the reporting of some successful weight loss programmes. ...
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The literature is uncertain about the extent to which those who attend cardiac rehabilitation (CR) gain weight while trying to quit smoking. This study aimed to determine the extent of CR-based smoking cessation provision and whether CR, as delivered in routine practice, is associated with helping patients quit smoking and avoid weight gain. Data from the UK National Audit of Cardiac Rehabilitation database, between April 2013 and March 2016, were used. Smoking status is categorised as smokers and quitters assessed by patient self-report. Outcomes included body weight, blood pressure, depression, and physical activity. A multiple linear regression model was constructed to understand the effect of continuing smoking or quitting smoking on CR outcomes. CR outcome scores were adjusted by the baseline CR score for each characteristic. An e-survey collected information about the smoking cessation support offered to patients attending CR. A total of 2052 smokers (58.59 ± 10.49 years, 73.6% male) and 1238 quitters (57.63 ± 10.36 years, 75.8% male) were analysed. Overall, 92.6% of CR programmes in the United Kingdom (UK) offer smoking cessation support for CR attenders. Quitting smoking during CR was associated with a mean increase in body weight of 0.4 kg, which is much less than seen in systematic reviews. Quitters who attended CR also had better improvements in physical activity status and psychosocial health measures than smokers. As delivered in routine practice, CR programmes in the UK adhere to the guideline recommendations for smoking cessation interventions, help patients quit smoking, and avoid weight gain on completion of CR
... Nicotine, as an exogenous agonist on AChR, has a strong influence on the appetite, weight control, and food reward. Smokers are known to gain weight when they are quitting [10], while high-restrained eating is associated with elevated rates of smoking compared to the general population [11], and nicotine suppresses the appetite even in healthy non-smoking individuals [12]. Moreover, nicotinic agonists decrease food intake, body mass index (BMI, kg/m 2 ), and weight gain by activating the hypothalamic pro-opiomelanocortin (POMC) neuron pathway through the central activation of α3β4* nAChR [13,14]. ...
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Purpose: Obesity is thought to arise, in part, from deficits in the inhibitory control over appetitive behavior. Such motivational processes are regulated by neuromodulators, specifically acetylcholine (ACh), via α4β2* nicotinic ACh receptors (nAChR). These nAChR are highly enriched in the thalamus and contribute to the thalamic gating of cortico-striatal signaling, but also act on the mesoaccumbal reward system. The changes in α4β2* nAChR availability, however, have not been demonstrated in human obesity thus far. The aim of our study was, thus, to investigate whether there is altered brain α4β2* nAChR availability in individuals with obesity compared to normal-weight healthy controls. Methods: We studied 15 non-smoking individuals with obesity (body mass index, BMI: 37.8 ± 3.1 kg/m2; age: 39 ± 14 years, 9 females) and 16 normal-weight controls (non-smokers, BMI: 21.9 ± 1.7 kg/m2; age: 28 ± 7 years, 13 females) by using PET and the α4β2* nAChR selective (-)-[18F]flubatine, which was applied within a bolus-infusion protocol (294 ± 16 MBq). Volume-of-interest (VOI) analysis was performed in order to calculate the regional total distribution volume (VT). Results: No overall significant difference in VT between the individuals with obesity and the normal-weight volunteers was found, while the VT in the nucleus basalis of Meynert tended to be lower in the individuals with obesity (10.1 ± 2.1 versus 11.9 ± 2.2; p = 0.10), and the VT in the thalamus showed a tendency towards higher values in the individuals with obesity (26.5 ± 2.5 versus 25.9 ± 4.2; p = 0.09). Conclusion: While these first data do not show greater brain α4β2* nAChR availability in human obesity overall, the findings of potentially aberrant α4β2* nAChR availability in the key brain regions that regulate feeding behavior merit further exploration.
... For example, subjects who were current smoker at baseline but quit before the regular health examination were classified into the quit-smoking group, and those who current smoker at both baseline and regular health examination were classified into the continued-smoking group. We additionally divided each of these into weight-loss, weight-maintenance, and weight-gain group, depending upon whether they had had a 5% or greater weight change at their regular health examination after two years compared to their baseline [23,24]. ...
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Background Smoking or weight loss is a risk of tuberculosis (TB) development. However, the impact of weight change after smoking cessation on the occurrence of TB remains elusive. We aimed to determine the relationship between weight change after smoking cessation and the risk of TB development. Methods We conducted a population-based cohort study using the national database in Republic of Korea. Of the 10,490,491 subjects who underwent health check-up in 2009, we enrolled 9,953,124 subjects without a previous TB history and followed them until 2017. We divided all study participants into the following three groups: never, former, and current smokers. The primary endpoint was newly developed TB. Results Among 9,953,124 subjects analyzed, 5,922,845 (59.5%) were never smokers, 1,428,209 (14.4%) were former smokers, and 2,602,080 (26.1%) were current smokers. The risk of TB development was significantly higher in current smokers than in never smokers (adjusted hazard ratio (aHR) 1.158; 95% confidence interval [CI] 1.131–1.186). Among current smokers, individuals who stopped smoking and maintained weight after baseline evaluation had a significantly lower risk of TB development compared with those who continued to smoke (aHR 0.771; 95% CI 0.741–0.892). However, even after smoking cessation, individuals who lost weight were at a significantly higher risk of TB development compared with those who continued to smoke (aHR 1.327; 95% CI 1.119–1.715). Conclusions Our findings suggest that smoking is a risk factor for TB and weight maintenance (neither gaining or losing) after quitting smoking might reduce the risk of TB development.
Article
Objectives: In this study, we aim to investigate changes in the prevalence and risk factors of metabolic syndrome before and after the COVID-19 epidemic. Methods: A cross-sectional survey was conducted using data from the 2018-2021 National Health and Nutrition Examination Survey, and 21,159 people were selected for analysis. SPSS version 29.0 program was used to analyze data, and frequency analysis and chi-square test were performed to determine the frequency and ratio of demographic and health behavioral factors before and after the COVID-19 epidemic, and the distribution of metabolic syndrome prevalence. The risk of occurrence by metabolic syndrome prevalence factor was analyzed through logistic regression. Results: As a result of the study, the prevalence of metabolic syndrome increased after the COVID-19 epidemic, and among the five diagnostic criteria, waist circumference, fasting blood sugar, triglycerides, and HDL-cholesterol, excluding blood pressure, increased significantly. In addition, the risk of metabolic syndrome was 1.16 times higher after the COVID-19 epidemic compared to before, and even after controlling for variables such as demographic factors, it was significantly higher at 1.14 times compared to before. Conclusions: Through this study, the prevalence of metabolic syndrome increased during the COVID-19 epidemic due to changes in lifestyle habits, such as decreased activity. If times like the COVID-19 epidemic repeat in the future, we recommend adding and promoting measures that can help manage chronic diseases such as metabolic syndrome when creating national action guidelines to prevent infectious diseases.
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In past decades the prevalence of overweight and obesity had grown rapidly. There are numerous factors contributing to this unfavorable change in people’s health. This review article investigates the environmental factors which may play a role in the prevalence of overweight and obesity and additionally the novel factors which appeared after the beginning of the COVID-19 pandemic, which caused the increase in BMI during the lockdown period. Most of the studies reveal that the COVID-19 pandemic and lockdown contributed to the growth of BMI in numerous countries and, eventually the prevalence of overweight and obesity increased. Studies suggest that the physical activity was decreased while sleep time and screen time were increased and the amount of food consumed increased, additionally more processed food with long shelf life was consumed. The diverse environmental factors may have an impact on obesity and overweight development taking into account policy and local school policy issues, socioeconomic status, lifestyle including physical activity, diet habits, and amongst others, more trivial causes such as uninteresting neighborhoods, lack of sense of security outside the place of residence or a long distance from shops. Still, this is the object of debate if air pollution is an environmental risk factor influencing the unfavorable trends towards increasing body weight.
Article
Nicotine, a major addictive component in tobacco, plays an important role in the changes of body weight upon smoking and its cessation. Here we showed that nicotine-treated mice exhibited weight loss and nicotine withdrawal led to weight gain. Using TMT-based proteomic analysis, we obtained the different hypothalamic protein profiles in response to nicotine and its withdrawal. A total of ~5000 proteins were identified from the hypothalamus with 50 altered proteins upon 28-day nicotine treatment and 28 altered proteins upon 15-day nicotine withdrawal. Of the altered proteins, CASP3, LCMT2, GRIN2D, CCNT2, FADS3 and MRPS18B were inversely changed in response to nicotine and withdrawal, coincidence with the change of body weight. Of them, CASP3, LCMT2, GRIN2D and CCNT2 were found to be associated with several GO terms and KEGG pathways linking with cell apoptosis, neurotransmission and metabolism. Further Western blot and RT-qPCR analyses confirmed that the levels of the 4 proteins CASP3, LCMT2, GRIN2D and CCNT2, instead of their mRNA transcripts, altered in response to nicotine and withdrawal. Thus this study provides nicotine- and withdrawal-induced hypothalamic protein profiles and suggests potential roles of these altered proteins in the change of body weight. Significance Cigarette smoking is one of important factors harming human health. Most smokers tend to have lower body weights and smoking cessation often lead to overweight or obesity, which is an important reason for smokers to insist on smoking. It is known that nicotine, a critical component in tobacco, is associated with the alteration in body weight by affecting hypothalamic function. Through TMT-based proteomic analysis, this study identified differential hypothalamic protein profiles in response to nicotine treatment and its withdrawal, and 4 nicotine- and withdrawal-induced contrary proteins CASP3, LCMT2, GRIN2D and CCNT2 are involved in several enriched GO terms and KEGG pathways, which are associated with cell apoptosis, neurotransmission and metabolism. Our study may provide novel targets for further investigation of the molecular mechanisms of nicotine- and withdrawal-induced alteration in body weight.
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Cost-effectiveness analysis, even with its inherent methodological problems, consistently shows that when smoking cessation interventions are effective they are nvariably also cost-effective. This is largely due to their relative low cost and the big impact that stopping smoking has on health outcomes. This is also the case for pharmacotherapy for smoking cessation, including nicotine replacement therapy (NRT), bupropion (Zyban) and varenicline (Champix). There is evidence that varenicline may be more cost-effective than other pharmacotherapy. Evidence is less conclusive about the relative cost-effectiveness of NRT compared with bupropion. Combination therapy (several forms of NRT, or NRT and bupropion) is also cost-effective compared with brief advice or counselling alone. While it is likely that combination pharmacotherapy, as compared with monopharmacotherapy, is cost-effective it has not yet been directly evaluated. Findings from economic analyses from the UK and elsewhere confirm that smoking cessation interventions, including pharmacotherapy, are among the most cost-effective health care interventions available.
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Estimates of postcessation weight gain vary widely. This study determined the magnitude of weight gain in a cohort using both point prevalence and continuous abstinence criteria for cessation. Participants were 196 volunteers who participated in a smoking cessation program and who either continuously smoked (n = 118), were continuously abstinent (n = 51), or who were point prevalent abstinent (n = 27) (i.e., quit at the 1-year follow-up visit but not at others). Continuously abstinent participants gained over 13 lbs. (5.90 kg) at 1 year, significantly more than continuously smoking (M = 2.4 lb.) and point prevalent abstinent participants (M = 6.7 lbs., or 3.04 kg). Individual growth curve analysis confirmed that weight gain and the rate of weight gain (pounds per month) were greater among continuously smoking participants and that these effects were independent of gender, baseline weight, smoking and dieting history, age, and education. Results suggest that studies using point prevalence abstinence to estimate postcessation weight gain may be underestimating postcessation weight gain.
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Cigarette smoking has been associated with increased upper body fat deposition, as estimated by the waist to hip ratio, which has been shown to be associated with glucose intolerance and dyslipidemia in nonsmoking subjects. Whether smoking is at the origin of central adiposity and its related metabolic disturbances is unclear. Moreover, it is controversial whether smoking influences fuel metabolism. Therefore, young healthy male volunteers smoking more than 10 cigarettes/day for more than 5 yr (n = 14) were compared with nonsmokers (n = 13) matched for age, sex, body mass index, alcohol consumption, physical activity, as well as family history for hypertension, diabetes, obesity, and coronary heart disease. After an overnight fast, blood was drawn for chemistry, body composition was assessed by dual energy x-ray absorptiometry, and fuel metabolism was determined by indirect calorimetry. Nicotine uptake was estimated by 24-h urinary excretion of cotinine. Lean and fat body mass as well as their respective ...
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Challenges the commonly-held assumption that prevention of weight gain after smoking cessation will prevent smoking relapse. The successes or failures of recent pharmacological and nonpharmacological treatments aimed at preventing postcessation weight gain are evaluated. No behavioral treatment has been shown to be successful in attenuating cessation-induced weight gain in healthy ex-smokers, but prospective studies have not reported that weight gain after cessation directly predicts relapse and that adjunct weight-control treatment may be associated with greater smoking relapse. Rather than developing intensive strategies for combating weight gain after smoking cessation, a more prudent approach for researchers may be to re-examine the fundamental relationship among smoking, eating, body weight, and weight-related attitudes. (PsycINFO Database Record (c) 2012 APA, all rights reserved)