The Mortality Risk of Smoking and Obesity Combined
ABSTRACT Both smoking and obesity have been linked to increased mortality, but evaluating the joint effect has been limited. This nationwide, prospective mortality study of U.S. radiologic technologists was designed to evaluate the combined mortality risks of obesity and smoking.
Mortality risk was investigated in 64,120 women and 18,760 men who completed a baseline questionnaire (1983 to 1989). Body mass index (BMI) (weight adjusted for height, or kilograms divided by meters squared) was calculated from self-reported weight and height at baseline, with five categories: less than 18.5 (underweight), 18.5 to 24.9 (normal), 25.0 to 29.9 (overweight), 30.0 to 34.9 (moderately obese), and 35.0 and higher (very obese). Participants were followed from the questionnaire until the date of death or through 2002, whichever occurred first. The combined association among BMI and smoking and all-cause, cancer, and circulatory disease mortality by gender and attained age (less than 65 years, 65 years and older) was examined using Cox proportional hazards regression analyses (conducted in 2005). Person-years at risk averaged 16 years (women aged less than 65), 6 years (women aged 65 and older), 15 years (men aged less than 65), and 7 years (men aged 65 and older), totaling 1.35 million person-years.
In all gender/age groups, both obesity and smoking, particularly current smoking, contributed substantially to all-cause mortality, with 3.5- to 5-fold risks for very obese, current smokers compared to normal weight, never smokers. Current smoking was the predominant risk factor for cancer mortality. Combining obesity with current smoking increased circulatory disease mortality by 6- to 11-fold for people aged less than 65 years, compared to normal weight, never smokers. Obese former smokers (less than 65 years) had notably lower risks.
Obese smokers (aged less than 65 years) had strikingly high mortality risks, particularly from circulatory disease mortality.
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- "s difficulty complying with dietary advice may not be very high . A population ' s health is a complex multi - dimensional concept that changes over age , time , and across countries . We consider cigarette smoking and obesity , though there cer - tainly are other important risk factors . The interaction of risk factors is quite likely , as well . Freedman et al . ( 2006 ) found the mortality risk among obese smokers , even young obese smokers , far exceeded the sum of their individual risks . Considerable variation in mortality risk may also exist among individuals , even within a specific sub - population . For example , Wessel et al . ( 2004 ) note substantial differences in cardiorespiratory fitness"
Article: The future of death in America[Show abstract] [Hide abstract]
ABSTRACT: Population mortality forecasts are widely used for allocating public health expenditures, setting research priorities, and evaluating the viability of public pensions, private pensions, and health care financing systems. Although we know a great deal about patterns in and causes of mortality, most forecasts are still based on simple linear extrapolations that ignore covariates and other prior information. We adapt a Bayesian hierarchical forecasting model capable of including more known health and demographic information than has previously been possible. This leads to the first age- and sex-specific forecasts of American mortality that simultaneously incorporate, in a formal statistical model, the effects of the recent rapid increase in obesity, the steady decline in tobacco consumption, and the well known patterns of smooth mortality age profiles and time trends. Formally including new information in forecasts can matter a great deal. For example, we estimate an increase in male life expectancy at birth from 76.2 years in 2010 to 79.9 years in 2030, which is 1.8 years greater than the U.S. Social Security Administration projection and 1.5 years more than U.S. Census projection. For females, we estimate more modest gains in life expectancy at birth over the next twenty years from 80.5 years to 81.9 years, which is virtually identical to the Social Security Administration projection and 2.0 years less than U.S. Census projections. We show that these patterns are also likely to greatly affect the aging American population structure. We offer an easy-to-use approach so that researchers can include other sources of information and potentially improve on our forecasts too.Demographic Research 07/2011; 25(1):1-38. DOI:10.4054/DemRes.2011.25.1 · 1.20 Impact Factor
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- "). Both smoking and obesity are independent risk factors for cardiovascular disease morbidity and mortality in women (Wilson, D-Agostino, Sullivan, Parise, and Kannel, 2002; Freedman et al., 2006; Eckel and Krauss, 1998), and the combination of current smoking and obesity has been found to have a synergistic effect on the risk of mortality from circulatory disease in women under age 65 (Freedman and others, 2006). It has been estimated that 4.2% of women in the U.S. are simultaneously current smokers and obese (Healton, Vallone, McCausland, Xiao, and Green, 2006). "
ABSTRACT: Little is known about the relationship between relative body weight and transition from experimentation to regular smoking in young adult women. In the current study, data from 2494 participants in wave 4 of the Missouri Adolescent Female Twin Study (aged 18-29years) who reported ever smoking a cigarette were analyzed using logistic regression. Body mass index (BMI) at time of interview was categorized according to CDC adult guidelines, and regular smoking was defined as having ever smoked 100 or more cigarettes and having smoked at least once a week for two months in a row. Since the OR's for the overweight and obese groups did not differ significantly from one another in any model tested, these groups were combined. Forty-five percent of women who had ever smoked had become regular smokers. Testing of interactions between potential covariates and levels of the categorical BMI variable revealed a significant interaction between overweight/obesity and childhood sexual abuse (CSA; p<0.001) associated with regular smoking. Among women reporting CSA, the association between overweight/obesity and having become a regular smoker was negative (n=374; OR=0.48, 95% CI: 0.28-0.81). Both underweight and overweight/obesity were positively associated with transition to regular smoking among women who did not report CSA (n=2076; OR=1.57, 95% CI: 1.05-2.35 and OR=1.73, 95% CI: 1.35-2.20, respectively). These results suggest that experiencing CSA alters the association between BMI and regular smoking in women who have experimented with cigarettes.Addictive behaviors 11/2010; 35(11):983-8. DOI:10.1016/j.addbeh.2010.06.014 · 2.44 Impact Factor
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- "Obese individuals who smoke have a 14 year reduction in life expectancy at the age of 40 . A large prospective study has shown that smoking coupled with obesity contributes substantially to all-cause mortality, with 3.5 to 5-fold risks for severely obese current smokers compared to normal weight non-smokers . Obese smokers also have an increased risk of developing both Type 2 Diabetes  and cancer . "
ABSTRACT: Obese individuals who smoke have a 14 year reduction in life expectancy. Both obesity and smoking are independently associated with increased risk of malignancy. Natural killer cells (NK) are critical mediators of anti-tumour immunity and are compromised in obese patients and smokers. We examined whether NK cell function was differentially affected by cigarette smoke in obese and lean subjects. Clinical data and blood were collected from 40 severely obese subjects (BMI>40 kg/m(2)) and 20 lean healthy subjects. NK cell levels and function were assessed using flow cytometry and cytotoxicity assays. The effect of cigarette smoke on NK cell ability to kill K562 tumour cells was assessed in the presence or absence of the adipokines leptin and adiponectin. NK cell levels were significantly decreased in obese subjects compared to lean controls (7.6 vs 16.6%, p = 0.0008). NK function was also significantly compromised in obese patients (30% +/- 13% vs 42% +/-12%, p = 0.04). Cigarette smoke inhibited NK cell ability to kill tumour cell lines (p<0.0001). NK cells from obese subjects were even more susceptible to the inhibitory effects of smoke compared to lean subjects (33% vs 28%, p = 0.01). Cigarette smoke prevented NK cell activation, as well as perforin and interferon-gamma secretion upon tumour challenge. Adiponectin but not leptin partially reversed the effects of smoke on NK cell function in both obese (p = 0.002) and lean controls (p = 0.01). Obese subjects have impaired NK cell activity that is more susceptible to the detrimental effects of cigarette smoke compared to lean subjects. This may play a role in the increase of cancer and infection seen in this population. Adiponectin is capable of restoring NK cell activity and may have therapeutic potential for immunity in obese subjects and smokers.PLoS ONE 01/2010; 5(1):e8660. DOI:10.1371/journal.pone.0008660 · 3.23 Impact Factor