Alcohol consumption is a cause of breast cancer (BC), yet the association between changes in alcohol consumption during adulthood and the risk of BC has been examined little. This study aimed to investigate the association between midlife changes in alcohol consumption and the risk of BC. Within the European Prospective Investigation into Cancer and Nutrition cohort including 123,679 women, changes in alcohol intake were obtained by comparing middle-aged participants’ alcohol intake assessed at recruitment and during follow-up, 9.8 years (median) later. Missing information about follow-up alcohol intake and covariates was multiple imputed. In the primary analysis, changes in alcohol consumption were investigated continuously as a change in alcohol intake of 10 g/day, calculated by subtracting the baseline intake (g/day) from the follow-up intake (g/day) and divided by 10 in relation to the risk of subsequent postmenopausal BC, overall, and by hormonal receptor status: estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2). In a secondary analysis, changes in alcohol intake were categorized in nine combinations of three intake groups at baseline and follow-up (≤1 g/day, >1–8 g/day, and >8 g/day)., Multivariable Cox proportional hazards regression models were used to estimate hazard ratios (HRs) with 95

BACKGROUND:Limited evidence exists for effect modification of genetic characteristics on the associations of food consumption and incident type 2 diabetes (T2D). OBJECTIVES:We aimed to investigate whether the food-T2D association would vary by genetic susceptibility to metabolic traits. METHODS:We analyzed data from 9542 incident T2D cases and a subcohort of 12,477 participants nested within the 340,234-participant cohort recruited in 1991-1998 and followed up for 10.9 y on average in 8 European countries. Polygenic risk scores (PRSs) for higher body mass index, insulin resistance, and T2D were constructed. Fifteen dietary variables potentially associated with T2D, obtained with cohort-specific self-reported dietary assessment, were examined: fruits, green leafy vegetables, root vegetables, wholegrains, rice, legumes, nuts and seeds, fermented dairy, red meat, processed meat, fish, eggs and egg products, sugar-sweetened beverages, coffee, and tea. A cross-product term between each PRS and each food/beverage was evaluated by genotyping chip and country with Prentice-weighted Cox regression for incident T2D, and stratum-specific estimates were meta analyzed, followed by Benjamini-Yekutieli multiple-testing correction. RESULTS:Accounting for multiple tests of 3 PRSs × 15 dietary items, no evidence of statistical interaction was evident on either a multiplicative or additive scale, with exp(β for a multiplicative interaction) (95% confidence interval) ranging from 0.84 (0.64, 1.10) (root vegetables and PRS for T2D) to 1.45 (0.78-2.76) (fish and PRS for T2D). CONCLUSIONS:Genetic susceptibility to high-risk metabolic traits did not modify the diet-T2D associations in European populations. Acknowledging the limitations of current PRS-based methods to detect gene-diet interactions, research should continue into the potential for precision nutrition and tailored food-based dietary guidance for T2D prevention.

Supplementary Table from Cigarette Smoking and Endometrial Cancer Risk: Observational and Mendelian Randomization Analyses

BACKGROUND:n-6 (ω-6) Polyunsaturated fatty acids may exert divergent biological effects, but limited knowledge exists about their associations with mortality. OBJECTIVES:To investigate the associations between adipose tissue content of individual n-6 polyunsaturated fatty acids - a long-term marker of endogenous exposure to these fatty acids - and all-cause mortality. METHODS:We used a prospective cohort study design. We followed a random sample of 4663 participants from the Danish diet, cancer, and health cohort, which was established between 1993 and 1997. Information on all-cause mortality was retrieved from the nationwide Danish civil registration system. An adipose tissue biopsy was collected from the buttock at recruitment and analyzed for fatty acid composition using gas chromatography. Hazard ratios were obtained using Cox proportional hazard regression. RESULTS:During a median of 21 y of follow-up, 1160 participants died. The median adipose tissue contents of linoleic acid and arachidonic acid were 10.60% and 0.36%, respectively. In multivariable continuous analyses, we observed a statistically significant inverse association between adipose tissue content of linoleic acid and all-cause mortality (P < 0.001). In contrast, a statistically nonsignificant positive association was found in continuous analyses of adipose tissue content of arachidonic acid and all-cause mortality (P = 0.078). Comparing the highest with the lowest quartile, the hazard ratio for mortality was 0.76 (95% confidence interval [CI]: 0.64, 0.90) for linoleic acid and 1.28 (95% CI: 1.07, 1.53) for arachidonic acid in adipose tissue, respectively. CONCLUSIONS:Adipose tissue content of linoleic acid was inversely associated with all-cause mortality, whereas adipose tissue content of arachidonic acid was associated with a higher all-cause mortality.

BACKGROUND: Leaflet calcification contributes to the development and progression of aortic valve stenosis. Vitamin K activates inhibitors of vascular calcification and may modulate inflammation and skeletal bone loss. Therefore, we aimed to determine whether higher dietary intakes of vitamin K 1 are associated with a lower incidence of aortic stenosis. METHODS: In the Danish Diet, Cancer and Health study, participants aged 50 to 64 years completed a 192-item food frequency questionnaire at baseline, from which habitual intakes of vitamin K 1 were estimated. Participants were prospectively followed using linkage to nationwide registers to determine incident aortic valve stenosis (primary outcome) and aortic stenosis with subsequent complications (aortic valve replacement, heart failure, or cardiovascular disease–related mortality; secondary outcome). RESULTS: In 55 545 participants who were followed for a maximum of 21.5 years, 1085 were diagnosed with aortic stenosis and 615 were identified as having subsequent complications. Participants in the highest quintile of vitamin K 1 intake had a 23% lower risk of aortic stenosis (hazard ratio, 0.77 [95% CI, 0.63–0.94]) and a 27% lower risk of aortic stenosis with subsequent complications (hazard ratio, 0.73 [95% CI, 0.56–0.95]), compared with participants in the lowest quintile after adjusting for demographics and cardiovascular risk factors. CONCLUSIONS: In this study, a high intake of vitamin K 1 –rich foods was associated with a lower incidence of aortic stenosis and a lower risk of aortic stenosis with subsequent complications.

Background: The vast majority of populations are facing growth in the proportion of older persons. Hence, there is an interest in identifying factors associated with longer and healthier life in older ages. Lifestyle, including diet, is crucial for healthy life expectancy, but evidence to support more specific dietary guidelines easily implemented in real life is lacking. Whole grains are specific dietary components with unexplored potential in healthy ageing. Methods: Using an illness-death multistate model approach with a priori chosen confounder control, the association between whole-grain intake and expected time as “healthy” and “with disease” during 20 years of follow-up was assessed. Healthy ageing was defined as the absence of cancer, ischemic heart disease, stroke, type 2 diabetes, asthma, chronic obstructive pulmonary disease, and dementia. Results: Based on data from 22,606 men and 25,468 women from the Diet, Cancer and Health cohort withmean follow-up times of 14 to 17 years, respectively, a doubling in whole-grain intake was associated with 0.43 (95% CI: 0.33–0.52) and 0.15 (0.06–0.24) years more lived without disease, for men and women. When comparing extreme quartiles, men with the highest whole-grain intake lived on average one year more without disease than those consuming the least. Furthermore, whole-grain intake was inversely associated with life expectancy with disease. Conclusions: This study suggests that whole grains are associated with healthy ageing and inversely associated with life expectancy with disease after age 50. These findings should encourage guidelines for increased whole-grain intake, especially among those with low intake, to support disease-free good health in the last part of life.

Background Randomised trials of vitamin D supplementation for cardiovascular disease and all-cause mortality have generally reported null findings. However, generalisability of results to individuals with low vitamin D status is unclear. We aimed to characterise dose-response relationships between 25-hydroxyvitamin D (25[OH]D) concentrations and risk of coronary heart disease, stroke, and all-cause mortality in observational and Mendelian randomisation frameworks. Methods Observational analyses were undertaken using data from 33 prospective studies comprising 500 962 individuals with no known history of coronary heart disease or stroke at baseline. Mendelian randomisation analyses were performed in four population-based cohort studies (UK Biobank, EPIC-CVD, and two Copenhagen population-based studies) comprising 386 406 middle-aged individuals of European ancestries, including 33 546 people who developed coronary heart disease, 18 166 people who had a stroke, and 27 885 people who died. Primary outcomes were coronary heart disease, defined as fatal ischaemic heart disease (International Classification of Diseases 10th revision code I20-I25) or non-fatal myocardial infarction (I21-I23); stroke, defined as any cerebrovascular disease (I60-I69); and all-cause mortality. Findings Observational analyses suggested inverse associations between incident coronary heart disease, stroke, and all-cause mortality outcomes with 25(OH)D concentration at low 25(OH)D concentrations. In population-wide genetic analyses, there were no associations of genetically predicted 25(OH)D with coronary heart disease (odds ratio [OR] per 10 nmol/L higher genetically-predicted 25(OH)D concentration 0 center dot 98, 95% CI 0 center dot 95-1 center dot 01), stroke (1 center dot 01, [0 center dot 97-1 center dot 05]), or all-cause mortality (0 center dot 99, 0 center dot 95-1 center dot 02). Null findings were also observed in genetic analyses for causespecific mortality outcomes, and in stratified genetic analyses for all outcomes at all observed levels of 25(OH)D concentrations. Interpretation Stratified Mendelian randomisation analyses suggest a lack of causal relationship for 25(OH)D concentrations with both cardiovascular and mortality outcomes for individuals at all levels of 25(OH)D. Our findings suggest that substantial reductions in mortality and cardiovascular morbidity due to long-term low-dose vitamin D supplementation are unlikely even if targeted at individuals with low vitamin D status. Copyright (c) 2023 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license.

INTRODUCTION:A diet rich in marine n-3 polyunsaturated fatty acids (PUFAs) may lower the risk of coronary heart disease and ischemic stroke. However, the association between intake of marine n-3 PUFAs and risk of hemorrhagic stroke has only been sparsely explored. We aimed to investigate the associations between intake of the major marine n-3 PUFAs, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) and their sum, in relation to incident hemorrhagic stroke and its subtypes, intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH). METHODS:We analyzed data from the Danish Diet, Cancer and Health Cohort, which was established between 1993 and 1997. Information on dietary intake of marine n-3 PUFAs was obtained through a validated food frequency questionnaire. Potential hemorrhagic stroke cases were identified by linkage to the Danish National Patient Register and subsequently validated. Hazard ratios obtained by Cox proportional hazard regression analyses were used as measures of association. RESULTS:A total of 394 subjects among 55,519 individuals developed hemorrhagic stroke during a median follow-up period of 13.5 years. In multivariable analyses including adjustment for established risk factors, we observed weak and statistically nonsignificant inverse associations between intake of EPA, DHA, and EPA + DHA and the rate of incident hemorrhagic stroke. In analyses of hemorrhagic stroke subtypes, we found indications of lower rates of ICH among participants in the highest quartile of EPA, DHA, and EPA + DHA compared with those in the lowest quartile and indications of lower rates of SAH in the highest quartile of EPA intake compared to the lowest quartile, but the findings were statistically nonsignificant. CONCLUSIONS:Inversely statistically nonsignificant associations were found between EPA, DHA, and EPA + DHA and hemorrhagic stroke.

[This corrects the article DOI: 10.1016/j.lanepe.2024.101091.].

Purpose We aimed to investigate the associations between parental BMI and offspring BMI trajectories and to explore whether the parent-offspring BMI growth trajectory association differed according to family SEP or social mobility. Methods We used data from the Avon Longitudinal Study of Parents and Children (ALSPAC). Children’s weight and height were collected from 1 to 18 years. Parents’ height and weight were reported pre-pregnancy. We assessed family SEP by measuring parents’ and grandparents’ educational attainment, social class, and social mobility by changes in education attainment across generations. Multilevel models were used to develop trajectories and assess patterns of change in offspring BMI, to associate parental BMI with these trajectories, and explore whether these associations differed by family SEP and social mobility. Results 13,612 children were included in the analyses. The average BMI of offspring whose parents were overweight or obese was higher throughout childhood and adolescence, compared to those with parents of normal BMI. Parental and grandparental low SEP were associated with higher child BMI, but there was little evidence of modification of parent-offspring associations. For example, at age 15 years the predicted mean BMI difference between children of overweight or obese mothers versus normal-weight mothers was 12.5% (95%CI: 10.1% to 14.7%) and 12.2% (95%CI: 10.3% to 13.7%) for high and low grandparental SEP, respectively. Discussion These findings strengthen the evidence that higher parental BMI and lower family SEP were associated with higher offspring BMI, but we did not observe strong evidence that family SEP modifies the parental-offspring BMI association.

Background The relationship between combined genetic predisposition and lifestyle and the risk of incident atrial fibrillation (AF) is unclear. Therefore, we aimed to assess a possible interaction between lifestyle and genetics on AF risk. Methods We included AF cases and a randomly drawn subcohort of 4040 participants from the Danish Diet, Cancer and Health cohort. Lifestyle risk factors were assessed, a score was calculated, and participants were categorised as having a poor, intermediate, or ideal lifestyle. We calculated a genetic risk score comprising 142 variants, and categorised participants into low (quintile 1), intermediate (quintiles 2–4) or high (quintile 5) genetic risk of AF. Results 3094 AF cases occurred during a median follow-up of 12.9 years. Regardless of genetic risk, incidence rates per 1000 person-years were gradually higher with worse lifestyle. For participants with high genetic risk, the incidence rates of AF per 1000 person-years were 5.0 (95% CI 3.4 to 7.3) among individuals with ideal lifestyle, 6.6 (95% CI 5.4 to 8.1) among those with intermediate lifestyle and 10.4 (95% CI 9.2 to 11.8) among participants with poor lifestyle. On an additive scale, there was a positive statistically significant interaction between genetic risk and lifestyle (relative excess risk due to interaction=0.86, 95% CI 0.68 to 1.03, p<0.001). Conclusions The rates of AF increased gradually with worse lifestyle within each category of genetic risk. We found a positive interaction on an additive scale between genetic risk and lifestyle, suggesting that risk factor modification is especially important in individuals with a high genetic risk of AF.

Background:Transportation noise has been linked with cardiometabolic outcomes, yet whether it is a risk factor for atrial fibrillation (AF) remains inconclusive. We aimed to assess whether transportation noise was associated with AF in a large, pooled Nordic cohort. Methods:We pooled data from 11 Nordic cohorts, totaling 161,115 participants. Based on address history from five years before baseline until end of follow-up, road, railway, and aircraft noise was estimated at a residential level. Incident AF was ascertained via linkage to nationwide patient registries. Cox proportional hazards models were utilized to estimate associations between running 5-year time-weighted mean transportation noise (Lden) and AF after adjusting for sociodemographics, lifestyle, and air pollution. Findings:We identified 18,939 incident AF cases over a median follow-up of 19.6 years. Road traffic noise was associated with AF, with a hazard ratio (HR) and 95% confidence interval (CI) of 1.02 (1.00-1.04) per 10-dB of 5-year mean time-weighted exposure, which changed to 1.03 (1.01-1.06) when implementing a 53-dB cut-off. In effect modification analyses, the association for road traffic noise and AF appeared strongest in women and overweight and obese participants. Compared to exposures ≤40 dB, aircraft noise of 40.1-50 and > 50 dB were associated with HRs of 1.04 (0.93-1.16) and 1.12 (0.98-1.27), respectively. Railway noise was not associated with AF. We found a HR of 1.19 (1.02-1.40) among people exposed to noise from road (≥45 dB), railway (>40 dB), and aircraft (>40 dB) combined. Interpretation:Road traffic noise, and possibly aircraft noise, may be associated with elevated risk of AF. Funding:NordForsk.

Alcohol consumption is a risk factor for breast cancer (BC), yet little is known about longitudinal alcohol consumption patterns and risk of BC. This study aimed to investigate whether trajectory profiles of alcohol consumption across adulthood were associated with risk of first primary malignant BC in postmenopausal women. At baseline, 28,720 pre-and postmenopausal women aged 50-65 years from the Danish Diet, Cancer and Health Cohort reported their average alcohol intake over the past 12 months and their average alcohol intake at the ages of 20, 30, 40, and 50 years. Alcohol consumption trajectories were estimated using latent class mixed models. BC cases were identified through record linkage to the Danish Cancer Registry. To examine associations between alcohol consumption trajectories and BC, we fitted a proportional hazard model adjusted for potential confounding factors using data from 24,543 postmenopausal women without missing covariate information. We identified 4 alcohol consumption trajectory profiles. During a median follow-up of 16.5 years, 1,591 cases of BC occurred. A mean alcohol consumption trajectory of > 10 g/day was associated with higher risk of BC (HR: 1.65, 95%CI: 1.35-2.03) compared to a mean alcohol consumption trajectory of < 6 g/day. We found no association between trajectory profiles characterized by lower alcohol intakes in early adulthood followed by increasing consumption of alcohol in adulthood compared to a consistently low intake of alcohol. Postmenopausal women drinking consistently high amounts of alcohol throughout adulthood had a higher risk of BC compared to women with a consistently low intake of alcohol.

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.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).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 trend = 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 cases = 101); for sugar-sweetened soft drinks, this association was null (HR 1.00, 95% CI 0.95-1.06; n cases = 127, p heterogeneity = 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 trend = 0.02 vs. non-consumers).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.

BACKGROUND:Omega-3 fatty acids derived from seafood acids may influence cardiac arrhythmogenesis, whereas the role of the major plant-derived omega-3 fatty acid, alpha-linolenic acid (ALA), on atrial fibrillation (AF) is largely unknown. OBJECTIVES:We aimed to investigate the association between ALA intake and risk of incident AF overall and in subjects with a low intake of marine omega-3 fatty acids. METHODS:We followed a total of 54,260 middle-aged men and women enrolled into the Danish Diet, Cancer, and Health cohort for development of AF using nationwide registries. Intake of ALA was assessed using a validated food frequency questionnaire and modeled as a restricted cubic spline. Statistical analyses were conducted using Cox proportional hazards regression. RESULTS:We identified a total of 4902 incident AF events during a median of 16.9 y of follow-up. In multivariable analyses, we observed indications of a statistically nonsignificant inverse association between ALA intake and risk of AF up to an ALA intake of 2.5 g/d, whereas no appreciable association was found for higher intakes of ALA. A statistically significant dose-dependent negative association was found between ALA intake and risk of AF in individuals consuming < 250 mg marine omega-3 fatty acids daily, whereas no association was found in those with a higher intake of marine omega-3 fatty acids. CONCLUSIONS:Intake of ALA was associated with a lower risk of AF in individuals consuming a low intake of marine omega-3 fatty acids. This finding is novel and warrants further investigation.

AIMS:Obesity is a major risk factor for atrial fibrillation (AF). Compared with stable weight, gaining weight was associated with a higher risk of incident AF in observational studies. The results, however, are conflicting regarding weight loss and risk of AF. This study aimed to assess the association between 5-year weight changes and risk of incident AF. METHODS AND RESULTS:The study was based on participants from the Danish Diet, Cancer, and Health Cohort. Body mass index (BMI) was assessed at a baseline examination and at a second examination 5 years later. Diagnoses of AF and co-morbidities were retrieved from the Danish National Patient Registry. In total, 43 758 participants without prior AF were included. The median age was 61 years and 54% were female. During a median follow-up of 15.7 years, 5312 individuals had incident AF (incidence rate 8.6/1000 person-years). Compared with stable weight, weight gain between 2.5 and 5 BMI units (kg/m2) was associated with a higher risk of AF [hazard ratio (HR) 1.24, 95% confidence interval (CI) 1.09-1.41]. Weight gain of 5 or more BMI units (kg/m2) was associated with a HR of 1.95 (95% CI 1.48-2.56) of incident AF. However, there was no statistically significant association between weight loss and risk of AF. CONCLUSION:Five-year weight gain was associated with greater risk of AF compared with stable weight in the Danish Diet, Cancer, and Health Cohort. There was no statistically significant association between weight loss and risk of AF.

PDF - 84KB, Joint effects of smoking and occupational exposure to aromatic amines and polycyclic aromatic hydrocarbons on the risk of bladder cancer (754 cases and 833 controls).

Background Whether cancer risk associated with a higher body mass index (BMI), a surrogate measure of adiposity, differs among adults with and without cardiovascular diseases (CVD) and/or type 2 diabetes (T2D) is unclear. The primary aim of this study was to evaluate separate and joint associations of BMI and CVD/T2D with the risk of cancer. Methods This is an individual participant data meta-analysis of two prospective cohort studies, the UK Biobank (UKB) and the European Prospective Investigation into Cancer and nutrition (EPIC), with a total of 577,343 adults, free of cancer, T2D, and CVD at recruitment. We used Cox proportional hazard regressions to estimate multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for associations between BMI and incidence of obesity-related cancer and in turn overall cancer with a multiplicative interaction between BMI and the two cardiometabolic diseases (CMD). HRs and 95% CIs for separate and joint associations for categories of overweight/obesity and CMD status were estimated, and additive interaction was quantified through relative excess risk due to interaction (RERI). Results In the meta-analysis of both cohorts, BMI (per ~ 5 kg/m 2 ) was positively associated with the risk of obesity-related cancer among participants without a CMD (HR: 1.11, 95%CI: 1.07,1.16), among participants with T2D (HR: 1.11, 95% CI: 1.05,1.18), among participants with CVD (HR: 1.17, 95% CI: 1.11,1.24), and suggestively positive among those with both T2D and CVD (HR: 1.09, 95% CI: 0.94,1.25). An additive interaction between obesity (BMI ≥ 30 kg/m 2 ) and CVD with the risk of overall cancer translated into a meta-analytical RERI of 0.28 (95% CI: 0.09–0.47). Conclusions Irrespective of CMD status, higher BMI increased the risk of obesity-related cancer among European adults. The additive interaction between obesity and CVD suggests that obesity prevention would translate into a greater cancer risk reduction among population groups with CVD than among the general population.

Abstract Background Diet may impact important risk factors for endometrial cancer such as obesity and inflammation. However, evidence on the role of specific dietary factors is limited. We investigated associations between dietary fatty acids and endometrial cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC). Methods This analysis includes 1,886 incident endometrial cancer cases and 297,432 non-cases. All participants were followed up for a mean of 8.8 years. Multivariable Cox proportional hazard models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) of endometrial cancer across quintiles of individual fatty acids estimated from various food sources quantified through food frequency questionnaires in the entire EPIC cohort. The false discovery rate (q-values) was computed to control for multiple comparisons. Results Consumption of n-6 γ-linolenic acid was inversely associated with endometrial cancer risk (HR comparing 5th with 1st quintileQ5−Q1=0.77, 95% CI = 0.64; 0.92, ptrend=0.01, q-value = 0.15). This association was mainly driven by γ-linolenic acid derived from plant sources (HRper unit increment=0.94, 95%CI= (0.90;0.98), p = 0.01) but not from animal sources (HRper unit increment= 1.00, 95%CI = (0.92; 1.07), p = 0.92). In addition, an inverse association was found between consumption of n-3 α-linolenic acid from vegetable sources and endometrial cancer risk (HRper unit increment= 0.93, 95%CI = (0.87; 0.99), p = 0.04). No significant association was found between any other fatty acids (individual or grouped) and endometrial cancer risk. Conclusion Our results suggest that higher consumption of γ-linolenic acid and α-linoleic acid from plant sources may be associated with lower risk of endometrial cancer.

C-statistics by tumor histology for variable lag-times since blood donation