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Background: Physical activity and BMI have been individually associated with cancer survivorship but have not yet been studied in combinations in colorectal cancer patients. Here, we investigate individual and combined associations of physical activity and BMI groups with colorectal cancer survival outcomes., Methods: Self-reported physical activity levels (MET hrs/wk) were assessed using an adapted version of the International Physical Activity Questionnaire (IPAQ) at baseline in 931 patients with stage I-III colorectal cancer and classified into 'highly active' and'not-highly active'(≥ / < 18 MET hrs/wk). BMI (kg/m 2 ) was categorized into 'normal weight', 'overweight', and 'obese'. Patients were further classified into combined physical activity and BMI groups. Cox-proportional hazard models with Firth correction were computed to assess associations [hazard ratio (HR), 95% profile HR likelihood confidence interval (95% CI) between individual and combined physical activity and BMI groups with overall and disease-free survival in colorectal cancer patients., Results: 'Not-highly active' compared to 'highly active' and 'overweight'/ 'obese' compared to 'normal weight' patients had a 40-50% increased risk of death or recurrence (HR: 1.41 (95% CI: 0.99-2.06), p = 0.03; HR: 1.49 (95% CI: 1.02-2.21) and HR: 1.51 (95% CI: 1.02-2.26), p = 0.04, respectively). 'Not-highly active' patients had worse disease-free survival outcomes, regardless of their BMI, compared to 'highly active/normal weight' patients. 'Not-highly active/obese' patients had a 3.66 times increased risk of death or recurrence compared to 'highly active/normal weight' patients (HR: 4.66 (95% CI: 1.75-9.10), p = 0.002). Lower activity thresholds yielded smaller effect sizes., Conclusion: Physical activity and BMI were individually associated with disease-free survival among colorectal cancer patients. Physical activity seems to improve survival outcomes in patients regardless of their BMI., (© 2023. The Author(s).)

Background: Obesity, defined by body mass index (BMI), measured at colorectal cancer (CRC) diagnosis has been associated with postoperative complications and survival outcomes. However, BMI does not allow for a differentiation between fat and muscle mass. Computed tomography (CT)-defined body composition more accurately reflects different types of tissue and their associations with health-related quality of life (HRQoL) during the first year of disease, but this has not been investigated yet. We studied the role of visceral and subcutaneous fat area (VFA and SFA) and skeletal muscle mass (SMM) on longitudinally assessed HRQoL in CRC patients., Methods: A total of 138 newly diagnosed CRC patients underwent CT scans at diagnosis and completed questionnaires prior to and six and twelve months post-surgery. We investigated the associations of VFA, SFA, and SMM with HRQoL at multiple time points., Results: A higher VFA was associated with increased pain six and twelve months post-surgery (β = 0.06, p = 0.04 and β = 0.07, p = 0.01) and with worse social functioning six months post-surgery (β = -0.08, p = 0.01). Higher SMM was associated with increased pain twelve months post-surgery (β = 1.03, p < 0.01)., Conclusions: CT-quantified body composition is associated with HRQoL scales post-surgery. Intervention strategies targeting a reduction in VFA and maintaining SMM might improve HRQoL in CRC patients during the first year post-surgery., Competing Interests: The authors declared that they have no competing interests.

Objective: Obesity, inflammation, and circulating 25-hydroxyvitamin D (25-OHD) have distinct roles in cancer prognosis. The interplay of these factors was investigated by evaluating the associations of body mass index (BMI) with circulating 25-OHD levels in cancer survivors and determining whether associations were modified by inflammation, defined by C-reactive protein (CRP) levels., Methods: Data on cancer survivors were aggregated from the US National Health and Nutrition Examination Survey (2001-2010). Multivariable linear regression models were used to evaluate the associations of BMI with circulating 25-OHD. Analyses were stratified by CRP levels: low < 1.0 mg/L, moderate 1.0-3.0 mg/L, and high > 3.0-9.9 mg/L., Results: Among 1,305 cancer survivors (mean age = 60.8 years, mean BMI = 28.0 kg/m 2 ), circulating 25-OHD levels were 8.74 nmol/L lower (95% CI: 4.71 to 12.77) in cancer survivors with BMI ≥ 30.0 kg/m 2 compared with those with BMI < 25.0 kg/m 2 . This association was, however, limited to those with moderate CRP (-9.90 nmol/L, 95% CI: -16.45 to -3.36) and high CRP (-11.61 nmol/L, 95% CI: -18.71 to -5.05), but not among those with low CRP levels (-5.31 nmol/L, 95% CI:-12.66 to 2.04)., Conclusions: A greater understanding of the interplay between 25-OHD and inflammation in cancer survivors with obesity should allow for targeted secondary prevention and help improve prognosis in these patients., (© 2017 The Obesity Society.)

Obesity is a well-established cause of postmenopausal breast cancer. However, early life adiposity is inversely associated with breast cancer incidence. To understand these conflicting relations, we use validated measures to assess adiposity in childhood and late adolescence, as well as weight change, in relation to total invasive breast cancer incidence and receptor subtypes. We conducted a prospective observational study among 74,177 women from the Nurses' Health Study from 1980-2012, with updated risk factors every 2 years during which 4,965 incident invasive breast cancers occurred. Overall, weight at age 18 was inversely associated with both premenopausal (HR per 30 kg = 0.52, 95% CI = 0.39-0.71) and postmenopausal (HR per 30 kg = 0.81, 95% CI = 0.72-0.92) breast cancer which was largely explained by adiposity at age 10. Long-term weight gain from age 18 both during premenopause and postmenopause were positively associated with postmenopausal breast cancer risk. However, premenopausal weight gain was not related to premenopausal breast cancer risk. Furthermore, weight gain since age 18 was positively associated with ER+/PR+ postmenopausal breast cancer (HR per 30 kg = 1.50, 95% CI = 1.36-1.65) but not ER+/PR- (HR per 30 kg = 0.96, 95% CI = 0.78-1.19) or ER-/PR- (HR per 30 kg = 1.16, 95% CI = 0.95-1.42) postmenopausal breast cancer. Overall, 17% of ER+/PR+ postmenopausal breast cancer and 14% of total postmenopausal breast cancer are attributable to weight gain of > 5 kg since age 18., (© 2017 UICC.)

Current guidelines recommend weight loss in obese cancer survivors. Weight loss, however, has adverse effects on bone health in obese individuals without cancer but this has not been evaluated in breast cancer survivors. We investigated the associations of intentional weight loss with bone mineral density (BMD) and bone turn-over markers in overweight/obese postmenopausal breast cancer survivors. Participants were overweight/obese breast cancer survivors (N = 81) with stage I, II or IIIA disease enrolled in the St. Louis site of a multi-site Exercise and Nutrition to Enhance Recovery and Good health for You (ENERGY) study; a randomized-controlled clinical trial designed to achieve a sustained ≥7 % loss in body weight at 2 years. Weight loss was achieved through dietary modification with the addition of physical activity. Generalized estimating equations were used to assess differences in mean values between follow-up and baseline. Mean weight decreased by 3 and 2.3 % between baseline and 6-month follow-up, and 12-month follow-up, respectively. There were decreases in osteocalcin (10.6 %, p value < 0.001), PINP (14.5 %, p value < 0.001), NTx (19.2 % p value < 0.001), and RANK (48.5 %, p value < 0.001), but not BALP and CTX-1 levels between baseline and 12-month follow-up. No significant changes occurred in mean T-scores, pelvis and lumbar spine BMD between baseline and 12-month follow-up. A 2.3 % weight loss over 12 months among overweight/obese women with early-stage breast cancer does not appear to have deleterious effect on bone health, and might even have beneficial effect. These findings warrant confirmation, particularly among breast cancer survivors with a larger magnitude of weight loss.

BACKGROUND: Mammographic breast density (MBD) is a strong risk factor and an intermediate phenotype for breast cancer, yet there are limited studies on how environmental pollutants are associated with MBD. OBJECTIVE: We investigated associations of perfluorooctane sulfonate (PFOS), perfluorooctanoic acid (PFOA), and perfluorohexane sulfonate (PFHxS) levels with measures of MBD and evaluated if early life factors modified any associations. METHODS: Metabolon performed metabolomics analysis using ultrahigh-performance liquid chromatography/tandem accurate mass spectrometry in fasting blood from 705 premenopausal women completing their annual screening mammogram in St. Louis, Missouri. We calculated least square means (LSM) of mammographic volumetric percent density (VPD), dense volume (DV), and nondense volume (NDV) by quartiles (Q) of PFOS, PFOA, and PFHxS from multivariable linear regression modeling overall and stratified by recruitment period, race, age at menarche, and body shape at age 10. Models were adjusted for age, age at menarche, body fat percentage, race, family history of breast cancer, oral contraceptive use, alcohol consumption, parity/age at first birth, and body shape at age 10. RESULTS: PFOS, PFOA, and PFHxS were not significantly associated with VPD or NDV. PFHxS was significantly positively associated with DV (Q1=67.64 cm³, Q2=69.91 cm³, Q3=69.06 cm³, Q4=75.79 cm³; 푝-trend=0.03). PFOS was positively associated with DV (Q1=65.45 cm³, Q2=70.74 cm³, Q3=73.31 cm³, Q4=73.52 cm³; 푝-trend=0.06) with DV being 8.1%, 12%, and 12.3% higher in Q2, Q3, and Q4 compared to Q1. Among women who were underweight/normal weight at age 10, PFOS was positively associated with VPD (Q1=9.02%, Q2=9.11%, Q3=9.48%, Q4=9.92%; 푝-trend=0.04) while there was an inverse association among women who were overweight/obese at age 10 (Q1=7.46%, Q2=6.94%, Q3=6.78%, Q4=5.47%; 푝-trend=0.005) (푝-interaction=0.04). DISCUSSION: We report novel associations of PFHxS and PFOS with DV in premenopausal women. PFOS, PFOA, and PFHxS were not associated with VPD and NDV. In addition, body shape at age 10 may modify the associations of PFOS with MBD. Further studies are needed to validate our findings and to evaluate the associations of other per- and polyfluoroalkyl substances (PFAS), as well as mixtures of PFAS, with MBD. [ABSTRACT FROM AUTHOR]

Obesity is well established as a cause of postmenopausal breast cancer incidence and mortality. In contrast, adiposity in early life reduces breast cancer incidence. However, whether short-term weight change influences breast cancer risk is not well known. We followed a cohort of 77,232 women from 1980 to 2006 (1,445,578 person-years), with routinely updated risk factor information, documenting 4196 incident cases of invasive breast cancer. ER and PR status were obtained from pathology reports and medical records yielding a total of 2033 ER+/PR+ tumors, 595 ER-/PR- tumors, 512 ER+/PR- tumors. The log incidence breast cancer model was used to assess the association of short-term weight gain (over past 4 years) while controlling for average BMI before and after menopause. Short-term weight change was significantly associated with breast cancer risk (RR 1.20; 95 % CI 1.09-1.33) for a 4-year weight gain of ≥15 lbs versus no change (≤5 lbs) (P_trend < 0.001). The association was stronger for premenopausal women (RR 1.38; 95 % CI 1.13-1.69) (P_trend = 0.004) than for postmenopausal women (RR 1.10; 95 % CI 0.97-1.25) (P_trend = 0.063). Short-term weight gain during premenopause had a stronger association for ER+/PR- (RR per 25 lb weight gain = 2.19; 95 % CI 1.33-3.61, P = 0.002) and ER-/PR- breast cancer (RR per 25 lb weight gain = 1.61; 95 % CI 1.09-2.38, P = 0.016) than for ER+/PR+ breast cancer (RR per 25 lb weight gain = 1.13; 95 % CI 0.89-1.43, P = 0.32). There are deleterious effects of short-term weight gain, particularly during pre-menopause, even after controlling for average BMI before and after menopause. The association was stronger for ER+/PR- and ER-/PR- than for ER+/PR+ breast cancer.

Background: Early life adiposity and changes in adiposity over the life course are associated with mammographic breast density among postmenopausal women. However, the underlying mechanisms are unknown; therefore, we comprehensively examined the associations of early life body mass index (BMI) and changes in BMI from ages 10, 18 to age at mammogram with growth factor, RANK pathway, and sex hormone gene expression in 372 postmenopausal women. Methods: We estimated early life BMI at age 10 using the validated 9‐level Stunkard pictogram. We calculated BMI at other ages (18, 30, and current age at mammogram) by dividing weight in kilograms at these ages with height in meters squared. Sequencing for gene expression was performed using the NanoString nCounter system. After adjusting for confounders, we estimated associations using multivariable linear regressions. Results: A 10 kg/m2 increase in early life BMI at age 10 was associated with a 17.2% decrease in RANKL gene expression (95% confidence interval [CI] = −30.8, −0.9) but was not associated with changes in other markers. BMI changes from ages 10, 18 to age at mammogram were associated with an increase in BMP2 and decreases in RANK, RANKL, and TNFRSF13B gene expression but were not associated with gene expression of other markers. A 10 kg/m2 increase in early life BMI from age 10 to current age was associated with a 7.8% increase in BMP2 (95% CI = −1.4, 17.8), an 8.5% decrease in RANK (95% CI = −13.9, −2.8), a 10.4% decrease in RANKL (95% CI = −16.9, −3.3), and an 8.5% decrease in TNFRSF13B gene expression (95% CI = −13.8, −2.8). Conclusion: The results provide new insights into the biological mechanisms underlying the associations of adiposity changes from early life to adulthood and early life adiposity with mammographic breast density in postmenopausal women. [ABSTRACT FROM AUTHOR]

Ovarian cancer is the deadliest gynecologic malignancy, yet the effects on survival of modifiable pre-diagnosis lifestyle factors, such as obesity and physical activity, remain largely unexplored. Our objective was to evaluate the effect of pre-diagnosis BMI and physical activity on ovarian cancer mortality using prospectively collected data. Data on women who developed ovarian cancer after enrollment into the NIH-AARP Diet and Health Study were analyzed. Cancer incidence was ascertained through linkage state cancer registries and consisted of 741 cases of epithelial ovarian cancer. Higher pre-diagnosis BMI was associated with increased overall and ovarian cancer-specific mortality. Comparing women with BMI 25–29.9, 30–34.9 and ≥ 35 to normal weight women, the HRs of overall mortality were 1.18 (95%CI 0.96–1.45), 1.05 (0.82–1.36) and 1.59 (1.14–2.18, p-trend = 0.02). The findings were similar for ovarian cancer-specific mortality comparing women with BMI ≥ 35 to normal weight women (BMI <25) with a HR of 1.47 (95%CI 1.03–2.09, p-trend 0.08). Pre-diagnosis physical activity was not associated with mortality, with HRs for overall mortality of 1.06 (95%CI 0.79–1.43), 0.94 (0.72–1.23), 0.98 (0.76–1.25), and 0.98 (0.75–1.28, p-trend = 0.91), comparing women who engaged in vigorous physical activity 1–3 times/month, 1–2 times/week, 3–4 times/week and 5 times/week, respectively, with those who never/rarely engaged in such activity. Women who were obese before developing ovarian cancer had increased mortality than those who were normal weight, but physical activity before diagnosis was not associated with mortality in this study population. These results suggest that maintaining a healthy weight is a powerful preventative tool. • Limited prospective data exists on the effect of pre-diagnosis obesity or physical activity on ovarian cancer mortality. • Higher BMI is associated with increased overall and ovarian cancer mortality; physical activity level was not associated. • Findings suggest that having a normal weight before ovarian cancer diagnosis confers survival advantage. [ABSTRACT FROM AUTHOR]