Body mass index and esophageal and gastric cancer: A pooled analysis of 10 population-based cohort studies in Japan

The effect of body mass index (BMI) on esophageal and gastric carcinogenesis might be heterogeneous, depending on subtype or subsite. However, findings from prospective evaluations of BMI associated with these cancers among Asian populations have been inconsistent and limited, especially for esophageal adenocarcinoma and gastric cardia cancer. We performed a pooled analysis of 10 population-based cohort studies to examine this association in 394,247 Japanese individuals. We used Cox proportional hazards regression to estimate study-specific hazard ratios (HRs) and 95% confidence intervals (CIs), then pooled these estimates to calculate summary HRs with a random effects model. During 5,750,107 person-years of follow-up, 1569 esophageal cancer (1038 squamous cell carcinoma and 86 adenocarcinoma) and 11,095 gastric (728 cardia and 5620 noncardia) cancer incident cases were identified. An inverse association was observed between BMI and esophageal squamous cell carcinoma (HR per 5-kg/m² increase 0.57, 95% CI 0.50–0.65), whereas a positive association was seen in gastric cardia cancer (HR 1.15, 95% CI 1.00–1.32). A nonsignificant and significant positive association for overweight or obese (BMI ≥25 kg/m²) relative to BMI <25 kg/m² was observed with esophageal adenocarcinoma (HR 1.32, 95% CI 0.80–2.17) and gastric cardia cancer (HR 1.24, 95% CI 1.05–1.46), respectively. No clear association with BMI was found for gastric noncardia cancer. This prospective study—the largest in an Asian country—provides a comprehensive quantitative estimate of the association of BMI with upper gastrointestinal cancer and confirms the subtype- or subsite-specific carcinogenic impact of BMI in a Japanese population.     

Central adiposity,obesity during early adulthood,and pancreatic cancer mortality in a pooled analysis of cohort studies

BackgroundBody mass index (BMI), a measure of obesity typically assessed in middle age or later, is known to be positively associated with pancreatic cancer. However, little evidence exists regarding the influence of central adiposity, a high BMI during early adulthood, and weight gain after early adulthood on pancreatic cancer risk.DesignWe conducted a pooled analysis of individual-level data from 20 prospective cohort studies in the National Cancer Institute BMI and Mortality Cohort Consortium to examine the association of pancreatic cancer mortality with measures of central adiposity (e.g. waist circumference; n = 647 478; 1947 pancreatic cancer deaths), BMI during early adulthood (ages 18–21 years) and BMI change between early adulthood and cohort enrollment, mostly in middle age or later (n = 1 096 492; 3223 pancreatic cancer deaths). Multivariable hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated using Cox proportional hazards regression models.ResultsHigher waist-to-hip ratio (HR = 1.09, 95% CI 1.02–1.17 per 0.1 increment) and waist circumference (HR = 1.07, 95% CI 1.00–1.14 per 10 cm) were associated with increased risk of pancreatic cancer mortality, even when adjusted for BMI at baseline. BMI during early adulthood was associated with increased pancreatic cancer mortality (HR = 1.18, 95% CI 1.11–1.25 per 5 kg/m²), with increased risk observed in both overweight and obese individuals (compared with BMI of 21.0 to <23 kg/m², HR = 1.36, 95% CI 1.20–1.55 for BMI 25.0 < 27.5 kg/m², HR = 1.48, 95% CI 1.20–1.84 for BMI 27.5 to <30 kg/m², HR = 1.43, 95% CI 1.11–1.85 for BMI ≥30 kg/m²). BMI gain after early adulthood, adjusted for early adult BMI, was less strongly associated with pancreatic cancer mortality (HR = 1.05, 95% CI 1.01–1.10 per 5 kg/m²).ConclusionsOur results support an association between pancreatic cancer mortality and central obesity, independent of BMI, and also suggest that being overweight or obese during early adulthood may be important in influencing pancreatic cancer mortality risk later in life.     

Prospective study of adiposity and weight change in relation to prostate cancer incidence and mortality

BACKGROUND.

Adiposity has been linked inconsistently with prostate cancer, and few studies have evaluated whether such associations vary by disease aggressiveness.

METHODS.

The authors prospectively examined body mass index (BMI) and adult weight change in relation to prostate cancer incidence and mortality in 287,760 men ages 50 years to 71 years at enrollment (1995–1996) in the National Institutes of Health‐AARP Diet and Health Study. At baseline, participants completed questionnaires regarding height, weight, and cancer screening practices, including digital rectal examinations and prostate‐specific antigen tests. Cox regression analysis was used to calculate relative risks (RR) and 95% confidence intervals (95% CIs).

RESULTS.

In total, 9986 incident prostate cancers were identified during 5 years of follow‐up, and 173 prostate cancer deaths were ascertained during 6 years of follow‐up. In multivariate models, higher baseline BMI was associated with significantly reduced total prostate cancer incidence, largely because of the relationship with localized tumors (for men in the highest BMI category [≥40 kg/m²] vs men in the lowest BMI category [<25 kg/m²]: RR, 0.67; 95% CI, 0.50–0.89; P = .0006). Conversely, a significant elevation in prostate cancer mortality was observed at higher BMI levels (BMI <25 kg/m²: RR, 1.0 [referent group]; BMI 25–29.9 kg/m²: RR, 1.25; 95% CI, 0.87–1.80; BMI 30–34.9 kg/m²: RR, 1.46; 95% CI, 0.92–2.33; and BMI ≥35 kg/m²: RR, 2.12; 95% CI, 1.08–4.15; P = .02). Adult weight gain from age 18 years to baseline also was associated positively with fatal prostate cancer (P = .009), but not with incident disease.

CONCLUSIONS.

Although adiposity was not related positively to prostate cancer incidence, higher BMI and adult weight gain increased the risk of dying from prostate cancer. Cancer 2007. Published 2007 by the American Cancer Society.     

Role of BMI and age in predicting pathologic vertebral fractures in newly diagnosed multiple myeloma patients: A retrospective cohort study

Vertebral fractures affect approximately 30% of myeloma patients and lead to a poor impact on survival and life quality. In general, age and body mass index (BMI) are reported to have an important role in vertebral fractures. However, the triangle relationship among age, BMI, and vertebral fractures is still unclear in newly diagnosed multiple myeloma (NDMM) patients. This study recruited consecutive 394 patients with NDMM at Taipei Veterans General Hospital between January 1, 2005 and December 31, 2015. Risk factors for vertebral fractures in NDMM patients were collected and analyzed. The survival curves were demonstrated using Kaplan‐Meier estimate. In total, 301 (76.4%) NDMM patients were enrolled in the cohort. In the median follow‐up period of 18.0 months, the median survival duration in those with vertebral fractures ≥ 2 was shorter than those with vertebral fracture < 2 (59.3 vs 28.6 months; P = 0.017). In multivariate Poisson regression, BMI < 18.5 kg/m² declared increased vertebral fractures compared with BMI ≥ 24.0 kg/m² (adjusted RR, 2.79; 95% CI, 1.44–5.43). In multivariable logistic regression, BMI < 18.5 kg/m² was an independent risk factor for vertebral fractures ≥ 2 compared with BMI ≥ 24.0 kg/m² (adjusted OR, 6.05; 95% CI, 2.43–15.08). Among age stratifications, patients with both old age and low BMI were at a greater risk suffering from increased vertebral fractures, especially in patients > 75 years and BMI < 18.5 kg/m² (adjusted RR, 12.22; 95% CI, 3.02–49.40). This is the first study that demonstrated that age had a significant impact on vertebral fractures in NDMM patients with low BMI. Elder patients with low BMI should consider to routinely receive spinal radiographic examinations and regular follow‐up.     

Body mass index,calcium supplementation and risk of colorectal adenomas

Calcium supplementation (1,200 mg/day) did not significantly reduce colorectal adenomas in our recent randomized, controlled trial (Vitamin D/Calcium Polyp Prevention Study, VCPPS, 2004–2013) in contrast to our previous trial (Calcium Polyp Prevention Study, CPPS, 1988–1996). To reconcile these findings, we identified participant characteristics that differed between the study populations and modified the effect of calcium supplementation on adenomas or high-risk findings (advanced or multiple adenomas). Compared to the CPPS, more participants in the VCPPS were obese (body mass index (BMI) ≥30 kg/m²; 37.5% vs. 24.4%) and fewer had normal BMI (BMI <25 kg/m²; 18.5% vs. 31%). BMI appeared to modify the effect of calcium supplementation on adenomas and especially on high risk-findings: in the VCPPS, there was a 44% reduction in high-risk findings among individuals whose BMI was normal (RR = 0.56, 95% CI = 0.26–1.23), but not among overweight (RR = 1.09, 95% CI = 0.62–1.91) or obese (RR = 1.54, 95% CI = 0.92–2.57) individuals (p_interaction = 0.03). Similarly, in the CPPS, there was a 56% reduction in high-risk findings among individuals whose BMI was normal (RR = 0.44, 95% CI = 0.26–0.74), but not among overweight (RR = 0.87, 95% CI = 0.55–1.39) or obese (RR = 1.02, 95% CI = 0.57–1.82) individuals (p_interaction = 0.02). Standardization of each trial's findings to the BMI distribution in the other attenuated calcium's protective effect on adenomas in the CPPS but enhanced it in the VCPPS. In conclusion, 1,200 mg/day calcium supplementation may reduce risk of colorectal adenomas among those with normal BMI but not in overweight or obese individuals; and differences in BMI distribution partially account for the apparent difference in calcium efficacy between the two trials.     

A meta-analysis on alcohol drinking and esophageal and gastric cardia adenocarcinoma risk

BackgroundIn order to provide a precise quantification of the association between alcohol drinking and esophageal and gastric cardia adenocarcinoma risk, we conducted a meta-analysis of available data.Patients and methodsWe identified 20 case–control and 4 cohort studies, including a total of 5500 cases. We derived meta-analytic estimates using random-effects models, taking into account correlation between estimates, and we carried out a dose–risk analysis using nonlinear random-effects meta-regression models.ResultsThe relative risk (RR) for drinkers versus nondrinkers was 0.96 [95% confidence interval (CI) 0.85–1.09] overall, 0.87 (95% CI 0.74–1.01) for esophageal adenocarcinoma and 0.89 (95% CI 0.76–1.03) for gastric cardia adenocarcinoma. Compared with nondrinkers, the pooled RRs were 0.86 for light (≤1 drink per day), 0.90 for moderate (1 to <4 drinks per day), and 1.16 for heavy (≥4 drinks per day) alcohol drinking. The dose–risk model found a minimum at 25 g/day, and the curve was <1 up to 70 g/day.ConclusionsThis meta-analysis provides definite evidence of an absence of association between alcohol drinking and esophageal and gastric cardia adenocarcinoma risk, even at higher doses of consumption.     

Obesity and incidence of lung cancer: A meta‐analysis

To date, the relationship between obesity and the incidence of lung cancer remains unclear and inconclusive. Thus, we conducted a meta‐analysis of published studies to provide a quantitative evaluation of this association. Relevant studies were identified through PubMed and EMBASE databases from 1966 to December 2011, as well as through the reference lists of retrieved articles. A total of 31 articles were included in this meta‐analysis. Overall, excess body weight (body mass index, BMI ≥ 25 kg/m²) was inversely associated with lung cancer incidence (relative risk, RR = 0.79; 95% confidence interval, CI: 0.73–0.85) compared with normal weight (BMI = 18.5‐24.9 kg/m²). The association did not change with stratification by sex, study population, study design, and BMI measurement method. However, when stratified by smoking status, the inverse association between excess body weight and lung cancer incidence in current (RR = 0.63, 95% CI: 0.57–0.70) and former (RR = 0.73, 95% CI: 0.58–0.91) smokers was strengthened. In non‐smokers, the association was also statistically significant (RR = 0.83, 95% CI: 0.70–0.98), although the link was weakened to some extent. The stratified analyses also showed that excess body weight was inversely associated with squamous cell carcinoma (RR = 0.68, 95% CI: 0.58–0.80) and adenocarcinoma (RR = 0.79, 95% CI: 0.65–0.96). No statistically significant link was found between excess body weight and small cell carcinoma (RR = 0.99, 95% CI: 0.66–1.48). The results of this meta‐analysis indicate that overweight and obesity are protective factors against lung cancer, especially in current and former smokers.     

Height and Body Mass Index in Relation to Esophageal Cancer; 23-year Follow-up of Two Million Norwegian Men and Women

Objective: Associations between body mass index (BMI) and stature and cancers at different sites have been explored in a number of studies. For esophageal cancer there seems to be different effects of BMI for different histological subtypes. We explored these relations in a Norwegian cohort. Material and methods: Height and weight were measured in 2 million Norwegians during 1963-2001. Duringfollow-up, 2245 histologically verified esophageal cancer cases were registered. Relative risks (RR) of esophageal cancer were estimated using proportional Cox regression. Results: Compared with normal weighted (BMI 18.5-24.9 kg/m²) an increased risk of esophageal adenocarcinoma (OA) was observed in overweight men (BMI 25-29 kg/m²): RR=1.80 (95% CI: 1.48-2.19) and in obese men (BMI 30kg/m²): RR=2.58 (95% CI: 1.81-3.68). The corresponding risk estimates for women were RR=1.64 (95% CI: 1.08-2.49) and RR=2.06 (95% CI: 1.25-3.39). The opposite relation was observed for esophageal squamous cell carcinoma (OSCC). For overweight men the RR of OSCC was 0.72 (95% CI: 0.63-0.82) and 0.68 (95% CI: 0.50-0.93) for obese. The corresponding RR estimates for women were 0.52 (95% CI: 0.42-0.65) and 0.43 (95% CI: 0.32-0.59). In addition, the lowest men had the highest risk of esophageal cancer in general. Adjustment for smoking did not change these relations. Conclusion: BMI had opposite relations to the two most common histological groups of esophageal cancer. While low BMI increased the risk of OSCC, high BMI increased the risk of OA. An increased risk of esophageal cancer was found in the lowest men.     

Body Mass Index (BMI), BMI Change,and Overall Survival in Patients With SCLC and NSCLC: A Pooled Analysis of the International Lung Cancer Consortium

IntroductionThe relationships between morbid obesity, changes in body mass index (BMI) before cancer diagnosis, and lung cancer outcomes by histology (SCLC and NSCLC) have not been well studied.MethodsIndividual level data analysis was performed on 25,430 patients with NSCLC and 2787 patients with SCLC from 16 studies of the International Lung Cancer Consortium evaluating the association between various BMI variables and lung cancer overall survival, reported as adjusted hazard ratios (aHRs) from Cox proportional hazards models and adjusted penalized smoothing spline plots.ResultsOverall survival of NSCLC had putative U-shaped hazard ratio relationships with BMI based on spline plots: being underweight (BMI < 18.5 kg/m²; aHR = 1.56; 95% confidence interval [CI]:1.43–1.70) or morbidly overweight (BMI > 40 kg/m²; aHR = 1.09; 95% CI: 0.95–1.26) at the time of diagnosis was associated with worse stage-specific prognosis, whereas being overweight (25 kg/m² ≤ BMI < 30 kg/m²; aHR = 0.89; 95% CI: 0.85–0.95) or obese (30 kg/m² ≤ BMI ≤ 40 kg/m²; aHR = 0.86; 95% CI: 0.82–0.91) was associated with improved survival. Although not significant, a similar pattern was seen with SCLC. Compared with an increased or stable BMI from the period between young adulthood until date of diagnosis, a decreased BMI was associated with worse outcomes in NSCLC (aHR = 1.24; 95% CI: 1.2–1.3) and SCLC patients (aHR=1.26 (95% CI: 1.0–1.6). Decreased BMI was consistently associated with worse outcome, across clinicodemographic subsets.ConclusionsBoth being underweight or morbidly obese at time of diagnosis is associated with lower stage-specific survival in independent assessments of NSCLC and SCLC patients. In addition, a decrease in BMI at lung cancer diagnosis relative to early adulthood is a consistent marker of poor survival.     

Association between body mass index and the colorectal cancer risk in Japan: pooled analysis of population-based cohort studies in Japan

BackgroundObesity has been recognized as important risk factors for colorectal cancer. However, limited evidence is available on colorectal cancer and body mass index (BMI) in Asian population.MethodsWe conducted a pooled analysis of eight population-based prospective cohorts studies in Japan with more than 300 000 subjects to evaluate an impact of obesity in terms of BMI on colorectal cancer risk with unified categories. We estimated summary hazard ratio (HR) by pooling of study-specific HR for BMI categories with random effect model.ResultsWe found a significant positive association between BMI and colorectal cancer risk in male and female. Adjusted HRs for 1 kg/m² increase were 1.03 [95% confidence interval (CI) 1.02–1.04] for males and 1.02 (95% CI 1.00–1.03) for females. The association was stronger in colon, especially in proximal colon, relative to rectum. Males showed a stronger association than females. Population attributable fraction for colorectal cancer by BMI ≥25 kg/m² was 3.62% (95% CI 1.91–5.30) for males and 2.62% (95% CI 0.74–4.47) for females.ConclusionsWe found significant association between BMI and colorectal cancer risk by pooling of data from cohort studies with considerable number of subjects among Japanese population. This information is important in cancer control planning, especially in Asian population.     

Anthropometric and reproductive factors and risk of esophageal and gastric cancer by subtype and subsite: Results from the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort

Obesity has been associated with upper gastrointestinal cancers; however, there are limited prospective data on associations by subtype/subsite. Obesity can impact hormonal factors, which have been hypothesized to play a role in these cancers. We investigated anthropometric and reproductive factors in relation to esophageal and gastric cancer by subtype and subsite for 476,160 participants from the European Prospective Investigation into Cancer and Nutrition cohort. Multivariable hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox models. During a mean follow-up of 14 years, 220 esophageal adenocarcinomas (EA), 195 esophageal squamous cell carcinomas, 243 gastric cardia (GC) and 373 gastric noncardia (GNC) cancers were diagnosed. Body mass index (BMI) was associated with EA in men (BMI ≥30 vs. 18.5–25 kg/m²: HR = 1.94, 95% CI: 1.25–3.03) and women (HR = 2.66, 95% CI: 1.15–6.19); however, adjustment for waist-to-hip ratio (WHR) attenuated these associations. After mutual adjustment for BMI and HC, respectively, WHR and waist circumference (WC) were associated with EA in men (HR = 3.47, 95% CI: 1.99–6.06 for WHR >0.96 vs. <0.91; HR = 2.67, 95% CI: 1.52–4.72 for WC >98 vs. <90 cm) and women (HR = 4.40, 95% CI: 1.35–14.33 for WHR >0.82 vs. <0.76; HR = 5.67, 95% CI: 1.76–18.26 for WC >84 vs. <74 cm). WHR was also positively associated with GC in women, and WC was positively associated with GC in men. Inverse associations were observed between parity and EA (HR = 0.38, 95% CI: 0.14–0.99; >2 vs. 0) and age at first pregnancy and GNC (HR = 0.54, 95% CI: 0.32–0.91; >26 vs. <22 years); whereas bilateral ovariectomy was positively associated with GNC (HR = 1.87, 95% CI: 1.04–3.36). These findings support a role for hormonal pathways in upper gastrointestinal cancers.     

Body mass index, effect modifiers, and risk of pancreatic cancer: a pooled study of seven prospective cohorts

Objective

To investigate whether the positive association of body mass index (BMI, kg/m²) with risk of pancreatic cancer is modified by age, sex, smoking status, physical activity, and history of diabetes.

Methods

In a pooled analysis of primary data of seven prospective cohorts including 458,070 men and 485,689 women, we identified 2,454 patients with incident pancreatic cancer during an average 6.9 years of follow-up. Cox proportional hazard regression models were used in data analysis.

Results

In a random-effects meta-analysis, for every 5 kg/m² increment in BMI, the summary relative risk (RR) was 1.06 (95% confidence interval (CI) 0.99–1.13) for men and 1.12 (95% CI 1.05–1.19) for women. The aggregate analysis showed that compared with normal weight (BMI: 18.5 to <25), the adjusted RR was 1.13 (95% CI 1.03–1.23) for overweight (BMI: 25 to <30) and 1.19 (95% CI 1.05–1.35) for obesity class I (BMI: 30 to <35). Tests of interactions of BMI effects by other risk factors were not statistically significant. Every 5 kg/m² increment in BMI was associated with an increased risk of pancreatic cancer among never and former smokers, but not among current smokers (P-interaction = 0.08).

Conclusion

The present evidence suggests that a high BMI is an independent risk factor of pancreatic cancer.     

An update of the WCRF/AICR systematic literature review and meta-analysis on dietary and anthropometric factors and esophageal cancer risk

BackgroundIn the 2007 World Cancer Research Fund/American Institute for Cancer Research Second Expert Report, the expert panel judged that there was strong evidence that alcoholic drinks and body fatness increased esophageal cancer risk, whereas fruits and vegetables probably decreased its risk. The judgments were mainly based on case–control studies. As part of the Continuous Update Project, we updated the scientific evidence accumulated from cohort studies in this topic.MethodsWe updated the Continuous Update Project database up to 10 January 2017 by searching in PubMed and conducted dose–response meta-analyses to estimate summary relative risks (RRs) and 95% confidence intervals (CIs) using random effects model.ResultsA total of 57 cohort studies were included in 13 meta-analyses. Esophageal adenocarcinoma risk was inversely related to vegetable intake (RR per 100 g/day: 0.89, 95% CI: 0.80–0.99,n = 3) and directly associated with body mass index (RR per 5 kg/m²: 1.47, 95% CI: 1.34–1.61,n = 9). For esophageal squamous cell carcinoma, inverse associations were observed with fruit intake (RR for 100 g/day increment: 0.84, 95% CI: 0.75–0.94,n = 3) and body mass index (RR for 5 kg/m² increment: 0.64, 95% CI: 0.56–0.73,n = 8), and direct associations with intakes of processed meats (RR for 50 g/day increment: 1.59, 95% CI: 1.11–2.28,n = 3), processed and red meats (RR for 100 g/day increment: 1.37, 95% CI: 1.04–1.82,n = 3) and alcohol (RR for 10 g/day increment: 1.25, 95% CI: 1.12–1.41,n = 6).ConclusionsEvidence from cohort studies suggested a protective role of vegetables and body weight control in esophageal adenocarcinomas development. For squamous cell carcinomas, higher intakes of red and processed meats and alcohol may increase the risk, whereas fruits intake may play a protective role.     

Obesity Is Associated With Increased Relative Risk of Diffuse Large B-Cell Lymphoma: A Meta-Analysis of Observational Studies

BackgroundThe relation between body mass index (BMI) and incidence of diffuse large B-cell lymphoma (DLBCL) has been suggested, but no systematic review has been undertaken.Material and MethodsWe performed a literature search through December 2012. Meta-analyses were performed to quantify the relative risk (RR) of DLBCL incidence in overweight and obese persons compared with normal weight individuals using the random-effects model. Subset analyses were performed according to study design, sex, and geographic region. Overweight was defined as a BMI 25 to 29.9 kg/m², and obesity was defined as a BMI of 30 kg/m². Meta-regression, using an unrestricted maximum likelihood model, was performed to evaluate the linear association between BMI and odds of DLBCL.ResultsOur study included 6 case-control and 10 cohort studies. The RR of DLBCL in overweight individuals was 1.14 (95% confidence interval [CI], 1.04-1.24; P = .004), and in obese individuals, RR was 1.29 (95% CI, 1.16-1.43; P < .001). The RR of DLBCL in overweight men and women was 1.22 and 1.27, respectively. In overweight individuals, both prospective and case-control studies showed an RR of 1.13. The RR of DLBCL in obese men and women was 1.40 and 1.34, respectively. In obese individuals, the RR in prospective studies was 1.25 and in case-control studies it was 1.33. Meta-regression analysis showed a 14% increase in DLBCL incidence for each 10 kg/m² increase in BMI.ConclusionAn increased BMI is associated with higher RR of DLBCL regardless of sex. Also, there seems to be a linear association between BMI and DLBCL incidence.     

Body mass index and incidence of localized and advanced prostate cancer--a dose-response meta-analysis of prospective studies

BackgroundThe relationship between obesity and risk of prostate cancer (PCa) is unclear; however, etiologic heterogeneity by subtype of PCa (localized, advanced) related to obesity was suggested. Therefore, we conducted a dose–response meta-analysis of prospective studies to assess the association between body mass index (BMI) and risk of localized and advanced PCa.Materials and methodsRelevant prospective studies were identified by a search of Medline and Embase databases to 03 October 2011. Twelve studies on localized PCa (1 033 009 men, 19 130 cases) and 13 on advanced PCa (1 080 790 men, 7067 cases) were identified. We carried out a dose–response meta-analysis using random-effects model.ResultsFor localized PCa, we observed an inverse linear relationship with BMI [P_trend < 0.001, relative risk (RR): 0.94 (95% confidence interval, 95% CI, 0.91–0.97) for every 5 kg/m² increase]; there was no evidence of heterogeneity (P_{heterogeneity} = 0.27). For advanced PCa, we observed a linear direct relationship with BMI (P_trend = 0.001, RR: 1.09 (95% CI 1.02–1.16) for every 5 kg/m² increase); there was weak evidence of heterogeneity (P_{heterogeneity} = 0.08). Omitting one study that contributed substantially to the heterogeneity yielded a pooled RR of 1.07 (95% CI 1.01–1.13) for every 5 kg/m² increase (P_{heterogeneity} = 0.26).ConclusionsThe quantitative summary of the accumulated evidence indicates that obesity may have a dual effect on PCa—a decreased risk for localized PCa and an increased risk for advanced PCa.     

Body mass index and risk of gastric cancer: A 30‐year follow‐up study in the Linxian general population trial cohort

Although a number of previous studies have noted either positive or no association for body mass index (BMI) and gastric cancer risk, little evidence exists in the Chinese population. We prospectively examined the associations of BMI with risk of gastric cancer in the Linxian General Population Trial cohort, with 29 584 healthy adults enrolled in 1985 and followed through to the end of 2014. Body weight and height were measured during physical examination at baseline and BMI was calculated as weight in kilograms divided by height in meters squared. Body mass index from 138 subjects was missing, and a total of 29 446 participants were included in the final analysis. Cox proportional hazards models were used to estimate hazard ratios and 95% confidence intervals. During 30 years of follow‐up, we confirmed 1716 newly diagnosed gastric cardia adenocarcinoma (GCA) cases and 626 new gastric non‐cardia adenocarcinoma (GNCA) cases. Overall, compared to the lowest quartile (BMI <20.32 kg/m²), subjects in the fourth quartile (BMI ≥23.31 kg/m²) subjects had lower risk of developing GNCA (hazard ratio, 0.65; 95% confidence interval, 0.51–0.83). Age‐ and sex‐specific analyses showed that this protective effect was only observed in men and older (52 + years) persons. No associations were observed for BMI with GCA incidence. Higher BMI was associated with decreased risk of GNCA in this population, particularly in men and older persons. Future studies are needed to confirm these findings. The trial is registered with ClinicalTrials.gov: NCT00342654.     

An update of the WCRF/AICR systematic literature review on esophageal and gastric cancers and citrus fruits intake

Purpose

The 2007 World Cancer Research Fund/American Institute for Cancer Research expert report concluded that foods containing vitamin C probably protect against esophageal cancer and fruits probably protect against gastric cancer. Most of the previous evidence was from case–control studies, which may be affected by recall and selection biases. More recently, several cohort studies have examined these associations. We conducted a systematic literature review of prospective studies on citrus fruits intake and risk of esophageal and gastric cancers.

Methods

PubMed was searched for studies published until 1 March 2016. We calculated summary relative risks and 95 % confidence intervals (95 % CI) using random-effects models.

Results

With each 100 g/day increase of citrus fruits intake, a marginally significant decreased risk of esophageal cancer was observed (summary RR 0.86, 95 % CI 0.74–1.00, 1,057 cases, six studies). The associations were similar for squamous cell carcinoma (RR 0.87, 95 % CI 0.69–1.08, three studies) and esophageal adenocarcinoma (RR 0.93, 95 % CI 0.78–1.11, three studies). For gastric cancer, the nonsignificant inverse association was observed for gastric cardia cancer (RR 0.75, 95 % CI 0.55–1.01, three studies), but not for gastric non-cardia cancer (RR 1.02, 95 % CI 0.90–1.16, four studies). Consistent summary inverse associations were observed when comparing the highest with lowest intake, with statistically significant associations for esophageal (RR 0.77, 95 % CI 0.64–0.91, seven studies) and gastric cardia cancers (RR 0.62, 95 % CI 0.39–0.99, three studies).

Conclusions

Citrus fruits may decrease the risk of esophageal and gastric cardia cancers, but further studies are needed.

     

Body mass,tobacco and alcohol and risk of esophageal,gastric cardia,and gastric non-cardia adenocarcinoma among men and women in a nested case-control study

Objectives: To prospectively assess the influence of body mass index (BMI), tobacco, and alcohol on the occurrence of esophageal, gastric cardia, and non-cardia gastric adenocarcinoma, and to detect any sex differences that could explain the male predominance of these tumors.Methods: A case-control study nested in the General Practitioner Research Database in the United Kingdom, 1994–2001. Odds ratios (ORs) were calculated with 95% confidence intervals (CI), including multivariate analysis.Results: During follow-up of 4,340,207 person-years, we identified 287 esophageal adenocarcinomas, 195 gastric cardia adenocarcinomas, 327 gastric non-cardia adenocarcinomas, and 10,000 controls. A positive association was found between overweight (BMI > 25 kg/m²) and esophageal adenocarcinoma (OR 1.67, 95% CI 1.22–2.30), and gastric cardia adenocarcinoma (OR 1.46, 95% CI 0.98–2.18), but not non-cardia gastric adenocarcinoma. The association between BMI and esophageal and gastric cardia adenocarcinoma were dose-dependent and seemingly independent of reflux. No strong sex differences were identified. Smokers, particularly females, were at increased risk of all studied adenocarcinomas, while no association with alcohol was found.Conclusions: Overweight increases risk of esophageal and gastric cardia adenocarcinoma, while tobacco smoking increases risk of esophageal, gastric cardia, and non-cardia gastric adenocarcinoma. The male predominance is not explained by sex differences in risk factor profiles of the studied exposures.Grant support: AstraZeneca R&D and the Swedish Cancer Society.     

Prospective study of body mass index,physical activity and thyroid cancer

Increased body size and physical inactivity are positively related to risk of several cancers, but only few epidemiologic studies have investigated body‐mass index (BMI) and physical activity in relation to thyroid cancer. We examined the relations of BMI and physical activity to thyroid cancer in a prospective cohort of 484,326 United States men and women, followed from 1995/1996 to 2003. During 3,490,300 person‐years of follow‐up, we documented 352 newly incident cases of thyroid cancer. The multivariate relative risks (RR) of thyroid cancer for BMI values of 18.5–24.9 (reference), 25.0–29.9 and ≥30 kg m^?2 were 1.0, 1.27 and 1.39 [95% confidence interval (CI) = 1.05–1.85]. Adiposity predicted papillary thyroid cancers (RR comparing extreme BMI categories = 1.47; 95% CI = 1.03–2.10) and, based on small numbers, suggestively predicted follicular thyroid cancers (RR = 1.49; 95% CI = 0.79–2.82) and anaplastic thyroid cancers (RR = 5.80; 95% CI = 0.99–34.19). No relation with BMI was noted for medullary thyroid cancers (RR = 0.97; 95% CI = 0.27–3.43). The positive relation of BMI to total thyroid cancer was evident for men but not for women. However, the test of interaction (p = 0.463) indicated no statistically significant gender difference. Physical activity was unassociated with thyroid cancer. The RRs of total thyroid cancer for low (reference), intermediate, and high level of physical activity were 1.0, 1.01 and 1.01 (95% CI = 0.76–1.34, p for trend = 0.931), respectively. Our results support an adverse effect of adiposity on risk for developing total and papillary, and possibly follicular thyroid cancers. Based on only 15 cases, adiposity was unrelated to medullary thyroid cancers. Physical activity was unrelated to total thyroid cancer.     

The association between metabolic health,obesity phenotype and the risk of breast cancer

Beyond the current emphasis on body mass index (BMI), it is unknown whether breast cancer risk differs between metabolically healthy and unhealthy normal weight or overweight/obese women. The Sister Study is a nationwide prospective cohort study. Data came from 50,884 cohort participants aged 35 to 74 years enrolled from 2003 through 2009. Cox proportional hazards models were used to estimate multivariable adjusted hazard ratios (HR) and 95% confidence intervals (CIs) for breast cancer risk. Metabolic abnormalities considered included: high waist circumference (≥88 cm); elevated blood pressure (≥130/85 mm Hg or antihypertensive medication); previously diagnosed diabetes or antidiabetic drug treatment; and cholesterol‐lowering medication use. During follow‐up (mean, 6.4 years), 1,388 invasive breast cancers were diagnosed at least 1 year after enrollment. Compared to women with BMI <25 kg/m² with no metabolic abnormalities (metabolically healthy normal weight phenotype), women with a BMI <25 kg/m² and ≥1 metabolic abnormality (metabolically unhealthy, normal weight phenotype) had increased risk of postmenopausal breast cancer (HR = 1.26, 95% CI: 1.01–1.56), as did women with a BMI ≥25 kg/m² and no metabolic abnormalities (metabolically healthy overweight/obese phenotype) (HR = 1.24, 95% CI: 0.99–1.55). Furthermore, risk of postmenopausal breast cancer was consistently elevated in women with normal BMI and central obesity (normal weight central obesity phenotype) regardless of the criterion used to define central obesity, with HR for waist circumference ≥88 cm, waist circumference ≥80 cm, and waist‐hip ratio ≥0.85 of 1.58, 95% CI: 1.02–2.46; 1.38, 95% CI: 1.09–1.75; and 1.38, 95% CI: 1.02–1.85, respectively. There was an inverse association between premenopausal breast cancer and metabolically healthy overweight/obese phenotype (HR = 0.71, 95% CI: 0.52–0.97). Our findings suggest that postmenopausal women who are metabolically unhealthy or have central adiposity may be at increased risk for breast cancer despite normal BMI.