Body mass index,cholesterol level and risk of lung cancer in Lithuanian men

Objective

Our objective was to investigate the association between body mass index (BMI), total serum cholesterol (TSC) level and risk of lung cancer in a Lithuanian population-based cohort study.

Materials and methods

The study included 6729 men initially free from cancer. During the follow-up (1978–2008), 358 lung cancer cases were identified. Cox proportional hazards models were used to estimate hazard ratios (HR) and corresponding 95% confidence intervals (95% CI).

Results

Following adjustment for age, smoking, alcohol consumption, and education, BMI 25–29.9 and ≥30.0 kg/m² hazard ratios (HR) were significantly associated with decreasing risk for lung cancer, HR = 0.73; 95% CI: 0.59, 0.91 and 0.62; 95% CI: 0.45, 0.87, respectively (p_trend = 0.001) compared to BMI <25 kg/m². Inverse association between BMI and lung cancer was observed among current smokers. We found no evidence that BMI was associated with decreased lung cancer risk in never smokers, although small sample size precluded meaningful analysis. Not significantly lower risk of lung cancer among participants in the 5th quintile compared with the 1st quintile of TSC concentrations was observed. HR per 1 mmol/l increase of TSC was 0.90; 95% CI: 0.82, 1.00. Findings suggest consistent effects of BMI and TSC when follow-up was 1993–2008.

Conclusion

Our results show an inverse dose-dependent association between lung cancer risk and BMI in Lithuanian men, especially among current smokers. The inverse association could not be attributed to preclinical cancer effect hypothesis. TSC level was not statistically significantly related to a lung cancer incidence.     

体质指数与结肠癌的关系探讨

背景与目的：肥胖被证实为增加结直肠癌的重要因素。有研究表明,无论对于男性还是女性,体质指数（body mass index,BMI）都与结肠癌的发病率有密切关系。因此,本研究探讨BMI与我国结肠癌发病的关系。为结肠癌的预防提供参考。方法：用病例．对照研究方法分析707例首次确诊的结肠癌患者和709名健康人的BMI情况,比较两组人群BMI的情况。结果：首次确诊的结肠癌患者平均BMI为（24．52±4．56）kg／m^2,健康对照人群平均BMI为（23．75±3．14）kg／m^2,结肠癌患者的BMI明显高于健康对照人群（t=-3．72,P〈0．001）。根据性别和年龄的不同进行分组后,可以看出结肠癌患者的BMI比健康对照组高。logistic回归分析,BMI的升高是结肠癌发生的危险因素,OR值为1．059（95％CI。1．029～1．090）。结论：汉族人结肠癌的发生与BMI有关。     

Prospective study of height, body mass index and risk of breast cancer.

The associations of breast cancer risk with height and body mass index have been examined in 291 cases of breast cancer that occurred among 25,967 Norwegian women during a mean follow-up of approximately 14 years (range 12-16 years). There was an overall increased risk of breast cancer with increasing body height, and the relative risk of women in the fourth quartile of height (mean = 170 cm) was 1.43 (95% confidence limits, 1.18-1.73) compared to women in the lowest quartile (mean = 155 cm), after adjusting for age, parity, age at first birth, and county of residence. Simultaneously, there was an overall inverse relation between body mass index (BMI) and breast cancer risk, which, however, was confined to women 50 years or younger. After adjustment for age, parity, age at first birth, and county of residence, the relative risk of women (less than or equal to 50 years) in the highest quartile of BMI (mean Quetelet = 30) was 0.63 (95% confidence limits, 0.48-0.82), compared to women in the lowest (mean Quetelet = 21). We propose that the lower breast cancer risk in shorter women may reflect caloric restriction during the pre- and peripubertal period, which may affect hyperplastic growth, and lead to a reduced number of breast tissue cells. The negative association with BMI may be related to a lower rate of cell division of breast tissue among obese premenopausal women.     

Childhood body mass index growth trajectories and endometrial cancer risk

Previously, we found that excess weight already in childhood has positive associations with endometrial cancer; however, associations with changes in body mass index (BMI) during childhood are not well understood. Therefore, we examined whether growth in childhood BMI is associated with endometrial cancer and its sub‐types. A cohort of 155,505 girls from the Copenhagen School Health Records Register with measured weights and heights at the ages of 6–14 years and born 1930–1989 formed the analytical population. BMI was transformed to age‐specific z scores. Using linear spline multilevel models, each girl's BMI growth trajectory was estimated as the deviance from the average trajectory for three different growth periods (6.25–7.99, 8.0–10.99, 11.0–14.0 years). Via a link to health registers, 1,020 endometrial cancer cases were identified, and Cox regressions were performed. A greater gain in BMI during childhood was positively associated with endometrial cancer but no differences between the different growth periods were detected in models adjusted for baseline BMI. The hazard ratios for the associations with overall growth during childhood per 0.1 z score increase were 1.15 (95% confidence interval [CI]: 1.07–1.24) for all endometrial cancers, 1.12 (95% CI: 1.04–1.21) for estrogen‐dependent cancers, 1.16 (95% CI: 1.06–1.26) for endometrioid adenocarcinomas and 1.46 (95% CI: 1.16–1.84) for non‐estrogen‐dependent cancers. Growth in BMI in early life is positively linked to later endometrial cancer risk. We did not identify any sensitive childhood growth period, which suggests that excess gain in BMI during the entire childhood period should be avoided.     

Childhood body mass index and the risk of prostate cancer in adult men

Background:

Prostate cancer aetiology is poorly understood. It may have origins early in life; previously we found a positive association with childhood height. The effects of early life body mass index (BMI; kg m⁻²) on prostate cancer remain equivocal. We investigated if childhood BMI, independently and adjusted for height, is positively associated with adult prostate cancer.

Methods:

Subjects were a cohort of 125 208 boys formed from the Copenhagen School Health Records Register, born 1930–1969 with height and weight measurements at 7–13 years. Cases were identified through linkage to the Danish Cancer Registry. Cox proportional hazards regressions were performed.

Results:

Overall, 3355 men were diagnosed with prostate cancer. Body mass index during childhood was positively associated with adult prostate cancer. The hazard ratio of prostate cancer was 1.06 (95% confidence interval (CI): 1.01–1.10) per BMI z-score at age 7, and 1.05 (95% CI: 1.01–1.10) per BMI z-score at age 13. Estimates were similar and significant at all other ages. However, adjustment for childhood height attenuated the associations at all but the youngest ages as most estimates became nonsignificant.

Conclusions:

These results suggest that at most childhood ages, BMI does not confer an additional risk for prostate cancer beyond that of height.     

Relation of body mass index to cancer risk in 362,552 Swedish men

Background Obesity has been linked with increased risk for cancers of the colon, kidney, breast, endometrium and gallbladder. For other cancer sites, the relationship with obesity is less well quantified, and the effect of weight change on cancer risk is unclear. Methods We examined the health records of 362,552 Swedish men who underwent at least one physical examination from 1971 to 1992, and were followed until death or the end of 1999. Incident cancer cases were identified by linkage to the Swedish cancer registry. Poisson regression models were used to estimate relative risks of cancer for both body-mass index (BMI) at baseline exam and, in a subgroup of 107,815 men, change in BMI after six years of follow-up, adjusting for age and smoking status. Results Compared to men of normal weight, obese men had a significantly increased risk of all cancers combined (RR = 1.1; 95% CI = 1.0–1.2). The risks were most pronounced for esophageal adenocarcinoma (RR = 2.7; 95% CI = 1.3–5.6), renal cell carcinoma (RR = 1.8; 95% CI = 1.4–2.4), malignant melanoma (RR = 1.4; 95% CI = 1.1–1.7), and cancers of the colon (RR = 1.7; 95% CI = 1.5–2.0), rectum (RR = 1.4; 95% CI = 1.1–1.7), and liver (RR = 3.6; 95% CI = 2.6–5.0). Risk of esophageal squamous cell carcinoma was elevated for underweight men whose BMI was less than 18.5 (RR = 3.1; 95% CI = 1.1–8.3). An excess risk for cancers of the pancreas and connective tissue was observed only among nonsmokers. Compared to men whose weight remained stable, men with more than a 15% increase in BMI after six years of follow-up had an elevated risk of pancreas and renal cell cancers. Conclusions Obesity and weight gain increase the risk for several forms of cancer in men, and underscore the need for further study into carcinogenic mechanisms and preventive interventions.     

Quetelet's index and risk of colon cancer in college alumni.

BACKGROUND: While previous studies suggest that overweight, middle-aged men may face increased risk of colon cancer, it is unclear whether their weights as young adults influence this risk. It is also unknown whether their level of physical activity affects their risk of developing colon cancer. PURPOSE: To determine the relationship between being overweight in middle-age or young adulthood and colon cancer risk, we prospectively studied alumni of Harvard University. We also investigated whether being overweight influences risk differently for men with different levels of physical activity. METHODS: In 1962 or 1966 (1962/1966), alumni completed questionnaires on weight, height, other sociodemographic characteristics, and medical history. We obtained information on weight and height at college entry from university archives. Alumni (n = 17,595) were followed from 1962/1966 to 1988 for colon cancer occurrence, ascertained from follow-up questionnaires in 1977 and 1988 and death certificates. RESULTS: Between 1962/1966 and 1988, 302 cases of colon cancer were diagnosed. Colon cancer risk increased with higher levels of Quetelet's index (weight [kg]/height [m]2) in 1962/1966. Relative risk per unit increase, adjusted for age, physical activity, and parental history of cancer, was 1.08 (95% confidence interval [CI], 1.04-1.13). Quetelet's index at college entry did not predict risk as well (adjusted relative risk per unit increase, 1.05; 95% CI, 1.00-1.10). The heaviest fifth of alumni during both college time and in 1962/1966 had almost two and one-half times the risk of the lightest fifth of alumni (adjusted relative risk, 2.40; 95% CI, 1.40-4.13). When alumni were classified according to activity level in 1962/1966, higher levels of Quetelet's index were significantly associated with colon cancer risk only among those who were less active. CONCLUSIONS: Overweight during middle-age or young adulthood is associated with higher colon cancer risk; in overweight, physically active men, however, the risk of colon cancer may not be increased.     

Tobacco smoking, body mass index, hypertension, and kidney cancer risk in central and eastern Europe

In a case–control study of kidney cancer in four central European countries, with 1097 incident cases and 1476 controls, we found an increased risk for self-reported hypertension and for obesity. Additional unknown risk factors are likely to be responsible for the high rates of kidney cancer in this region.     

The impact of height and body mass index on the risk of testicular cancer in 600,000 Norwegian men

The present study aimed at exploring the relations between body mass index (BMI) and stature and testicular cancer in a huge Norwegian cohort with measured height and weight. Height and weight were measured in 600,000 Norwegian men aged 14–44 years during 1963–2001. Results from parts of the study cohort have been reported previously. During follow-up, 1,357 testicular cancers were registered. Relative risks (RRs) of testicular cancer were estimated using Cox proportional hazards regression. The risk of testicular cancer decreased with adult BMI. Compared with men with normal BMI, overweight and obese men had a relative risk of cancer of 0.89 (95% CI: 0.77–1.03) and 0.83 (95% CI: 0.58–1.17). The relative risk of testicular cancer per unit increase in BMI was 0.97 (95% CI: 0.95–1.00). The risk of testicular cancer was not associated with adolescent BMI. A moderate increase in risk of seminomas was seen with increasing adult height. Compared with men with height 170–79 cm, men with height 180 cm and above had a relative risk of 1.17 (95% CI: 1.00–1.37).     

体质量指数与结直肠癌预后的关系

目的:探讨体质量指数与结直肠癌患者预后的关系.方法:回顾性分析2010年1月至2011年12月新疆医科大学附属肿瘤医院收治的353例行根治手术的结直肠癌患者临床病理资料.将患者分为低体重组(BMI<18.5kg/m2)、正常体重组(18.5kg/m2≤BMI<23kg/m2)、超重组(23kg/m2≤BMI<27.5kg/m2)、肥胖组(BMI≥27.5kg/m2).比较四组临床因素,分析BMI与结直肠癌患者5年生存率的关系.结果:BMI与患者术前CA199有统计学差异(P=0.020),对5年生存率无显著影响(P=0.254).民族、pT分期、术前放化疗、肿瘤分化程度均是结直肠癌独立预后因素(P<0.05).结论:BMI对结直肠癌患者的预后无显著影响.     

Interleukin-6-related genotypes, body mass index, and risk of multiple myeloma and plasmacytoma.

Interleukin-6 (IL-6) promotes normal plasma cell development and proliferation of myeloma cells in culture. We evaluated IL-6 genotypes and body mass index (BMI) in a case-control study of multiple myeloma and plasmacytoma. DNA samples and questionnaires were obtained from incident cases of multiple myeloma (n = 134) and plasmacytoma (n = 16; plasma cell neoplasms) ascertained from the Los Angeles County population-based cancer registry and from siblings or cousins of cases (family controls, n = 112) and population controls (n = 126). Genotypes evaluated included IL-6 promoter gene single nucleotide polymorphisms (SNP) at positions -174, -572, and -597; one variable number of tandem repeats (-373 A(n)T(n)); and one SNP in the IL-6 receptor (IL-6ralpha) gene at position -358. The variant allele of the IL-6 promoter SNP -572 was associated with a roughly 2-fold increased risk of plasma cell neoplasms when cases were compared with family [odds ratio (OR), 1.8; 95% confidence interval (95% CI), 0.7-4.7] or population controls (OR, 2.4; 95% CI, 1.2-4.7). The -373 9A/9A genotype was associated with a decreased risk compared with the most common genotype (OR for cases versus family controls, 0.4; 95% CI, 0.1-1.7; OR for cases versus population controls, 0.3; 95% CI, 0.1-0.9). No other SNPs were associated with risk. Obesity (BMI >or= 30 kg/m(2)) increased risk nonsignificantly by 40% and 80% when cases were compared with family controls or population controls, respectively, relative to persons with a BMI of <25 kg/m(2). These results suggest that IL-6 promoter genotypes may be associated with increased risk of plasma cell neoplasms.     

Serum dehydroepiandrosterone and dehydroepiandrosterone sulfate and the subsequent risk of developing colon cancer.

This purpose of this study was to evaluate whether serum dehydroepiandrosterone (DHEA) and its sulfate conjugate, dehydroepiandrosterone sulfate (DHEAS), are associated with the likelihood of developing colon cancer. A nested case-control study was conducted using the serum bank and cancer registry in Washington County, Maryland. From a population of 20,305 county residents who donated blood in 1974, incident cases of colon cancer that occurred from 1975 to 1991 (n = 117) were matched to one cancer-free control by age, race, and sex. Serum specimens that were stored at -70 degrees C since 1974 were assayed for DHEA and DHEAS. Compared with the controls, the mean serum concentrations of cases were 3% lower for DHEA (P = 0.90) and 13% lower for DHEAS (P = 0.60). When DHEA levels were analyzed according to fourths, no noteworthy associations were observed. Compared with the lowest fourth, the highest fourth of serum DHEAS was nonsignificantly associated with a halving in the risk of colon cancer (odds ratio, 0.50; 95% confidence limits, 0.18, 1.37; Ptrend = 0.22), and further analyses showed the potential protective association was confined largely to males (highest-versus-lowest fourth odds ratio, 0.26; 95% confidence limits, 0.06, 1.16; Ptrend = 0.06). This prospective study does not provide strong evidence that circulating DHEA and DHEAS concentrations are associated with the risk of colon cancer. Among men, DHEAS was associated with a decreased risk of colon cancer, but the association was within the bounds of chance. Further studies are needed to either support or refute the potentially promising lead hinted at by the results for DHEAS.     

Methylation scores for smoking,alcohol consumption and body mass index and risk of seven types of cancer

Methylation marks of exposure to health risk factors may be useful markers of cancer risk as they might better capture current and past exposures than questionnaires, and reflect different individual responses to exposure. We used data from seven case-control studies nested within the Melbourne Collaborative Cohort Study of blood DNA methylation and risk of colorectal, gastric, kidney, lung, prostate and urothelial cancer, and B-cell lymphoma (N cases = 3123). Methylation scores (MS) for smoking, body mass index (BMI), and alcohol consumption were calculated based on published data as weighted averages of methylation values. Rate ratios (RR) and 95% confidence intervals for association with cancer risk were estimated using conditional logistic regression and expressed per SD increase of the MS, with and without adjustment for health-related confounders. The contribution of MS to discriminate cases from controls was evaluated using the area under the curve (AUC). After confounder adjustment, we observed: large associations (RR = 1.5-1.7) with lung cancer risk for smoking MS; moderate associations (RR = 1.2-1.3) with urothelial cancer risk for smoking MS and with mature B-cell neoplasm risk for BMI and alcohol MS; moderate to small associations (RR = 1.1-1.2) for BMI and alcohol MS with several cancer types and cancer overall. Generally small AUC increases were observed after inclusion of several MS in the same model (colorectal, gastric, kidney, urothelial cancers: +3%; lung cancer: +7%; B-cell neoplasms: +8%). Methylation scores for smoking, BMI and alcohol consumption show independent associations with cancer risk, and may provide some improvements in risk prediction.     

The association of physical activity and body mass index with the risk of large bowel polyps.

PURPOSE AND METHOD: Several studies have suggested that physical inactivity and obesity increase the risk for colorectal neoplasia. In this study, we investigated the association of physical activity and body mass index (BMI) with the risk of different types of large bowel polyps. We did an observational analysis nested within a randomized double-blind placebo-controlled chemoprevention trial among patients with one or more recently resected histologically confirmed colorectal adenoma. Nine hundred thirty patients were randomized to calcium (1,200 mg/d, as carbonate) or placebo. Follow-up colonoscopies were conducted approximately 1 and 4 years after the qualifying examination. At study entry, we obtained each subject's current body weight and height, which we used to calculate BMI. After the second study colonoscopy, we asked subjects questions about their leisure time physical activity. Seven hundred eighty-seven subjects completed at least part of the physical activity questionnaire. RESULTS: We found no association between measures of physical activity or BMI and tubular adenomas or hyperplastic polyps. However, among men, there were strong inverse associations observed between physical activity and advanced neoplastic polyps. Compared with men whose total daily energy expenditure was in the lowest tertile, those in the highest tertile had a risk ratio of 0.35 (95% confidence interval, 17-0.72); there was no similar reduction observed among women (risk ratio, 1.21; 95% confidence interval, 0.36-4.03; P for interaction = 0.04). DATA INTERPRETATIONS: We found a significant inverse relationship between several measures of physical activity and risk of advanced colorectal neoplasms, particularly among men. No associations were found between BMI and hyperplastic polyps, tubular adenomas, or advanced neoplastic polyps.     

Alcohol consumption and risk of lung cancer: the Framingham Study

BACKGROUND: Reports on the association between alcohol consumption and the risk of lung cancer have been inconsistent. The purpose of this study was to assess this association in a cohort study. METHODS: This study included 4265 participants in the original population-based Framingham Study cohort and 4973 subjects in the offspring cohort. Alcohol consumption data were collected periodically for both cohorts. We used the risk sets method to match control subjects to each case patient based on age, sex, smoking variables, and year of birth. We used a conditional logistic regression model to estimate the relative risk of lung cancer according to alcohol consumption. RESULTS: Alcohol consumption was generally light to moderate (i.e., <12 g/day) in both cohorts. During mean follow-ups of 32.8 years in the original and 16.2 years in the offspring cohorts, 269 cases of lung cancer occurred. In categories of total alcohol consumption of 0, 0.1-12, 12.1-24, and greater than 24 g/day, the crude incidence rates of lung cancer were 7.4, 13.6, 16.4, and 25.2 cases per 10 000 person-years, respectively, in the original cohort and 6.6, 4.3, 7.9, and 12.3 cases per 10 000 person-years, respectively, in the offspring cohort. However, after adjustment for age, sex, pack-years of smoking, smoking status, and year of birth in a multivariable conditional logistic regression model, relative risks for lung cancer from the lowest to the highest category of alcohol consumption were 1.0 (referent), 1.0 (95% confidence interval [CI] = 0.5 to 2.1), 1.0 (95% CI = 0.5 to 2.3), and 1.1 (95% CI = 0.5 to 2.3), respectively, in the original cohort and 1.0, 1.4 (95% CI = 0.5 to 3.6), 1.1 (95% CI = 0.3 to 3.6), and 2.0 (95% CI = 0.7 to 5.7), respectively, in the offspring cohort. CONCLUSION: Alcohol consumption among subjects in the Framingham Study, most of whom were light to moderate drinkers, was not statistically significantly associated with the risk of lung cancer.     

Serum total and HDL cholesterol and risk of prostate cancer

Background  

Studies suggest a decreased risk of high-grade prostate cancer in men with lower circulating total cholesterol and that statins may protect against aggressive disease. Confirmation in additional populations and examination of associations for lipoprotein subfractions are needed.     

Serum cotinine level as predictor of lung cancer risk.

BACKGROUND: No prospective studies are available on serum cotinine level as a marker of lung cancer risk. METHODS: We analyzed serum cotinine level among 1,741 individuals enrolled since the 1970s in a prospective study of Norwegian volunteers who developed lung cancer during the follow-up and 1,741 matched controls free from lung cancer. Serum cotinine was measured with a competitive immunoassay. Regression dilution was corrected for based on repeated measures on samples from 747 subjects. RESULTS: Mean serum cotinine level was higher in cases than in controls. Compared with subjects with a cotinine level of < or = 5 ng/mL, the odds ratio of lung cancer was increasing linearly, reaching 55.1 (95% confidence interval, 35.7-85.0) among individuals with a serum cotinine level of > 378 ng/mL. There was no clear suggestion of a plateau in risk at high exposure levels. Odds ratios were very similar in men and women. We found no association between serum cotinine level (range, 0.1-9.9 ng/mL) and lung cancer risk among self-reported nonsmokers and long-term quitters (79 cases and 350 controls). DISCUSSION: The association between tobacco smoking and lung cancer risk might be stronger than is estimated from questionnaire-based studies. Serum cotinine level is a predictor of risk of lung cancer among smokers. The reported plateau in risk at high doses is likely due mainly to artifacts. There is no difference between men and women in the carcinogenicity of tobacco smoking.