Prevalence of site-specific obesity-related cancers according to exposure group.

Background:Obesity and cardiometabolic dysfunction have been associated with cancer risk and severity. Underlying mechanisms remain unclear. Objectives:The aim of this study was to examine associations of obesity and related cardiometabolic traits with incident cancer. Methods:FHS (Framingham Heart Study) and PREVEND (Prevention of Renal and Vascular End-Stage Disease) study participants without prevalent cancer were studied, examining associations of obesity, body mass index (BMI), waist circumference, visceral adipose tissue (VAT) and subcutaneous adipose tissue depots, and C-reactive protein (CRP) with future cancer in Cox models. Results:Among 20,667 participants (mean age 50 years, 53% women), 2,619 cancer events were observed over a median follow-up duration of 15 years. Obesity was associated with increased risk for future gastrointestinal (HR: 1.30; 95% CI: 1.05-1.60), gynecologic (HR: 1.62; 95% CI: 1.08-2.45), and breast (HR: 1.32; 95% CI: 1.05-1.66) cancer and lower risk for lung cancer (HR: 0.62; 95% CI: 0.44-0.87). Similarly, waist circumference was associated with increased risk for overall, gastrointestinal, and gynecologic but not lung cancer. VAT but not subcutaneous adipose tissue was associated with risk for overall cancer (HR: 1.22; 95% CI: 1.05-1.43), lung cancer (HR: 1.92; 95% CI: 1.01-3.66), and melanoma (HR: 1.56; 95% CI: 1.02-2.38) independent of BMI. Last, higher CRP levels were associated with higher risk for overall, colorectal, and lung cancer (P < 0.05 for all). Conclusions:Obesity and abdominal adiposity are associated with future risk for specific cancers (eg, gastrointestinal, gynecologic). Although obesity was associated with lower risk for lung cancer, greater VAT and CRP were associated with higher lung cancer risk after adjusting for BMI.

Aims Recent studies suggest an association between cardiovascular disease (CVD) and cancer incidence/mortality, but the pathophysiological mechanisms underlying these associations are unclear. We aimed to examine biomarkers previously associated with CVD and study their association with incident cancer and cancer-related death in a prospective cohort study. Methods and results We used a proteomic platform to measure 71 cardiovascular biomarkers among 5032 participants in the Framingham Heart Study who were free of cancer at baseline. We used multivariable-adjusted Cox models to examine the association of circulating protein biomarkers with risk of cancer incidence and mortality. To account for multiple testing, we set a 2-sided false discovery rate <0.05. Growth differentiation factor-15 (also known as macrophage inhibitory cytokine-1) was associated with increased risk of incident cancer [hazards ratio (HR) per 1 standard deviation increment 1.31, 95% CI 1.17-1.47], incident gastrointestinal cancer (HR 1.85, 95% CI 1.37-2.50), incident colorectal cancer (HR 1.94, 95% CI 1.29-2.91), and cancer-related death (HR 2.15, 95% CI 1.72-2.70). Stromal cell-derived factor-1 showed an inverse association with cancer-related death (HR 0.75, 95% CI 0.65-0.86). Fibroblast growth factor-23 showed an association with colorectal cancer (HR 1.55, 95% CI 1.20-2.00), and granulin was associated with haematologic cancer (HR 1.61, 95% CI 1.30-1.99). Other circulating biomarkers of inflammation, immune activation, metabolism, and fibrosis showed suggestive associations with future cancer diagnosis. Conclusion We observed several significant associations between circulating CVD biomarkers and cancer, supporting the idea that shared biological pathways underlie both diseases. Further investigations of specific mechanisms that lead to both CVD and cancer are warranted.

BACKGROUND:The extent to which co-occurrence of cardiovascular disease (CVD) and cancer is due to shared risk factors or other mechanisms is unknown.OBJECTIVES:We investigated the association of standard CVD risk factors, CVD biomarkers, preexisting CVD, and ideal CV health metrics with the development of future cancer.METHODS:We prospectively followed Framingham Heart Study and PREVEND participants free of cancer at baseline, and ascertained histology-proven cancer. We studied the association of baseline CV risk factors, 10-year atherosclerotic CVD risk score, established CVD biomarkers, prevalent CVD, and AHA Life's Simple 7 CV health score with incident cancer using multivariable Cox models. Analyses of interim CVD events with incident cancer used time-dependent covariates.RESULTS:Among 20,305 participants (mean age 50 ± 14 years, 54% women), 2,548 incident cancer cases occurred over a median follow-up of 15.0 (13.3-15.0) surveillance years. Traditional CVD risk factors including age, sex, and smoking status were independently associated with cancer (P <0.001 for all). Estimated 10-year atherosclerotic CVD risk was also associated with future cancer (HR 1.16 per 5% increase in risk, 95% CI 1.14-1.17, P<0.001). We found that natriuretic peptides (NP) (tertile 3 vs 1: HR 1.40, 95% CI 1.03-1.91, p=0.035) was associated with incident cancer, but not high sensitivity troponin (hs-cTn) (p=0.47). Prevalent CVD and the development of interim CV events were not associated with higher risk of subsequent cancer. However, ideal CV health was associated with lower future cancer risk (HR 0.95 per 1-point increase in AHA health score, 95% CI 0.92-0.99, p=0.009).CONCLUSIONS:CVD risk as captured by traditional CVD risk factors, 10-year atherosclerotic CVD risk score, and NP concentrations are associated with increased risk of future cancer. Conversely, a heart healthy lifestyle is associated with a reduced risk of future cancer. Our data suggest that the association between CVD and future cancer is attributable to shared risk factors.

Background/objective Obesity has been associated with the risk of developing certain cancers. A limited number of studies have examined effects of various anthropometric measures of body composition on cancer risk. The aim of this study was to estimate the sex-specific effects of various anthropometric measures on risk of obesity-related cancers (ObCa). Subjects/methods Data on body mass index (BMI), waist circumference (WC), waist-to-height ratio (WHtR), and hip circumference (HC) among 3818 45–69-year olds in the Framingham Offspring Study were included. Cox proportional hazards models were used to estimate adjusted risks of 16 obesity-related cancers, with the most common being postmenopausal breast, endometrial, and colon cancers. Results Obesity as measured by BMI in both men and women was a predictor of ObCa; those in the highest quintile (Q5) of BMI (>30.07 in women; >30.80 kg/m 2 in men) had more than twice the risk of ObCa (HR = 2.07; 95% CI: 1.06–4.07 (women) and HR = 2.25; 95% CI: 1.08–4.69 (men)). Waist-related measures (WC, WHtR) were stronger predictors of ObCa in men than in women, and HC confounded the relations between waist size and cancer risk. After adjusting for HC, men in Q5 of WC had more than a threefold increased risk of ObCa (HR: = 3.22; 95% CI: 1.39–7.45). Comparable effects in women were weak and non-statistically significant. Results were similar for WHtR. Finally, an inverse J-shaped relation was found between HC and ObCa after adjusting for WC among men but not in women. Conclusions These results suggest that obesity as measured by BMI is a predictor of obesity-related cancer risk in men and women. They also suggest that waist and hip circumference measures are interrelated and confound the independent effects of each measure. Among men, a large waist size and a small hip size are independent predictors of cancer risk.

Abstract Cardiovascular abnormalities were identified prospectively in all 70 persons who developed complete right bundle-branch block (RBBB) in The Framingham Study during 18 years of biennial fol...

Introduction: Obesity and cardiometabolic dysfunction may be shared risk factors for development of cancer. We sought to examine the association of obesity and abdominal adiposity with incident cancer. Methods: We studied participants of the Framingham Heart Study and Prevention of Renal and Vascular End-Stage Disease study. We examined the association of obesity, body-mass index (BMI), waist circumference (WC), and visceral adiposity (VAT) with future cancer in Cox models. We adjusted for age, sex, diabetes, systolic blood pressure, hypertension treatment, smoking status (current, former, never), and cholesterol ratio. Results: Among 20,667 individuals (mean age 50, 53% women) free of cancer at baseline, we observed 2,619 incident cancer events over a mean follow-up of 13.3±3.3 years. Obesity (BMI≥30 kg/m 2 ) was associated with 30% increased hazard of future gastrointestinal cancer (HR 1.30, 95% CI 1.05-1.60, P=0.01), 62% increased hazard of gynecologic cancers (HR 1.62, 95% CI 1.08-2.45, P=0.02), and by contrast, 38% lower risk of lung cancer (HR 0.62, 95% CI 0.44-0.87, P=0.006). We found similar associations of future cancer with continuous BMI and WC ( Figure ). Among 3,077 individuals with CT scans, VAT was associated with incident cancer (HR 1.16, 95% CI 1.03-1.31, P=0.01 per 1-SD change in VAT). After adjusting for BMI, higher VAT was associated with greater risk of lung cancer (HR 1.92, 95% CI 1.01-3.65, P=0.045). Conclusions: We observed that obesity and abdominal adiposity were associated with future cancer events, including gastrointestinal and gynecologic cancers. Interestingly, obesity was associated with lower risk of lung cancer. However, greater VAT was associated with greater lung cancer risk after adjusting for BMI. These findings highlight the importance of specific obesity-related phenotypes and adipose depots in better understanding the association between obesity and cancer.

Introduction: Emerging data support a potential link between CVD and cancer, but whether this is due to shared risk factors or other mechanisms is unknown. We sought to investigate the association ...

Overweight and diabetes are known cancer risk factors. This study examines independent and combined effects of weight gain and metabolic dysfunction during middle-adult years on obesity-related cancer risk. Subjects (n = 3850) aged 45–69 years at exams 3–5 in the Framingham Offspring Study were classified according to current and prior (~14 years earlier) weight status, interim weight change and prevalent metabolic dysfunction. Cancer risk among subjects who were overweight at baseline and remained overweight, as well as those who became overweight during follow-up, was compared with risk among normal-weight individuals. Gaining ≥0.45 kg (≥1.0 pound)/year (vs. maintaining stable weight) over ~14 years increased cancer risk by 38% (95% confidence interval (CI), 1.09, 1.76); combined with metabolic dysfunction, weight gain increased cancer risk by 77% (95% CI, 1.21, 2.59). Compared with non-overweight adults, men and women who became overweight during midlife had 2.18-fold and 1.60-fold increased cancer risks; those who were overweight from baseline had non-statistically significant 28 and 33% increased cancer risks, respectively, despite having a midlife body mass index that was 3.4 kg/m2 higher than those who gained weight later. Midlife weight gain was a strong cancer risk factor. This excess risk was somewhat stronger among those with concurrent metabolic dysfunction.

Excess body fat, diabetes, and metabolic syndrome are associated with the development of certain cancers. Weight gain during the middle‐adult years is linked with the development of metabolic dysfunction although not all individuals who gain weight develop these complications. The objective of this study was to examine prospectively the independent and combined effects of weight change and metabolic dysfunction on obesity‐related cancer risk. We used data for 3,850 45–69 year‐old individuals who were followed every four years in the Framingham Offspring Study. For each subject, weight (pounds) was regressed on age (years) starting at the baseline visit and ending (~12–20 years later) at the first exam at which they had complete data for fasting glucose and lipid levels (generally exam 3). The slope of weight change (per year) was used to classify each subject as gaining ≥ 1lb/year over 12–20 years, losing ≥ 1lb/year, or remaining weight stable (neither gaining nor losing ≥ 1lb/year per year). Since the risk of obesity‐related cancer may be linked with the duration and intensity of chronic inflammation, long‐term weight gain during the middle‐adult years may better capture the risk of adiposity on obesity‐related cancers. Thus, in a second analysis, we classified subjects into one of three groups based on weight status over the 12–20 year exposure period: those who were of normal weight throughout (including those who lost weight), those who were overweight/obese at baseline and remained so, and those who were of normal weight at baseline and became overweight/obese. Subjects with metabolic dysfunction (MetDys) were those identified with impaired fasting glucose/diabetes, dyslipidemia (elevated serum triglycerides or low HDL‐cholesterol), or hypertension. MetDys for each subject was classified as having 2 or more (vs. 0 or 1) metabolic abnormalities prior to the start of follow up for incident cancer. Primary obesity‐related cancers included postmenopausal breast, endometrial, and colorectal cancers. Cox proportional hazards were used to evaluate the effect of weight change with and without MetDys, adjusting for potential confounding by sex, age, height, education, smoking, alcohol intake, and physical activity. Subjects gaining ≥ 1lb/year had statistically significant increases in obesity‐related cancer risk: HR=1.8 (95%CI: 1.2–2.6) and HR=1.3 (95%CI: 1.0–1.7) for those with and without concurrent MetDys, respectively. Those with stable weights (or who lost weight), regardless of prevalent MetDys, had no increased cancer risk. Compared with the referent group (normal weight with one or fewer metabolic abnormalities), subjects who became obese during the middle‐adult years and whose weight gain was accompanied by greater MetDys had a two‐fold increased risk of developing obesity‐related cancer (HR=2.1; 95%CI: 1.2–3.6); weight gain not accompanied by MetDys still led to a 70% increase risk of cancer (HR=1.7; 95%CI: 1.3–2.4). Normal‐weight subjects with MetDys also a 60% increased risk (HR=1.6; 95%CI: 1.1–2.4) of developing an obesity‐related cancer. This study demonstrates that individuals who gain weight during the middle‐adult years, especially when their weight gain is accompanied by metabolic dysfunction, are at much higher risk for developing an obesity‐related cancer. Support or Funding Information NHLBI, Framingham Heart Study, (NHLBI/NIH Contract #N01‐HC‐25195) and the Boston University School of Medicine

CONTEXTCellular characteristics of fat quality have been associated with cardiometabolic risk and can be estimated by computed tomography (CT) attenuation.OBJECTIVEThe aim was to determine the association between CT attenuation (measured in Hounsfield units [HU]) and clinical outcomes.METHODSThis was a prospective community-based cohort study using data from the Framingham Heart Study (n = 3324, 48% women, mean age 51 years) and Cox proportional hazard models.MAIN OUTCOMESThe primary outcomes of interest were incident cardiovascular disease (CVD) and all-cause mortality. The secondary outcomes of interest were incident cancer, non-CVD death, and cancer death.RESULTSThere were 111 incident CVD events, 137 incident cancers, 85 deaths including 69 non-CVD deaths, and 45 cancer deaths in up to 23 047 person-years of follow-up. A 1-SD increment in visceral adipose tissue (VAT) HU was inversely associated with incident CVD in the age- and sex-adjusted model (hazard ratio [HR] 0.78, P = .02) but not after multivariable adjustment (HR 0.83, P = .11). VAT HU was directly associated with all-cause mortality (multivariable HR 1.40, P = .003), which maintained significance after additional adjustment for body mass index (HR 1.53, P < .001) and VAT volume (HR 1.99, P < .001). Non-CVD death remained significant in all 3 models, including after adjustment for VAT volume (HR 1.97, P < .001). VAT HU was also associated with cancer mortality (HR 1.93, P = .002). Similar results were obtained for sc adipose tissue HU.CONCLUSIONSFat quality, as estimated by CT attenuation, is associated with all-cause mortality, non-CVD death, and cancer death. These associations highlight how indirect indices of fat quality can potentially add to a better understanding of obesity-related complications.

Abstract Background: It is unknown whether the risk for obesity-related cancers differs between metabolically unhealthy and healthy overweight/obese adults. Methods: Data on body mass index (BMI), waist circumference (WC), waist-to-height ratio (WHtR), and random blood glucose in Framingham Heart Study adults (n = 3,763) ages 55 to 69 years were used to estimate risks of obesity-related cancers (n = 385), including postmenopausal breast, female reproductive, colon, liver, gallbladder, pancreas, and kidney cancers, as well as esophageal adenocarcinomas. Multivariable-adjusted Cox proportional hazards models were used to estimate risk for obesity-related cancers associated with body fat and metabolic health (as defined by glucose levels) among subjects in three risk groups (vs. referent group with normal weight/normal glucose): normal weight/elevated glucose, overweight/normal glucose, and overweight/elevated glucose. Results: Overweight adults [BMI ≥ 25 or WHtR ≥ 0.51 (men) and ≥0.57 (women)] with elevated glucose (≥125 mg/dL) had a statistically significant 2-fold increased risk of developing obesity-related cancer, whereas overweight adults with normal glucose had a 50% increased risk. Normal-weight adults with elevated glucose had no excess cancer risk. The effects of BMI and WHtR were independent of one another. Finally, overweight women with elevated blood glucose had a 2.6-fold increased risk [95% confidence interval (CI), 1.4–4.9] of female reproductive (cervical, endometrial, uterine cancers) and postmenopausal breast cancers, whereas overweight women with normal glucose levels had only a 70% increased risk (95% CI, 1.1–2.5). Conclusion: These results suggest that cancer risk may be lower among metabolically healthy overweight/obese older adults than among overweight/obese adults with metabolic dysfunction. Impact: Metabolic dysfunction and obesity act synergistically to increase cancer risk. Cancer Epidemiol Biomarkers Prev; 23(10); 2057–65. ©2014 AACR.

Objectives The aim of this study was to determine whether ectopic fat depots are prospectively associated with cardiovascular disease, cancer, and all-cause mortality.Background The morbidity associated with excess body weight varies among individuals of similar body mass index. Ectopic fat depots may underlie this risk differential. However, prospective studies of directly measured fat are limited.Methods Participants from the Framingham Heart Study (n = 3,086; 49% women; mean age of 50.2 years) underwent assessment of fat depots (visceral adipose tissue, pericardial adipose tissue, and periaortic adipose tissue) using multidetector computed tomography and were followed up longitudinally for a median of 5.0 years. Cox proportional hazards regression models were used to examine the association of each fat depot (per 1 SD increment) with the risk of incident cardiovascular disease, cancer, and all-cause mortality after adjustment for standard risk factors, including body mass index.Results Overall, there were 90 cardiovascular events, 141 cancer events, and 71 deaths. After multivariable adjustment, visceral adipose tissue was associated with cardiovascular disease (hazard ratio: 1.44; 95% confidence interval: 1.08 to 1.92; p = 0.01) and cancer (hazard ratio: 1.43; 95% confidence interval: 1.12 to 1.84; p = 0.005). Addition of visceral adipose tissue to a multivariable model that included body mass index modestly improved cardiovascular risk prediction (net reclassification improvement of 16.3%). None of the fat depots were associated with all-cause mortality.Conclusions Visceral adiposity is associated with incident cardiovascular disease and cancer after adjustment for clinical risk factors and generalized adiposity. These findings support the growing appreciation of a pathogenic role of ectopic fat. (C) 2013 by the American College of Cardiology Foundation

Objectives To relate cancer since entry into the Framingham Heart Study with the risk of incident Alzheimer’s disease and to estimate the risk of incident cancer among participants with and without Alzheimer’s disease. Design Community based prospective cohort study; nested age and sex matched case-control study. Setting Framingham Heart Study, USA. Participants 1278 participants with and without a history of cancer who were aged 65 or more and free of dementia at baseline (1986-90). Main outcome measures Hazard ratios and 95% confidence intervals for the risks of Alzheimer’s disease and cancer. Results Over a mean follow-up of 10 years, 221 cases of probable Alzheimer’s disease were diagnosed. Cancer survivors had a lower risk of probable Alzheimer’s disease (hazard ratio 0.67, 95% confidence interval 0.47 to 0.97), adjusted for age, sex, and smoking. The risk was lower among survivors of smoking related cancers (0.26, 0.08 to 0.82) than among survivors of non-smoking related cancers (0.82, 0.57 to 1.19). In contrast with their decreased risk of Alzheimer’s disease, survivors of smoking related cancer had a substantially increased risk of stroke (2.18, 1.29 to 3.68). In the nested case-control analysis, participants with probable Alzheimer’s disease had a lower risk of subsequent cancer (0.39, 0.26 to 0.58) than reference participants, as did participants with any Alzheimer’s disease (0.38) and any dementia (0.44). Conclusions Cancer survivors had a lower risk of Alzheimer’s disease than those without cancer, and patients with Alzheimer’s disease had a lower risk of incident cancer. The risk of Alzheimer’s disease was lowest in survivors of smoking related cancers, and was not primarily explained by survival bias. This pattern for cancer is similar to that seen in Parkinson’s disease and suggests an inverse association between cancer and neurodegeneration.

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Breast and prostate cancer are two commonly diagnosed cancers in the United States. Prior work suggests that cancer causing genes and cancer susceptibility genes can be identified.

BACKGROUND: It is unclear whether the increased risk of colon cancer associated with obesity differs for men and women, by distribution of body fat, or by location of the tumor. The primary goal of this study was to address these questions. METHODS: Eligible subjects from the Framingham Study cohort were classified according to body mass index (BMI) and waist size during two age periods: 30–54 y (n=3764) and 55–79 y (n=3802). All eligible men and women were cancer-free at baseline and had complete information on the following potential confounders: age, sex, education, height, activity, smoking, and alcohol. There were 157 incident lifetime cases of colon cancer among those followed beginning at 30–54 y of age and 149 lifetime cases among those whose follow up began at 55–79 y. Subjects were stratified further by gender, activity, and tumor location. The Cox Proportional Hazards Models were used to adjust for possible confounding by the above-described factors. RESULTS: A BMI ≥30 led to a 50% increased risk (95% CI: 0.92–2.5) of colon cancer among middle-aged (30–54 y) and a 2.4-fold increased risk (95% CI: 1.5–3.9) among older (55–79 y) adults. The BMI effect was stronger for men than for women and for cases occurring in the proximal colon. These adverse effects generally diminished when waist was added to the multivariable models. A larger waist size (≥99.1 cm (39 in) and 101.6 cm (40 in) for women and men, respectively) was associated with a two-fold increased risk of colon cancer; this risk increased linearly with increasing waist size and was evident for both proximal and distal colon cancer. There was no attenuation of these effects when BMI was added to the multivariable models. A larger waist had a particularly adverse effect among sedentary subjects (relative risk (RR)=4.4 for middle-aged adults; RR=3.0 for older adults). CONCLUSION: These findings suggest that waist circumference is a stronger predictor of colon cancer risk than is BMI, and that central obesity is responsible for an increased risk of cancer of both the proximal and distal colon.

OBJECTIVE:Adult weight gain has been associated with a twofold risk of postmenopausal breast cancer. Data are limited regarding whether weight gain at specific periods of marked changes in estrogen- and insulin-related hormones have different risk associations. This study assesses the relation of adult weight change overall and at specific, hormonally relevant times with diagnosis of a first breast cancer after age 55 (late onset).METHODS:Framingham study data were used to assess premenopausal (25-44 yr), perimenopausal (45-55 yr), postmenopausal (after 55 yr), and adult lifetime (from 25 yr) weight change in relation to late-onset breast cancer in 2,873 women followed for up to 48 yr, with 206 late-onset breast cancers.RESULTS:Adult lifetime weight gain was associated with an increased risk of late-onset breast cancer (P trend = 0.046). Weight gain during specific time periods was not associated with breast cancer. Data suggested a possible decreased risk of breast cancer with weight loss from ages 25 to 44 and 45 to 55 yr (relative risk = 0.4 [0.2-1.2] and 0.5 [0.3-0.9], respectively).CONCLUSION:These data confirm prior reports of an association between adult lifetime weight gain and increased risk of late-onset breast cancer and support current recommendations to avoid adult weight gain.

The association between alcohol consumption and bladder cancer is controversial. We used data from 10 125 participants in the Framingham Heart Study to assess the association between total and beverage-specific alcohol consumption and the risk of bladder cancer. For each case of bladder cancer, up to five control subjects were selected and matched on major confounders using a risk set method. We used conditional logistic regression to assess the risk of bladder cancer according to categories of alcohol consumption. During a mean follow-up of 27.3 +/- 10.1 years, there were 126 incident cases of bladder cancer. There was no statistically significant association between alcohol consumption and risk of bladder cancer (P-trend = .3). In beverage-specific analyses, beer consumption was associated with a reduced risk of bladder cancer (P-trend = .03), whereas wine (P-trend = .7) and spirit (P-trend = .2) consumption were not. Our data suggest that total and beverage-specific alcohol consumption are not associated with an increased risk of bladder cancer.