Faculty Bibliography

High sugar intake may increase cancer risk by promoting insulin-glucose dysregulation, oxidative stress, inflammation, and body adiposity, but epidemiologic evidence is unclear. Associations between dietary sugars and lifestyle-related cancer risk from longitudinal studies were evaluated. We systematically searched PubMed, Embase, and CINAHL and identified 37 prospective cohort studies (1990-2017) reporting multivariable adjusted risk estimates for dietary sugars in relation to cancer. Of 15 and 14 studies on total sugar and sucrose respectively, 11 reported a null association in relation to cancer. Of 14 studies on fructose, 8 reported null associations, and 2 reported protective and 4 reported detrimental associations. In two of five studies on added sugars, a 60-95% increased cancer risk was observed with higher intakes. In 8 of 15 studies, a 23% to 200% higher cancer risk was observed with higher sugary beverage consumption. In conclusion, most studies were indicative of a null association, but suggestive detrimental associations were reported for added sugars and sugary beverages. Expected final online publication date for the Annual Review of Nutrition Volume 38 is August 21, 2018. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

Ultra-processed foods provide 58 % of energy intake and 89 % of added sugars in the American diet. Nevertheless, the association between ultra-processed foods and excess weight has not been investigated in a US sample. The present investigation therefore aims to examine the association between ultra-processed foods and excess weight in a nationally representative sample of US adults. We performed a cross-sectional analysis of anthropometric and dietary data from 15 977 adults (20-64 years) participating in the National Health and Nutrition Examination Survey 2005-2014. Dietary data were collected by 24-h recall. Height, weight and waist circumference (WC) were measured. Foods were classified as ultra-processed/non-ultra-processed according to the NOVA classification. Multivariable linear and logistic regression was used to evaluate the association between ultra-processed food consumption (% energy) and BMI, WC and odds of BMI≥25 kg/m2, BMI≥30 kg/m2 and abdominal obesity (men: WC≥102 cm, women: WC≥88 cm). Prevalence of BMI≥25 kg/m2, BMI≥30 kg/m2 and abdominal obesity was 69·2, 36·1 and 53·0 %, respectively. Consuming ≥74·2 v. ≤36·5 % of total energy from ultra-processed foods was associated with 1·61 units higher BMI (95 % CI 1·11, 2·10), 4·07 cm greater WC (95 % CI 2·94, 5·19) and 48, 53 and 62 % higher odds of BMI≥25 kg/m2, BMI≥30 kg/m2 and abdominal obesity, respectively (OR 1·48; 95 % CI 1·25, 1·76; OR 1·53; 95 % CI 1·29, 1·81; OR 1·62; 95 % CI 1·39, 1·89, respectively; P for trend<0·001 for all). A significant interaction between being female and ultra-processed food consumption was found for BMI (F 4,79=4·89, P=0·002), WC (F 4,79=3·71, P=0·008) and BMI≥25 kg/m2 (F 4,79=5·35, P<0·001). As the first study in a US population, our findings support that higher consumption of ultra-processed food is associated with excess weight, and that the association is more pronounced among women.

Case-control studies suggest that higher whole grain and lower refined grain intakes are associated with reduced cancer risk, but longitudinal evidence is limited. The objective of this prospective cohort study is to evaluate associations between whole and refined grains and their food sources in relation to adiposity-related cancer risk. Participants were adults from the Framingham Offspring cohort (N = 3,184; ≥18 yr). Diet, measured using a food frequency questionnaire, medical and lifestyle data were collected at exam 5 (1991-95). Between 1991 and 2013, 565 adiposity-related cancers were ascertained using pathology reports. Cox proportional hazards models were used to estimate adjusted hazard ratios and 95% confidence intervals for associations of whole and refined grains with risk of adiposity-related cancers combined and with risk of breast and prostate cancers in exploratory site-specific analyses. Null associations between whole and refined grains and combined incidence of adiposity-related cancers were observed in multivariable-adjusted models (HR: 0.94; 95% CI: 0.71-1.23 and HR: 0.98; 95% CI: 0.70-1.38, respectively). In exploratory analyses, higher intakes of whole grains (oz eq/day) and whole grain food sources (servings/day) were associated with 39% and 47% lower breast cancer risk (HR: 0.61; 95% CI: 0.38-0.98 and HR: 0.53; 95% CI: 0.33-0.86, respectively). In conclusion, whole and refined grains were not associated with adiposity-related cancer risk. Whole grains may protect against breast cancer, but findings require confirmation within a larger sample and in other ethnic groups.

BACKGROUND:Higher sugar consumption may increase cancer risk by promoting insulin-glucose dysregulation, oxidative stress, hormonal imbalances, and excess adiposity. This prospective study investigates the association between dietary sugars(fructose and sucrose) and sugary foods and beverages in relation to combined and site-specific (breast, prostate, colorectal) adiposity-associated cancers. METHODS:The analytic sample consisted of 3,184 adults, aged 26-84y, from the Framingham Offspring cohort. Diet data was first collected between 1991-1995 using a food frequency questionnaire. Intakes of fructose, sucrose, sugary foods and sugary beverages (fruit juice and sugar-sweetened beverages) were derived. Participants were followed up until 2013 to ascertain cancer incidence; 565 doctor-diagnosed adiposity-related cancers, including 124 breast, 157 prostate and 68 colorectal cancers occurred. Multivariable-adjusted Cox proportional hazards models were used to evaluate associations. Tests for interaction with BMI and waist circumference were conducted. RESULTS:No associations were observed between fructose, sucrose, sugary food consumption and combined incidence of adiposity-related cancers or the examined site-specific cancers. While total consumption of sugary beverages was not associated with site-specific cancer risk, higher intakes of fruit juice were associated with 58% increased prostate cancer risk(HR:1.58;95%CI:1.04-2.41) in multivariable-adjusted models. In exploratory stratified analyses, higher sugary beverage intakes increased overall adiposity-related cancer risk by 59% in participants with excessive central adiposity(HR:1.59;95%CI:1.01-2.50)(p-trend=0.057). CONCLUSIONS:In this cohort of American adults, higher sugary beverage consumption was associated with increased cancer risk among participants with central adiposity. IMPACT/CONCLUSIONS:These analyses suggest that avoiding sugary beverages represents a simple dietary modification that may be used as an effective cancer control strategy.

BACKGROUND:High parental self-efficacy (PSE) has been associated with healthy diets and higher levels of physical activity (PA) in children; however, data on PSE in relation to body weight and body composition are scarce. The objective of this study was to investigate associations of PSE with measures of diet, PA, body composition, and physical fitness in early childhood. METHOD/METHODS:We used baseline data from the MINISTOP trial in healthy Swedish children ( n = 301; 4.5 ± 0.15 years). PSE was assessed using a questionnaire, dietary data were collected using a mobile technology-assisted methodology, and PA was obtained (sedentary behavior and moderate-to-vigorous) by accelerometry. Body composition was measured using the pediatric option for BodPod and cardiorespiratory fitness by the 20 m shuttle run. Linear regression was conducted to evaluate cross-sectional associations of the outcomes in relation to total PSE and scores computed for the individual PSE factors: (1) diet, (2) limit setting of unhealthful behaviors, and (3) PA. RESULTS:Higher scores of total PSE and the diet factor were associated with higher fruit intake (β = 0.82 g/point and 1.99 g/point; p = .014 and .009, respectively) and lower consumption of unhealthy snacks (β = -0.42 g/point and -0.89 g/point; p = .012 and .020, respectively) after adjustment for parental body mass index and education, respondent, and child's sex and age. No associations were observed between PSE and PA, body composition, or cardiorespiratory fitness. CONCLUSIONS:Our study noted that PSE should be considered in conjunction with other strategies for a sustainable impact on childhood obesity.

BACKGROUND AND OBJECTIVE/OBJECTIVE:Adiposity in pre- and postnatal life may influence menarcheal age. Existing evidence is primarily cross-sectional, failing to address temporality, for which the role of adiposity in early life remains unclear. The current study sought to systematically review longitudinal studies evaluating the associations between birth weight and infant/childhood weight status/weight gain in relation to menarcheal age. METHODS:PubMed, EMBASE, Web of Science, Global Health (Ovid) and CINAHL were systematically searched. Selected studies were limited to English-language articles presenting multi-variable analyses. Seventeen studies reporting risk estimates for birth weight (n = 3), infant/childhood weight gain/weight status (n = 4) or both (n = 10), in relation to menarcheal age were included. RESULTS:Lower vs. higher birth weight was associated with earlier menarche in nine studies and later menarche in one study, while three studies reported a null association. Greater BMI or weight gain over time and greater childhood weight were significantly associated with earlier menarche in nine of nine and six of seven studies, respectively. CONCLUSIONS:Studies suggested that lower birth weight and higher body weight and weight gain in infancy and childhood may increase the risk of early menarche. The pre- and postnatal period may thus be an opportune time for weight control interventions to prevent early menarche, and its subsequent consequences.

Higher carbohydrate intake, glycaemic index (GI), and glycaemic load (GL) are hypothesised to increase cancer risk through metabolic dysregulation of the glucose-insulin axis and adiposity-related mechanisms, but epidemiological evidence is inconsistent. This prospective cohort study investigates carbohydrate quantity and quality in relation to risk of adiposity-related cancers, which represent the most commonly diagnosed preventable cancers in the USA. In exploratory analyses, associations with three site-specific cancers: breast, prostate and colorectal cancers were also examined. The study sample consisted of 3184 adults from the Framingham Offspring cohort. Dietary data were collected in 1991-1995 using a FFQ along with lifestyle and medical information. From 1991 to 2013, 565 incident adiposity-related cancers, including 124 breast, 157 prostate and sixty-eight colorectal cancers, were identified. Cox proportional hazards models were used to evaluate the role of carbohydrate nutrition in cancer risk. GI and GL were not associated with risk of adiposity-related cancers or any of the site-specific cancers. Total carbohydrate intake was not associated with risk of adiposity-related cancers combined or prostate and colorectal cancers. However, carbohydrate consumption in the highest v. lowest quintile was associated with 41 % lower breast cancer risk (hazard ratio (HR) 0.59; 95 % CI 0.36, 0.97). High-, medium- and low-GI foods were not associated with risk of adiposity-related cancers or prostate and colorectal cancers. In exploratory analyses, low-GI foods, were associated with 49 % lower breast cancer risk (HR 0.51; 95 % CI 0.32, 0.83). In this cohort of Caucasian American adults, associations between carbohydrate nutrition and cancer varied by cancer site. Healthier low-GI carbohydrate foods may prevent adiposity-related cancers among women, but these findings require confirmation in a larger sample.