Hébert, James R.

(1) Background. Cognitive dysfunction is prevalent among cancer survivors. Inflammation may contribute to impaired cognition, and diet represents a novel strategy to mitigate cognitive decline. The purpose was to (1) assess the impact of an educational cooking class on cancer survivor eating habits and their inflammatory potential and (2) determine the relationship between diet and cognitive function. (2) Methods. This was a non-randomized interventional study of a virtual educational cooking class in post-treatment, adult cancer survivors. Energy-adjusted Dietary Inflammatory Index (E-DII™) scores and subjective cognitive function were assessed at baseline and 1 month post-intervention. (3) Results. Of 22 subjects, all were female, White, and primarily had breast cancer (64%). There was a significant decrease in E-DII scores, which became more anti-inflammatory, one month after intervention (−2.3 vs. −2.7, p = 0.005). There were significant increases in cognition, including perceived cognitive impairment (COG-PCI, p < 0.001), comments from others (COG-OTH, p < 0.001), and quality of life (COG-QOL, p < 0.001). A change in calories was a significant predictor of a change in perceived cognitive ability (COG-PCA) after adjustment (β = 0.007, p = 0.04; 95% CI (0.000, 0.014)). (4) Conclusions. Educational cooking classes may be an effective way to impact diet-derived inflammation; additional research is needed to assess the long-term effects of dietary changes on cognition.

Inflammation plays a central role in pancreatic cancer etiology and can be modulated by diet. We aimed to examine the association between the inflammatory potential of diet, assessed with the Dietary Inflammatory Index (DII®), and pancreatic cancer risk in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial prospective cohort. Our study included 101,449 participants aged 52–78 years at baseline who completed both baseline questionnaire and a diet history questionnaire. Energy‐adjusted DII (E‐DII) scores were computed based on food and supplement intake. Cox proportional hazards models and time dependent Cox models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) with participants in the lowest E‐DII quintile (most anti‐inflammatory scores) as referent. After a median 8.5 years of follow‐up, 328 pancreatic cancer cases were identified. E‐DII scores were not associated with pancreatic cancer risk in the multivariable model (HRQ5vsQ1 = 0.94; 95% CI = 0.66–1.35; p‐trend = 0.43). Time significantly modified the association (p‐interaction = 0.01). During follow up <4 years, there was suggestive evidence of an inverse association between E‐DII and pancreatic cancer (HRQ5vsQ1 = 0.60; 95% CI = 0.35–1.02; p‐trend = 0.20) while there was a significant positive trend in the follow up ≥4 years (HRQ5vsQ1 = 1.31; 95% CI = 0.83–2.08; p‐trend = 0.03). Similar results were observed for E‐DII from food only. Our study does not support an association between inflammatory potential of diet and pancreatic cancer risk; however, heterogeneous results were obtained with different follow‐up times. These divergent associations may result from the influences of undetected disease in the short‐term.

We conducted a retrospective cohort study to investigate the colorectal cancer (CRC) incidence and mortality prevention achievable in clinical practice with an optimized colonoscopy protocol targeting near‐complete polyp clearance. The protocol consisted of: ( i ) telephonic reinforcement of bowel preparation instructions; ( ii ) active inspection for polyps throughout insertion and circumferential withdrawal; and ( iii ) timely updating of the protocol and documentation to incorporate the latest guidelines. Of 17,312 patients provided screening colonoscopies by 59 endoscopists in South Carolina, USA from September 2001 through December 2008, 997 were excluded using accepted exclusion criteria. Data on 16,315 patients were merged with the South Carolina Central Cancer Registry and Vital Records Registry data from January 1996 to December 2009 to identify incident CRC cases and deaths, incident lung cancers and brain cancer deaths (comparison control cancers). The standardized incidence ratios (SIR) and standardized mortality ratios (SMR) relative to South Carolina and US SEER‐18 population rates were calculated. Over 78,375 person‐years of observation, 18 patients developed CRC versus 104.11 expected for an SIR of 0.17, or 83% CRC protection, the rates being 68% and 91%, respectively among the adenoma‐ and adenoma‐free subgroups (all p < 0.001). Restricting the cohort to ensure minimum 5‐year follow‐up (mean follow‐up 6.64 years) did not change the results. The CRC mortality reduction was 89% ( p < 0.001; four CRC deaths vs . 35.95 expected). The lung cancer SIR was 0.96 ( p = 0.67), and brain cancer SMR was 0.92 ( p = 0.35). Over 80% reduction in CRC incidence and mortality is achievable in routine practice by implementing key colonoscopy principles targeting near‐complete polyp clearance.

OBJECTIVE To examine elevated depressive symptoms and antidepressant use in relation to diabetes incidence in the Women’s Health Initiative. RESEARCH DESIGN AND METHODS A total of 161,808 postmenopausal women were followed for over an average of 7.6 years. Hazard ratios (HRs) estimating the effects of elevated depressive symptoms and antidepressant use on newly diagnosed incident diabetes were obtained using Cox proportional hazards models adjusted for known diabetes risk factors. RESULTS Multivariable-adjusted HRs indicated an increased risk of incident diabetes with elevated baseline depressive symptoms (HR 1.13 [95% CI 1.07–1.20]) and antidepressant use (1.18 [1.10–1.28]). These associations persisted through year 3 data, in which respective adjusted HRs were 1.23 (1.09–1.39) and 1.31 (1.14–1.50). CONCLUSIONS Postmenopausal women with elevated depressive symptoms who also use antidepressants have a greater risk of developing incident diabetes. In addition, longstanding elevated depressive symptoms and recent antidepressant medication use increase the risk of incident diabetes.