Physical activity is known to reduce risks of heart disease and all-cause mortality,¹ as well as risks of colon, breast, and endometrial cancers.² Less is known, however, about whether physical activity reduces risk of other cancers, which, together, constitute 75% of incident cancers in the United States³ and 61% of cancers worldwide.⁴ Physical inactivity is highly prevalent, with an estimated 51% of people in the United States⁵ and 31% of people worldwide not attaining recommended physical activity levels.⁶ Any decrease in risk of cancer associated with physical activity may therefore be relevant to public health and cancer prevention efforts.

Obesity and components of energy imbalance, that is, excessive energy intake and suboptimal levels of physical activity, are established risk factors for cancer incidence. Accumulating evidence suggests that these factors also may be important after the diagnosis of cancer and influence the course of disease, as well as overall health, well-being, and survival. Lifestyle and medical interventions that effectively modify these factors could potentially be harnessed as a means of cancer control. However, for such interventions to be maximally effective and sustainable, broad sweeping scientific discoveries ranging from molecular and cellular advances, to developments in delivering interventions on both individual and societal levels are needed. This review summarizes key discussion topics that were addressed in a recent Institute of Medicine Workshop entitled, “The Role of Obesity in Cancer Survival and Recurrence”; discussions included (i) mechanisms associated with obesity and energy balance that influence cancer progression; (ii) complexities of studying and interpreting energy balance in relation to cancer recurrence and survival; (iii) associations between obesity and cancer risk, recurrence, and mortality; (iv) interventions that promote weight loss, increased physical activity, and negative energy balance as a means of cancer control; and (v) future directions. Cancer Epidemiol Biomarkers Prev; 21(8); 1244–59. ©2012 AACR.

Background: Colorectal cancer, the third most common cancer in the United States, has a natural history that usually encompasses several decades. Dietary components have been implicated in the etiology of colorectal cancer, perhaps through their effect on inflammation.Methods: We examined the ability of the dietary inflammatory index (DII) to predict colorectal cancer in the Iowa Women's Health Study. The DII was computed based on dietary intake assessed by a 121-item food frequency questionnaire in this cohort of 34,703 women, ages 55 to 69 years, free of any self-reported prior malignancy at enrollment in 1986. Incident colorectal cancer cases were identified through linkage with the State Health Registry of Iowa (a Surveillance, Epidemiology, and End Results program member). Cox proportional hazards regression was used to estimate HRs. Through the end of 2010, 1,636 incident colorectal cancers were identified, including 1,329 colon and 325 rectal cancers.Results: Multivariable analysis, adjusting for body mass index, smoking status, pack-years of smoking, hormone replacement therapy, education, diabetes, and total energy intake, revealed positive associations between higher DII and colorectal cancer risk [HR for DIIcontinuous: 1.07 per unit increase in DII (corresponding to 0.5 SD unit increase); 95% confidence interval (CI), 1.01–1.13; HR for DIIquintiles: Q5 vs. Q1 = 1.20; 95% CI, 1.01–1.43]. HRs for DII were similar for colon cancer and rectal cancer, though not statistically significant for rectal cancer.Conclusions: These results indicate that a proinflammatory diet, as indicated by higher DII scores, was associated with higher risk of developing colorectal cancer.Impact: Proinflammatory diets are associated with increased risk of colorectal cancer. Cancer Epidemiol Biomarkers Prev; 23(11); 2383–92. ©2014 AACR.

Background: The MLL 11q23 translocation arises in utero and is present in 75% of infant leukemias. That MLL+ acute myeloid leukemia (AML) can arise following chemotherapy with DNA topoisomerase II (DNAt2) inhibitors suggests that these substances, which also occur naturally in foods, may contribute toward infant leukemia. We hypothesized that maternal consumption of dietary DNAt2 inhibitors during pregnancy would increase the risk of infant leukemia, particularly AML(MLL+). Methods: This Children's Oncology Group case-control study consisted of 240 incident cases of infant acute leukemia [AML and acute lymphoblastic leukemia (ALL)] diagnosed during 1996 to 2002 and 255 random digit dialed controls. Maternal diet during pregnancy was determined through a food frequency questionnaire. An index of specific foods identified a priori to contain DNAt2 inhibitors as well as vegetables and fruits were created and analyzed using unconditional logistic regression. Results: There was little evidence of an association between the specific DNAt2 index and leukemia overall and by subtype. An exception was AML(MLL+); odds ratios (95% confidence intervals) comparing the second to fourth quartiles to the first were 1.9 (0.5-7.0), 2.1 (0.6-7.7), and 3.2 (0.9-11.9), respectively (P for trend = 0.10). For the vegetable and fruit index, there were significant or near-significant inverse linear trends for all leukemias combined, ALL(MLL+), and AML(MLL−). Conclusion: Overall, maternal consumption of fresh vegetables and fruits during pregnancy was associated with a decreased risk of infant leukemia, particularly MLL+. However, for AML(MLL+) cases, maternal consumption of specific DNAt2 inhibitors seemed to increase risk. Although based on small numbers, these data provide some support for distinct etiologic pathways in infant leukemia.

Background: Most longitudinal studies of nondemented persons have reported greater cognitive decline among APOE ε4 carriers vs noncarriers. However, most studies involved elderly samples (aged 65+) and were not large enough to examine the three APOE alleles separately. Methods: Change in cognitive function was examined over a 6-year period using three neuropsychological tests among four APOE genotype groups (ε2/2 + ε2/3, ε3/3 (referent), ε4/2 + ε4/3, ε4/4). The population-based sample included 1,693 African Americans and 6,202 Caucasians initially ages 47 to 68. Results: There was increasingly greater cognitive decline from the ε2 group to the ε4/4 group in Caucasians for two of the three tests. The combination of APOE ε4 with hypercholesterolemia or diabetes showed the greatest cognitive decline. Among African Americans, only the test measuring psychomotor speed showed associations with APOE genotype. Conclusions:APOE ε4 is associated with greater cognitive decline in middle-aged Caucasian individuals, with a reduced decline among ε2 carriers. This suggests that the processes by which APOE genotype mediates dementia risk are operative well in advance of overt dementia.

Ectional and longitudinal associations between light-intensity activity and physical function in older cancer survivors at increased risk for age- and treatment-related comorbidities, including accelerated functional decline. Methods The analysis included data from 641 breast, prostate, and colorectal cancer survivors (54% female) age 65 yr and older who participated in a 1-yr home-based diet and exercise intervention designed to reduce the rate of physical function decline. ANCOVA was used to compare means of physical function across levels of PA intensity (low–light [LLPA]: 1.5–2.0 METs; high–light [HLPA]: 2.1–2.9 METs; MVPA: ≥3.0 METs). Results In cross-sectional analyses, increasing tertiles of light-intensity activity were associated with higher scores for all three measures of physical function (all P values <0.005), after adjusting for age, sex, body mass index, comorbidity, symptoms, and MVPA. Associations were stronger for HLPA than for LLPA. Compared with survivors who had decreased MVPA or maintained stable MVPA and HLPA at the postintervention follow-up, those who had increased HLPA, but had decreased MVPA or maintained stable MVPA, reported higher physical function scores (LS means [95% confidence interval]: SF-36 Physical Function Subscale: −5.58 [−7.96 to −3.20] vs −2.54 [−5.83 to 0.75], P = 0.14; Basic Lower Extremity Function: −2.00 [−3.45 to −0.55] vs 0.28 [−1.72 to 2.28], P = 0.07; Advanced Lower Extremity Function: −2.58 [−4.00 to −1.15] vs 0.44 [−1.52 to 2.40], P = 0.01). Conclusions Our findings suggest that increasing light-intensity activities, especially HLPA, may be a viable approach to reducing the rate of physical function decline in individuals who are unable or reluctant to initiate or maintain adequate levels of moderate-intensity activities....