Search

Context The incidence and remission of nonalcoholic fatty liver disease (NAFLD) are sparsely studied outside Asia. Objective This prospective study aimed to investigate NAFLD incidence and remission, and their predictors among a general Finnish population. Methods The applied cohort included 1260 repeatedly studied middle-aged participants with data on liver ultrasound and no excessive alcohol intake. Hepatic steatosis was assessed by liver ultrasound with a 7.2-year study interval. Comprehensive data on health parameters and lifestyle factors were available. Results At baseline, 1079 participants did not have NAFLD, and during the study period 198 of them developed NAFLD. Of the 181 participants with NAFLD at baseline, 40 achieved NAFLD remission. Taking multicollinearity into account, key predictors for incident NAFLD were baseline age (odds ratio 1.07; 95% CI, 1.02-1.13; P =.009), waist circumference (WC) (2.77, 1.91-4.01 per 1 SD; P <.001), and triglycerides (2.31, 1.53-3.51 per 1 SD; P <.001) and alanine aminotransferase (ALAT) (1.90, 1.20-3.00 per 1 SD; P =.006) concentrations as well as body mass index (BMI) change (4.12, 3.02-5.63 per 1 SD; P <.001). Predictors of NAFLD remission were baseline aspartate aminotransferase (ASAT) concentration (0.23, 0.08-0.67 per 1 SD; P =.007) and WC change (0.38, 0.25-0.59 per 1 SD; P <.001). Conclusion During follow-up, NAFLD developed for every fifth participant without NAFLD at baseline, and one-fifth of those with NAFLD at baseline had achieved NAFLD remission. NAFLD became more prevalent during the follow-up period. From a clinical perspective, key factors predicting NAFLD incidence and remission were BMI and WC change independent of their baseline level. [ABSTRACT FROM AUTHOR]

Context: The influence of dietary pattern trajectories from youth to adulthood on adult glucose metabolism is unknown.Objective: To identify dietary pattern trajectories from youth to adulthood and examine their associations with adult impaired fasting glucose (IFG).Methods: Thirty-one-year population-based cohort study among 1007 youths aged 3-18 years at baseline in Finland. Diet intake was assessed in 1980, 1986, 2001, 2007, and 2011. Group-based trajectory modelling was used to identify dietary pattern (identified by factor analysis) trajectories. Adult IFG was measured by the latest available data from 2001, 2007, and 2011.Results: Among 1007 participants, 202 (20.1%) developed IFG and 27 (2.7%) developed type 2 diabetes in adulthood (mean follow-up of 30.7 years; mean [SD] age 40.5 [5.0] years). Three dietary patterns were identified at baseline and were retained in 1986 and 2001: "Traditional Finnish," "High carbohydrate," and "Vegetables and dairy products." Three different patterns were identified in 2007, which remained similar in 2011: "Traditional Finnish and high carbohydrate," "Red meat," and "Healthy." Trajectories of increased or stably medium "red meat" pattern scores from youth to adulthood were detrimentally associated with IFG (relative risk 1.46, 95% CI 1.12-1.90 for Medium (M)-stable/M-large increase vs low-stable trajectory) after adjusting for confounders. This association was slightly reduced after further adjusting for long-term dietary fiber intake.Conclusion: Trajectories of an increased or stably moderate adherence to a "red meat" dietary pattern from youth to adulthood are associated with higher risk of adult IFG. This association is partly explained by low dietary fiber intake. [ABSTRACT FROM AUTHOR]

Background: Despite reporting lower levels of alcohol consumption, people with lower socio-economic status (SES) experience greater alcohol-related harm. Whether differential biases in the measurement of alcohol use could explain this apparent paradox is unknown. Using alcohol biomarkers to account for measurement error, we examined whether differential exposure to alcohol could explain the socio-economic differences in alcohol mortality.Methods: Participants from eight representative health surveys (n = 52 164, mean age 47.7 years) were linked to mortality data and followed up until December 2016. The primary outcome was alcohol-attributable mortality. We used income and education as proxies for SES. Exposures include self-reported alcohol use and four alcohol biomarkers [serum gamma-glutamyl transferase (available in all surveys), carbohydrate-deficient transferrin, alanine aminotransferase and aspartate aminotransferase (available in subsamples)]. We used shared frailty Cox proportional hazards to account for survey heterogeneity.Results: During a mean follow-up of 20.3 years, totalling 1 056 844 person-years, there were 828 alcohol-attributable deaths. Lower SES was associated with higher alcohol mortality despite reporting lower alcohol use. Alcohol biomarkers were associated with alcohol mortality and improved the predictive ability when used in conjunction with self-reported alcohol use. Alcohol biomarkers explained a very small fraction of the socio-economic differences in alcohol mortality, since hazard ratios either slightly attenuated (percent attenuation range 1.0-12.1%) or increased.Conclusions: Using alcohol biomarkers in addition to self-reported alcohol use did not explain the socio-economic differences in alcohol mortality. Differential bias in the measurement of alcohol use is not a likely explanation for the alcohol-harm paradox. [ABSTRACT FROM AUTHOR]

Background: Epidemiologic data are inconsistent regarding the vitamin E-lung cancer association, and no study to our knowledge has examined serologic changes in vitamin E status in relation to subsequent risk.Methods: In a cohort of 22 781 male smokers in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study, we ascertained 3184 lung cancer cases during up to 28 years of observation. Cox proportional hazards models examined whether higher serum alpha-tocopherol concentrations at baseline, 3 years, or the interval change were associated with lower lung cancer risk. All statistical tests were two-sided.Results: After adjustment for age, body mass index, smoking intensity and duration, serum total cholesterol, and trial intervention group, we found lower lung cancer risk in men with high baseline alpha-tocopherol (fifth quintile [Q5] vs Q1, hazard ratio [HR] = 0.76, 95% confidence interval [CI] = 0.66 to 0.87, Ptrend < .001). A similar reduction in risk was seen for serum alpha-tocopherol at 3 years (Q5 vs Q1, HR = 0.78, 95% CI = 0.67 to 0.91, Ptrend = .004). The inverse risk association appeared stronger for younger men and those who had smoked fewer years but was similar across trial intervention groups. We also found reduced risk among men not supplemented with vitamin E who had a lower serum alpha-tocopherol at baseline and greater increases in concentrations at 3 years (third tertile vs first tertile of serum alpha-tocopherol change, HR = 0.74, 95% CI = 0.59 to 0.91, P = .005).Conclusions: Higher vitamin E status, as measured by serum alpha-tocopherol concentration, as well as repletion of a low vitamin E state, was related to decreased lung cancer risk during a 28-year period. Our findings provide evidence supporting the importance of adequate physiological vitamin E status for lung cancer risk reduction. [ABSTRACT FROM AUTHOR]

Introduction: The Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study demonstrated that β-carotene supplementation increases lung cancer incidence in smokers. Further, cigarettes with higher tar and nicotine content are associated with a higher risk of lung cancer. However, no studies have examined whether the increased risk associated with β-carotene supplementation in smokers varies by the tar or nicotine content of cigarettes.Methods: The ATBC Study was a randomized, double-blind intervention trial conducted in southwest Finland. A total of 29 133 male smokers, aged 50-69 years, were enrolled and randomly assigned to one of four groups (α-tocopherol, β-carotene, both, or placebo). Cox proportional hazards models were used to estimate the hazard ratio (HR) and 95% confidence intervals (CI) of lung cancer risk by β-carotene trial assignment stratified by a priori categories of cigarette tar and nicotine content.Results: The β-carotene supplementation group had significantly higher risk of developing lung cancer in all categories of tar content (yes vs. no β-carotene supplementation-ultralight cigarettes [≤7 mg tar]: HR = 1.31, 95% CI = 0.91 to 1.89; nonfiltered cigarettes [≥21 mg tar]: HR = 1.22, 95% CI = 0.91 to 1.64; p for interaction = .91). Similarly, there was no interaction with nicotine content (yes vs. no β-carotene supplementation-ventilated cigarettes [≤0.8 µg nicotine]: HR = 1.23, 95% CI = 0.98 to 1.54; nonfiltered cigarettes [≥1.3 µg nicotine]: HR = 1.22, 95% CI = 0.91 to 1.64; p for interaction = .83).Conclusion: These findings support the conclusion that supplementation with β-carotene increases the risk of lung cancer in smokers regardless of the tar or nicotine content of cigarettes smoked. Our data suggest that all smokers should continue to avoid β-carotene supplementation.Implications: Previous studies demonstrated that β-carotene supplementation increases risk of lung cancer in smokers. This study moves the field forward by examining the potential for modification of risk of lung cancer with different levels of tar and nicotine in cigarettes smoked, as interaction with carcinogens in these components of cigarette smoke is hypothesized to be the mechanism by which β-carotene increases risk. Our study provides evidence that the increased risk of lung cancer in smokers who take β-carotene supplements is not dependent upon the tar or nicotine level of cigarettes smoked and suggests that all smokers should continue to avoid β-carotene supplementation. [ABSTRACT FROM AUTHOR]

Background: Declining participation rates in health examination surveys may impair the representativeness of surveys and introduce bias into the comparison of results between population groups if participation rates differ between them. Changes in the characteristics of non-participants over time may also limit comparability with earlier surveys. Methods: We studied the association of socio-economic position with participation, and its changes over the past 25years. Occupational class and educational level are used as indicators of socio-economic position. Data from six cross-sectional FINRISK surveys conducted between 1987 and 2012 in Finland were linked to national administrative registers, which allowed investigation of the differences between survey participants and nonparticipants. Results: Our results show that individuals with low occupational class or low level of education were less likely to participate than individuals with high occupational class or high level of education. Participation rates decreased in all subgroups of the population but the decline was fastest among those with low level of education. Conclusions: The differences in participation rates must be taken into account to avoid biased estimates because socio-economic position has also been shown to be strongly related to health, health behaviour and biological risk factors. Particular attention should be paid to the recruitment of the less-educated population groups. [ABSTRACT FROM AUTHOR]

Background: Health examination surveys (HESs) provide valuable data on health and its determinants at the population level. Comparison of HES results within and between countries and over time requires measurements which are free of bias due to differences in or adherence to measurement procedures and/or measurement devices. Methods: In the European HES (EHES) Pilot Project, 12 countries conducted a pilot HES in 2010-11 using standardized measurement protocols and centralized training. External evaluation visits (site visits) were performed by the EHES Reference Centre staff to evaluate the success of standardization and quality of data collection. Results: In general, standardized EHES protocols were followed adequately in all the pilot surveys. Small deviations were observed in the posture of participants during the blood pressure and height measurement; in the use of a tourniquet when drawing blood samples; and in the calibration of measurement devices. Occasionally, problems with disturbing noise from outside or people coming into the room during the measurements were observed. In countries with an ongoing national HES or a long tradition of conducting national HESs at regular intervals, it was more difficult to modify national protocols to fulfil EHES requirements. Conclusions: The EHES protocols to standardize HES measurements and procedures for collection of blood samples are feasible in crosscountry settings. The prerequisite for successful standardization is adequate training. External and internal evaluation activities during the survey fieldwork are also needed to monitor compliance to standards. [ABSTRACT FROM AUTHOR]

Introduction: Genetic variations in DBH-gene and its surroundings have been shown to associate with smoking behavior including smoking cessation in several studies. In this study we replicate and measure the effect size for association between DBH polymorphism rs3025343 and smoking cessation in a large population-based sample while examining environmental factors that could relate to the association.Methods: We studied 11 926 adult subjects from four surveys of the National FINRISK Study. The analysis was restricted to either current or former smokers. Logistic and linear regression analyses were conducted to investigate the relationships of the single nucleotide polymorphism (SNP), covariates, smoking cessation, and smoking severity (cotinine, CPD). Gene-environment interactions were tested by likelihood-ratio test.Results: The association between rs3025343 and smoking cessation (prevalence odds ratio, OR = 1.12, p = .094, 95%CI = 0.98-1.30) was replicated identically with the GWAS study of The Tobacco and Genetics Consortium (OR = 1.12, 95%CI = 1.08-1.18). None of our tested phenotypes significantly influenced the association between rs3025343 and smoking cessation. Overall, marital status, education, depression, alcohol use, self-rated health, and chronic obstructive pulmonary disease (COPD) showed phenotypic associations with smoking cessation, but the association of various phenotypes with smoking cessation did not vary by genotype.Conclusions: The current study replicates the effect size for the association between rs3025343 and smoking cessation despite lack of overall significance due to smaller sample size. We could not show environmental influences on the association of rs3025343 with smoking cessation.Implications: Our study replicates the direction and strength of the association of DBH polymorphism rs3025343 with smoking cessation. We could not detect environmental influences on the strength of the association of rs3025343 with smoking cessation, but the limited power of our analysis needs to be taken into account. [ABSTRACT FROM AUTHOR]

Background: a number of nutrients have been found to be associated with better muscle strength and mass; however, the role of the whole diet on muscle strength and mass remains still unknown. Objective: to examine whether the healthy Nordic diet predicts muscle strength, and mass 10 years later among men and women. Methods: about 1,072 participants belong to the Helsinki Birth Cohort Study, born 1934-44. Diet was assessed with a validated food-frequency questionnaire during 2001-04. The Nordic diet score (NDS) was calculated. The score included Nordic fruits, vegetables, cereals, ratio of polyunsaturated to saturated fatty acids, low-fat milk, fish, red meat, total fat and alcohol. Higher scores indicated better adherence to the healthy Nordic diet. Hand grip strength, leg strength (knee extension) and muscle mass were measured during the follow-up, between 2011 and 2013. Results: in women, each 1-unit increase in the NDS was related to 1.83 N greater leg strength (95% confidence interval [CI] 0.14-3.51; P = 0.034), and 1.44 N greater hand grip strength (95% CI: 0.04-2.84; P = 0.044). Women in the highest quartile of the NDS had on average 20.0 N greater knee extension results, and 14.2 N greater hand grip results than those in the lowest quartile. No such associations were observed among men. The NDS was not significantly related to muscle mass either in men or women. Conclusions: adherence to the healthy Nordic diet seems to protect from weaker muscle strength in old women. Therefore, the healthy Nordic diet may help to prevent disability. [ABSTRACT FROM AUTHOR]

Background: Gastrin, which induces gastric acid secretion, and a structurally similar hormone, cholecystokinin (CCK)-a potent acid inhibitor, may each play a role in gastric cancer. However, few studies have investigated this hypothesis in humans. We therefore investigated whether serum gastrin or CCK concentrations at baseline were associated with the incidence of gastric non-cardia adenocarcinomas (GNCA), oesophagogastric junctional adenocarcinomas (EGJA) or gastric carcinoid tumours over 24 years of follow-up in a study nested within the all-male Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study of Finnish smokers.Methods: Totals of 283 incident GNCA, 96 EGJA and 10 gastric carcinoid cases, and 778 matched controls, were included in our analysis. Gastrin and CCK were measured using specific radioimmunoassays. Odds ratios (OR) and 95% confidence intervals (95% CI) were estimated by multivariable logistic regression with adjustment for all known or suspected confounding factors, including Helicobacter pylori seropositivity.Results: Those with high gastrin (Q4 vs Q1), had an increased risk of GNCA (fully adjusted OR: 1.92; 95% CI: 1.21, 3.05) and gastric carcinoids, though the small number of carcinoid cases meant the fully adjusted model was unstable (age-adjusted continuous model OR: 4.67; 95% CI: 2.67, 8.15). CCK was associated with risk of GNCA only for those in Q3 relative to Q1 (OR: 0.56; 95% CI: 0.33, 0.96), and no significant trend was observed.Conclusions: Our data suggest that high serum concentrations of gastrin may be associated independently with an increased risk of gastric cancer; the role of CCK in cancer risk is less clear. [ABSTRACT FROM AUTHOR]

Background: Due to vitamin D intake below recommendation (10 mg/day) and low (<50nmol/l) serum 25- hydroxycholecalciferol (25(OH)D) concentration in Finnish population, the fortification of liquid dairy products with 0.5 mg vitamin D/100g and fat spreads with 10 mg/100g started in Finland in December 2002. In 2010, the fortification recommendation was doubled. The aim of this study was to investigate whether the vitamin D intake and status have improved among Finnish adults as a consequence of these nutrition policy actions. A further aim was to study the impact of vitamin supplement use to the total vitamin D intake. Methods: A cross-sectional survey was conducted every 5 years. The National FINDIET Survey was conducted in Finland as part of the National FINRISK health monitoring study. Dietary data were collected by using a computer-assisted 48-h dietary recall. In 2002, dietary data comprised 2007, in 2007, 1575 and 2012, 1295 working aged (25-64 years) Finns. Results: The mean D-vitamin intake increased from 5 mg/day to 17 mg/day in men and from 3 mg/day to 18 mg/day in women from 2002 to 2012. The most important food sources of vitamin D were milk products, fat spreads and fish dishes. The share of milk products was 39% among younger men and 38% among younger women, and 29% among older men and 28% among older women. Fat spreads covered on average 28% of vitamin D intake, except for younger men for which it covered 23%. Fish dishes provided 28% of vitamin D intake for older men and women, and approximately 18% for younger ones. In January-April 2012, the average serum 25-hydroxycholecalciferol (25(OH)D) concentration for men was 63 nmol/l for men and for women 67 nmol/l for women. Conclusions: The fortification of commonly used foods with vitamin D and vitamin D supplementation seems to be an efficient way to increase the vitamin D intake and the vitamin D status in the adult population. [ABSTRACT FROM AUTHOR]

Background: High alcohol consumption is a major cause of morbidity, yet alcohol is associated with both favourable and adverse effects on cardiometabolic risk markers. We aimed to characterize the associations of usual alcohol consumption with a comprehensive systemic metabolite profile in young adults.Methods: Cross-sectional associations of alcohol intake with 86 metabolic measures were assessed for 9778 individuals from three population-based cohorts from Finland (age 24-45 years, 52% women). Metabolic changes associated with change in alcohol intake during 6-year follow-up were further examined for 1466 individuals. Alcohol intake was assessed by questionnaires. Circulating lipids, fatty acids and metabolites were quantified by high-throughput nuclear magnetic resonance metabolomics and biochemical assays.Results: Increased alcohol intake was associated with cardiometabolic risk markers across multiple metabolic pathways, including higher lipid concentrations in HDL subclasses and smaller LDL particle size, increased proportions of monounsaturated fatty acids and decreased proportion of omega-6 fatty acids, lower concentrations of glutamine and citrate (P < 0.001 for 56 metabolic measures). Many metabolic biomarkers displayed U-shaped associations with alcohol consumption. Results were coherent for men and women, consistent across the three cohorts and similar if adjusting for body mass index, smoking and physical activity. The metabolic changes accompanying change in alcohol intake during follow-up resembled the cross-sectional association pattern (R2 = 0.83, slope = 0.72 ± 0.04).Conclusions: Alcohol consumption is associated with a complex metabolic signature, including aberrations in multiple biomarkers for elevated cardiometabolic risk. The metabolic signature tracks with long-term changes in alcohol consumption. These results elucidate the double-edged effects of alcohol on cardiovascular risk. [ABSTRACT FROM AUTHOR]

Background: Vitamin D has been discussed in the context of cardiovascular disease, cancer, bone health and other outcomes. Epidemiological studies have reported on the importance of vitamin D in cancer prevention and treatment. The discovery of vitamin D-associated metabolites through agnostic metabolomics analyses offers a new approach for elucidating disease aetiology and health-related pathway identification.Methods: Baseline serum 25-hydroxy-vitamin D [25(OH)D] and 940 serum metabolites were measured in 392 men from eight nested cancer case-control studies in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study of Finnish male smokers (aged 50-69 years). The metabolomic profiling was conducted using mass spectrometry. We used linear regression to estimate the standardized beta-coefficient as the effect metric for the associations between metabolites and 25(OH)D levels.Results: A majority of the metabolites associated with 25(OH)D were of lipid origin, including 3-carboxy-4-methyl-5-propyl-2-furanpropanoic acid (CMPF) [beta-estimate 0.38 per 1 standard deviation (SD) increment], stearoyl-arachidonoyl-glycerophosphoethanolamine (GPPE) (-0.38 per SD) and two essential fatty acids: eicosapentaenoate (EPA; 0.17 per SD) and docosahexaenoate (DHA; 0.13 per SD). Each of these lipid metabolites was associated with 25(OH)D at the principal components corrected P-value of 3.09 × 10-4 CONCLUSIONS: The large number of metabolites, particularly lipid compounds, found to be associated with serum 25(OH)D provide new biological clues relevant to the role of vitamin D status and human health outcomes. The present findings should be re-examined in other metabolomics studies of diverse populations. [ABSTRACT FROM AUTHOR]

Background: It has been suggested that high fish consumption improves mental well-being. The aim of this study was to assess whether high fish consumption or omega-3 polyunsaturated fatty acid (PUFA) intake was associated with reduced self-reported psychological distress.Methods: We used three cross-sectional data sets, the nationwide Health 2000 Survey (n = 5840), the Fishermen Study on Finnish fishermen and their family members (n = 1282) and the Finntwin16 Study on young adults (n = 4986). Data were based on self-administered questionnaires, interviews, health examinations and blood samples. Psychological distress was measured using the 12-item and 21-item General Health Questionnaires (GHQs). Fish consumption was measured by a food frequency questionnaire (FFQ, g/day) and independent frequency questions (times/month). Dietary intake (g/day) and serum concentrations (% from fatty acids) of PUFAs were determined. Relationships were analysed using regression analysis.Results: Regardless of the measure, fish consumption and omega-3 PUFA dietary intake were not associated with distress in any of the data sets. In contrast to the hypothesis, high serum docosahexaenoic acid was associated with high distress in the Fisherman Study men. Some non-linear associations were detected between serum omega-3 PUFAs or fish consumption (times/month) and distress. In the Fishermen Study, the associations were modified by alcohol consumption, smoking and physical activity.Conclusions: Our results do not support the hypothesis that fish consumption or omega-3 PUFA intake are associated with reduced psychological distress in the general population or in a population with high fish consumption. [ABSTRACT FROM AUTHOR]

Adiposity is associated with pancreatic cancer; however, the underlying mechanism(s) is uncertain. Leptin is an adipokine involved inmetabolic regulation, and obese individuals have higher concentrations.We conducted a pooled, nested case-control study of cohort participants from the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial, the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study, and the Cancer Prevention Study II Nutrition Cohort to investigate whether prediagnostic serum leptin was associated with pancreatic cancer. A total of 731 pancreatic adenocarcinoma cases that occurred between 1986 and 2010 were included (maximum follow-up, 23 years). Incidence density-selected controls (n = 909) were matched to cases by cohort, age, sex, race, and blood draw date. Conditional logistic regression was used to calculate odds ratios and 95%confidence intervals. Sex-specific quintiles were based on the distribution of the controls. Overall, serumleptinwas not associated with pancreatic cancer (quintile 5 vs. quintile 1: odds ratio = 1.13, 95%confidence interval: 0.75, 1.71; Ptrend = 0.38). Therewas a significant interaction by follow-up time (P = 0.003), such that elevated risk was apparent only during follow-up of more than 10 years after blood draw (quintile 5 vs. quintile 1: odds ratio = 2.55, 95% confidence interval: 1.23, 5.27; Ptrend = 0.004). Our results support an association between increasing leptin concentration and pancreatic cancer; however, long follow-up is necessary to observe the relationship. Subclinical disease may explain the lack of association during early follow-up. [ABSTRACT FROM AUTHOR]

Background: Non-communicable diseases (NCDs) cause 63% of deaths worldwide. The leading NCD risk factor is raised blood pressure, contributing to 13% of deaths. A large proportion of NCDs are preventable by modifying risk factor levels. Effective prevention programmes and health policy decisions need to be evidence based. Currently, self-reported information in general populations or data from patients receiving healthcare provides the best available information on the prevalence of obesity, hypertension, diabetes, etc. in most countries. Methods: In the European Health Examination Survey Pilot Project, 12 countries conducted a pilot survey among the working-age population. Information was collected using standardized questionnaires, physical measurement and blood sampling protocols. This allowed comparison of self-reported and measured data on prevalence of overweight, obesity, hypertension, high blood cholesterol and diabetes. Results: Self-reported data under-estimated population means and prevalence for health indicators assessed. The self-reported data provided prevalence of obesity four percentage points lower for both men and women. For hypertension, the self-reported prevalence was 10 percentage points lower, only in men. For elevated total cholesterol, the difference was 50 percentage point among men and 44 percentage points among women. For diabetes, again only in men, the self-reported prevalence was 1 percentage point lower than measured. With self-reported data only, almost 70% of population at risk of elevated total cholesterol is missed compared with data from objective measurements. Conclusions: Health indicators based on measurements in the general population include undiagnosed cases, therefore providing more accurate surveillance data than reliance on self-reported or healthcare-based information only. [ABSTRACT FROM AUTHOR]

Background: Health examination surveys (HESs), including both questionnaire and physical measurements, and in most cases also collection of biological samples, can provide objective health indicators. This information complements data from health interview surveys and administrative registers, and is important for evidence-based planning of health policies and prevention activities. HESs are valuable data sources for research. The first national HESs in Europe were conducted in the late 1950s and early 1960s. They have recently been carried out in an increasing number of countries, but there has been no joint standardization between the countries. Methods: The European Health Examination Survey Pilot Project was conducted in 2009–2012. The European Health Examination Survey Pilot Reference Centre was established and pilot surveys were conducted in 12 countries. Results: European standardized protocols for key measurements on main chronic disease risk factors (height, weight, waist circumference, blood pressure, blood lipids and fasting glucose or HbA1c) were prepared. European-level training and external quality assessment were organized. Although the level of earlier experience, infrastructures, economic status and cultural settings varied between the pilot countries, it was possible to standardize measurements of HESs across the populations. Obtaining high participation rates was challenging. Conclusion: HESs provide high-quality and representative population data to support policy decisions and research. For future national HESs, centralized coordination, training and external quality assessment are needed to ensure comparability of the results. Further studies on effects of different survey methods on comparability of the results and on recruitment and motivation of survey participants are needed. [ABSTRACT FROM PUBLISHER]

Fruit and vegetable intake may protect against pancreatic cancer, since fruits and vegetables are rich in potentially cancer-preventive nutrients. Most case-control studies have found inverse associations between fruit and vegetable intake and pancreatic cancer risk, although bias due to reporting error cannot be ruled out. In most prospective studies, inverse associations have been weaker and imprecise because of small numbers of cases. The authors examined fruit and vegetable intake in relation to pancreatic cancer risk in a pooled analysis of 14 prospective studies from North America, Europe, and Australia (study periods between 1980 and 2005). Relative risks and 2-sided 95% confidence intervals were estimated separately for the 14 studies using the Cox proportional hazards model and were then pooled using a random-effects model. Of 862,584 men and women followed for 7−20 years, 2,212 developed pancreatic cancer. The pooled multivariate relative risks of pancreatic cancer per 100-g/day increase in intake were 1.01 (95% confidence interval (CI): 0.99, 1.03) for total fruits and vegetables, 1.01 (95% CI: 0.99, 1.03) for total fruits, and 1.02 (95% CI: 0.99, 1.06) for total vegetables. Associations were similar for men and women separately and across studies. These results suggest that fruit and vegetable intake during adulthood is not associated with a reduced pancreatic cancer risk. [ABSTRACT FROM AUTHOR]

Greater exposure to retinol (vitamin A) may prevent prostate cancer, although under some conditions it could promote cell growth and de-differentiation. The authors prospectively examined prostate cancer risk and serum retinol levels, measured by using high-performance liquid chromatography, at baseline (n = 29,104) and after 3 years (n = 22,843) in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study cohort. Cox proportional hazards models were used to estimate the relative risk of total (n = 2,041) and aggressive (n = 461) prostate cancer by quintiles of baseline and 3-year serum retinol concentrations and by change in serum retinol levels from baseline to 3 years. Men with higher retinol concentrations at baseline were more likely to develop prostate cancer (quintile 5 vs. quintile 1 hazard ratio = 1.19, 95% confidence interval: 1.03, 1.36; Ptrend = 0.009). The results were similar for aggressive disease. Joint categorization based on baseline and 3-year retinol levels showed that men who were in the highest quintile at both time points had the greatest increased risk (baseline/3-year quintile 5/quintile 5 vs. quintile 1/quintile 1 hazard ratio = 1.31, 95% confidence interval: 1.08, 1.59). In this largest study to date of vitamin A status and subsequent risk of prostate cancer, higher serum retinol was associated with elevated risk, with sustained high exposure conferring the greatest risk. Future studies may clarify the underlying biologic mechanisms of the retinol-prostate cancer association. [ABSTRACT FROM PUBLISHER]

Background In the late 1960s, coronary heart disease (CHD) mortality among Finnish men was the highest in the world. From 1972 to 2007, risk factor surveys have been carried out to monitor risk factor trends and assess their contribution to declining mortality in Finland. [ABSTRACT FROM PUBLISHER]

Background: The mitogenic and growth-stimulatory effects of insulin-like growth factors appear to play a role in prostate carcinogenesis, yet any direct association of circulating insulin levels and risk of prostate cancer remains unclear. [ABSTRACT FROM PUBLISHER]

Background: Results of several case-control studies suggest that high consumption of meat (all meat, red meat, or processed meat) is associated with an increased risk of renal cell cancer, but only a few prospective studies have examined the associations of intakes of meat, fat, and protein with renal cell cancer. Methods: We conducted a pooled analysis of 13 prospective studies that included 530469 women and 244483 men and had follow-up times of up to 7-20 years to examine associations between meat, fat, and protein intakes and the risk of renal cell cancer. All participants had completed a validated food frequency questionnaire at study entry. Using the primary data from each study, we calculated the study-specific relative risks (RRs) for renal cell cancer by using Cox proportional hazards models and then pooled these RRs by using a random-effects model. All statistical tests were two-sided. Results: A total of 1478 incident cases of renal cell cancer were identified (709 in women and 769 in men). We observed statistically significant positive associations or trends in pooled age-adjusted models for intakes of total fat, saturated fat, monounsaturated fat, polyunsaturated fat, cholesterol, total protein, and animal protein. However, these associations were attenuated and no longer statistically significant after adjusting for body mass index, fruit and vegetable intake, and alcohol intake. For example, the pooled age-adjusted RR of renal cell cancer for the highest vs the lowest quintile of intake for total fat was 1.30 (95% confidence interval [Cl] = 1.08 to 1.56; Ptrend = .001) and for total protein was 1.17 (95% Cl = 0.99 to 1.38; Ptrend = .02). By comparison, the pooled multivariable RR for the highest vs the lowest quintile of total fat intake was 1.10 (95% Cl = 0.92 to 1.32; Ptrend = .31) and of total protein intake was 1.06 (95% Cl = 0.89 to 1.26; Ptrend = .37). Intakes of red meat, processed meat, poultry, or seafood were not associated with the risk of renal cell cancer. Conclusions: Intakes of fat and protein or their subtypes, red meat, processed meat, poultry, and seafood are not associated with risk of renal cell cancer. [ABSTRACT FROM AUTHOR]