3.29 Smoking and body weight

Last updated: March 2015
Suggested citation:Letcher, T, Greenhalgh, EM & Winstanley, MH. 3.29 Smoking and body weight. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/3-29-smoking-and-body-weight

 

The relationship between smoking and reduced body weight is widely recognised by smokers, and generally overestimated.

3.29.1 Does smoking cause smokers to weigh less than non-smokers?

While it is true that smokers weigh, on average, less than people who have quit smoking and those who have never smoked, the effect is modest and accrues over decades of smoking.1 For example, some studies have found only a small effect for daily smoking on body weight among some groups of young smokers.2 A US longitudinal study examining the relationship between trajectories of cigarette smoking from early adolescence to young adulthood and obesity in the mid-30s has found that heavy/continuous smokers and those who started smoking in late adolescence had a significantly lower likelihood of obesity compared with nonsmokers,3 however starting smoking does not appear to be associated with short-term weight loss.1

The relationship between smoking and body weight is likely to be due to a range of effects of nicotine on the metabolism.4

It has been suggested that the typically lower body mass index (BMI) of smokers is due to higher total energy expenditure compared with never smokers.5 However, evidence regarding the relative roles of energy intake and expenditure is scant.5 Some research suggests the involvement of plasma leptin, which plays a key role in energy intake and expenditure regulation.6

There is also evidence to suggest that increased cigarette consumption among smokers can be associated with higher BMI.7 For example, a case–control study of over 1000 18–65 year olds found that for those of normal weight, smoking prevalence decreased as BMI increased.8 This trend was reversed among overweight, obese or morbidly obese individuals: smoking prevalence was significantly higher among the morbidly obese compared with those who were overweight or obese. Morbidly obese individuals were twice as likely to smoke as those of normal weight.8

It has been suggested that such findings are due to the contribution of other risk behaviours such as physical inactivity, poor nutrition and higher alcohol consumption among overweight individuals;8 for example, there is some evidence of a positive association between physical activity and smoking, significantly mediating the relationship between smoking and BMI.7

Recent research has found that while smokers tend to have a lower BMI than non-smokers, their fat distribution is more likely to be in the abdominal region (central adiposity or 'male pattern' fat distribution).1, 9 Individuals with the pattern of central fat accumulation are at greater risk of developing a range of cardiovascular1 and metabolic problems related to obesity9 including coronary artery disease.10

The association between smoking and abdominal adiposity may be dose dependent: a large cross-sectional population-based survey among Swiss people aged 35–75 years found that smokers' mean waist circumference and percentage body fat increased with cigarettes smoked per day.11 In addition, there is some evidence that adolescent smoking is associated with abdominal obesity in adulthood: Finnish research found that smoking at least 10 cigarettes daily when aged 16 to 18 years is a risk factor for adult abdominal obesity among both genders and for overweight in females.12

3.29.2 Smoking cessation and weight gain

Sustained cessation is associated with a mean weight gain of about 5–6 kg in the first year of abstinence,4, 13 an issue of concern to some smokers. However the relationship between smoking and body weight is not clear cut. A prospective study of the association between smoking and weight gain among an adult Spanish cohort found that active smokers as well as those who stopped smoking during follow-up (median period 4.2 years) experienced significantly greater weight gains than never smokers.14 For further discussion on implications for cessation, see Chapter 7, Section 7.1.2 .

3.29.3 Relative contribution of smoking and obesity to morbidity

Over the last decade, obesity has come to have an equal or even greater contribution to the burden of disease than smoking, and is associated with a greater negative impact on quality of life.15 This is based on US estimates of quality-adjusted life-years (QALYs) lost due to obesity and smoking between 1993 and 2008 and is related to a population obesity increase of 85% and a smoking prevalence decrease of 18.5% among US adults over this time.15 Overall, obesity had a greater effect on morbidity than mortality, while smoking has a negative impact on mortality; this has been demonstrated among US and Western European populations.15,16 Western European data also indicate that people in higher BMI categories spend more years living with disability, whereas life expectancy with disability may not be related to smoking status.16 In Australasia, a report published in 2014 cited dietary risks (accounting for 11% of the total burden), high body mass index (9%) and smoking (8%) as the leading risk factors for disease.17

Childhood and adolescent behaviours and cardiovascular (CVD) risk factor profiles are important determinants of CVD risk factor prevalence later in life. A Finnish study following a cohort of 1809 people aged 3–18 years found the six-year progression of carotid atherosclerosis increased significantly with the number of childhood cardiovascular risk factors, including lipid levels, high blood pressure, obesity, diabetes, smoking and physical inactivity.18 A large prospective cohort study following people aged 18–26 years between 1995 and 1996 and 2001 and 2002 found that overweight and obese adolescents were more likely than those of normal weight to report a diagnosis of high blood pressure and cholesterol by the time they were young adults, regardless of BMI in young adulthood.19 Adolescent smoking and physical activity levels did not independently predict these CVD risk factors.

There is some evidence of a dose–response relationship between pregnancy smoking exposure and overweight and obesity in children. A UK cross-sectional survey of 3038 children aged 5–11 years found that overweight and obesity prevalence estimates were higher for those with mothers who smoked heavily (10+ cigarettes daily) during pregnancy.20 See Section 3.8.5 for further discussion on the long-term effects of smoking during pregnancy.

3.29.4 Smoking compared to and in combination with obesity: contribution to mortality

Since being overweight is strongly associated with many disease entities, it has also given rise to the question of whether it is better to be a leaner smoker or a heavier non-smoker. A large international study has investigated the connection between smoking, body weight and mortality from coronary heart disease.21 The study concludes that although smokers have on average a lower BMI than non-smokers, it is of nowhere near sufficient magnitude to offset the risk of dying from CVD as a result of smoking. The authors conclude that 'it is unquestionably better to quit smoking and gain weight than to continue to smoke'.(p. 834)21 Similarly, smoking appears to offset the CVD risk factor benefits associated with parental longevity such as trends towards lower BMI, weight and waist circumference observed among women in Swiss population-based research.22

Studies covering tens of thousands of deaths provide reliable evidence on mortality from persistent smoking and from adult obesity.23,24 An increase of 10% in the prevalence of smoking and of 2 BMI points in overweight populations reduce the life span in men comparably, each by about one year.23 An increase in life expectancy of about 10 years can be gained through smoking cessation, much greater than a smoker could expect to gain from weight control.23

While smoking and adiposity are independent predictors of mortality, the combination of current or recent smoking with a BMI ≥35 or a large waist circumference is related to an especially high mortality risk (5 to 8 times that of never smokers within normal weight range).25 US all-cause mortality data from 51–72 year olds indicates an increase in mortality rates with greater BMI or waist circumference, and an increase from never to former to current smoking.25 Obese smokers have a 14-year reduction in life expectancy at age 40 compared with lean non-smokers, as well as an increased risk of developing type 2 diabetes and cancer.26

The evidence regarding how smoking and obesity might interact to reduce life expectancy and the degree of interaction is not clear.26 For example, overweight or obesity in late adolescence has been found to increase the risk of all-cause adult mortality regardless of smoking status: obesity and overweight in late adolescence were as hazardous as heavy (>10 cigarettes/day) and light (1–10/day) smoking, respectively, with no interaction between BMI and smoking status.27 US research comparing the burden of mortality due to smoking, education levels and obesity in those aged 55+ years found smoking and low education decreased population life expectancy more than did obesity, with highest life expectancy at age 55 found in highly educated non-smokers, slightly higher than normal BMI.28

Among modifiable dietary, lifestyle and metabolic risk factors, smoking and high blood pressure were responsible for the largest number of deaths in the US in 2005, accounting for about 1 in 5 or 6 adult deaths.29 In comparison, overweight/obesity caused about 9% of deaths, physical inactivity and high blood glucose about 8%, and high LDL cholesterol almost 5%.29

Estimates based on Swedish national data forecast a continued decline in premature deaths among males due to reductions in smoking over the last four decades, despite large increases in overweight and obesity over this time. However, one-third of the survival benefit from reduced smoking was estimated to be offset by the parallel increase in obesity.27

Australian longitudinal research has identified central obesity and smoking as key independent risk factors predicting mortality from coronary heart disease and cardiovascular disease, with no added influence of measured lipids or blood pressure.30 When combined with cigarette smoking, waist-to-hip ratio was as effective as the Framingham risk score (incorporating the contribution of blood pressure, total cholesterol, high density lipoprotein cholesterol and diabetes) in predicting coronary heart disease and cardiovascular disease deaths.30 Similarly, US longitudinal research examining modifiable risk factors for cardiovascular disease found a low-risk profile (not smoking, moderate or high cardiorespiratory fitness, and healthy waist circumference) among men to be associated with a reduced risk of coronary heart disease, cardiovascular disease mortality and all-cause death31 while among women five lifestyle factors independently and significantly predicted mortality: 55% of deaths during follow-up were attributed to the combination of smoking, overweight, physical inactivity and poor diet; 28% of deaths were attributed to smoking.32

Some evidence suggests that natural killer (NK) cells may be a mechanism by which obesity and smoking are associated with an increased risk of malignancy and mortality.26 Crucial in mediating anti-tumour immunity, there is a marked reduction in the numbers and function of NK cells in obese individuals, and increased susceptibility of the cells to the harmful effects of cigarette smoke.26

There is a lack of agreement about how to adjust for potential confounders including smoking status in the association between body mass index (BMI) and mortality.33 Research using 50 cohort data sets from about 30 international studies to examine the relationship between BMI and mortality and any interaction with smoking status found that excluding smokers' data or disregarding smoking status did not affect the association between BMI and mortality.33 Worldwide, mean adult BMI increased between 1980 and 2008, although trends differed significantly between countries.34 In Australia, the prevalence of overweight and obesity in adults had increased to 62.8% in 2011-12, from 61.2% in 2007-08 and 56.3% in 1995.35 Obesity and smoking are significantly more common in the most disadvantaged areas. In 2007-08 almost one-fifth of people who were overweight or obese were also current smokers.

Overweight or obese smokers were twice as likely to have heart disease as people who were within the normal weight range and who had never smoked, 2.2 times as likely to have Type 2 diabetes, and 2.8 times as likely to have bronchitis.36 

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References

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