An estimated 4 in 10 cancers are preventable through modifiable risk factors. This review summarizes the epidemiologic evidence linking physical activity, sedentary behavior, and obesity with cancer risk. We explore the possible biologic mechanisms underpinning the associations between these lifestyle factors and cancer incidence, including effects on endogenous sex steroids and metabolic hormones, insulin sensitivity, and chronic inflammation.

Endometrial cancer is the sixth most common cancer in women worldwide and the most common gynecologic malignancy in the developed world. This chapter explores the current epidemiologic evidence on the association between obesity and endometrial cancer risk and mortality. Using body mass index (BMI) as a measure of obesity, we found that obesity (defined as BMI > 30 and < 35 kg/m) was associated with a 2.6-fold increase in endometrial cancer risk, while severe obesity (BMI > 35 kg/m) was associated with a 4.7-fold increase compared to normal-weight women (BMI < 25 kg/m). Increased central adiposity also increased endometrial cancer risk by 1.5- to twofold. Among both healthy and endometrial cancer patient populations, obesity was associated with a roughly twofold increase in endometrial cancer-specific mortality. This risk reduction was also observed for obesity and all-cause mortality among endometrial cancer patients. In the few studies that assessed risk associated with weight change, an increased endometrial cancer risk with weight gain and weight cycling was observed, whereas some evidence for a protective effect of weight loss was found. Furthermore, early-life obesity was associated with a moderately increased risk of endometrial cancer later in life. There are several mechanisms whereby obesity is hypothesized to increase endometrial cancer risk, including increased endogenous sex steroid hormones, insulin resistance, chronic inflammation and adipokines. Further research should focus on histological subtypes or molecular phenotypes of endometrial tumors and population subgroups that could be at an increased risk of obesity-associated endometrial cancer. Additionally, studies on weight gain, loss or cycling and weight loss interventions can provide mechanistic insight into the obesity-endometrial cancer association. Sufficient evidence exists to recommend avoiding obesity to reduce endometrial cancer risk.

This study examined the effects of server race, customer race, and their interaction on restaurant tips while statistically controlling for customers' perceptions of service quality and other variables. The findings indicate that consumers of both races discriminated against Black service providers by tipping them less than White service providers. Furthermore, this server race effect on tipping was moderated by perceived service quality and dining party size. The theoretical and practical implications of these findings are discussed. Particularly noteworthy is the possibility that the server race effect on tipping represents an adverse impact against Black servers that makes the use of tipping to compensate employees a violation of employment discrimination law in the United States.

Purpose: To prescribe different physical activity (PA) intensities using activity trackers to increase PA, reduce sedentary time, and improve health outcomes among breast cancer survivors. The maintenance effect of the interventions on study outcomes was also assessed. Methods: The Breast Cancer and Physical Activity Level pilot trial randomized 45 breast cancer survivors to a home-based, 12-wk lower (300 min•wk−1 at 40%-59% of HR reserve) or higherintensity PA (150 min•wk−1 at 60%-80% of HR reserve), or no PA intervention/control. Both intervention groups received Polar A360® activity trackers. Study outcomes assessed at baseline, 12 and 24 wk included PA and sedentary time (ActiGraph GT3X+), health-related fitness (e.g., body composition, cardiopulmonary fitness/VO2max), and patient-reported outcomes (e.g., quality of life). Intention-to-treat analyses were conducted using linear mixed models and adjusted for baseline outcomes. Results: Increases in moderate-vigorous intensity PA (least squares adjusted group difference [LSAGD], 0.6; 95% confidence interval [CI], 0.1-1.0) and decreases in sedentary time (LSAGD, −1.2; 95% CI, −2.2 to −0.2) were significantly greater in the lowerintensity PA group versus control at 12 wk. Increases in VO2max at 12 wk in both interventions groups were significantly greater than changes in the control group (lower-intensity PA group LSAGD, 4.2; 95% CI, 0.5-8.0 mL•kg−1•min−1; higher-intensity PA group LSAGD, 5.4; 95% CI, 1.7-9.1mL•kg−1•min−1). Changes in PA and VO2max remained at 24wk, but differences between the intervention and control groups were no longer statistically significant. Conclusions: Increases in PA time and cardiopulmonary fitness/VO2max can be achieved with both lower-and higher-intensity PA interventions in breast cancer survivors. Reductions in sedentary time were also noted in the lower-intensity PA group.

Epidemiological studies suggest that adults and children who are habitual short sleepers tend to have a higher body mass index, fat percentage and abdominal circumference when compared to average-duration sleepers. Reduced or disturbed sleep is also associated with certain predictors of type 2 diabetes, such as glucose intolerance, insulin resistance, reduced insulin response to glucose and a reduction in the disposition index. Current experimental evidence suggests that sleep restriction may lead to increased food intake but does not appear to result in decreased energy expenditure. Furthermore, sleep restriction has been reported to increase evening cortisol levels, which may decrease insulin sensitivity the next morning. This notion was further supported by studies, which noted decreases in the effectiveness of insulin-mediated glucose uptake the following morning. Further evidence suggests that short sleepers have glucose responses that are similar to average-duration sleepers, but at the cost of an increase in insulin release, which may be the result of decreased insulin sensitivity over time. Recent studies also provide evidence that sleep restriction enhances susceptibility to food stimuli, especially for energy-dense, high-carbohydrate foods. In summary, inadequate sleep, in both quality and quantity, should be regarded as a plausible risk factor for the development of obesity and type 2 diabetes. In addition to other health promotion measures, a good night's sleep should be seen as a critical health component by clinicians in the prevention and treatment of obesity and type 2 diabetes.