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.     

Body size and composition and prostate cancer risk: systematic review and meta-regression analysis

The evidence that measures of obesity and stature are associated with prostate cancer is weak and inconsistent. We performed a systematic review and meta-analysis of the relationship between body mass index (BMI), height, weight, waist circumference and waist-to-hips ratio (WHR) and the risk of prostate cancer. Study-specific dose-response slopes were obtained, and random effects rate ratios (RRs) were computed from linear meta-regression models. We included 55,521 cases identified among 2,818,767 men from 31 cohort studies, and 13,232 cases and 16,317 controls from 25 case–control studies. The overall RR for BMI was 1.05 per 5 kg/m² increment, 95% CI 1.01–1.08. For studies that reported results by stage of disease, the RRs were stronger for advanced disease (RR 1.12 per 5 kg/m² increment, 95% CI 1.01–1.23) compared with localized disease (RR 0.96 per 5 kg/m² increment, 95% CI 0.89–1.03), p = 0.02. Height was also positively associated with risk (RR 1.05 per 10 cm increment, 95% CI 1.02–1.09), but the evidence was weak for weight (RR 1.01 per 10 kg increment, 95% CI 0.97–1.04), waist circumference (RR 1.03 per 10 cm increment, 95% CI 0.99–1.07), and WHR (RR 1.11 per 0.1 unit increment, 95% CI 0.95–1.30). Stronger associations were observed among cohort studies compared with case–control studies for BMI (p = 0.006), height (p < 0.001) and weight (p = 0.02). This meta-analysis indicates that obesity is weakly associated with an increased risk of prostate cancer (particularly advanced stage tumors). While increased stature may also increase risk, there is little evidence for an association with central obesity.     

Body mass index and physical activity as risk factors for pancreatic cancer: the Multiethnic Cohort Study

Objective To examine body mass index (BMI) and physical activity as risk factors for pancreatic cancer. Methods Eight-year prospective data from 77,255 men and 90,175 women including 237 and 235 pancreatic cancer cases, respectively, in the Hawaii-Los Angeles Multiethnic Cohort Study were analyzed. Participants completed a questionnaire that included questions on body weight, height, and physical activity. Cox proportional hazards models were calculated to estimate relative risks (RR) of pancreatic cancer by levels of BMI and total physical activity (as metabolic equivalents (METs)) adjusted for several potential confounders. Results Obesity (BMI ≥ 30 kg/m²) was associated with an increased pancreatic cancer risk in men (RR = 1.51 (95% CI: 1.02–2.26)), but a reduced risk in women (RR = 0.65 (95% CI: 0.43–0.99)). In men the risk was higher in never smokers than in current or former smokers, though differences were not statistically significant. Physical activity was not associated with pancreatic cancer risk in either men or women. Conclusion The findings suggest, that a BMI of ≥ 30 kg/m² may be a risk factor for pancreatic cancer in men. No evidence of an effect of physical activity on risk was found.     

Height and Body Mass Index in Relation to Colorectal and Gallbladder Cancer in Two Million Norwegian Men and Women

Objectives: The present study aimed at exploring the relations between BMI and stature and colorectal and gallbladder cancer in a huge Norwegian cohort with measured height and weight.Material and methods: Height and weight were measured in two million Norwegian men and women aged 20–74 during 1963–2001. During follow-up, 47,117 colorectal and 1715 gallbladder cancer cases were registered. Relative risks (RRs) of colorectal and gallbladder cancer were estimated using Cox proportional hazards regression.Results: The risk of colon cancer increased with increasing BMI in men; the RR of colon cancer per unit increase in BMI was 1.04 (95% CI: 1.04–1.05). For mucinous colorectal adenocarcinomas, the risk increased to a larger extent with increasing BMI in both sexes. The RR of colorectal cancer associated with 10 cm increase in height was 1.14 (95% CI: 1.11–1.16) in men and 1.17 (95% CI: 1.14–1.20) in women. The risk of gallbladder cancer increased with increasing BMI in women; the overall RR associated with one unit increase in BMI was 1.06 (95% CI: 1.04–1.07). There was no association between height and gallbladder cancer in either sex.Conclusion: The risk of colon cancer increased with increasing BMI in men, and the risk of gallbladder cancer increased with increasing BMI in women. In both sexes, the risk of colon cancer increased with increasing height.     

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.     

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.     

A meta-analysis of body mass index and esophageal and gastric cardia adenocarcinoma

BackgroundThe incidence rates of esophageal and gastric cardia adenocarcinoma (EGCA) have increased over recent years in several countries, and overweight/obesity has been suggested to play a major role in these trends. In fact, higher body mass index (BMI) has been positively associated with EGCA in several studies.Material and methodsWe conducted a meta-analysis of case–control and cohort studies on the BMI and EGCA updated to March 2011. We estimated overall relative risks (RRs) and 95% confidence intervals (CI) for BMI between 25 and 30 and BMI ≥ 30 kg/m², when compared with normo-weight subjects, using random-effects models.ResultsWe identified 22 studies, including almost 8000 EGCA cases. The overall RR was 1.71 (95% CI 1.50–1.96) for BMI between 25 and 30, and was 2.34 (95% CI 1.95–2.81) for BMI ≥ 30 kg/m². The continuous RR for an increment of 5 kg/m² of BMI was 1.11 (95% CI 1.09–1.14). The association was stronger for esophageal adenocarcinoma (RR for BMI ≥ 30 kg/m² = 2.73, 95% CI 2.16–3.46) than for gastric cardia adenocarcinoma (RR for BMI ≥ 30 kg/m² = 1.93, 95% CI 1.52–2.45). No substantial differences emerged across strata of sex and geographic areas.ConclusionOverweight and obesity are strongly related to EGCA, particularly to espophageal adenocarcinoma.     

A prospective study of waist circumference and body mass index in relation to colorectal cancer incidence

OBJECTIVES: To study the association between waist circumference and colorectal cancer, and whether it is independent of body mass index (BMI). METHODS: Between 1997 and 2005, 953 incident colorectal cancer cases (546 men and 407 women) were identified among 95,151 participants (44,068 men and 51,083 women) from the Cancer Prevention Study-II Nutrition Cohort. RESULTS: Waist circumference was associated with increased colorectal cancer incidence in both men (multivariable adjusted rate ratio (RR) 1.68, 95% confidence interval (CI) 1.12-2.53 for waist circumference > or =120 cm compared to <95 cm, p trend = 0.006) and women (RR 1.75, 95% CI 1.20-2.54 for > or =110 compared to <85 cm, p trend = 0.003). High levels of BMI were also associated with increased risk. After adjustment for BMI, waist circumference remained associated with a nonstatistically significant increase in colorectal cancer incidence in both men (RR 1.41, 95% CI 0.81-2.45 for > or =120 compared to <95 cm, p trend = 0.10) and women (RR 1.48, 95% CI 0.89-2.48 for > or =110 compared to <85 cm, p trend = 0.13). CONCLUSIONS: Our results confirm that waist circumference is associated with increased colorectal cancer incidence, possibly partially independent of BMI.     

Postmenopausal endometrial cancer risk and body size in early life and middle age: prospective cohort study

Background:

Greater adiposity in early life has been linked to increased endometrial cancer risk in later life, but the extent to which this association is mediated through adiposity in later life is unclear.

Methods:

Among postmenopausal women who had never used menopausal hormone therapies and reported not having had a hysterectomy, adjusted relative risks (RRs) of endometrial cancer were estimated using Cox regression.

Results:

Among 249 791 postmenopausal women with 7.3 years of follow-up on average (1.8 million person-years), endometrial cancer risk (n=1410 cases) was strongly associated with current body mass index (BMI) at baseline (RR=1.87 per 5 kg m⁻² increase in BMI, 95% confidence interval (CI): 1.77–1.96). Compared with women thinner than average at age 10, the increased risk among women plumper at age 10 (RR=1.27, 95% CI: 1.09–1.49) disappeared after adjustment for current BMI (RR=0.90, 95% CI: 0.77–1.06). Similarly, compared with women with clothes size 12 or less at age 20, the increased risk among women with clothes size 16 or larger (RR=1.87, 95% CI: 1.61–2.18) was not significant after adjustment for current BMI (RR=1.03, 95% CI: 0.88–1.22).

Conclusion:

Among women who have never used hormone therapy for menopause, the association between body size in early life and endometrial cancer risk in postmenopausal women can be largely explained by women''s current BMI.     

Body fatness at an early age and risk of colorectal cancer

While there is convincing evidence that excess body fatness in adulthood is positively associated with colorectal cancer risk, the association between body fatness at an early age (≤30 years) and the risk of colorectal cancer has been equivocal. The present meta‐analysis was performed to clarify this association. PubMed and Web of Science databases were searched for relevant studies that investigated this association. The risk estimates from each study were transformed into a continuous variable for each 5 kg/m² increase in body mass index (BMI). A random effects model was used to calculate the summary relative risks (RRs) with 95% confidence intervals (CIs). A total of 15 observational studies (13 cohort studies and two case‐control studies) were included in this meta‐analysis. Each 5 kg/m² increase in BMI was significantly associated with a 13% (RR 1.13, 95% CI 1.08, 1.19), 17% (RR 1.17, 95% CI 1.09, 1.25) and 8% (RR 1.08, 95% CI 1.04, 1.11) higher risk of colorectal cancer overall, in men, and in women, respectively. Substantial heterogeneity was observed across studies. Based on the anatomic subsite, each 5 kg/m² increase in BMI was significantly associated with a 14% (RR 1.14, 95% CI 1.07, 1.22) higher risk of colon cancer, whereas no association (RR 1.03, 95% CI 0.95, 1.13) was observed with rectal cancer. In summary, body fatness at an early age may affect colon cancer risk later in life. Prevention of overweight and obesity in young individuals should be emphasized to prevent early‐onset colon cancer attributed to excess body fatness.     

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.     

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.     

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.     

Prospective study of body mass index, height, physical activity and incidence of bladder cancer in US men and women

We evaluated prospectively the association between body mass index (BMI), height, recreational physical activity and the risk of bladder cancer among US adults. Data were used from 2 ongoing cohorts, the Health Professionals Follow-up Study and the Nurses' Health Study, with 3,542,012 years of follow-up and 866 incident bladder cancer cases (men = 507; women = 359) for the anthropometric analysis and 1,890,476 years of follow-up and 706 incident bladder cancer cases (men = 502; women = 204) for the physical activity analysis. Cox proportional hazard models were used to estimate incidence rate ratios (RR) and 95% confidence intervals (CI) between BMI, height, physical activity and bladder cancer risk adjusting for age, pack-years of cigarette smoking and current smoking. Estimates from each cohort were pooled using a random-effects model. We observed no association between baseline BMI and bladder cancer risk, even when we compared a BMI of > or =30 kg/m(2) to a BMI of 18-22.9 kg/m(2) [pooled multivariate (MV) RR, 1.16; 95% CI: 0.89-1.52]. A weak, but statistically significant, association was observed for the same comparison after excluding bladder cancer cases diagnosed within the first 4 years of follow-up (pooled MV RR, 1.33; 95% CI: 1.01-1.76). Height was not related to bladder cancer risk (pooled MV RR, 0.82; 95% CI: 0.65-1.03, top vs. bottom quintile). Total recreational physical activity also was not associated with the risk of bladder cancer (pooled MV RR, 0.97; 95% CI: 0.77-1.24, top vs. bottom quintile). Our findings do not support a role for BMI, height or physical activity in bladder carcinogenesis.     

Body mass index and colon cancer: an evaluation of the modifying effects of estrogen (United States)

Objective: The association between body mass index (BMI) and colon cancer has been reported to be different for men and women. No prior literature has examined if estrogen influences these differences. Methods: Using data from an incident population-based case (n = 1972) and control (n = 2386) study of colon cancer we evaluated if estrogen modifies the association between BMI and risk of colon cancer. Results: Women who were estrogen-negative (postmenopausal women not taking hormone replacement therapy, HRT) were at increased risk of colon cancer regardless of indicator of estrogen status used (i.e. estrogen-negative compared to estrogen-positive women defined as either being premenopausal or postmenopausal women using HRT, OR 1.54, 95% CI 1.23–1.93; no recent exposure to estrogens compared to current or HRT use within the past 2 years, OR 1.58, 95% CI 1.24–2.00; postmenopausal women not currently using HRT compared to postmenopausal women taking HRT, OR 1.65, 95% CI 1.29–2.12). BMI (kg/m²) was not associated with an increased risk of colon cancer among women who were estrogen-negative. However, women who were estrogen-positive experienced a greater than two-fold increase in colon cancer risk if they had a BMI of > 30 relative to those who had a BMI of <23 (for estrogen-positive, OR, 2.50, 95% CI 1.51–4.13; premenopausal, OR 2.19, 95% CI 0.94–5.07; postmenopausal using HRT, OR 3.36, 95% CI 1.58–7.13). Among men the colon cancer risk associated with BMI decreased with advancing age. Physical activity modified the increased colon cancer risk associated with a large BMI. Conclusions: These data suggest the importance of estrogen in colon cancer etiology. Being estrogen-negative resulted in a significant increased risk of colon cancer. However, BMI significantly increased the risk of colon cancer among women who were estrogen-positive. We hypothesize that estrogen up-regulates IGF-I receptors and IRS-I levels in the colon, which in turn increases susceptibility to obesity-induced increased levels of insulin. We further hypothesize that androgens may have similar effects in men given the decline in colon cancer risk associated with BMI with advancing age.     

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.     

The U-shaped association between body mass index and gastric cancer risk in the Helicobacter pylori Biomarker Cohort Consortium: A nested case–control study from eight East Asian cohort studies

The association between body mass index (BMI) and noncardia gastric cancer (NCGC) risk remains controversial. The purpose of our study was to examine the association of BMI with NCGC risk with consideration of Helicobacter pylori (HP) biomarkers. This international nested case–control study, composed of 1,591 incident NCGC cases and 1,953 matched controls, was established from eight cohorts in China, Japan and Korea, where the majority of NCGCs are diagnosed worldwide. HP antibody biomarkers were measured in blood collected at cohort enrollment by multiplex serology. The NCGC risk according to baseline BMI was estimated using logistic regression to produce odds ratios (ORs) and 95% confidence intervals (CIs). We found a U-shaped association between BMI category and NCGC risk. Compared to those with reference BMI (22.6–25.0 kg/m²), those with lower and higher BMI had an increased NCGC risk (BMI <18.5 kg/m², OR = 1.56, 95% CI = 1.04–2.34; BMI >27.5 kg/m², OR = 1.48, 95% CI = 1.15–1.91; adjusted for age, sex and smoking). The U-shaped association was persistent among subjects with HP infection and high-risk biomarkers (HP+ CagA+: BMI <18.5 kg/m², OR = 1.60, 95% CI = 1.00–2.55; BMI >27.5 kg/m², OR = 1.59, 95% CI = 1.21–2.11; and Omp+ HP0305+: BMI <18.5 kg/m², OR = 1.88, 95% CI = 1.04–3.42; BMI >27.5 kg/m², OR = 1.70, 95% CI = 1.20–2.42, respectively). Our study provides evidence of significantly increased NCGC risk among individuals with low or high BMI, including in subjects with high-risk HP biomarkers (HP+ CagA+, Omp+ HP0305+) in the high-risk area of East Asia.     

Prospective study on metabolic factors and risk of prostate cancer

BACKGROUND:

There are inconsistent data regarding the association between metabolic factors, separately and combined, and the risk of prostate cancer and death from prostate cancer.

METHODS:

In the Metabolic Syndrome and Cancer Project (Me‐Can), data on body mass index (BMI); blood pressure; and blood levels of glucose, cholesterol, and triglycerides were collected for 289,866 men. Cox proportional hazard models were used to calculate relative risks (RRs) by exposures in quintiles as well as for z scores (with a mean of 0 and a standard deviation of 1) together with a composite sum of scores to assess the combined effect of metabolic factors. RRs were corrected for random errors in measurement.

RESULTS:

During a mean follow‐up of 12 years, 6673 men were diagnosed with prostate cancer and 961 died of the disease. Men with high levels of glucose and triglycerides were found to have a decreased risk of prostate cancer: top versus bottom quintile of glucose: RR, 0.82 (95% confidence interval [95% CI], 0.62‐1.08; P value for trend = .03) and top versus bottom quintile of triglycerides: RR, 0.88 (95% CI, 0.74‐1.04; P value for trend = .001). High BMI, elevated blood pressure, and a high composite z score were found to be associated with an increased risk of death from prostate cancer: top versus bottom quintile of BMI: RR, 1.36 (95% CI, 1.08‐1.71); systolic blood pressure: RR, 1.62 (95% CI, 1.07‐2.45); and per 1‐unit increase of the composite z score: RR, 1.13 (95% CI, 1.03‐1.25).

CONCLUSIONS:

The authors found no evidence of an association between high levels of metabolic factors and the risk of prostate cancer, but high BMI, elevated blood pressure, and a composite score of all metabolic factors were associated with an increased risk of death from prostate cancer. Cancer 2012. © 2012 American Cancer Society.     

Overall and abdominal obesity and prostate cancer risk in a West African population: An analysis of the Ghana Prostate Study

Obesity has been associated with an increased risk of advanced prostate cancer. However, most studies have been conducted among North American and European populations. Prostate cancer mortality appears elevated in West Africa, yet risk factors for prostate cancer in this region are unknown. We thus examined the relationship between obesity and prostate cancer using a case-control study conducted in Accra, Ghana in 2004 to 2012. Cases and controls were drawn from a population-based sample of 1037 men screened for prostate cancer, yielding 73 cases and 964 controls. An additional 493 incident cases were recruited from the Korle-Bu Teaching Hospital. Anthropometric measurements were taken at enrollment. We used logistic regression to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for associations between body mass index (BMI), waist circumference (WC), waist-hip ratio (WHR) and prostate cancer, adjusting for potential confounders. The mean BMI was 25.1 kg/m² for cases and 24.3 kg/m² for controls. After adjustment, men with BMI ≥ 30 kg/m² had an increased risk of prostate cancer relative to men with BMI < 25 kg/m² (OR 1.86, 95% CI 1.11-3.13). Elevated WC (OR 1.76, 95% CI 1.24-2.51) and WHR (OR 1.46, 95% CI 0.99-2.16) were also associated with prostate cancer. Associations were not modified by smoking status and were evident for low- and high-grade disease. These findings indicate that overall and abdominal obesity are positively associated with prostate cancer among men in Ghana, implicating obesity as a potentially modifiable risk factor for prostate cancer in this region.     

Metabolic factors and the risk of colorectal cancer in 580,000 men and women in the metabolic syndrome and cancer project (Me‐Can)

BACKGROUND:

The metabolic syndrome (MetS) has been related to an increased risk of colorectal cancer, but the modest size of previous studies precluded detailed characterization of the role of individual MetS factors and their interaction on risk.

METHODS:

In the Metabolic Syndrome and Cancer Project (Me‐Can), data on body mass index (BMI), blood pressure, and blood levels of glucose, cholesterol, and triglycerides were available for 578,700 men and women. The mean age of participants at baseline was 44 years, and the mean follow‐up was 12 years. Relative risks (RR) of colorectal cancer per 1 standard deviation increment in Z score of factors and for a combined MetS score, were calculated from Cox regression models, including adjustment for potential confounders.

RESULTS:

During follow‐up, 2834 men and 1861 women were diagnosed with colorectal cancer. The RR of colorectal cancer for the MetS score was 1.25 (95% confidence interval [CI], 1.18‐1.32) in men, and 1.14 (95% CI, 1.06‐1.22) in women. Significant associations also were observed in men for BMI (RR, 1.07; 95% CI, 1.02‐1.13), blood pressure (RR, 1.10; 95% CI, 1.02‐1.18), and triglycerides (RR, 1.17; 95% CI, 1.06‐1.28) and, in women, for BMI (RR, 1.08; 95% CI, 1.01‐1.15). There was no significant positive interaction between the metabolic factors on risk.

CONCLUSIONS:

The combination of metabolic factors and some separate factors was related to an increased risk of colorectal cancer, but there was no interaction between metabolic factors. Cancer 2011;. © 2010 American Cancer Society.