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1.
J Hum Hypertens ; 2020 Oct 13.
Artigo em Inglês | MEDLINE | ID: mdl-33051584

RESUMO

A healthy diet reduces risk for high blood pressure. A small body size at birth increases risk for high blood pressure. Our aim was to study whether birth weight modifies the association between a healthy Nordic diet, characterized by high intake of Nordic vegetables, fruits, and berries, whole-grain rye, oat, and barley, and rapeseed oil, and blood pressure. Finnish men and women (n = 960) born in 1934-1944 attended clinical visits including clinical measurements, and questionnaires in 2001-2004 and 2011-2013. Linear regression was applied to investigate the interactions between birth weight and Nordic diet (measured by the Baltic sea diet score (BSDS)) on blood pressure change during the 10-year follow-up. Baseline Nordic diet and birth weight showed a significant interaction on systolic blood pressure (SBP) (p = 0.02), and pulse pressure (PP) (p < 0.01) over a 10-year follow-up. In the lowest birth weight category (women < 2951 g, men < 3061 g), predicted SBP decreased across BSDS thirds (lowest (T1): 155 mmHg, highest (T3): 145 mmHg, p for linearity = 0.01) as did predicted PP (T1: 71 mmHg, T3: 63 mmHg, p < 0.01). In the middle birth weight category, predicted SBP increased across BSDS thirds (T1: 151 mmHg, T3: 155 mmHg, p = 0.02) as did predicted PP (T1: 67 mmHg, T3: 71 mmHg, p < 0.01). In the highest birth weight category, no associations were found. Higher adherence to a healthy Nordic diet was associated with lower SBP and PP in individuals with low birth weight but with higher SBP and PP in those with average birth weight.

2.
Artigo em Inglês | MEDLINE | ID: mdl-32873601

RESUMO

INTRODUCTION: Observational and intervention studies have verified that weight loss predicts a reduced type 2 diabetes (T2D) risk. At the population level, knowledge on the prediction of self-report intentional weight loss (IWL) on T2D incidence is, however, sparse. We studied the prediction of self-report IWL on T2D incidence during a 15-year follow-up in a general adult population. RESEARCH DESIGN AND METHODS: The study sample from the representative Finnish Health 2000 Survey comprised 4270 individuals, aged 30-69 years. IWL was determined with questions concerning dieting attempts and weight loss during the year prior to baseline. Incident T2D cases during a 15-year follow-up were drawn from national health registers. The strength of the association between IWL and T2D incidence was estimated with the Cox model. RESULTS: During the follow-up, 417 incident cases of T2D occurred. IWL predicted an increased risk of T2D incidence (HR 1.44; 95% CI 1.11 to 1.87, p=0.008) in a multivariable model. In interaction analyses comparing individuals with and without IWL, a suggestively elevated risk emerged in men, the younger age group, among less-educated people and in individuals with unfavorable values in several lifestyle factors. CONCLUSIONS: Self-report IWL may predict an increased risk of T2D in long-term, probably due to self-implemented IWL tending to fail. The initial prevention of weight gain and support for weight maintenance after weight loss deserve greater emphasis in order to prevent T2D.

3.
Int J Epidemiol ; 2020 Sep 30.
Artigo em Inglês | MEDLINE | ID: mdl-32995840

RESUMO

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.

4.
Nutr Diabetes ; 10(1): 26, 2020 07 23.
Artigo em Inglês | MEDLINE | ID: mdl-32703940

RESUMO

BACKGROUND/OBJECTIVES: Maternal pre-pregnancy overweight/obesity and gestational diabetes (GDM) are associated with increased fat deposition in adult offspring. The purpose of this study was to identify if maternal pre-pregnancy overweight (body mass index (BMI) ≥ 25 kg/m2) or GDM are associated with dietary quality or intake in adult offspring. SUBJECTS/METHODS: Participants (n = 882) from two longitudinal cohort studies (ESTER Maternal Pregnancy Disorders Study and the Arvo Ylppö Longitudinal Study) completed a validated food-frequency questionnaire at a mean age of 24.2 years (SD 1.3). Diet quality was evaluated by a Recommended Finnish Diet Index (RDI). The study sample included offspring of normoglycaemic mothers with pre-pregnancy overweight/obesity (ONO = 155), offspring of mothers with GDM regardless of BMI (OGDM = 190) and offspring of mothers with normal weight and no GDM (controls; n = 537). RESULTS: Among men, daily energy and macronutrient intakes were similar in ONO and controls. However, after adjusting for current offspring characteristics, including BMI, daily carbohydrate intake relative to total energy intake was higher in ONO-men [2.2 percentages of total energy intake (95% confidence interval 0.4, 4.0)]. In ONO-women, macronutrient intakes relative to total energy intake were similar with controls, while total daily energy intake seemed lower [-587.2 kJ/day (-1192.0, 4.4)]. After adjusting for confounders, this difference was attenuated. Adherence to a healthy diet, as measured by RDI, was similar in ONO and controls [mean difference: men 0.40 (-0.38, 1.18); women 0.25 (-0.50, 1.00)]. In OGDM vs. controls, total energy and macronutrient intakes were similar for both men and women. Also adherence to a healthy diet was similar [RDI: men 0.09 (-0.62, 0.80); women -0.17 (-0.93, 0.59)]. CONCLUSIONS: Our study suggested higher daily carbohydrate intake in male offspring exposed to maternal pre-pregnancy overweight/obesity, compared with controls. Prenatal exposure to GDM was not associated with adult offspring dietary intakes.

6.
J Biol Rhythms ; 35(5): 501-511, 2020 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-32579418

RESUMO

Individuals with a later chronotype (evening types) tend to have unhealthier behaviors and increased morbidity and mortality as compared with those with an earlier chronotype (morning types). However, the role of genetics in explaining evening types' adverse health and health behavior is unclear. Our aim was to study genetic associations of chronotype among 8433 Finns from the cross-sectional National FINRISK 2007 and 2012 studies. First, we studied associations between chronotype and 20 key clock genes with a candidate-gene approach and then performed a full genome-wide association study (GWAS) of chronotype. We also developed a genetic risk score (GRS) for chronotype based on 313 single nucleotide polymorphisms (SNPs) that have previously been associated with chronotype. Chronotype was assessed with a shortened version of Horne and Östberg's Morningness-Eveningness Questionnaire (sMEQ), and for comparison, we also used the single self-evaluation question on chronotype from the questionnaire. Linear and logistic regression was used for statistical analysis assuming additive effects. The clock gene analysis revealed 1 independent association signal within NR1D2 (lead SNP rs4131403) that was associated with chronotype (p < 0.05; as based on both chronotype assessment methods). The GWAS analysis did not yield any genome-wide significant associations (p > 5 × 10-8). However, higher GRS was associated with evening chronotype (p < 0.001; as based on both chronotype assessment methods). In conclusion, our findings indicated novel genetic associations between chronotype and the NR1D2 clock gene, which has previously been associated with carbohydrate and lipid metabolism. Furthermore, the GRS was able to capture the genetic aspect of chronotype in our study population. These findings expand our knowledge of the genetic basis of chronotype.

7.
Public Health Nutr ; 23(7): 1266-1272, 2020 05.
Artigo em Inglês | MEDLINE | ID: mdl-32204746

RESUMO

OBJECTIVE: To investigate whether vitamin D status predicts weight gain or increase in waist circumference during the 11-year follow-up in general adult population. DESIGN: A population-based longitudinal study. SETTING: The study was conducted using data from the nationally representative Health 2000/2011 Survey. The analyses were based on regression models adjusted for sociodemographic and lifestyle factors. PARTICIPANTS: Weight, waist circumference and vitamin D status (serum 25-hydroxyvitamin D concentration analysed with radioimmunoassay) were measured from 2924 participants aged 30-64 years at baseline. RESULTS: In men, low vitamin D status at baseline predicted ≥10 % increase in waist circumference during the follow-up when adjusted for age only (OR for sufficient v. deficient S-25(OH)D 0·41; 95 % CI 0·25, 0·67; P for trend <0·01), but the association with weight gain was only borderline significant. After adjustment for potential confounders, low vitamin D status remained a significant predictor of increase in waist circumference, but the association with weight gain was further attenuated. In women, vitamin D status at baseline did not predict weight gain or increase in waist circumference. CONCLUSIONS: Our results suggest that vitamin D insufficiency may be a risk factor of abdominal obesity among men but not among women. In men, it may also increase the risk of weight gain. Further studies are required to confirm these findings and examine potential mechanisms behind them. There is also a possibility that vitamin D is a biomarker of healthy lifestyle rather than an independent risk factor for obesity.


Assuntos
Obesidade/epidemiologia , Deficiência de Vitamina D/epidemiologia , Vitamina D/sangue , Circunferência da Cintura , Ganho de Peso , Adulto , Feminino , Seguimentos , Inquéritos Epidemiológicos , Humanos , Estilo de Vida , Estudos Longitudinais , Masculino , Pessoa de Meia-Idade , Estado Nutricional , Obesidade/sangue , Fatores de Risco , Fatores Sexuais , Vitamina D/análogos & derivados , Deficiência de Vitamina D/sangue
8.
Ann Epidemiol ; 42: 12-18, 2020 02.
Artigo em Inglês | MEDLINE | ID: mdl-32024597

RESUMO

PURPOSE: We identify the individual and joint contributions of excess weight and cigarette smoking to national-level type II diabetes (T2D) incidence and to educational and gender disparities therein filling an important gap in T2D epidemiology. METHODS: Based on the FINRISK surveys conducted in 1997, 2002, and 2007 and linked to the Finnish National Drug Reimbursement Register through 2011, we used a regression-counterfactual approach to estimate the percentage of diagnosed drug-treated incident T2D cases attributable to excess body weight and cigarette smoking. Body mass index (BMI) and waist circumference were evaluated. RESULTS: T2D incidence was 10.24 in men and 7.04 in women per 1000 person-years. Excess baseline BMI (≥25.0 kg/m2) explained 69% and 63%, and smoking explained 9% and 14% of T2D incidence, in men and women, respectively. Most of the gender difference was explained by the risk factors. Approximately 90% in men and 98% in women of the higher T2D incidence among those in the lower versus upper third of the educational distribution was explained by excess BMI. The results were similar for waist circumference and lifetime maximum BMI. CONCLUSIONS: Excess body weight is the main risk factor contributing to national-level T2D incidence and disparities by educational attainment and gender in a high-income population.


Assuntos
Fumar Cigarros/efeitos adversos , Diabetes Mellitus Tipo 2/epidemiologia , Obesidade Abdominal/epidemiologia , Adulto , Idoso , Índice de Massa Corporal , Escolaridade , Feminino , Finlândia/epidemiologia , Humanos , Incidência , Masculino , Pessoa de Meia-Idade , Vigilância da População , Características de Residência , Fatores Sexuais , Fatores Socioeconômicos
9.
J Natl Cancer Inst ; 112(10): 1003-1012, 2020 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-31917448

RESUMO

BACKGROUND: Although 20 pancreatic cancer susceptibility loci have been identified through genome-wide association studies in individuals of European ancestry, much of its heritability remains unexplained and the genes responsible largely unknown. METHODS: To discover novel pancreatic cancer risk loci and possible causal genes, we performed a pancreatic cancer transcriptome-wide association study in Europeans using three approaches: FUSION, MetaXcan, and Summary-MulTiXcan. We integrated genome-wide association studies summary statistics from 9040 pancreatic cancer cases and 12 496 controls, with gene expression prediction models built using transcriptome data from histologically normal pancreatic tissue samples (NCI Laboratory of Translational Genomics [n = 95] and Genotype-Tissue Expression v7 [n = 174] datasets) and data from 48 different tissues (Genotype-Tissue Expression v7, n = 74-421 samples). RESULTS: We identified 25 genes whose genetically predicted expression was statistically significantly associated with pancreatic cancer risk (false discovery rate < .05), including 14 candidate genes at 11 novel loci (1p36.12: CELA3B; 9q31.1: SMC2, SMC2-AS1; 10q23.31: RP11-80H5.9; 12q13.13: SMUG1; 14q32.33: BTBD6; 15q23: HEXA; 15q26.1: RCCD1; 17q12: PNMT, CDK12, PGAP3; 17q22: SUPT4H1; 18q11.22: RP11-888D10.3; and 19p13.11: PGPEP1) and 11 at six known risk loci (5p15.33: TERT, CLPTM1L, ZDHHC11B; 7p14.1: INHBA; 9q34.2: ABO; 13q12.2: PDX1; 13q22.1: KLF5; and 16q23.1: WDR59, CFDP1, BCAR1, TMEM170A). The association for 12 of these genes (CELA3B, SMC2, and PNMT at novel risk loci and TERT, CLPTM1L, INHBA, ABO, PDX1, KLF5, WDR59, CFDP1, and BCAR1 at known loci) remained statistically significant after Bonferroni correction. CONCLUSIONS: By integrating gene expression and genotype data, we identified novel pancreatic cancer risk loci and candidate functional genes that warrant further investigation.

10.
J Sci Med Sport ; 23(6): 596-602, 2020 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-31928882

RESUMO

OBJECTIVES: To assess the stability and determinants of total and context specific sitting in a follow-up of adults. DESIGN: Longitudinal study. METHODS: Participants in the DILGOM cohort (n=3735, men 45%), reported daily sitting in five contexts (work-related, in vehicle, at home by the TV, at home at the computer, and elsewhere) in 2007 and 2014. Sociodemographic background, lifestyle and health were assessed in 2007. Total sitting comprised the sum of context specific sitting. Changes in, and determinants of context specific sitting, stratified by baseline age into young middle-aged (<53 years); late middle-aged (53-68 years) and older-aged (>68 years) were estimated by generalized linear mixed models. RESULTS: In 2007, total daily sitting was 7h 26min, 6h 16min, and 6h 3min in young middle-aged, late middle-aged and older-aged groups, respectively. Over 7 years, total sitting decreased on average by 26min. Sitting at the computer increased by 7-17min. The late middle-aged group also increased sitting by the TV, and decreased total, work-related, vehicle and elsewhere sitting. Occupational status determined context specific sitting, but somewhat differently in young and late middle-aged groups. Poor self-rated health determined less work-related and more sitting by the TV in the young, whereas good health determined less work-related sitting in the late middle-aged group. CONCLUSIONS: Self-reported sitting is a fairly stable behavior, with the exception for the late middle-aged group, where all context specific and total sitting changed significantly. Occupational status and health determined changes in sitting; however, somewhat differently by age group.


Assuntos
Estilo de Vida , Comportamento Sedentário , Postura Sentada , Adulto , Idoso , Feminino , Finlândia , Humanos , Estudos Longitudinais , Masculino , Pessoa de Meia-Idade , Inquéritos e Questionários , Fatores de Tempo
11.
Clin Gastroenterol Hepatol ; 18(4): 995-997.e2, 2020 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-31255807

RESUMO

Alcoholic liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD) are the major causes for nonviral liver cirrhosis in the population. Whereas the typical NAFLD patient is one with abdominal obesity, metabolic syndrome (MetS), and no or minimal alcohol use, the patient with pure alcoholic liver cirrhosis has, according to cohort studies, typically consumed >5-10 daily alcohol drinks for several years.1 However, both alcohol use and components of the MetS are continuous variables and, as such, not dichotomic. Recent evidence suggests harmful synergistic effects of obesity, MetS, and alcohol intake for the risk of future liver disease.2 Consequently, given an increasing population prevalence of overweight and obese alcohol users, expectedly, there will be many patients that do not fit either the typical NAFLD or typical ALD phenotype, but share features of both disease entities. Current case-finding strategies focusing on either pure NAFLD or pure ALD3,4 may underestimate the true risk in individuals who will develop liver disease as the result of interaction between alcohol and metabolic disorders.1.

12.
Hepatology ; 71(3): 835-848, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-31323122

RESUMO

BACKGROUND AND AIMS: The effects of alcohol use in nonalcoholic fatty liver disease are unclear. We investigated the impact of alcohol use in fatty liver disease on incident liver, cardiovascular, and malignant disease, as well as death. APPROACH AND RESULTS: Our study comprised 8,345 persons with hepatic steatosis (fatty liver index >60) who participated in health-examination surveys (FINRISK 1992-2012 or Health 2000), with available data on baseline alcohol intake. Main exclusions were baseline clinical liver disease, viral hepatitis, ethanol intake >50 g/day, and current abstainers. Data were linked with national registers for hospital admissions, malignancies, and death regarding liver, cardiovascular, and malignant disease, as well as all-cause death. Adjustment were for multiple confounders. Alcohol consumption showed a dose-dependent risk increase for incident advanced liver disease and malignancies. Consuming 10-19 g/day of alcohol in general or 0-9 g/day as nonwine beverages doubled the risk for advanced liver disease compared to lifetime abstainers. In contrast, alcohol intake up to 49 g/day was associated with a 22%-40% reduction of incident cardiovascular disease (CVD). We observed a J-shaped association between alcohol intake and all-cause death with a maximal risk reduction of 21% (95% confidence interval, 5%-34%) at alcohol intake of 0-9 g/day compared to lifetime abstainers. However, these benefits on CVD and mortality were only observed in never smokers. Alcohol intake >30 g/day yielded increased risk estimates for mortality compared to lifetime abstainers. In a subpopulation with longitudinal data, alcohol intake remained stable over time in >80% of subjects. CONCLUSIONS: Even low alcohol intake in fatty liver disease is associated with increased risks for advanced liver disease and cancer. Low to moderate alcohol use is associated with reduced mortality and CVD risk but only among never smokers.

13.
J Gastroenterol Hepatol ; 35(2): 291-298, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-31260143

RESUMO

BACKGROUND AND AIM: Liver disease is traditionally categorized as alcoholic and non-alcoholic. We studied various risk factors predictive of advanced non-viral liver disease in general population and analyzed the interaction between these factors and alcohol consumption. METHODS: Persons without underlying liver disease who participated in the Health2000 or FINRISK studies 1992-2012 comprised a cohort of 41 260 individuals. Pattern of alcohol consumption and metabolic, lifestyle-related, and anthropometric parameters were analyzed with Cox regression analysis using severe liver disease hospitalization, cancer, or death as end-point. Viral liver diseases were excluded. RESULTS: A total of 355 liver events occurred during the mean 12.4-year follow-up (511 789 person-years). In the multivariate model, age (hazard ratio [HR] 1.03, P = 0.0083 for men; HR 1.04, P = 0.0198 for women), waist-to-hip ratio (WHR) (HR 1.52, P = 0.0006 for men; HR 1.58, P = 0.0167 for women), patatin-like phospholipase-containing domain 3 mutations (HR 1.9, P = 0.024 for men; HR 2.7, P = 0.0109 for women), and weekly binge drinking (HR 2.4, P = 0.0024 for men; HR 7.4, P < 0.0001 for women) predicted development of severe liver disease. Among men, diabetes (HR 2.7, P = 0.0002), average alcohol consumption (HR for 10 g/day 1.1, P = 0.0022), non-married status (HR 1.9, P = 0.0397 for single; HR 2.4, P = 0.0002 for widowed/separated), and serum high-density lipoprotein (HR 2.2, P = 0.0022) and non-high-density lipoprotein cholesterol (HR 1.2, P = 0.0237) were additional risk factors. Alcohol intake increased the risk especially among persons with high WHR (P for interaction 0.009). CONCLUSIONS: Age, patatin-like phospholipase-containing domain 3 haplotype, and WHR increase the risk for development of severe liver disease. We found strong synergism between alcohol and central obesity. Binge drinking is an additional risk factor.

14.
J Natl Cancer Inst ; 112(2): 191-199, 2020 Feb 01.
Artigo em Inglês | MEDLINE | ID: mdl-31077299

RESUMO

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.

15.
Int J Cancer ; 146(3): 861-873, 2020 02 01.
Artigo em Inglês | MEDLINE | ID: mdl-31037736

RESUMO

Alcohol consumption is an established risk factor for colorectal cancer (CRC). However, while studies have consistently reported elevated risk of CRC among heavy drinkers, associations at moderate levels of alcohol consumption are less clear. We conducted a combined analysis of 16 studies of CRC to examine the shape of the alcohol-CRC association, investigate potential effect modifiers of the association, and examine differential effects of alcohol consumption by cancer anatomic site and stage. We collected information on alcohol consumption for 14,276 CRC cases and 15,802 controls from 5 case-control and 11 nested case-control studies of CRC. We compared adjusted logistic regression models with linear and restricted cubic splines to select a model that best fit the association between alcohol consumption and CRC. Study-specific results were pooled using fixed-effects meta-analysis. Compared to non-/occasional drinking (≤1 g/day), light/moderate drinking (up to 2 drinks/day) was associated with a decreased risk of CRC (odds ratio [OR]: 0.92, 95% confidence interval [CI]: 0.88-0.98, p = 0.005), heavy drinking (2-3 drinks/day) was not significantly associated with CRC risk (OR: 1.11, 95% CI: 0.99-1.24, p = 0.08) and very heavy drinking (more than 3 drinks/day) was associated with a significant increased risk (OR: 1.25, 95% CI: 1.11-1.40, p < 0.001). We observed no evidence of interactions with lifestyle risk factors or of differences by cancer site or stage. These results provide further evidence that there is a J-shaped association between alcohol consumption and CRC risk. This overall pattern was not significantly modified by other CRC risk factors and there was no effect heterogeneity by tumor site or stage.


Assuntos
Neoplasias Colorretais/etiologia , Etanol/efeitos adversos , Idoso , Consumo de Bebidas Alcoólicas/efeitos adversos , Estudos de Casos e Controles , Feminino , Humanos , Estilo de Vida , Masculino , Pessoa de Meia-Idade , Razão de Chances , Estudos Prospectivos , Fatores de Risco
16.
Prev Med ; 131: 105970, 2020 02.
Artigo em Inglês | MEDLINE | ID: mdl-31883872

RESUMO

Sugar-sweetened beverage (SSB) intake is associated with metabolic disorders. The reduction of SSB intake has been promoted to prevent death and disability from chronic diseases. We investigated the association between SSB intake and the risk of coronary events and death, and assessed if substitution of coffee, tea, milk, fruit juice and artificially-sweetened beverages (ASB) for SSBs was associated with a reduced risk of coronary events and death. This was a follow-up study in which data from six studies were pooled and standard observational analyses were performed. Diet intake was assessed at baseline by food-frequency questionnaires. Hazard ratios (HRs) with 95% confidence intervals for the incidence of coronary events and deaths were calculated by Cox proportional hazards regression. The effect of substituting another beverage for SSBs was calculated by taking the difference in the individual effect estimates. During the median 8.2-year follow-up, 4248 coronary events and 1630 coronary deaths were documented among 284,345 individuals. 355 ml daily increase of SSB intake was associated with an increased risk of coronary events (HR: 1.08; 95%CI: 1.02, 1.14) and possibly coronary death (HR: 1.05; 95%CI: 0.96, 1.16). Substitution analyses suggested that replacing SSBs with coffee (HR: 0.93; 95%CI: 0.87, 1.00) or ASB (HR: 0.89; 95%CI: 0.83, 0.97), might be associated with a lower risk of developing coronary events. We found that SSB intake was associated with an increased risk of coronary events and possibly coronary death. Our findings also suggest that replacing SSB's with ASBs or coffee may lower the risk of developing CHD.

17.
Community Dent Oral Epidemiol ; 48(2): 143-151, 2020 04.
Artigo em Inglês | MEDLINE | ID: mdl-31868961

RESUMO

OBJECTIVE: To study whether diets based on the Nordic food culture and dietary recommendations are related to periodontal disease development. METHODS: The data were based on the Health 2000 and 2011 Surveys (BRIF8901). The participants were aged 30-49 in 2000, periodontally healthy, without diabetes or rheumatoid arthritis. Analyses were made in the total study population (n = 240) and among nonsmokers (n = 193) in 2011. Periodontal condition was determined in a clinical examination, and the number of teeth with deepened (≥4 mm) periodontal pockets in 2011 was used as an outcome. The diet was measured using a validated food frequency questionnaire and the quality of the diet using the Baltic Sea Diet Score (BSDS) and the Recommended Finnish Diet Score (RFDS) in 2000. Incidence rate ratios (IRRs) and 95% confidence intervals (CIs) were estimated using Poisson regression models. RESULTS: Low scores (indicating poor diet) in both the BSDS and the RFDS were associated with the development of deepened periodontal pockets. Among nonsmokers, the associations between low dietary scores and the number of teeth with deepened periodontal pockets were stronger than among the whole study population. CONCLUSIONS: Among middle-aged adults, poor-quality diet appears to be associated with the development of periodontal disease.


Assuntos
Dieta , Doenças Periodontais/etiologia , Bolsa Periodontal , Adulto , Feminino , Finlândia , Seguimentos , Humanos , Masculino , Pessoa de Meia-Idade , Inquéritos e Questionários
18.
Hepatol Commun ; 3(12): 1704-1705, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31832576

RESUMO

A pathophysiologic risk score consisting of insulin resistance and genetic risk predicts incident liver outcomes in NAFLD. Such scores may represent a viable strategy for risk stratification in NAFLD.

19.
PLoS Biol ; 17(10): e3000443, 2019 10.
Artigo em Inglês | MEDLINE | ID: mdl-31626640

RESUMO

Obesity is associated with changes in the plasma lipids. Although simple lipid quantification is routinely used, plasma lipids are rarely investigated at the level of individual molecules. We aimed at predicting different measures of obesity based on the plasma lipidome in a large population cohort using advanced machine learning modeling. A total of 1,061 participants of the FINRISK 2012 population cohort were randomly chosen, and the levels of 183 plasma lipid species were measured in a novel mass spectrometric shotgun approach. Multiple machine intelligence models were trained to predict obesity estimates, i.e., body mass index (BMI), waist circumference (WC), waist-hip ratio (WHR), and body fat percentage (BFP), and validated in 250 randomly chosen participants of the Malmö Diet and Cancer Cardiovascular Cohort (MDC-CC). Comparison of the different models revealed that the lipidome predicted BFP the best (R2 = 0.73), based on a Lasso model. In this model, the strongest positive and the strongest negative predictor were sphingomyelin molecules, which differ by only 1 double bond, implying the involvement of an unknown desaturase in obesity-related aberrations of lipid metabolism. Moreover, we used this regression to probe the clinically relevant information contained in the plasma lipidome and found that the plasma lipidome also contains information about body fat distribution, because WHR (R2 = 0.65) was predicted more accurately than BMI (R2 = 0.47). These modeling results required full resolution of the lipidome to lipid species level, and the predicting set of biomarkers had to be sufficiently large. The power of the lipidomics association was demonstrated by the finding that the addition of routine clinical laboratory variables, e.g., high-density lipoprotein (HDL)- or low-density lipoprotein (LDL)- cholesterol did not improve the model further. Correlation analyses of the individual lipid species, controlled for age and separated by sex, underscores the multiparametric and lipid species-specific nature of the correlation with the BFP. Lipidomic measurements in combination with machine intelligence modeling contain rich information about body fat amount and distribution beyond traditional clinical assays.


Assuntos
Tecido Adiposo/metabolismo , Distribuição da Gordura Corporal/estatística & dados numéricos , Lipidômica , Aprendizado de Máquina , Obesidade/diagnóstico , Biomarcadores/sangue , Índice de Massa Corporal , Estudos de Coortes , Feminino , Finlândia , Humanos , Metabolismo dos Lipídeos , Masculino , Modelos Estatísticos , Obesidade/sangue , Fatores Sexuais , Esfingomielinas/sangue , Circunferência da Cintura , Relação Cintura-Quadril
20.
PLoS One ; 14(10): e0223692, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31644575

RESUMO

BACKGROUND: GlycA is a nuclear magnetic resonance (NMR) spectroscopy biomarker that predicts risk of disease from myriad causes. It is heterogeneous; arising from five circulating glycoproteins with dynamic concentrations: alpha-1 antitrypsin (AAT), alpha-1-acid glycoprotein (AGP), haptoglobin (HP), transferrin (TF), and alpha-1-antichymotrypsin (AACT). The contributions of each glycoprotein to the disease and mortality risks predicted by GlycA remain unknown. METHODS: We trained imputation models for AAT, AGP, HP, and TF from NMR metabolite measurements in 626 adults from a population cohort with matched NMR and immunoassay data. Levels of AAT, AGP, and HP were estimated in 11,861 adults from two population cohorts with eight years of follow-up, then each biomarker was tested for association with all common endpoints. Whole blood gene expression data was used to identify cellular processes associated with elevated AAT. RESULTS: Accurate imputation models were obtained for AAT, AGP, and HP but not for TF. While AGP had the strongest correlation with GlycA, our analysis revealed variation in imputed AAT levels was the most predictive of morbidity and mortality for the widest range of diseases over the eight year follow-up period, including heart failure (meta-analysis hazard ratio = 1.60 per standard deviation increase of AAT, P-value = 1×10-10), influenza and pneumonia (HR = 1.37, P = 6×10-10), and liver diseases (HR = 1.81, P = 1×10-6). Transcriptional analyses revealed association of elevated AAT with diverse inflammatory immune pathways. CONCLUSIONS: This study clarifies the molecular underpinnings of the GlycA biomarker's associated disease risk, and indicates a previously unrecognised association between elevated AAT and severe disease onset and mortality.


Assuntos
Biomarcadores , alfa 1-Antitripsina/sangue , Suscetibilidade a Doenças , Feminino , Glicoproteínas , Humanos , Espectroscopia de Ressonância Magnética , Masculino , Morbidade , Mortalidade , Orosomucoide/efeitos adversos , Modelos de Riscos Proporcionais
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