Post-diagnosis adiposity, physical activity, sedentary behaviour, dietary factors, supplement use and colorectal cancer prognosis: Global Cancer Update Programme (CUP Global) summary of evidence grading.

Based on the World Cancer Research Fund Global Cancer Update Programme, we performed systematic reviews and meta-analyses to investigate the association of post-diagnosis adiposity, physical activity, sedentary behaviour, and dietary factors with colorectal cancer prognosis. We searched PubMed and Embase until 28th February, 2022. An independent expert committee and expert panel graded the quality of evidence. A total of 167 unique publications were reviewed, and all but five were observational studies. The quality of the evidence was graded conservatively due to the high risk of several biases. There was evidence of non-linearity in the associations between body mass index and colorectal cancer prognosis. The associations appeared reverse J-shaped, and the quality of this evidence was graded as limited (likelihood of causality: limited-no conclusion). The evidence on recreational physical activity and lower risk of all-cause mortality (relative risk [RR] highest vs. lowest: 0.69, 95% confidence interval [CI]: 0.62-0.77) and recurrence/disease-free survival (RR: 0.80, 95% CI: 0.70-0.92) was graded as limited-suggestive. There was limited-suggestive evidence for the associations between healthy dietary and/or lifestyle patterns (including diets that comprised plant-based foods), intake of whole grains and coffee with lower risk of all-cause mortality, and between unhealthy dietary patterns and intake of sugary drinks with higher risk of all-cause mortality. The evidence for other exposures on colorectal cancer outcomes was sparse and graded as limited-no conclusion. Analyses were conducted excluding cancer patients with metastases without substantial changes in the findings. Well-designed intervention and cohort studies are needed to support the development of lifestyle recommendations for colorectal cancer patients.

The association of sleep with metabolic pathways and metabolites: evidence from the Dietary Approaches to Stop Hypertension (DASH)-sodium feeding study.

INTRODUCTION: Sleep is increasingly being viewed as an issue of public health concern, yet few epidemiologic studies have explored associations between sleep habits and metabolomic profile. OBJECTIVES: To assess the association between sleep and blood metabolites. METHODS: We examined the association between sleep and 891 fasting plasma metabolites in a subgroup of 106 participants from the Dietary Approaches to Stop Hypertension (DASH)-Sodium feeding trial (1997-1999). We produced two sleep variables to analyze, sleep midpoint (median time between bedtime and waketime) and sleep duration, as well as bedtime and wake time. Metabolites were measured using liquid and gas chromatography, coupled with mass spectrometry. We assessed associations between sleep variables and log transformed metabolites using linear mixed-effects models. We combined the resulting p-values using Fisher's method to calculate associations between sleep and 38 metabolic pathways. RESULTS: Sixteen pathways were associated (p < 0.05) with midpoint. Only the γ-glutamyl amino acid metabolism pathway reached Bonferroni-corrected threshold (0.0013). Eighty-three metabolites were associated with midpoint (FDR < 0.20). Similar associations were found for wake time. Neither bed time nor duration were strongly associated. The top metabolites (pathways given in brackets) associated with sleep were erythrulose (advanced glycation end-product) (positive association) and several γ-glutamyl pathway metabolites, including CMPF (fatty acid, dicarboxylate), isovalerate (valine, leucine and isoleucine and fatty acid metabolism) and HWESASXX (polypeptide) (inverse association). CONCLUSION: Within our study, several metabolites that have previously been linked to inflammation and oxidative stress (processes involved in diseases such as cardiovascular disease and cancer) were found to be associated with sleep.

A Cohort Study of Adolescent and Midlife Diet and Pancreatic Cancer Risk in the NIH-AARP Diet and Health Study.

Given the long latency period of pancreatic cancer, exploring the influence of early and midlife exposures will further advance our understanding of the disease. We assessed associations between diet and pancreatic cancer incidence in the National Institutes of Health (NIH)-AARP (formerly American Association of Retired Persons) Diet and Health Study. In 1996, a total of 303,094 participants completed 2 food frequency questionnaires that assessed diet at ages 12-13 years and 10 years previously. We used Cox proportional hazards regression to estimate adjusted hazard ratios and 95% confidence intervals. Through the end of 2006, a total of 1,322 pancreatic cancer cases occurred (average follow up time = 10.1 years). When comparing the highest tertiles with the lowest, carbohydrate intake during adolescence (hazard ratio (HR) = 0.87, 95% confidence interval (CI): 0.76, 0.99), but not 10 years before baseline, was inversely associated with pancreatic cancer risk. Total fat intake 10 years before baseline was significantly associated with increased risk (HR = 1.17, 95% CI: 1.02, 1.34), while risk was higher for high fat intake during both adolescence and midlife. Calcium intake 10 years before baseline was associated with reduced risk (HR = 0.87, 95% CI: 0.76, 0.99), as was a change from low intake in adolescence to high intake in midlife (HR = 0.71, 95% CI: 0.54, 0.93). Our study found a number of dietary factors present during adolescence and midlife to be associated with pancreatic cancer.

Epidemiological evidence of a relationship between type-1 diabetes mellitus and cancer: a review of the existing literature.

This review explores the epidemiological evidence relating to type-1 diabetes (T1DM) and cancer incidence and mortality. Mortality rates among those with T1DM are higher in every age group compared with the general population; the majority of this mortality is due to factors related to the consequences of diabetes, such as cardiovascular and renal disease. For over 100 years, researchers have explored the relationships between diabetes and cancer and although there is now a large body of work on the subject, consensus has not been reached. Such research has tended to focus upon type-2 diabetes, with the result that very little is known about T1DM and cancer. As incidence of T1DM increases, by around 3% annually among children, the need for further research into its impact upon cancer incidence and mortality increases. Within this review, findings varied by study method utilised, T1DM definition used and study region and outcome measure explored. None of the case-control studies found a statistically significant link between the two diseases, whereas both of the meta-analyses did. Cohort studies produced mixed results. There were also mixed findings among research that defined T1DM in the same way (e.g. defining individuals with the disease as those diagnosed with diabetes before 30 years of age). The review found a number of studies which explored cause-specific cancer mortality among those with diabetes; such studies also had mixed findings. This inconsistency within results suggests the need for further research to understand better the potential relationships between T1DM and cancer.

Pancreatic cancer incidence trends: evidence from the Surveillance, Epidemiology and End Results (SEER) population-based data.

Background: Annual pancreatic cancer incidence rates have been increasing. We examine pancreatic cancer incidence trends by demographics and histologic type. Methods: Data from the Surveillance, Epidemiology and End Results (SEER) registries were available to assess temporal trends and pancreatic cancer rates from 1974 to 2013. Results: Pancreatic cancer incidence rates declined between the 1970s and 1990s but increased from 1994 to 2013 among White males. Among non-Hispanic White and Hispanic males, the annual percent change (APC) in incidence between 1992 and 2013 was 0.84% and 0.73%, respectively. Rates also rose among White non-Hispanic, Hispanic and Asian females (APC = 0.81%, 0.56% and 1.23%, respectively) and even more rapidly among females aged 25-34 years (APC > 2.5%). Rates among Black males and females remained unchanged, but higher compared with the other racial/ethnic groups. By histologic type, the increases were greatest for non-secretory endocrine cancers ( > 6%), followed by ductal adenocarcinomas (∼5%) and adenocarcinoma, NOS (∼1.4%)-the largest histologic subgroup of pancreatic cancer. Rates for mucinous adenocarcinomas and poorly specified pancreatic cancer decreased. Overall, incidence rates during 2000-13 were higher among males than females [MF incidence rate ratio (IRR) = 1.28]. The IRR was >1.00 at all ages ≥ 35, but rates among females were higher at younger ages (IRRs 15-24: 0.66, 25-34: 0.81). The MF IRRs for most of the histologic types were elevated among males apart from solid pseudopapillary adenocarcinoma and cystic carcinomas (IRR = 0.22, confidence interval: 0.14-0.34 and 0.52, 0.41-0.65, respectively). Conclusion: Pancreatic cancer has been increasing overall, but patterns differ by demographic group and histologic type. Many of the trends parallel changing prevalence of lifestyle risk factors such as smoking, overweight and obesity, and diabetes in the USA, particularly for pancreatic adenocarcinoma, and improved diagnosis methods during the past 40 years.

Impaired glucose metabolism among those with and without diagnosed diabetes and mortality: a cohort study using Health Survey for England data.

BACKGROUND: The extent that controlled diabetes impacts upon mortality, compared with uncontrolled diabetes, and how pre-diabetes alters mortality risk remain issues requiring clarification. METHODS: We carried out a cohort study of 22,106 Health Survey for England participants with a HbA1C measurement linked with UK mortality records. We estimated hazard ratios (HRs) of all-cause, cancer and cardiovascular disease (CVD) mortality and 95% confidence intervals (CI) using Cox regression. RESULTS: Average follow-up time was seven years and there were 1,509 deaths within the sample. Compared with the non-diabetic and normoglycaemic group (HbA1C <5.7% [<39 mmol/mol] and did not indicate diabetes), undiagnosed diabetes (HbA1C ≥6.5% [≥48 mmol/mol] and did not indicate diabetes) inferred an increased risk of mortality for all-causes (HR 1.40, 1.09-1.80) and CVD (1.99, 1.35-2.94), as did uncontrolled diabetes (diagnosed diabetes and HbA1C ≥6.5% [≥48 mmol/mol]) and diabetes with moderately raised HbA1C (diagnosed diabetes and HbA1C 5.7-<6.5% [39-<48 mmol/mol]). Those with controlled diabetes (diagnosed diabetes and HbA<5.7% [<39 mmol/mol]) had an increased HR in relation to mortality from CVD only. Pre-diabetes (those who did not indicate diagnosed diabetes and HbA1C 5.7-<6.5% [39-<48 mmol/mol]) was not associated with increased mortality, and raised HbA1C did not appear to have a statistically significant impact upon cancer mortality. Adjustment for BMI and socioeconomic status had a limited impact upon our results. We also found women had a higher all-cause and CVD mortality risk compared with men. CONCLUSIONS: We found higher rates of all-cause and CVD mortality among those with raised HbA1C, but not for those with pre-diabetes, compared with those without diabetes. This excess differed by sex and diabetes status. The large number of deaths from cancer and CVD globally suggests that controlling blood glucose levels and policies to prevent hyperglycaemia should be considered public health priorities.

Diabetes mellitus and mortality from all-causes, cancer, cardiovascular and respiratory disease: evidence from the Health Survey for England and Scottish Health Survey cohorts.

BACKGROUND: Diabetes mellitus is associated with differing rates of all-cause and cause-specific mortality compared with the general population; although the strength of these associations requires further investigation. The effects of confounding factors, such as overweight and obesity and the presence of co-morbid cardiovascular disease (CVD), upon such associations also remain unclear. There is thus a need for studies which utilise data from nationally-representative samples to explore these associations further. METHODS: A cohort study of 204,533 participants aged 16+ years (7,199 with diabetes) from the Health Survey for England (HSE) (1994-2008) and Scottish Health Survey (SHeS) (1995, 1998 and 2003) linked with UK mortality records. Odds ratios (ORs) of all-cause and cause-specific mortality and 95% confidence intervals were estimated using logistic and multinomial logistic regression. RESULTS: There were 20,051 deaths (1,814 among those with diabetes). Adjusted (age, sex, and smoking status) ORs for all-cause mortality among those with diabetes was 1.68 (95%CI 1.57-1.79). Cause-specific mortality ORs were: cancer 1.26 (1.13-1.42), respiratory diseases 1.25 (1.08-1.46), CVD 1.96 (1.80-2.14) and 'other' causes 2.06 (1.84-2.30). These were not attenuated significantly after adjustment for generalised and/or central adiposity and other confounding factors. The odds of mortality differed between those with and without comorbid CVD at baseline; the ORs for the latter group were substantially increased. CONCLUSIONS: In addition to the excess in CVD and all-cause mortality among those with diabetes, there is also increased mortality from cancer, respiratory diseases, and 'other' causes. This increase in mortality is independent of obesity and a range of other confounding factors. With falling CVD incidence and mortality, the raised risks of respiratory and cancer deaths in people with diabetes will become more important and require increased health care provision.