Body mass index and risk of ovarian cancer

BACKGROUND:

Convincing epidemiologic evidence links excess body mass to increased risks of endometrial and postmenopausal breast cancers, but the relation between body mass index (BMI) and ovarian cancer risk remains inconclusive. Potential similarities regarding a hormonal mechanism in the etiology of female cancers highlight the importance of investigating associations according to menopausal hormone therapy (MHT) use. However, to the authors' knowledge, data addressing whether the relation between BMI and ovarian cancer differs by MHT use are very sparse.

METHODS:

The authors prospectively investigated the association between BMI and ovarian cancer among 94,525 US women who were followed between 1996 through 1997 to December 31, 2003. During 7 years of follow‐up, 303 epithelial ovarian cancer cases were documented.

RESULTS:

Compared with normal weight women (BMI of 18.5‐24.9 kg/m²), the multivariate relative risk (MVRR) of ovarian cancer for obese women (BMI of ≥30 kg/m²) in the cohort as a whole was 1.26 (95% confidence interval [95% CI], 0.94‐1.68). Among women who never used MHT, the MVRR for obese versus normal weight women was 1.83 (95% CI, 1.18‐2.84). In contrast, no relation between BMI and ovarian cancer was apparent among women who ever used MHT (MVRR = 0.96; 95% CI, 0.65‐1.43; P interaction = 0.02). Exploratory analyses also suggested a positive association between BMI and ovarian cancer among women without a family history of ovarian cancer (MVRR comparing obese vs normal weight women = 1.36; 95% CI, 1.00‐1.86), but no relation with BMI was apparent among women with a positive family history of ovarian cancer (MVRR = 0.74; 95% CI, 0.34‐1.62 [P interaction = .02]).

CONCLUSIONS:

Based on the results of the current study, the authors suspect that obesity is associated with enhanced ovarian cancer risk through a hormonal mechanism. Cancer 2009. Published 2009 by the American Cancer Society.     

Dietary patterns and risk of prostate cancer in U.S. men.

We prospectively investigated the associations between dietary patterns and risk of prostate cancer in the Health Professionals Follow-up Study. Between 1986 and 2000, 3,002 incident prostate cancer cases were identified in our cohort. Using factor analysis, two major dietary patterns were identified, a prudent and a western dietary pattern. Dietary patterns were not appreciably associated with risk of total prostate cancer. For the highest versus the lowest quintiles, the multivariable relative risk (RR) for the prudent pattern was 0.94 [95% confidence interval (CI), 0.83-1.06], and for the western pattern, the multivariable RR was 1.03 (95% CI, 0.92-1.17). Neither were these associated with risk of advanced prostate cancer [highest versus lowest quintile, prudent pattern (RR, 1.01; 95% CI, 0.68-1.49); western pattern (RR, 1.13; 95% CI, 0.77-1.67)]. Higher western pattern scores were suggestively associated with a greater risk of advanced prostate cancer among older men [highest versus lowest quintile (RR, 1.35; 95% CI, 0.97-1.90)], but not after adding processed meat to the model [highest versus lowest quintile (RR, 1.11; 95% CI, 0.75-1.65)]. We did not find any evidence for a protective association between prudent pattern and risk of prostate cancer. The lack of association between a western dietary pattern as identified by factor analysis in our cohort and prostate cancer risk suggests that dietary risk factors for prostate cancer are likely to differ from those for other conditions, such as cardiovascular disease and type 2 diabetes, that have been associated with a western dietary pattern in this cohort.     

Body mass index and cancer risk in Korean men and women

Obesity is associated with diverse health risks, but the role of body weight (BMI) as a risk factor for all and site-specific cancers remains controversial and risks for cancer associated with obesity have not been well-characterized in Asians. Body weight and risk for cancer were examined in a 14-year prospective cohort study of 1,213,829 Koreans aged 30-95 years insured by the National Health Insurance Corporation who had a biennial medical evaluation in 1992-1995. Incidence rates for all cancers and site-specific cancers were examined in relation to BMI. Age- and smoking-status adjusted hazard ratios (HR) with 95% confidence intervals (CI) were examined using the Cox proportional hazards model. For both sexes, the average baseline BMI was 23.2 kg/m(2), and the association of risk for all-cancers with BMI was positive. Obese men (BMI >or= 30 kg/m(2)) were at increased risk for developing the following cancers: stomach (1.31, 1.05-1.64), colon (1.42, 1.02-1.98), liver (1.63, 1.27-2.10) and gallbladder (1.65, 1.11-2.44). Obese women (BMI >or= 30 kg/m(2)) were at increased risk for developing liver cancer (1.39, 1.00-1.94), pancreatic cancer (1.80, 1.14-2.86) and breast cancer among women aged >or=50 years old (1.38, 1.00-1.90). The HRs were comparable in never and ever smokers for all cancers and all specific sites except for lung cancer. For all cancers common to both sexes, the association was significantly weaker (p < 0.01) in females. Our study provides further confirmation of the excess cancer risk associated with obesity. Rising obesity in Asian populations raises concern that increasing numbers of avoidable cancer cases will occur among Asians.     

Body mass index in relation to serum prostate‐specific antigen levels and prostate cancer risk

High Body mass index (BMI) has been directly associated with risk of aggressive or fatal prostate cancer. One possible explanation may be an effect of BMI on serum levels of prostate‐specific antigen (PSA). To study the association between BMI and serum PSA as well as prostate cancer risk, a large cohort of men without prostate cancer at baseline was followed prospectively for prostate cancer diagnoses until 2015. Serum PSA and BMI were assessed among 15,827 men at baseline in 2010–2012. During follow‐up, 735 men were diagnosed with prostate cancer with 282 (38.4%) classified as high‐grade cancers. Multivariable linear regression models and natural cubic linear regression splines were fitted for analyses of BMI and log‐PSA. For risk analysis, Cox proportional hazards regression models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) and natural cubic Cox regression splines producing standardized cancer‐free probabilities were fitted. Results showed that baseline Serum PSA decreased by 1.6% (95% CI: ?2.1 to ?1.1) with every one unit increase in BMI. Statistically significant decreases of 3.7, 11.7 and 32.3% were seen for increasing BMI‐categories of 25 < 30, 30 < 35 and ≥35 kg/m², respectively, compared to the reference (18.5 < 25 kg/m²). No statistically significant associations were seen between BMI and prostate cancer risk although results were indicative of a positive association to incidence rates of high‐grade disease and an inverse association to incidence of low‐grade disease. However, findings regarding risk are limited by the short follow‐up time. In conclusion, BMI was inversely associated to PSA‐levels. BMI should be taken into consideration when referring men to a prostate biopsy based on serum PSA‐levels.     

Vitamin E supplements and risk of prostate cancer in U.S. men.

Supplementation with alpha-tocopherol (a form of vitamin E) was associated with decreased risk of prostate cancer in a randomized trial among Finnish smokers. We examined the association between vitamin E supplement use and prostate cancer incidence in the Cancer Prevention Study II Nutrition Cohort. Participants in the study completed a detailed questionnaire at enrollment in 1992-1993. Historical information was also available from a questionnaire completed in 1982 at enrollment in a previous cohort. Through August 31, 1999, we documented 4,281 cases of incident prostate cancer among 72,704 men. Multivariate-adjusted rate ratios (RRs) were calculated using Cox Proportional Hazards models. Regular vitamin E supplement use (>/=4 times per week) was not associated with overall risk of prostate cancer or with risk of advanced prostate cancer at diagnosis. No trend was seen with increasing dose of vitamin E. Men who reported regular vitamin E use in both 1982 and in 1992-1993 were not at lower risk of prostate cancer. Among current smokers, there was a suggestion of slightly reduced risk with regular vitamin E supplement use [RR = 0.87, 95% confidence interval (CI) = 0.67-1.11]. Our results do not support an important role for vitamin E supplements in prostate cancer prevention.     

Serum selenium and risk of prostate cancer in U.S. blacks and whites

Prostate cancer is the fourth most common cancer in men worldwide and the most common cancer in men in the United States, with reported incidence rates for U.S. blacks being the highest in the world. The etiology of prostate cancer and an explanation for the racial disparity in incidence in the United States remain elusive. Epidemiologic studies suggest that selenium, an essential trace element, may protect against the disease. To further explore this hypothesis, we measured serum selenium in 212 cases and 233 controls participating in a multicenter, population-based case-control study that included comparable numbers of U.S. black and white men aged 40-79 years. Serum selenium was inversely associated with risk of prostate cancer (comparing highest to lowest quartiles, OR = 0.71, 95% CI 0.39-1.28; p for trend = 0.11), with similar patterns seen in both blacks and whites. Cubic regression spline analysis of continuous serum selenium indicated a reduced risk of prostate cancer above concentrations of 0.135 microg/ml (median among controls) compared to a reference value set at the median of the lowest selenium quartile. Because both the selenoenzyme GPX and vitamin E can function as antioxidants, we also explored their joint effect. Consistent with other studies, the inverse association with selenium was strongest among men with low serum alpha-tocopherol concentrations. In conclusion, our results suggest a moderately reduced risk of prostate cancer at higher serum selenium concentrations, a finding that can now be extended to include U.S. blacks. Since selenium exposure varies widely throughout the world, further research on optimal concentrations for cancer prevention is justified.     

Body mass index, weight change, and risk of prostate cancer in the Cancer Prevention Study II Nutrition Cohort.

BACKGROUND: Obesity has been associated with aggressive prostate cancer. The extent of this association, which varies by stage and grade, remains unclear. The role of recent weight change had not been previously examined. METHODS: We examined body mass index (BMI) and weight change in relation to incident prostate cancer by disease stage and grade at diagnosis among 69,991 men in the Cancer Prevention Study II Nutrition Cohort. Participants provided information on height and weight in 1982, and again at enrollment in 1992. During follow-up through June 30, 2003 (excluding the first 2 years of follow-up), we documented 5,252 incident prostate cancers. Cox proportional hazards models were used to estimate rate ratios (RR) and 95% confidence intervals (95% CI). RESULTS: The association between BMI in 1992 and risk of prostate cancer differed by stage and grade at diagnosis. BMI was inversely associated with risk of nonmetastatic low-grade prostate cancer (RR, 0.84; 95% CI, 0.66-1.06), but BMI was positively associated with risk of nonmetastatic high-grade prostate cancer (RR, 1.22; 95% CI, 0.96-1.55) and risk of metastatic or fatal prostate cancer (RR, 1.54; 95% CI, 1.06-2.23). Compared with weight maintenance, men who lost >11 pounds between 1982 and 1992 were at a decreased risk of nonmetastatic high-grade prostate cancer (RR, 0.58; 95% CI, 0.42-0.79). CONCLUSION: Obesity increases the risk of more aggressive prostate cancer and may decrease either the occurrence or the likelihood of diagnosis of less-aggressive tumors. Men who lose weight may reduce their risk of prostate cancer.     

Body size and composition and prostate cancer risk.

Reported associations between body measurements and the risk of prostate cancer are weak and inconsistent, possibly because some measures used do not differentiate between adipose and nonadipose tissue, body components that would theoretically have different associations with prostate cancer. Some studies have addressed this problem by estimating lean body mass from subjects' age, height, and weight. In a prospective cohort study of men 27-75 years of age at recruitment in 1990-1994, body measurements were taken by trained interviewers. Nonadipose and adipose mass were calculated from bioelectric impedance analysis. Incident prostate cancers were ascertained by use of the population cancer registry. Altogether 16,336 men contributed 113,535 person-years and 477 cancers, of which 79 were "aggressive," to the analysis. We found no overall association between prostate cancer and any anthropometric measurement. Analysis stratified by cancer aggressiveness revealed modest associations between measures of adiposity and the risk of aggressive disease. On the basis of the WHO cut points and compared with men in the normal range of body mass index, the risk ratio for obese men was 2.2 (95% confidence interval, 1.2-4.1). For each 10-kg increase in fat mass, the risk ratio was 1.4 (95% confidence interval, 1.0-1.8). Energy imbalance may play a role in the development of aggressive prostate cancer.     

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.     

Body mass index and colorectal cancer risk: A Mendelian randomization study

Traditional observational studies have reported a positive association between higher body mass index (BMI) and the risk of colorectal cancer (CRC). However, evidence from other approaches to pursue the causal relationship between BMI and CRC is sparse. A two-sample Mendelian randomization (MR) study was undertaken using 68 single nucleotide polymorphisms (SNPs) from the Japanese genome-wide association study (GWAS) and 654 SNPs from the GWAS catalogue for BMI as sets of instrumental variables. For the analysis of SNP-BMI associations, we undertook a meta-analysis with 36 303 participants in the Japanese Consortium of Genetic Epidemiology studies (J-CGE), comprising normal populations. For the analysis of SNP-CRC associations, we utilized 7636 CRC cases and 37 141 controls from five studies in Japan, and undertook a meta-analysis. Mendelian randomization analysis of inverse-variance weighted method indicated that a one-unit (kg/m²) increase in genetically predicted BMI was associated with an odds ratio of 1.13 (95% confidence interval, 1.06-1.20; P value <.001) for CRC using the set of 68 SNPs, and an odds ratio of 1.07 (1.03-1.11, 0.001) for CRC using the set of 654 SNPs. Sensitivity analyses robustly showed increased odds ratios for CRC for every one-unit increase in genetically predicted BMI. Our MR analyses strongly support the evidence that higher BMI influences the risk of CRC. Although Asians are generally leaner than Europeans and North Americans, avoiding higher BMI seems to be important for the prevention of CRC in Asian populations.     

Body mass index and risk of colorectal cancer according to fatty acid synthase expression in the nurses' health study

Fatty acid synthase (FASN) plays an important role in energy metabolism of fatty acids and is overexpressed in some colon cancers. We investigated whether associations between body mass index (BMI) and risk of colorectal cancer varied according to FASN expression. During follow-up of 109,051 women in the ongoing prospective Nurses' Health Study, a total of 1351 incident colon and rectal cancers were diagnosed between 1986 and 2004. We constructed tissue microarrays of the available resected tumor samples (n = 536), and FASN expression was analyzed by immunohistochemistry. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated using Cox proportional hazards regression models. All statistical tests were two-sided. High BMI was associated with an increased risk of FASN-negative (no or weak expression) colorectal cancer compared with normal BMI (high BMI [≥ 30 kg/m(2)], ie, obese vs normal BMI [18.5-22.9 kg/m(2)], HR = 2.25, 95% CI = 1.49 to 3.40, P(trend) < .001) but not with FASN-positive (moderate to strong expression) colorectal cancer. A statistically significant heterogeneity in colorectal cancer risks was observed between FASN-negative and FASN-positive tumors (P(heterogeneity) = .033). The age-adjusted incidence rates for FASN-positive and FASN-negative colorectal cancers were 10.9 and 7.1, respectively, per 100,000 person-years. This molecular pathological epidemiology study supports a role of energy metabolism in colorectal cancer pathogenesis.     

Body mass index and weight change in men with prostate cancer: progression and mortality

Purpose

Body mass index (BMI) is a modifiable lifestyle factor that has been associated with an increased risk of fatal prostate cancer and biochemical recurrence. The main purpose of the present study was to investigate the association between the exposure BMI at the time of a prostate cancer diagnosis and weight change after diagnosis, and the outcomes of prostate cancer progression and mortality in a large cohort study.

Methods

Data from 4,376 men diagnosed with clinically localized prostate cancer between 1997 and 2002 were analyzed. BMI and weight change were self-reported in 2007. Hazard ratios (HRs) with 95 % confidence intervals (CIs) were estimated in complete-case analysis (n = 3,214) using Cox proportional hazards models.

Results

Progression was experienced among 639 (14.6 %) of the study participants, and in total, 450 (10.3 %) deaths of any cause and 134 (3.1 %) prostate cancer-specific deaths were recorded during follow-up. Obese men had a 47 % increased rate of overall mortality compared to normal weight men (HR 1.47, 95 % CI 1.03–2.10). No statistically significant associations were found for BMI and prostate cancer progression or prostate cancer-specific mortality. A weight loss >5 % after diagnosis almost doubled the rate of overall mortality compared to maintaining a stable weight (HR 1.94, 95 % CI 1.41–2.66), while a weight gain >5 % was associated with an almost doubled increased rate of prostate cancer-specific mortality (HR 1.93, 95 % CI 1.18–3.16).

Conclusions

Being obese was associated with an increased rate of overall mortality, and gaining weight after a prostate cancer diagnosis was associated with an increased rate of prostate cancer-specific mortality.     

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.     

Body mass index and risk of colorectal cancer according to tumor lymphocytic infiltrate

Higher body mass index (BMI), higher body adiposity and obesity have been associated with increased risk of colorectal cancer. Evidence suggests that excess energy balance may influence systemic immune and inflammatory status. Thus, we hypothesized that the positive association between BMI and colorectal cancer risk might differ according to colorectal carcinoma subtypes according to levels of histopathological lymphocytic reaction to tumor. We collected biennial questionnaire data on weight and baseline height information in two prospective cohort studies, the Nurses' Health Study (1980‐2010) and the Health Professionals Follow‐up Study (1986‐2010). Utilizing duplication‐method Cox proportional hazards regression models, we prospectively assessed the association between BMI and risk of colorectal cancer subtypes according to the degree of Crohn's‐like lymphoid reaction, peritumoral lymphocytic reaction, intratumoral periglandular reaction, tumor‐infiltrating lymphocytes, the overall lymphocytic reaction score, or T‐cell [CD3⁺, CD8⁺, CD45RO (PTPRC)⁺ or FOXP3⁺] density in tumor tissue. Statistical significance level was adjusted for multiple hypotheses testing by Bonferroni correction. During follow up of 1,708,029 men and women (over 3,346,752 person‐years), we documented 1,436 incident rectal and colon cancer cases with available formalin‐fixed paraffin‐embedded tumor tissue materials and pathological immunity data. BMI was significantly associated with higher risk of overall colorectal cancer (P_trend < 0.001); however, the association of BMI with colorectal carcinoma risk did not significantly differ by the level of lymphocytic reaction or T‐cell infiltration in tumor tissue status (P_{heterogeneity} > 0.10). BMI may be associated with risk of colorectal cancer regardless of levels of lymphocytic response to tumor.     

Body mass index and risk of breast cancer. A prospective study of 23,826 Norwegian women

The association between body mass index (BMI) and the incidence rate of breast cancer has been examined in 236 cases of breast cancer that developed among 23,826 Norwegian women during 11 to 14 years of follow-up. At the time of height and weight measurement they were 35 to 51 years of age, and at the end of follow-up their age was between 46 and 63 years. There was an overall age-adjusted incidence rate ratio (IRR) of 0.52 (95% confidence limits, 0.34 and 0.77) for women in the highest quartile of BMI compared to women in the lowest quartile, which was confined to an effect observed among women who were diagnosed at age 50 or earlier (IRR = 0.36). The association with BMI displayed an inverse dose-related trend (chi 2 for trend = 14.22, p less than 0.001). The negative trend was particularly pronounced among non-smoking women (chi 2 = 14.63), and no clear trend associate with BMI was observed among women who smoked 10 or more cigarettes per day (chi 2 = 0.41), indicating an interaction between BMI and cigarette smoking (chi 2 interaction = 3.86, p = 0.05). We thus suggest that there is a negative association between body mass index and risk of breast cancer among premenopausal women.     

Body mass index and pancreatic cancer risk: A meta-analysis of prospective studies

A number of studies have examined the association between body mass index (BMI) and risk of pancreatic cancer, but uncertainty about the relationship remains. We performed a meta-analysis to summarize the evidence from prospective studies investigating this association. We searched MEDLINE for studies published in any language from 1966 to November 2006. Prospective studies were included if they reported relative risks (RRs) with 95% confidence intervals (CIs) for the association between BMI and pancreatic cancer incidence or mortality. Study-specific RR estimates were combined by use of a random-effects model. A total of 21 independent prospective studies, involving 3,495,981 individuals and 8,062 pancreatic cancer cases, met the inclusion criteria. The estimated summary RR of pancreatic cancer per 5 kg/m(2) increase in BMI was 1.12 (95% CI, 1.06-1.17; p-heterogeneity = 0.13) in men and women combined, 1.16 (95% CI, 1.05-1.28; p-heterogeneity = 0.001) in men, and 1.10 (95% CI, 1.02-1.19; p-heterogeneity = 0.12) in women. There was no evidence of publication bias (p = 0.58). Findings from this meta-analysis of prospective studies support a positive association between BMI and risk of pancreatic cancer in men and women.     

Body mass index in relation to ovarian cancer survival.

Evidence for an association between indicators of adiposity and survival after ovarian cancer has been inconsistent. A prospective cohort study was conducted in China to examine the relationship between ovarian cancer survival and body mass index (BMI). From the 214 patients recruited in 1999 to 2000 with histopathologically confirmed invasive epithelial ovarian cancer, 207 patients or their close relatives (96.7% of cases) were traced and followed to 2003. Deaths were recorded and Cox proportional hazards regression was used to obtain hazard ratios (HR) and 95% confidence intervals (95% CI) from multivariate models. Reduced survival was observed among patients with BMI > or = 25 kg/m(2) at 5 years before diagnosis (P = 0.001). There were 98 (59.8%) of 164 patients with BMI <25 kg/m(2) survived to the time of interview compared with only 15 women (34.9%) among the 43 patients whose BMI was > or =25 kg/m(2). The HRs significantly increased with higher BMI at 5 years before diagnosis but not at diagnosis nor at age 21 years. The adjusted HR was 2.33 (95% CI, 1.12-4.87) for BMI of > or =25 versus <20 kg/m(2), with a significant dose-response relationship. The HR was 3.31 (95% CI, 1.26-8.73) among patients who had been overweight or obese at age 21 years, but a linear dose-response was not found. We conclude that premorbid BMI may have independent prognostic significance in ovarian cancer.     

Diabetes mellitus and risk of prostate cancer in the health professionals follow‐up study

History of diabetes may be associated with decreased prostate cancer (PCa) risk. Published studies have not always accounted for time since diabetes diagnosis or confounding and effect modification by lifestyle factors. The authors investigated the relationship between diabetes and PCa risk in men in the Health Professionals Follow‐Up Study from 1986 to 2004. During that time, 4,511 new PCa cases were identified. Multivariate hazard ratios (HR) were estimated using Cox regression. The HR of PCa comparing men with vs. without diabetes was 0.83 and 95% confidence interval (CI): 0.74, 0.94. PCa risk was not reduced in the first year after diabetes diagnosis (HR: 1.30, CI: 0.97, 1.72), was lower for men diagnosed for 1–6 years (HR: 0.82, CI: 0.66, 1.02), and was even lower for men who had been diagnosed for 6–15 (HR: 0.75, CI: 0.61, 0.93) or >15 years (HR: 0.78, CI: 0.63, 0.96). Reduced PCa risk was stronger in men diagnosed before 1994 (pre‐PSA era) vs. after 1994. The authors also demonstrated that obese and diabetic men had a lower HR for PCa than those who were either not obese and diabetic or obese and non‐diabetic. Results are consistent with the hypothesis that diabetes is associated with reduced PCa risk. Potential biological mechanisms are discussed. © 2008 Wiley‐Liss, Inc.     

Body mass index and smoking-related lung cancer risk in the Singapore Chinese Health Study

Background:

Smokers with low body mass index (BMI) may be more susceptible to lung cancer.

Methods:

We prospectively examined the association between baseline BMI and lung cancer risk in the Singapore Chinese Health Study, a cohort of 63 257 Chinese enrolled between 1993 and 1998.

Results:

After adjustment for smoking intensity and duration, BMI was inversely associated with risk of lung cancer among current smokers (P for trend=0.0004). Current smokers at different dosage of smoking with low BMI had significantly higher risk for lung cancer than those with high BMI. Hazard ratios (95% confidence intervals) of lung cancer for heavy smokers with BMI of ⩾28, 24–<28, 20–<24, and <20 kg m⁻² were 6.37 (2.10–19.30), 9.01 (5.04–16.10), 8.53 (6.35–11.5), and 11.12 (6.60–18.70), respectively, as compared with nonsmokers. BMI had no modifying effects on lung cancer risk among nonsmokers and former smokers.

Conclusion:

Smokers with lower BMI may experience an enhanced risk of lung cancer. The findings have significant public-health implication given the increase in smoking prevalence in developing countries, where people still have relatively low BMI.