The association of weight gain during adulthood with prostate cancer incidence and survival: a population-based cohort

Obese men appear to have an increased risk of being diagnosed with advanced prostate cancer and of dying from the disease. Few studies have examined the impact of weight gain during adulthood on prostate cancer risk and mortality and these have reported conflicting results. We analysed data from 20,991 Norwegian men who participated in two phases of the Nord‐Trøndelag Health Study in 1984/1986 (HUNT‐1, when aged at least 20 years) and 1995/1997 (HUNT‐2). Weight and height were measured at both HUNT‐1 and HUNT‐2, allowing each man's change in weight and body mass index (BMI) to be computed. During a median of 9.3 years of follow‐up after the end of HUNT‐2, 649 (3%) men developed prostate cancer. We observed no increase in prostate cancer incidence amongst men who put on weight between HUNT‐1 and HUNT‐2. In multivariable models, including adjustment for weight at HUNT‐2, the hazard ratio (HR) for prostate cancer per one standard deviation, SD (6.2 kg) gain in weight was 0.98 (95% confidence interval [95% CI] = 0.87–1.10, p‐trend = 0.70) and per one SD gain in BMI (1.9 kg/m²) was 0.99 (95% CI = 0.90–1.10, p‐trend = 0.88). Amongst men diagnosed with prostate cancer (any stage), there was no evidence that gain in weight before diagnosis was positively associated with subsequent all‐cause mortality (HR per one SD increase in weight = 0.98; 95% CI = 0.81–1.19, p‐trend = 0.86). We conclude that weight gain in adulthood had no effect on prostate cancer incidence or survival in this population.     

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.     

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.     

Investigating the prostate specific antigen,body mass index and age relationship: is an age–BMI-adjusted PSA model clinically useful?

Purpose

Previous studies indicate a possible inverse relationship between prostate-specific antigen (PSA) and body mass index (BMI), and a positive relationship between PSA and age. We investigated the associations between age, BMI, PSA, and screen-detected prostate cancer to determine whether an age–BMI-adjusted PSA model would be clinically useful for detecting prostate cancer.

Methods

Cross-sectional analysis nested within the UK ProtecT trial of treatments for localized cancer. Of 18,238 men aged 50–69 years, 9,457 men without screen-detected prostate cancer (controls) and 1,836 men with prostate cancer (cases) met inclusion criteria: no history of prostate cancer or diabetes; PSA < 10 ng/ml; BMI between 15 and 50 kg/m². Multivariable linear regression models were used to investigate the relationship between log-PSA, age, and BMI in all men, controlling for prostate cancer status.

Results

In the 11,293 included men, the median PSA was 1.2 ng/ml (IQR: 0.7–2.6); mean age 61.7 years (SD 4.9); and mean BMI 26.8 kg/m² (SD 3.7). There were a 5.1% decrease in PSA per 5 kg/m² increase in BMI (95% CI 3.4–6.8) and a 13.6% increase in PSA per 5-year increase in age (95% CI 12.0–15.1). Interaction tests showed no evidence for different associations between age, BMI, and PSA in men above and below 3.0 ng/ml (all p for interaction >0.2). The age–BMI-adjusted PSA model performed as well as an age-adjusted model based on National Institute for Health and Care Excellence (NICE) guidelines at detecting prostate cancer.

Conclusions

Age and BMI were associated with small changes in PSA. An age–BMI-adjusted PSA model is no more clinically useful for detecting prostate cancer than current NICE guidelines. Future studies looking at the effect of different variables on PSA, independent of their effect on prostate cancer, may improve the discrimination of PSA for prostate cancer.

     

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.     

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.     

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.     

Does obesity modify the relationship between physical activity and breast cancer risk?

Purpose

With only 5–10% of breast cancer cases attributed to genetic inheritance, prevention efforts have focused on modifiable risk factors. Physical activity plays a role in reducing breast cancer risk; however, the interaction between physical activity and other modifiable risk factors, such as obesity, has received little attention.

Methods

A systematic review and meta-analysis was conducted of studies examining the relationship between physical activity and breast cancer and how it may be modified by body mass index (BMI).

Results

A total of 29 papers were included: 18 were cohort and 11 were case–control studies. Overall, a significant reduction in the relative risk of breast cancer was found in postmenopausal women with high versus low levels of physical activity for women with a BMI <25 kg/m² (RR 0.85, 95% CI 0.79, 0.92) and ≥25 kg/m² (RR 0.87, 95% CI 0.81, 0.93) but not ≥30 kg/m² (RR: 0.93, 95% CI 0.76, 1.13). Physical activity was not associated with a significant reduction in risk of breast cancer in premenopausal women in any BMI group.

Conclusion

The results of this meta-analysis suggest that physical activity is associated with a larger breast cancer risk reduction among women who are normal weight or overweight than among women who are obese. Since the included studies used diverse methods for assessment of physical activity and categories of BMI, results should be interpreted with caution and additional work is needed.

     

Obesity,weight gain,and ovarian cancer risk in African American women

Although there is growing evidence that higher adiposity increases ovarian cancer risk, little is known about its impact in African American (AA) women, the racial/ethnic group with the highest prevalence of obesity. We evaluated the impact of body mass index (BMI) 1 year before diagnosis and weight gain since age 18 years on ovarian cancer risk in a population‐based case‐control study in AA women in 11 geographical areas in the US. Cases (n = 492) and age and site matched controls (n = 696) were identified through rapid case ascertainment and random‐digit‐dialing, respectively. Information was collected on demographic and lifestyle factors, including self‐reported height, weight at age 18 and weight 1 year before diagnosis/interview. Multivariable logistic regression was used to compute odds ratios (OR) and 95% confidence intervals (CI), adjusting for potential covariates. Obese women had elevated ovarian cancer risk, particularly for BMI ≥ 40 kg/m² compared to BMI <25 (OR = 1.72, 95% CI: 1.12‐2.66; p for trend: 0.03). There was also a strong association with weight gain since age 18 (OR: 1.52; 95% CI: 1.07–2.16; p for trend: 0.02) comparing the highest to lowest quartile. In stratified analyses by menopausal status, the association with BMI and weight gain was limited to postmenopausal women, with a 15% (95% CI: 1.05–1.23) increase in risk per 5 kg/m² of BMI and 6% (95% CI: 1.01–1.10) increase in risk per 5 kg of weight gain. Excluding hormone therapy users essentially did not change results. Obesity and excessive adult weight gain may increase ovarian cancer risk in post‐menopausal AA women.     

Obesity and non-Hodgkin lymphoma survival in an ethnically diverse population: the Multiethnic Cohort study

Purpose

Obesity increases mortality for several malignancies, but for non-Hodgkin lymphoma (NHL), the association between body mass index (BMI) and survival is unclear. We examined the association of pre-diagnostic BMI with overall and NHL-specific survival in the multiethnic cohort (MEC) study of African Americans, Native Hawaiians, Japanese Americans, Latinos, and Caucasians.

Methods

MEC participants free of NHL at cohort entry and diagnosed with NHL during follow-up were included in the analyses (n = 1,331). BMI was based on self-reported weight and height at cohort entry and after 6.1 years of cohort entry. Cox proportional hazards regression was used to calculate hazard ratios (HR) and 95 % confidence intervals (CI) with BMI as time-varying exposure in relation to all-cause and NHL-specific mortality while adjusting for known confounders.

Results

The mean age at NHL diagnosis was 70.5 (range 45–89) years. After a mean follow-up of 4.3 ± 3.5 years, 667 deaths including 450 NHL-specific deaths occurred. In multivariable models, obese patients (BMI ≥30.0 kg/m²) had higher all-cause (HR 1.46, 95 % CI 1.13–1.87) and NHL-specific (HR 1.77, 95 % CI 1.30–2.41) mortality compared with patients with high-normal BMI (22.5–24.9 kg/m²). For overweight patients (BMI = 25.0–29.9 kg/m²), the respective HRs were 1.21 (95 % CI 0.99–1.49) and 1.36 (95 % CI 1.06–1.75). Cases with low-normal BMI (<22.5 kg/m²) experienced a significant 45 % higher all-cause and a 40 % higher NHL-specific mortality. After stratification by NHL type, the adverse effect of BMI was stronger for chronic lymphocytic leukemia/small lymphocytic lymphoma than for diffuse large B cell lymphoma and follicular lymphoma.

Conclusions

Pre-diagnostic BMI may be a suitable prognostic marker for NHL patients.     

Factors associated with incident and fatal pancreatic cancer in a cohort of middle‐aged women

Risk factors for pancreatic cancer, other than smoking and diabetes, are not well‐established, especially for women. In a cohort of 1.3 million middle‐aged women, followed for 9.2 million person‐years for cancer incidence and 11.5 million person‐years for mortality, there were 1,338 incident pancreatic cancer cases and 1,710 deaths from the disease. Using proportional hazards models, we calculated adjusted relative risks (RRs) and 95% confidence intervals (CIs) by smoking, height, body mass index (BMI), alcohol consumption, physical activity and history of diabetes. Pancreatic cancer incidence was greater in current than never smokers (RR 2.39, CI 2.10–2.73), the risk increasing with the number of cigarettes smoked. The incidence of pancreatic cancer also increased with increasing BMI (RR 1.34, CI 1.13–1.57 for BMI ≥ 30 vs. 22.5–25 kg/m²), and with a history of diabetes (RR 1.58, CI 1.22–2.03, with vs. without such a history). These factors were also associated with increased mortality from pancreatic cancer. Height, alcohol consumption and physical activity showed little or no association with pancreatic cancer risk. © 2008 Wiley‐Liss, Inc.     

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.     

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 effects of body mass index on complications and survival outcomes in patients with cervical carcinoma undergoing curative chemoradiation therapy

BACKGROUND:

The effect of body mass index (BMI) on treatment outcomes for patients with locally advanced cervical carcinoma who receive definitive chemoradiation is unclear.

METHODS:

The cohort in this study included all patients with cervical carcinoma (n = 404) who had stage IB₁ disease and positive lymph nodes or stage ≥IB₂ disease and received treatment at the authors' facility between January 1998 and January 2008. The mean follow‐up was 47.2 months. BMI was calculated using the National Institute of Health online calculator. BMI categories were created according to the World Health Organization classification system. Primary outcomes were overall survival, disease‐free survival, and complication rate. Univariate and multivariate analyses were performed. Kaplan‐Meier survival curves were generated and compared using Cox proportional hazard models.

RESULTS:

On multivariate analysis, compared with normal weight (BMI 18.5‐24.9 kg/m²), a BMI <18.5 kg/m² was associated with decreased overall survival (hazard ratio, 2.37; 95% confidence interval, 1.28‐4.38; P < .01). The 5‐year overall survival rate was 33%, 60%, and 68% for a of BMI <18.5 kg/m², a BMI from 18.5 kg/m² to 24.9 kg/m², and a BMI >24.9 kg/m², respectively. A BMI <18.5 kg/m² was associated with increased risk of grade 3 or 4 complications compared with a BMI >24.9 kg/m² (radiation enteritis: 16.7% vs 13.6%, respectively; P = .03; fistula: 11.1% vs 8.8%, respectively; P = .05; bowel obstruction: 33.3% vs 4.4%, respectively; P < .001; lymphedema: 5.6% vs 1.2%, respectively; P = .02).

CONCLUSIONS:

Underweight patients (BMI <18.5 kg/m²) with locally advanced cervical cancer had diminished overall survival and more complications than normal weight and obese patients. Cancer 2011. © 2010 American Cancer Society.     

Body mass index at diagnosis and survival among colon cancer patients enrolled in clinical trials of adjuvant chemotherapy

BACKGROUND:

Although obesity is an established risk factor for developing colon cancer, its prognostic impact and relation to patient sex in colon cancer survivors remains unclear.

METHODS:

The authors examined the prognostic and predictive impact of the body mass index (BMI) in patients with stage II and III colon carcinoma (N = 25,291) within the Adjuvant Colon Cancer Endpoints (ACCENT) database. BMI was measured at enrollment in randomized trials of 5‐fluorouracil–based adjuvant chemotherapy. Association of BMI with the time to recurrence (TTR), disease‐free survival (DFS), and overall survival (OS) were determined using Cox regression models. Statistical tests were 2‐sided.

RESULTS:

During a median follow‐up of 7.8 years, obese and underweight patients had significantly poorer survival compared with overweight and normal‐weight patients. In a multivariable analysis, the adverse prognostic impact of BMI was observed among men but not among women (P_interaction = .0129). Men with class 2 and 3 obesity (BMI ≥35.0 kg/m²) had a statistically significant reduction in DFS (hazard ratio [HR], 1.16; 95% confidence interval [CI], 1.01‐1.33; P = .0297) compared with normal‐weight patients. Underweight patients had a significantly shorter TTR and reduced DFS (HR, 1.18; 95% CI, 1.09‐1.28; P < .0001) that was more significant among men (HR, 1.31; 95% CI, 1.15‐1.50; P < .0001) than among women (HR, 1.11; 95% CI, 1.01‐1.23; P = .0362; P_interaction = .0340). BMI was not predictive of a benefit from adjuvant treatment.

CONCLUSIONS:

Obesity and underweight status were associated independently with inferior outcomes in patients with colon cancer who received treatment in adjuvant chemotherapy trials. Cancer 2013. © 2013 American Cancer Society.     

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.     

The influence of high body mass index on the prognosis of patients with esophageal cancer after surgery as primary therapy

BACKGROUND:

High body mass index (BMI), a prevalent condition in the United States, is associated with esophageal adenocarcinoma (EAC). Its influence on a patient's outcome remains unclear. In the current study, the authors examined the impact of BMI on survival and complications in patients with esophageal cancer (EC) who underwent surgery as their primary therapy.

METHODS:

The authors retrospectively reviewed 301 consecutive EC patients who underwent surgery but received no adjunctive therapy. Patients were segregated into 2 subgroups based on their baseline BMI: normal/low (<25 kg/m²) and high (≥25 kg/m²).

RESULTS:

Seventy‐six (25%) patients had a BMI <25 kg/m² and 225 (75%) patients had a BMI ≥25 kg/m². In the high BMI group, there were more men (P < .001), fewer upper ECs (P = .021), a lower baseline clinical stage (P = .006), and frequent EAC (P < .001). Postoperative morbidity was similar in both groups, with the exception of gastrointestinal complications (P = .016). The 5‐year overall survival (OS) rates were 44% in the normal/low BMI group and 60% in the high BMI group (P = .017). The 5‐year disease‐free survival (DFS) rates were 41% in the normal/low BMI group and 60% in the high BMI group (P = .005). On multivariable analysis, age, weight loss, peripheral vascular disease (PVD), and both clinical and pathological stage of disease were found to be independent prognosticators for OS. Older age (hazard ratio [HR], 1.029; 95% confidence interval [95% CI], 1.009‐1.049 [P = .004]), weight loss (HR, 1.525; 95% CI, 1.034‐2.248 [P = .033]), and PVD (HR, 2.325; 95% CI, 1.039‐5.204 [P = .040]) were found to be associated with poor OS.

CONCLUSIONS:

High BMI is common in EC patients and the better OS/DFS noted in patients with a high BMI is because of the diagnosis of a low baseline clinical stage. Confirmation of these findings is warranted. Cancer 2010. © 2010 American Cancer Society.     

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.     

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.