AimTo investigate the prevalence of, and demographic associations with, uncorrected refractive error (URE) in an older British population.MethodsData from 4428 participants, aged 48–89 years, who ...attended an eye examination in the third health check of the European Prospective Investigation into Cancer-Norfolk study and had also undergone an ophthalmic examination were assessed. URE was defined as ≥1 line improvement of visual acuity with pinhole-correction in the better eye in participants with LogMar presenting visual acuity (PVA) <0.3 (PVA <6/12). Refractive error was measured using an autorefractor without cycloplegia. Myopia was defined as spherical equivalent ≤−0.5 dioptre, and hypermetropia ≥0.5 dioptre.ResultsAdjusted to the 2010 midyear British population, the prevalence of URE in this Norfolk population was 1.9% (95% CI 0.6% to 3.1%). Lower self-rated distance vision was correlated with higher prevalence of URE (ptrend<0.001). In a multivariate logistic regression model adjusting for age, gender, retirement status, educational level and social class, independent significant associations with URE were increasing age (ptrend<0.001) and having hypermetropic or myopic refractive error. Wearing distance spectacles was inversely associated with URE (OR 0.34, 95% CI 0.21 to 0.55, p<0.001). There were 3063 people (69.2%) who wore spectacles/contact lenses for distance vision. Spectacle wear differed according to type of refractive error (p<0.001), and use rose with increasing severity of refractive error (ptrend<0.001).ConclusionAlthough refractive error is common, the prevalence of URE was found to be low in this population reflecting a low prevalence of PVA<0.3.
Study objective: To investigate the independent association between individual and area based socioeconomic measures and fruit and vegetable consumption. Design: Cross sectional population based ...study. Setting and participants: 22 562 men and women aged 39–79 years living in the general community in Norfolk, United Kingdom, recruited using general practice age-sex registers. Outcome measures: Fruit and vegetable intake assessed using a food frequency questionnaire. Main results: Being in a manual occupational social class, having no educational qualifications, and living in a deprived area all independently predicted significantly lower consumption of fruit and vegetables. The effect of residential area deprivation was predominantly in those in manual occupational social class and no educational qualifications. Conclusions: Understanding some of the community level barriers to changing health related behaviours may lead to more effective interventions to improving health in the whole community, particularly those who are most vulnerable.
ObjectivesAssess the association between marine omega-3 polyunsaturated fatty acid (n-3 PUFA) intake from supplements, mainly cod liver oil, and coronary heart disease (CHD) ...mortality.DesignProspective cohort study, with three exposure measurements over 22 years.SettingNorfolk-based European Prospective Investigation into Cancer (EPIC-Norfolk, UK).Participants22 035 men and women from the general population, 39–79 years at recruitment.ExposureSupplement use was assessed in three questionnaires (1993–1998; 2002–2004; 2004–2011). Participants were grouped into non-supplement users (NSU), n-3 PUFA supplement users (SU+n3) and non–n-3 PUFA supplement users (SU-n3). Cox regression adjusted for time-point specific variables: age, smoking, prevalent illnesses, body mass index, alcohol consumption, physical activity and season and baseline assessments of sex, social class, education and dietary intake (7-day diet diary).Primary and secondary outcome measuresDuring a median of 19-year follow-up, 1562 CHD deaths were registered for 22 035 included participants.ResultsBaseline supplement use was not associated with CHD mortality, but baseline food and supplement intake of n-3 PUFA was inversely associated with CHD mortality after adjustment for fish consumption. Using time-varying covariate analysis, significant associations were observed for SU+n3 (HR: 0.74, 95% CI 0.66 to 0.84), but not for SU-n3 versus NSU. In further analyses, the association for SU+n3 persisted in those who did not take other supplements (HR: 0.83, 95% CI 0.71 to 0.97). Those who became SU+n3 over time or were consistent SU+n3 versus consistent NSU had a lower hazard of CHD mortality; no association with CHD was observed in those who stopped using n-3 PUFA-containing supplements.ConclusionsRecent use of n-3 PUFA supplements was associated with a lower hazard of CHD mortality in this general population with low fish consumption. Residual confounding cannot be excluded, but the findings observed may be explained by postulated biological mechanisms and the results were specific to SU+n3.
The aim of this study was to investigate for the first time the association between body fat and risk of amyotrophic lateral sclerosis (ALS) with an appropriate prospective study design.
The EPIC ...(European Prospective Investigation into Cancer and Nutrition) study included 518,108 individuals recruited from the general population across 10 Western European countries. At recruitment, information on lifestyle was collected and anthropometric characteristics were measured. Cox hazard models were fitted to investigate the associations between anthropometric measures and ALS mortality.
Two hundred twenty-two ALS deaths (79 men and 143 women) occurred during the follow-up period (mean follow-up = 13 years). There was a statistically significant interaction between categories of body mass index and sex regarding ALS risk (p = 0.009): in men, a significant linear decrease of risk per unit of body mass index was observed (hazard ratio = 0.93, 95% confidence interval 0.86-0.99 per kg/m(2)); among women, the risk was more than 3-fold increased for underweight compared with normal-weight women. Among women, a significant risk reduction increasing the waist/hip ratio was also evident: women in the top quartile had less than half the risk of ALS compared with those in the bottom quartile (hazard ratio = 0.48, 95% confidence interval 0.25-0.93) with a borderline significant p value for trend across quartiles (p = 0.056).
Increased prediagnostic body fat is associated with a decreased risk of ALS mortality.
Recent epidemiological investigations have reported on the association between telomere length (TL) and a number of malignancies, including B‐cell lymphoma (BCL). The reported results for BCLs are ...however inconsistent. We carried out a nested case–control study to determine whether TL is associated with future risk of BCL. Using quantitative polymerase chain reaction, the relative TL (i.e. the ratio of telomere repeat copy number to single gene copy number) was measured in mononuclear cell DNA of prediagnostic peripheral blood samples of 464 lymphoma cases and 464 matched controls (median time between blood collection and diagnosis, 4.6 years). Conditional logistic regression was used to analyze the association between TL and the risk of developing lymphoma and histologic subtypes. TL was significantly longer in cases compared to controls (p = 0.01). Multivariable models showed a significantly increased risk of BCL odds ratio (OR) = 1.66, 1.80 and 3.20 for quartiles 2–4, respectively, p‐trend = 0.001, diffuse large B‐cell lymphoma (DLBCL) (OR = 1.20, 2.48 and 2.36 for quartiles 2–4, respectively, p‐trend = 0.03) and follicular lymphoma (FL) (OR = 1.39, 1.90 and 2.69 for quartiles 2–4, respectively, p‐trend = 0.02) with increasing TL. This study suggests an association between longer leucocyte TL and increased risk of BCL which was most pronounced for DLBCL and FL.
What's new?
Can telomere length affect cancer risk? Earlier studies have disagreed. This study investigated whether the length of these repetitive DNA sequences at the ends of chromosome correlate with the risk of developing B‐cell lymphoma. Using data from the European Prospective Investigation into Cancer and Nutrition (EPIC), the authors conducted the largest prospective study to date on this question. They found that longer telomeres do indeed appear to signal an increased risk of B‐cell lymphoma.
Higher coffee intake has been purportedly related to a lower risk of liver cancer. However, it remains unclear whether this association may be accounted for by specific biological mechanisms.
We ...aimed to evaluate the potential mediating roles of inflammatory, metabolic, liver injury, and iron metabolism biomarkers on the association between coffee intake and the primary form of liver cancer-hepatocellular carcinoma (HCC).
We conducted a prospective nested case-control study within the European Prospective Investigation into Cancer and Nutrition among 125 incident HCC cases matched to 250 controls using an incidence-density sampling procedure. The association of coffee intake with HCC risk was evaluated by using multivariable-adjusted conditional logistic regression that accounted for smoking, alcohol consumption, hepatitis infection, and other established liver cancer risk factors. The mediating effects of 21 biomarkers were evaluated on the basis of percentage changes and associated 95% CIs in the estimated regression coefficients of models with and without adjustment for biomarkers individually and in combination.
The multivariable-adjusted RR of having ≥4 cups (600 mL) coffee/d compared with <2 cups (300 mL)/d was 0.25 (95% CI: 0.11, 0.62; P-trend = 0.006). A statistically significant attenuation of the association between coffee intake and HCC risk and thereby suspected mediation was confirmed for the inflammatory biomarker IL-6 and for the biomarkers of hepatocellular injury glutamate dehydrogenase, alanine aminotransferase, aspartate aminotransferase (AST), γ-glutamyltransferase (GGT), and total bilirubin, which-in combination-attenuated the regression coefficients by 72% (95% CI: 7%, 239%). Of the investigated biomarkers, IL-6, AST, and GGT produced the highest change in the regression coefficients: 40%, 56%, and 60%, respectively.
These data suggest that the inverse association of coffee intake with HCC risk was partly accounted for by biomarkers of inflammation and hepatocellular injury.
In the present study, we investigated the association between dietary intake of carbohydrates and the risk of type 2 diabetes. Incident cases of diabetes (n 749) were identified and compared with a ...randomly selected subcohort of 3496 participants aged 40–79 years. For dietary assessment, we used 7 d food diaries administered at baseline. We carried out modified Cox proportional hazards regression analyses and compared results obtained from the different methods of adjustment for total energy intake. Dietary intakes of total carbohydrates, starch, sucrose, lactose or maltose were not significantly related to diabetes risk after adjustment for confounders. However, in the residual method for energy adjustment, intakes of fructose and glucose were inversely related to diabetes risk. The multivariable-adjusted hazard ratios (HR) of diabetes comparing the extreme quintiles of intake were 0·79 (95 % CI 0·59, 1·07; P for trend = 0·03) for glucose and 0·62 (95 % CI 0·46, 0·83; P for trend = 0·01) for fructose. In the nutrient density method, only fructose was inversely related to diabetes risk (HR 0·65, 95 % CI 0·48, 0·88). The replacement of 5 % energy intake from SFA with an isoenergetic amount of fructose was associated with a 30 % lower diabetes risk (HR 0·69, 95 % CI 0·50, 0·96). Results of the standard and energy partition methods were similar to those of the residual method. These prospective findings suggest that the intakes of starch and sucrose are not associated, but that those of fructose and glucose are inversely associated with diabetes risk. Whether the inverse associations with fructose and glucose reflect the effect of substitution of these carbohydrate subtypes with other nutrients (i.e. SFA), their net higher intake or other nutrients associated with their intake remains to be established through further investigation.
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Sugars, and in particular fructose, consumption has been associated with increased systolic and diastolic blood pressure (BP), mediated by increased serum uric acid concentration, which ...interferes with the renin‐angiotensin mechanism and inhibits nitric oxide release from endothelial cells. Uric acid can also increase sodium sensitivity.
Investigating associations between dietary sugars and health endpoints is difficult because of measurement error in self‐reported intake. Dietary biomarkers may help us elucidate true associations.
We have assessed total sugars and total fructose intake (including fructose from sucrose) in a cross‐sectional analysis of 1366 participants (624 men, 742 women), 39 – 77 years of age, of the Norfolk cohort of the
European Prospective Investigation into Cancer
(EPIC) study using 7‐day diaries and sucrose and fructose measured in spot urines, as biomarkers of sugars intake. Other study measurements include serum uric acid and BP. Associations were investigated using linear regression analyses with log‐transformed variables, stratified by sex and adjusted for age and BMI. Urinary concentrations were adjusted by specific gravity.
Total sugars consumption (mean ± SD) was 111.7 ± 40.3 g/d, of which 44.3 ± 17.9 g/d was total fructose. Serum uric acid was 344 ± 66 µM. Serum uric acid concentration was not associated with systolic BP in men and women. Intake of total sugars and total fructose assessed by 7‐d diary or biomarker was not significantly associated with serum uric acid or with BP.
Our results do not support an association between fructose intake and increased BP.
Adjusted (age, BMI) systolic BP mm Hg (mean, 95% CI) by quintile of total fructose intake in 624 men and 742 women of EPIC Norfolk. Intake was measured by biomarker (urinary fructose) and 7DD (adjusted for total energy intake).
Men (n=624)
Women (n=742)
Intake
Biomarker
7DD
Biomarker
7DD
Q1
137.4 (136.3; 138.6)
136.9 (135.9; 138.0)
132.2 (131.0; 133.5)
131.2 (129.9; 132.6)
Q2
136.7 (135.6; 137.8)
137.1 (135.8; 138.3)
132.7 (131.4; 134.0)
131.8 (130.5; 133.1)
Q3
136.9 (135.7; 138.0)
137.1 (135.9; 138.3)
132.5 (131.3; 133.8)
133.5 (132.2; 134.8)
Q4
137.4 (136.2; 138.5)
136.8 (135.6; 138.1)
132.3 (131.0; 133.6)
132.2 (130.8; 133.5)
Q5
137.0 (135.8; 138.2)
137.5 (131.7; 132.9)
131.8 (130.3; 133.2)
132.9 (131.7; 134.0)
Meta-analysis of case-control genome-wide association studies (GWAS) for early onset and morbid obesity identified four variants in/near the PRL, PTER, MAF and NPC1 genes.
We aimed to validate ...association of these variants with obesity-related traits in population-based samples.
Genotypes and anthropometric traits were available in up to 31 083 adults from the Fenland, EPIC-Norfolk, Whitehall II, Ely and Hertfordshire studies and in 2042 children and adolescents from the European Youth Heart Study. In each study, we tested associations of rs4712652 (near-PRL), rs10508503 (near-PTER), rs1424233 (near-MAF) and rs1805081 (NPC1), or proxy variants (r (2)>0.8), with the odds of being overweight and obese, as well as with body mass index (BMI), percentage body fat (%BF) and waist circumference (WC). Associations were adjusted for sex, age and age(2) in adults and for sex, age, age group, country and maturity in children and adolescents. Summary statistics were combined using fixed effects meta-analysis methods.
We had 80% power to detect odds ratios of 1.046 to 1.092 for overweight and 1.067 to 1.136 for obesity. Variants near PRL, PTER and MAF were not associated with the odds of being overweight or obese, or with BMI, %BF or WC after meta-analysis (P>0.15). The NPC1 variant rs1805081 showed some evidence of association with %BF (β=0.013 s.d./allele, P=0.040), but not with any of the remaining obesity-related traits (P>0.3).
Overall, these variants, which were identified in a GWAS for early onset and morbid obesity, do not seem to influence obesity-related traits in the general population.
The Systematic COronary Risk Evaluation – Older Persons (SCORE-OP) algorithm is developed to assess 10-year risk of death due to cardiovascular disease (CVD) in individuals aged ≥65 years. We studied ...the performance of SCORE-OP in the European Prospective Investigation of Cancer Norfolk (EPIC-Norfolk) prospective population cohort.
10-year CVD mortality as predicted by SCORE-OP was compared with observed CVD mortality among individuals in the EPIC-Norfolk cohort. Persons aged 65–79 years without known CVD were included in the analysis. CVD mortality was defined as death due to ischemic heart disease, cardiac failure, cerebrovascular disease, peripheral-artery disease or aortic aneurysm. Predicted 10-year CVD mortality was calculated by the SCORE-OP algorithm, and compared to observed mortality rates. The area under the receiver operator characteristics curve (AUROC) was calculated to evaluate discriminative power. Calibration was evaluated by calculating ratios of predicted vs observed mortality and by Hosmer-Lemeshow tests.
A total of 6590 individuals (45.8% men), mean age 70.2 years (standard deviation 3.3) were included. The predicted mortality by SCORE-OP was 9.84% (95% confidence interval (CI) 9.76–9.92) and observed mortality was 10.2% (95% CI 9.52–11.04), ratio 0.96. AUROC was 0.63 (95% CI 0.60–0.65), and X2 was 3.3 (p = 0.92).
SCORE-OP overall accurately estimates the rate of CVD mortality in a general population aged 65–79 years. However, while calibration is excellent, the discriminative power of the SCORE-OP is limited, and as such cannot be readily implemented in clinical practice for this population.
•SCORE-OP overall accurately estimates the rate of CVD mortality in individuals aged 65–79 years in the general population.•SCORE-OP overestimates the rate of CVD mortality in younger (65–69 years) individuals.•SCORE-OP underestimates the rate of CVD mortality in older (70–79 years) individuals.•Discriminative performance of SCORE-OP was limited and warrants attention before SCORE-OP is implemented in daily practice.
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