NIHR Bristol Nutrition Biomedical Research Unit

Background: Clinically diagnosed eating disorders may have adverse cardiometabolic consequences, including overweight or obesity and high blood pressure. However, the link between problematic eating attitudes in early adolescence, which can lead to disordered eating behaviors, and future cardiometabolic health is, to our knowledge, unknown.Objective: We assessed whether variations in midchildhood eating attitudes influence the future development of overweight or obesity and high blood pressure.Design: Of 17,046 children who participated in the Promotion of Breastfeeding Intervention Trial (PROBIT), we included 13,557 participants (79.5% response rate) who completed the Children’s Eating Attitudes Test (ChEAT) at age 11.5 y and in whom we measured adiposity and blood pressure at ages 6.5, 11.5, and 16 y. We assessed whether ChEAT scores ≥85th percentile (indicative of problematic eating attitudes) compared with scores <85th percentile at age 11.5 y were associated with new-onset overweight, obesity, high systolic blood pressure, or high diastolic blood pressure between midchildhood and early adolescence.Results: After controlling for baseline sociodemographic confounders, we observed positive associations of problematic eating attitudes at age 11.5 y with new-onset obesity (OR: 2.18; 95% CI: 1.58, 3.02), new-onset high systolic blood pressure (OR: 1.34; 95% CI: 1.05, 1.70), and new-onset high diastolic blood pressure (OR: 1.25; 95% CI: 0.99, 1.58) at age 16 y. After further controlling for body mass index at age 6.5 y, problematic eating attitudes remained positively associated with new-onset obesity (OR: 1.80; 95% CI: 1.28, 2.53); however, associations with new-onset high blood pressure were attenuated (OR: 1.14; 95% CI: 0.89, 1.45 and OR: 1.09; 95% CI: 0.86, 1.39 for new-onset systolic and diastolic blood pressure, respectively).Conclusions: Problematic eating attitudes in midchildhood seem to be related to the development of obesity in adolescence, a relatively novel observation with potentially important public health implications for obesity control. PROBIT was registered at clinicaltrials.gov as NCT01561612 and isrctn.com as ISRCTN37687716.

PurposeThe insulin-like growth factor (IGF) system is modifiable by diet and lifestyle, and has been linked to prostate cancer development and progression.MethodsWe conducted a prospective cohort study of 621 men diagnosed with localized prostate cancer to investigate the associations of dietary and lifestyle changes with post-diagnosis circulating levels of IGF-I and IGFBP-3. We used analysis of covariance to estimate the associations, controlling for baseline IGF-I or IGFBP-3, respectively.ResultsMean IGF-I levels were 6.5% (95% CI −12.8, −0.3%, p = 0.04) lower in men who decreased their protein intake after diagnosis compared to men who did not change. Men who changed their fruit and vegetable intake had lower IGF-I levels compared to non-changers [Decreased intake: −10.1%, 95% CI −18.4, −1.8%, p = 0.02; Increased intake: −12.0%, 95% CI −18.4, −1.8%, p = 0.002]. IGFBP-3 was 14.6% (95% CI −24.5, −4.8%, p = 0.004) lower in men who achieved a healthy body mass index after diagnosis. Men who became inactive had 9.5% higher average IGF-I levels (95% CI 0.1, 18.9%, p = 0.05).ConclusionsDecreased protein intake and body mass index, and increased physical activity and fruit and vegetable intake, following a prostate cancer diagnosis were associated with reduced post-diagnosis serum IGF-I and IGFBP-3. Counterintuitively, reduced fruit and vegetable intake was also associated with reduced IGF-I, but with weak statistical support, possibly implicating chance. If confirmed in other studies, our findings may inform potential lifestyle interventions in prostate cancer. ProtecT was registered at International Standard Randomised Controlled Trial Registry, http://isrctn.org as ISRCTN20141297.

Prostate cancer is the most common cancer in men in developed countries, and is a target for risk reduction strategies. The effects of alcohol consumption on prostate cancer incidence and survival remain unclear, potentially due to methodological limitations of observational studies. In this study, we investigated the associations of genetic variants in alcohol‐metabolising genes with prostate cancer incidence and survival. We analysed data from 23,868 men with prostate cancer and 23,051 controls from 25 studies within the international PRACTICAL Consortium. Study‐specific associations of 68 single nucleotide polymorphisms (SNPs) in 8 alcohol‐metabolising genes (Alcohol Dehydrogenases (ADHs) and Aldehyde Dehydrogenases (ALDHs)) with prostate cancer diagnosis and prostate cancer‐specific mortality, by grade, were assessed using logistic and Cox regression models, respectively. The data across the 25 studies were meta‐analysed using fixed‐effect and random‐effects models. We found little evidence that variants in alcohol metabolising genes were associated with prostate cancer diagnosis. Four variants in two genes exceeded the multiple testing threshold for associations with prostate cancer mortality in fixed‐effect meta‐analyses. SNPs within ALDH1A2 associated with prostate cancer mortality were rs1441817 (fixed effects hazard ratio, HRfixed = 0.78; 95% confidence interval (95%CI):0.66,0.91; p values = 0.002); rs12910509, HRfixed = 0.76; 95%CI:0.64,0.91; p values = 0.003); and rs8041922 (HRfixed = 0.76; 95%CI:0.64,0.91; p values = 0.002). These SNPs were in linkage disequilibrium with each other. In ALDH1B1, rs10973794 (HRfixed = 1.43; 95%CI:1.14,1.79; p values = 0.002) was associated with prostate cancer mortality in men with low‐grade prostate cancer. These results suggest that alcohol consumption is unlikely to affect prostate cancer incidence, but it may influence disease progression.