The relationship between obesity and breast cancer risk and mortality

Obesity is an established risk factor for postmenopausal, but not premenopausal, development of breast cancer. Evidence for a positive association between obesity and breast cancer mortality is mounting. Avoiding adult weight gain and maintaining a healthy body weight may contribute importantly to decreasing breast cancer risk and mortality, especially in postmenopausal women.     

Are passive smoking,air pollution and obesity a greater mortality risk than major radiation incidents?

Background  

Following a nuclear incident, the communication and perception of radiation risk becomes a (perhaps the) major public health issue. In response to such incidents it is therefore crucial to communicate radiation health risks in the context of other more common environmental and lifestyle risk factors. This study compares the risk of mortality from past radiation exposures (to people who survived the Hiroshima and Nagasaki atomic bombs and those exposed after the Chernobyl accident) with risks arising from air pollution, obesity and passive and active smoking.     

The temporal pattern of reduction of mortality risk after smoking cessation

We investigated the excess mortality risks of former smokers according to the number of years since they quit smoking in a cohort of 21,112 men and women evaluated with coronary angiography and included in the Coronary Artery Surgery Study registry. There is a prompt decline in mortality risk within the first year of quitting. Thereafter, former smokers have a sustained, modestly elevated mortality risk for at least 20 years compared with people who never smoked. The pattern is similar in men and women, in 35-54, 55-64, and greater than or equal to 65 age groups, and in subcohorts of those with coronary artery disease and those without coronary artery disease.     

Eligibility for obesity treatment and risk of mortality in men

OBJECTIVE: To evaluate the risk of all-cause and cardiovascular disease (CVD) mortality associated with each outcome of the NIH obesity treatment algorithm and to examine the effects of cardiorespiratory fitness on the risk of mortality associated with these outcomes. RESEARCH METHODS AND PROCEDURES: The NIH obesity treatment algorithm was applied to 18,666 men (20 to 64 years of age) from the Aerobics Center Longitudinal Study in Dallas, TX, examined between 1979 and 1995. Risk of all-cause and CVD mortality was assessed using Cox proportional hazards regression. RESULTS: A total of 7029 men (37.7%) met the criteria for needing weight loss treatment [overweight (BMI = 25 to 29.9 kg/m2 or WC > 102 cm) with > or =2 CVD risk factors or obese (BMI > or = 30 kg/m2)]. Mortality surveillance through 1996 identified 435 deaths (151 from CVD) during 191,364 man-years of follow-up. Compared with the normal weight reference group, the hazard ratios (95% confidence interval) for death from all causes were 0.63 (0.45 to 0.88), 1.23 (0.98 to 1.54), 1.05 (0.60 to 1.85), and 1.71 (1.64 to 2.31) for men who were overweight with <2 CVD risk factors, overweight with > or = 2 CVD risk factors, obese with <2 CVD risk factors, and obese with > or =2 CVD risk factors, respectively. Corresponding hazard ratios for CVD mortality were 0.72 (0.38 to 1.37), 1.67 (1.12 to 2.50), 1.69 (0.67 to 4.30), and 3.31 (2.07 to 5.30). Including physical fitness as a covariate significantly attenuated all risk estimates. DISCUSSION: The NIH obesity treatment algorithm is useful in identifying men at increased risk of premature mortality; however, including an assessment of fitness would help improve risk stratification among all groups of patients.     

Underweight, overweight and obesity as risk factors for mortality and hospitalization

AIMS: The prevalence of overweight and obesity is increasing in many countries. We aimed to investigate differences in mortality and severe morbidity between underweight people (body mass index (BMI)<18.5), overweight people (BMI 25 to <30), obese people (BMI> or =30), and those with normal weights (BMI 18.5 to <25). METHODS: Random samples of the Swedish population aged 16-74 years in 1980-81 and 1988-89 were followed for 12 years with regard to all-cause mortality and mortality from circulatory diseases, all inpatient care, and inpatient care for circulatory and musculoskeletal diseases. Relative risks (RRs) for different levels of BMI were adjusted for age, longstanding illness, smoking, and educational level at baseline. In addition, analyses were made with delayed entry until the fourth-year after interview. RESULTS: Obesity and underweight, but not overweight, was associated with higher all-cause mortality. Among underweight men, the adjusted RR for all-cause mortality was 2.4 (95% confidence interval 1.6-3.6), and among underweight women it was 2.0 (1.5-2.7), but population attributable risks (PARs) were small, at 1.2% and 2.7%, respectively. Overweight was associated with increased risks for inpatient care for circulatory diseases, with PARs being 13.4% among men and 8.1% among women, and musculoskeletal diseases (PARs were 12.7% and 12.9%, respectively). Obese men and women had about 50% higher risks of all-cause mortality than normal-weight people, PARs being 3.2% and 3.8% respectively. CONCLUSIONS: This study supports the findings of other studies, in that overweight seems to be an exaggerated risk factor for all-cause mortality, but is related to other chronic disease. Underweight and obesity generally implies greater increases of RRs, but avoidance of overweight may have greater effect on the population level with regard to reduced cardiovascular and locomotor disease.     

高血压合并肥胖影响因素分析

目的探讨高血压合并肥胖者的主要影响因素,为高血压合并肥胖的防治提供理论依据。方法以社区医院门诊病人为基础进行病例对照研究,其中以门诊收治的高血压合并肥胖患者372人为病例组,在同一社区人群中选择血压和体重均正常者437人为对照组;对研究对象进行问卷调查和实验室检查。运用单因素与多因素分析方法,探讨高血压合并肥胖者的主要影响因素。结果高血压合并肥胖的发病危险随着年龄的增长而增加,男性高于女性;有家族遗传倾向者发病风险明显增高,父亲肥胖（OR=5.04,95%CI=3.12～8.14）,父亲高血压（OR=2.46,95%CI=1.81～3.35）,母亲肥胖（OR=2.55,95%CI=1.78～3.64）,母亲高血压（OR=2.14,95%CI=1.60～2.86）;膳食口味偏咸（OR=2.45,95%CI=1.82～3.29）与饮酒（OR=1.92,95%CI=1.37～2.68）等行为可以增加发病风险,而坚持骑车或步行上班（OR=0.64,95%CI=0.46～0.89）、饮用牛奶（OR=0.73,95%CI=0.55～0.97）等行为则可降低发病风险。病例组血脂异常率高于对照组（P〈0.01）,提示高血压合并肥胖可增加血脂紊乱的风险。结论将戒烟限酒、减少食盐的摄入量,适量运动、合理膳食作为高血压合并肥胖人群的主要预防措施;家族遗传倾向是高血压与肥胖发病的主要危险因素,应对此类高危人群加强一、二级预防。     

The effect of health shocks on smoking and obesity

Aim

To investigate whether negative changes in their own health (i.e. health shocks) or in that of a smoking or obese household member, lead smokers to quit smoking and obese individuals to lose weight.

Methods

The study is informed by economic models (‘rational addiction’ and ‘demand for health’ models) which offer hypotheses on the relationship between health shocks and health-related behaviour. Each hypothesis was tested applying a discrete-time hazard model with random effects using up to ten waves of the German Socioeconomic Panel (GSOEP) and statistics on cigarette, food and beverage prices provided by the Federal Statistical Office.

Results

Health shocks had a significant positive impact on the probability that smokers quit during the same year in which they experienced the health shock. Health shocks of a smoking household member between year t?2 and t?1 also motivated smoking cessation, although statistical evidence for this was weaker. Health shocks experienced by obese individuals or their household members had, on the other hand, no significant effect on weight loss, as measured by changes in Body Mass Index (BMI).

Conclusion

The results of the study suggest that smokers are aware of the risks associated with tobacco consumption, know about effective strategies to quit smoking, and are willing to quit for health-related reasons. In contrast, there was no evidence for changes in health-related behaviour among obese individuals after a health shock.     

Paternal smoking and increased risk of infant and under-5 child mortality in Indonesia

We examined the relationship between paternal smoking and child mortality. Among 361,021 rural and urban families in Indonesia, paternal smoking was associated with increased infant mortality (rural, odds ratio [OR] = 1.30; 95% confidence interval [CI] = 1.24, 1.35; urban, OR = 1.10; 95% CI = 1.01, 1.20), and under-5 child mortality (rural, OR = 1.32; 95% CI = 1.26, 1.37; urban, OR = 1.14; 95% CI = 1.05, 1.23). Paternal smoking diverts money from basic necessities to cigarettes and adversely affects child health; tobacco control should therefore be considered among strategies to improve child survival.     

Estimating health-adjusted life expectancy conditional on risk factors: results for smoking and obesity

Background  

Smoking and obesity are risk factors causing a large burden of disease. To help formulate and prioritize among smoking and obesity prevention activities, estimations of health-adjusted life expectancy (HALE) for cohorts that differ solely in their lifestyle (e.g. smoking vs. non smoking) can provide valuable information. Furthermore, in combination with estimates of life expectancy (LE), it can be tested whether prevention of obesity and smoking results in compression of morbidity.     

The combined effect of smoking tobacco and drinking alcohol on cause-specific mortality: a 30 year cohort study

Background  

Smoking and consuming alcohol are both related to increased mortality risk. Their combined effects on cause-specific mortality were investigated in a prospective cohort study.     

The effects of maternal smoking on fetal and infant mortality

Although maternal cigarette smoking has been shown to reduce the birth weight of an infant, previous findings on the relation between smoking and fetal and infant mortality have been inconsistent. This study used the largest data base ever available (360,000 birth, 2,500 fetal death, and 3,800 infant death certificates for Missouri residents during 1979-1983) to assess the impact of smoking on fetal and infant mortality. Multiple logistic regression was used to estimate the joint effects of maternal smoking, age, parity, education, marital status, and race on total mortality (infant plus fetal deaths). Compared with nonsmoking women having their first birth, women who smoked less than one pack of cigarettes per day had a 25% greater risk of mortality, and those who smoked one or more packs per day had a 56% greater risk. Among women having their second or higher birth, smokers experienced 30% greater mortality than nonsmokers, but there was no difference by amount smoked. The prevalence of smoking in this population was 30%. It was estimated that if all pregnant women stopped smoking, the number of fetal and infant deaths would be reduced by approximately 10%. The higher rate of mortality among blacks compared with whites could not be attributed to differences in smoking or the other four maternal characteristics studied. In fact, the black-white difference was greater among low-risk women (e.g., married multiparas aged 20 and over with high education) than among high-risk women (e.g., unmarried teenagers with low education).     

Interactive effects of main genotype, caloric intakes, and smoking status on risk of obesity

The aim of this study was to determine the strong candidate genes increasing susceptibility to obesity among previously reported obesity-related genes in Korean subjects and evaluate gene-environmental interactions in susceptibility to obesity. The study population comprised of 163 adolescents (95 boys and 68 girls) and their parents (97 men and 96 women).We used multivariable-adjusted logistic regression analysis, and classification and regression tree (CART) analysis incorporating both the genetic (ADRB2 R16G genotype) and environmental (overeating, smoking status, and parent's obese status) variables. The polymorphisms were genotyped with SNP-ITTM assays using the SNPstream 25KTM System (Orchid Biosciences, New Jersey, USA). Arg16 allele of ADRB2 R16G, smoking and overeating were linked to an increased risk of obesity in adults. CART analysis showed that smoking parents who overate and carried the Arg allele, ADRB2 R16G, had an odds ratio (OR) of 11.7 (95% confidence interval (CI), 2.13-64.04) for obesity compared to non-smoking parents who had none of these factors. Among children, the highest risk group for obesity was the overeater with obese parents (OR, 5.20; 95% CI, 1.86-14.53). The results of the study indicate that beta2-adrenoceptor polymorphism may contribute to the development of obesity through gene-environmental interactions. Further replication studies with larger sample size would be needed to confirm our study results.     

2型糖尿病患者肥胖状态与全因死亡风险的关联研究

目的 分析不同肥胖状态与2型糖尿病（T2DM）患者全因死亡风险的关联。方法 研究对象来自浙江农村社区T2DM队列,该队列2016年完成基线调查,本研究使用的随访数据截至 2021年12月31日,剔除随访期间失访或资料不全者,共纳入10 310例研究对象。根据BMI和腰围将研究对象分为低体重、正常体型、单纯中心性肥胖、单纯全身肥胖、复合超重和复合肥胖6种状态,采用Cox比例风险回归模型分析不同肥胖状态T2DM患者的全因死亡风险比（HR）值及其95%CI。结果 研究对象累计随访57 049.47人年,随访（5.53±0.89）人年,随访期间共死亡971例,死亡密度为1 702.03/10万人年。以正常体型患者为对照,调整混杂因素后低体重患者全因死亡风险增加104%（HR=2.04,95%CI：1.42~2.92）,单纯全身肥胖、复合超重、复合肥胖患者的全因死亡风险分别下降34%（HR=0.66,95%CI：0.53~0.82）、22%（HR=0.78,95%CI：0.66~0.92）、38%（HR=0.62,95%CI：0.49~0.78）,单纯中心性肥胖患者全因死亡风险差异无统计学意义。亚组分析显示,不同性别和不同年龄组低体重T2DM患者全因死亡风险增加,女性复合肥胖患者全因死亡风险较正常体型患者下降50%,而男性该肥胖状态患者全因死亡风险差异无统计学意义;≥65岁老年患者中,单纯全身肥胖、复合超重、复合肥胖患者的全因死亡风险均明显低于正常体型组（HR=0.61,95%CI：0.48~0.78;HR=0.76,95%CI：0.63~0.91;HR=0.56,95%CI：0.42~0.73）,而<65岁的各种肥胖状态患者全因死亡风险差异无统计学意义。敏感性分析结果未见明显变化。结论 T2DM患者全因死亡风险存在“肥胖悖论”现象,低体重患者的全因死亡风险明显高于正常体型者,全身型或复合型超重/肥胖患者的死亡风险明显降低。     

The contribution of smoking to sex differences in mortality

The contribution of smoking to sex differences in mortality is estimated on the basis of data from 12 studies of the mortality of nonsmoking men and women, together with mortality data for comparable general population samples. Most of the data are for samples drawn from the U.S. population from the late 1950s to 1980. The findings from different studies are generally consistent, once methodological factors are taken into account. The findings indicate that, for total mortality, the proportion of sex differences attributable to smoking decreases from about two-thirds at age 40 to about one-quarter at age 80. Over the adult age span, it appears that about half of the sex difference in total mortality is attributable to smoking. Findings for ischemic heart disease mortality show a similar pattern. For lung cancer, it appears that about 90 percent of the sex difference in mortality is attributable to smoking. The estimated contributions of smoking include both the effects of sex differences in smoking habits and the effects of sex differences in the increase in mortality caused by smoking. The quantitative results should be interpreted with caution, since several lines of argument suggest that multivariate analyses controlling for other relevant factors would produce lower estimates of the contribution of smoking to sex differences in mortality. Despite this limitation, the findings analyzed in this review, together with additional evidence from related research, strongly support the conclusion that cigarette smoking makes a major contribution to men's higher mortality, but other factors also play an important role.