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Purpose: Investigate the association between choline and betaine intake and all-cause mortality in a large Swedish cohort. Methods: Women (52,246) and men (50,485) attending the Västerbotten Intervention Programme 1990–2016 were included. Cox proportional hazard regression models adjusted for energy intake, age, BMI, smoking, education, and physical activity were used to estimate mortality risk according to betaine, total choline, phosphatidylcholine, glycerophosphocholine, phosphocholine, sphingomyelin, and free choline intakes [continuous (per 50 mg increase) and in quintiles]. Results: During a median follow-up of 16 years, 3088 and 4214 deaths were registered in women and men, respectively. Total choline intake was not associated with all-cause mortality in women (HR 1.01; 95% CI 0.97, 1.06; P = 0.61) or men (HR 1.01; 95% CI 0.98, 1.04; P = 0.54). Betaine intake was associated with decreased risk of all-cause mortality in women (HR 0.95; 95% CI 0.91, 0.98; P < 0.01) but not in men. Intake of free choline was negatively associated with risk of all-cause mortality in women (HR 0.98; 95% CI 0.96, 1.00; P = 0.01). No other associations were found between intake of the different choline compounds and all-cause mortality. In women aged ≥ 55 years, phosphatidylcholine intake was positively associated with all-cause mortality. In men with higher folate intake, total choline intake was positively associated with all-cause mortality. Conclusion: Overall, our results do not support that intake of total choline is associated with all-cause mortality. However, some associations were modified by age and with higher folate intake dependent on sex. Higher intake of betaine was associated with lower risk of all-cause mortality in women. [ABSTRACT FROM AUTHOR]

Purpose: Previously reported associations of protein-rich foods with stroke subtypes have prompted interest in the assessment of individual amino acids. We examined the associations of dietary amino acids with risks of ischaemic and haemorrhagic stroke in the EPIC study. Methods: We analysed data from 356,142 participants from seven European countries. Dietary intakes of 19 individual amino acids were assessed using validated country-specific dietary questionnaires, calibrated using additional 24-h dietary recalls. Multivariable-adjusted Cox regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) of ischaemic and haemorrhagic stroke in relation to the intake of each amino acid. The role of blood pressure as a potential mechanism was assessed in 267,642 (75%) participants. Results: After a median follow-up of 12.9 years, 4295 participants had an ischaemic stroke and 1375 participants had a haemorrhagic stroke. After correction for multiple testing, a higher intake of proline (as a percent of total protein) was associated with a 12% lower risk of ischaemic stroke (HR per 1 SD higher intake 0.88; 95% CI 0.82, 0.94). The association persisted after mutual adjustment for all other amino acids, systolic and diastolic blood pressure. The inverse associations of isoleucine, leucine, valine, phenylalanine, threonine, tryptophan, glutamic acid, serine and tyrosine with ischaemic stroke were each attenuated with adjustment for proline intake. For haemorrhagic stroke, no statistically significant associations were observed in the continuous analyses after correcting for multiple testing. Conclusion: Higher proline intake may be associated with a lower risk of ischaemic stroke, independent of other dietary amino acids and blood pressure. [ABSTRACT FROM AUTHOR]

Purpose: To investigate the association between fruit and vegetable intake (FVI) and the risk of developing prediabetes and type 2 diabetes (T2D) in a Swedish prospective cohort study. Methods: Subjects were 6961 men and women aged 35–56 years old at baseline, participating in the Stockholm Diabetes Prevention Program cohort. By design, the cohort was enriched by 50% with subjects that had family history of diabetes. Anthropometric measurements, oral glucose tolerance tests and questionnaires on lifestyle and dietary factors were carried out at baseline and two follow-up occasions. Cox proportional hazard models were used to estimate hazard ratios with 95% CIs. Results: During a mean follow-up time of 20 ± 4 years, 1024 subjects developed T2D and 870 prediabetes. After adjustments for confounders, the highest tertile of total FVI was associated with a lower risk of developing T2D in men (HR 0.76, 95% CI 0.60–0.96). There was also an inverse association between total fruit intake and prediabetes risk in men, with the HR for the highest tertile being 0.76 (95% CI 0.58–1.00). As for subtypes, higher intake of apples/pears was inversely associated with T2D risk in both sexes, whereas higher intakes of banana, cabbage and tomato were positively associated with T2D or prediabetes risk in either men or women. Conclusion: We found an inverse association between higher total FVI and T2D risk and between higher fruit intake and prediabetes risk, in men but not in women. Certain fruit and vegetable subtypes showed varying results and require further investigation. [ABSTRACT FROM AUTHOR]

Purpose: Experimental studies suggested that antioxidants could protect against skin carcinomas. However, epidemiological studies on antioxidant supplement use in relation to basal-cell carcinoma (BCC) and squamous-cell carcinoma (SCC) risks yielded inconsistent findings, and few prospective studies have been conducted to date. We aimed to investigate the associations between antioxidant supplement intake and keratinocyte cancer (KC) risk. Methods: E3N is an ongoing prospective cohort initiated in 1990 and involving 98,995 French women aged 40–65 years at recruitment. Intakes of dietary antioxidants were estimated via a validated dietary questionnaire in 1993 and self-reported antioxidant supplement use was collected in 1995. We used Cox models to compute hazard ratios (HRs) and 95% confidence intervals (CIs) adjusted for age and skin cancer risk factors. Results: Over 1995–2014, 2426 BCC and 451 SCC cases were diagnosed among 63,063 women. We found positive relationships between vitamin A supplement use and KC risk (HR = 1.37, 95% CI 1.15–1.62), particularly with BCC (HR = 1.40, 95% CI 1.17–1.69); and between vitamin E supplement use and risks of both BCC (HR = 1.21, 95% CI 1.03–1.52) and SCC (HR = 1.43, 95% CI 1.03–1.99). Intake of beta-carotene supplements was associated with an increased SCC risk (HR = 1.59, 95% CI 1.00–2.54). Vitamin C supplement use was not associated with KC risk. We found similar results when considering total antioxidant intake. Conclusions: Intakes of vitamin A or E supplements were associated with an increased KC risk in women. Further studies with information on doses and duration of supplement use and the ability to examine their underlying mechanisms are needed. [ABSTRACT FROM AUTHOR]

Purpose: There is existing evidence on the potential role of chronic inflammation in the pathogenesis of pancreatic cancer (PC) and on how risk may be modulated by dietary factors. Pro-inflammatory diets are suggested to be associated with increased risk of PC but, so far, evidence remains not conclusive. We examined the association between the dietary inflammatory potential and PC risk within the European Prospective Investigation into Cancer and Nutrition (EPIC) study, which includes 450,112 participants. Methods: After a 14-year follow-up, a total of 1239 incident PC cases were included in this study. The inflammatory potential of the diet was estimated using an Inflammatory Score of the Diet (ISD). Hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between the ISD and PC were estimated using multivariable Cox regression models, adjusted for known risk factors for PC. Results: Participants with higher ISDs had a higher risk of developing PCs. In the fully adjusted multivariate model, the risk of PC increased by 11% (HR 1.11, 95% CI 1.02–1.22) for 1 point each standard deviation increase in the ISD score. Neither obesity nor any other known risk factor for PC showed statistically significant interactions. Conclusion: To the best of our knowledge, this is the first prospective study reporting a positive relationship between the inflammatory potential of diet and PC. Since early diagnosis and treatment of pancreatic cancer might be challenging, prevention remains the major hope for reducing the burden of this disease. [ABSTRACT FROM AUTHOR]

Purpose: Epidemiologic evidence for specific types and sources of dietary fat and individual fatty acid with colorectal cancer (CRC) risk remains inconclusive. We aimed to comprehensively examine the associations of intakes of specific types (saturated, monounsaturated, polyunsaturated, and trans) and sources (animal, dairy, and vegetable) of dietary fat and individual fatty acid with CRC risk. Design: We prospectively followed 65,550 women from the Nurses' Health Study (1986–2014) and 45,684 men from the Health Professionals Follow-up Study (1986–2014). Dietary intake was assessed every 4 years using food frequency questionnaires. Self-reported CRC cases were confirmed through medical record review. Time-dependent Cox proportional hazards regression was used to estimate the hazard ratios (HRs) for intakes of dietary fats and fatty acids and CRC risk. Results: During 2,705,560 person-years of follow-up, 2726 incident CRC cases were confirmed. Intake of monounsaturated fat tended to be positively associated with the risk of CRC (HR comparing extreme quintiles 1.22; 95% CI 1.01, 1.47; p = 0.06 for trend). This positive association was mainly driven by monounsaturated fatty acids from animal sources (MUFA-As) (HR comparing extreme quintiles 1.23; 95% CI 1.02, 1.49; p = 0.02 for trend). The positive association between MUFA-As and CRC was attenuated after adjusting for red and processed meat consumption (HR comparing extreme quintiles 1.17; 95% CI 0.95, 1.44; p = 0.13 for trend). We did not find clear associations between other types and sources of dietary fat or individual fatty acid and CRC risk. Conclusions: Higher intake of MUFA-As was associated with higher CRC risk. This could be partly explained by confounding due to other components of red and processed meat. [ABSTRACT FROM AUTHOR]

Purpose: Our aim was to investigate prospective associations of consumption of total dairy and dairy types with incident prediabetes in a Dutch population-based study. Methods: Two enrolment waves of the Hoorn Studies were harmonized, resulting in an analytic sample of 2262 participants without (pre-) diabetes at enrolment (mean age 56 ± 7.3 years; 50% male). Baseline dietary intake was assessed by validated food frequency questionnaires. Relative risks (RRs) were calculated between dairy, fermented dairy, milk, yogurt (all total/high/low fat), cream and ice cream and prediabetes. Additionally, substituting one serving/day of dairy types associated with prediabetes with alternative dairy types was analysed. Results: During a mean 6.4 ± 0.7 years of follow-up, 810 participants (35.9%) developed prediabetes. High fat fermented dairy, cheese and high fat cheese were associated with a 17% (RR 0.83, 95% CI 0.69–0.99, ptrend = 0.04), 14% (RR 0.86, 95% CI 0.73–1.02, ptrend = 0.04) and 21% (RR 0.79, 95% CI 0.66–0.94, ptrend = 0.01) lower risk of incident prediabetes, respectively, in top compared to bottom quartiles, after adjustment for confounders. High fat cheese consumption was continuously associated with lower prediabetes risk (RRservings/day 0.94, 95% CI 0.88–1.00, p = 0.04). Total dairy and other dairy types were not associated with prediabetes risk in adjusted models, irrespective of fat content (RR ~ 1). Replacing high fat cheese with alternative dairy types was not associated with prediabetes risk. Conclusion: The highest intake of high fat fermented dairy, cheese and high fat cheese were associated with a lower risk of prediabetes, whereas other dairy types were not associated. Cheese seems to be inversely associated with type 2 diabetes risk, despite high levels of saturated fatty acids and sodium. [ABSTRACT FROM AUTHOR]

Purpose: Long-term associations of dietary glycemic index (GI) and glycemic load (GL) with mortality outcomes remain unclear. Methods: The present analysis included 72,783 participants of the Japan Public Health Center-based Prospective Study. Participants who responded to the 5-year follow-up questionnaire in 1995–1999 were followed-up until December 2015. We estimated the risk of total and cause-specific mortality associated with GI and GL using Cox proportional hazards regression models. Results: During 1,244,553 person years of follow-up, 7535 men and 4913 women died. GI was positively associated with all-cause mortality. As compared with the lowest quartile, the multivariable HR for those who had the highest quartile of GI was 1.14 (95% CI 1.08–1.20). The HRs for death comparing the highest with the lowest quartile were 1.28 (95% CI 1.14–1.42) for circulatory system diseases, 1.33 (95% CI 1.14–1.55) for heart disease, 1.32 (95% CI 1.11–1.57) for cerebrovascular disease, and 1.45 (95% CI 1.18–1.78) for respiratory diseases. GI was not associated with mortality risks of cancer and digestive diseases. GL showed a null association with all-cause mortality (highest vs lowest quartile; HR 1.04; 95% CI 0.96–1.12). However, among those who had the highest quartile of GL, the HRs for death from circulatory system diseases was 1.24 (95% CI 1.05–1.46), cerebrovascular disease was 1.34 (95% CI 1.03–1.74), and respiratory diseases was 1.35 (95% CI 1.00–1.82), as compared with the lowest quartile. Conclusion: In this large prospective cohort study, dietary GI and GL were associated with mortality risks. [ABSTRACT FROM AUTHOR]

Purpose: Cardiovascular disease (CVD) is a leading cause of mortality globally and is strongly influenced by dietary risk factors. The aim was to assess the association between egg consumption and risk of CVD risk/mortality, including coronary heart disease (CHD), stroke, and heart failure. Methods: MEDLINE, Embase, and Web of Science databases were searched through April 2020 for prospective studies. Two independent reviewers screened and extracted the data through standardized methods. Size effects were calculated as summary relative risks (SRRs) in a dose–response fashion through random-effects meta-analyses. Results: Thirty-nine studies including nearly 2 million individuals and 85,053 CHD, 25,103 stroke, 7536 heart failure, and 147,124 CVD cases were included. The summary analysis including 17 datasets from 14 studies conducted on CVD (incidence and/or mortality) showed that intake of up to six eggs per week is inversely associated with CVD events, when compared to no consumption [for four eggs per week, SRR = 0.95 (95% CI: 0.90; 1.00)]; a decreased risk of CVD incidence was observed for consumption of up to one egg per day [SRR = 0.94 (95% CI: 0.89; 0.99)]. The summary analysis for CHD incidence/mortality including 24 datasets from 16 studies showed a decreased risk up to two eggs per week [(SRR = 0.96 (95% CI: 0.91; 1.00)]. No associations were retrieved with risk of stroke. The summary analysis for heart failure risk including six datasets from four studies showed that intake of one egg per day was associated with increased risk raising for higher intakes compared to no consumption [for 1 egg per day, SRR = 1.15 (95% CI:1.02; 1.30)]. After considering GRADE criteria for strength of the evidence, it was rated low for all outcomes but stroke, for which it was moderate (yet referring to no risk). Conclusion: There is no conclusive evidence on the role of egg in CVD risk, despite the fact that higher quality studies are warranted to obtain stronger evidence for a possible protection of CVD associated with moderate weekly egg consumption compared to no intake; equally, future studies may strengthen the evidence for increased heart failure risk associated with high regular egg consumption. [ABSTRACT FROM AUTHOR]

Purpose: Lipid intakes such as saturated (SFA), monounsaturated (MUFA) and polyunsaturated (PUFA) fatty acids have been widely studied regarding cardiovascular health, but their relevance to cancer is unclear. Inconsistent epidemiological results may be explained by varied mechanisms involving PUFAs and redox balance, inflammatory status and cell signalling, along with interactions with other dietary components such as antioxidants, dietary fibre and more generally fruits and vegetable intakes. Therefore, this study aimed to investigate the associations between lipid intakes and cancer risk, and their potential modulation by vitamin C, vitamin E, dietary fibre and fruit and vegetable intakes. Methods: This prospective study included 44,039 participants aged ≥ 45 years from the NutriNet-Santé cohort (2009–2017). Dietary data were collected using repeated 24 h-dietary records. Multivariable Cox models were performed to characterize associations. Results: SFA intake was associated with increased overall [n = 1722 cases, HRQ5vsQ1 = 1.44 (1.10–1.87), p-trend = 0.008] and breast [n = 545 cases, HRQ5vsQ1 = 1.98 (1.24–3.17), p-trend = 0.01] cancer risks. n-6 PUFA [HRQ5vsQ1 = 0.56 (0.32–0.97), p-trend = 0.01] and MUFA (HRQ5vsQ1 = 0.41 [0.18-0.0.95), p-trend = 0.009] intakes were associated with a decreased risk of digestive cancers (n = 190 cases). Associations between n-6 PUFA, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) intakes and digestive cancer risk were modulated by dietary fibre, vitamin C and fruit and vegetable intakes. Conclusion: These findings suggested that SFA intake could increase overall and breast cancer risks while some unsaturated fatty acids could decrease digestive cancer risk. However, in line with mechanistic hypotheses, our results suggest that intakes of fruits and vegetables and their constituents (antioxidants, fibre) may interact with PUFAs to modulate these associations. [ABSTRACT FROM AUTHOR]

Purpose: The association between dietary acrylamide intake and estrogen receptor-positive (ER+) breast cancer risk in epidemiological studies is inconsistent. By analyzing gene-acrylamide interactions for ER+ breast cancer risk, we aimed to clarify the role of acrylamide intake in ER+ breast cancer etiology. Methods: The prospective Netherlands Cohort Study on diet and cancer includes 62,573 women, aged 55–69 years. At baseline, a random subcohort of 2589 women was sampled from the total cohort for a case–cohort analysis approach. Dietary acrylamide intake of subcohort members (n = 1449) and ER+ breast cancer cases (n = 844) was assessed with a food frequency questionnaire. We genotyped single nucleotide polymorphisms (SNPs) in genes in acrylamide metabolism, sex steroid systems, oxidative stress and DNA repair. Multiplicative interaction between acrylamide intake and SNPs was assessed with Cox proportional hazards analysis, based on 20.3 years of follow-up. Results: Unexpectedly, there was a statistically non-significant inverse association between acrylamide and ER+ breast cancer risk among all women but with no clear dose–response relationship, and no association among never smokers. Among the results for 57 SNPs and 2 gene deletions, rs1056827 in CYP1B1, rs2959008 and rs7173655 in CYP11A1, the GSTT1 gene deletion, and rs1052133 in hOGG1 showed a statistically significant interaction with acrylamide intake for ER+ breast cancer risk. Conclusions: This study did not provide evidence for a positive association between acrylamide intake and ER+ breast cancer risk. If anything, acrylamide was associated with a decreased ER+ breast cancer risk. The interaction with SNPs in CYP1B1 and CYP11A1 suggests that acrylamide may influence ER+ breast cancer risk through sex hormone pathways. [ABSTRACT FROM AUTHOR]

Purpose: The aim of the study was to assess associations between intake of combined soft drinks (sugar sweetened and artificially sweetened) and fruit and vegetable juices and the risk of hepatocellular carcinoma (HCC), intrahepatic bile duct (IHBC) and biliary tract cancers (GBTC) using data from the European Prospective Investigation into Cancer and Nutrition cohort of 477,206 participants from 10 European countries. Methods: After 11.4 years of follow-up, 191 HCC, 66 IHBC and 236 GBTC cases were identified. Hazard ratios and 95 % confidence intervals (HR; 95 % CI) were estimated with Cox regression models with multivariable adjustment (baseline total energy intake, alcohol consumption and intake pattern, body mass index, physical activity, level of educational attainment and self-reported diabetes status). Results: No risk associations were observed for IHBC or GBTC. Combined soft drinks consumption of >6 servings/week was positively associated with HCC risk: HR 1.83; 95 % CI 1.11-3.02, p = 0.01 versus non-consumers. In sub-group analyses available for 91 % of the cohort artificially sweetened soft drinks increased HCC risk by 6 % per 1 serving increment (HR 1.06, 95 % CI 1.03-1.09, n = 101); for sugar-sweetened soft drinks, this association was null (HR 1.00, 95 % CI 0.95-1.06; n = 127, p = 0.07). Juice consumption was not associated with HCC risk, except at very low intakes (<1 serving/week: HR 0.60; 95 % CI 0.38-0.95; p = 0.02 vs. non-consumers). Conclusions: Daily intake of combined soft drinks is positively associated with HCC, but a differential association between sugar and artificially sweetened cannot be discounted. This study provides some insight into possible associations of HCC with sugary drinks intake. Further exploration in other settings is required. [ABSTRACT FROM AUTHOR]