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OBJECTIVES: This study aimed to comprehensively analyze the time trends in average sleep duration and prevalence of short sleep, poor sleep quality, and high sleep debt among Chinese adults. STUDY DESIGN: This was a cross-sectional study. METHODS: The study used nationally representative data from Chinese Family Panel Survey (CFPS) among adults aged ≥18 years. Linear regression and logistic regression were used to calculate P-values for trends across waves, and absolute difference in prevalences were calculated by linear regression. Poisson regression analysis was used to calculate the prevalence ratios of sleep-related problems. RESULTS: In 2018, the estimated average sleep duration in adults was 7.6 h/d. A shorter sleep duration, higher proportion of short sleep, and poor sleep quality were observed in people aged ≥65 years, women, people with primary school education or below, and residents in Liaoning province. The average sleep duration slightly decreased from 8.2 h/d in 2010 to 7.6 h/d in 2016, and then remained stable from 2016 to 2018. The prevalence of short sleep duration has markedly increased from 11.8% in 2010 to 24.1% in 2016, and then there was a decline in prevalence from 2016 to 2018, although this decrease was not significant. The prevalence of high sleep debt among employed people increased from 6.2% in 2010 to 8.6% in 2018 (absolute difference, 2.4 p.p; P trend = 0.063). In addition, the prevalence of poor sleep quality increased from 15.6% in 2012 to 21.3% in 2018 (absolute difference of 5.7 p.p; P trend<0.001). For all the sleep-related variables, the degree of changes varied by sociodemographic subgroups. CONCLUSIONS: In this nationally representative survey of the Chinese population, the average sleep duration slightly decreased from 2010 to 2016, and then remained stable from 2016 to 2018. Poor sleep quality, and high sleep debt increased among most of the sociodemographic subgroups. Future studies are needed to understand the drivers of changes in sleep health among Chinese adults.
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Trastornos del Inicio y del Mantenimiento del Sueño , Trastornos del Sueño-Vigilia , Adulto , Femenino , Humanos , Estudios Transversales , Pueblos del Este de Asia , Sueño , Privación de Sueño , Trastornos del Sueño-Vigilia/epidemiología , Encuestas y CuestionariosRESUMEN
AIMS: The metabolic syndrome (MetS) and its consequences are one of the main public health challenges worldwide. We conducted a systematic review and dose-response meta-analysis of studies that examined the association between screen time and the MetS among children and adolescents. DATA SYNTHESIS: A systematic search was conducted using electronic databases, including PubMed, Scopus, ProQuest, and Cochrane Library, for studies published from 1963 up to 2 May 2022. In this systematic review and meta-analysis, observational studies with cross-sectional, case-control, and cohort design evaluating the association between screen time and MetS were included. Random effects models and linear and nonlinear dose-response meta-analyses were used to pool study results. RESULTS: Seven studies were included in the meta-analysis. The summary OR of MetS among children and adolescents for the highest vs. lowest time of screen time was 1.64 (95% CI: 1.32-2.03, with little evidence of heterogeneity, I2 = 9.3%, P-heterogeneity = 0.35, n = 7 studies) and 1.64 (95% CI: 1.27-2.12, I2 = 27.7%, n = 6) for cross-sectional studies. Results persisted across several additional subgroup analyses. There was a linear positive association between screen time and the risk of MetS (P dose-response <0.0001; P nonlinearity = 0.64) with an OR of 1.29 (95% CI: 1.12-1.46) per 2 h/day increment in screen time. CONCLUSION: The current dose-response meta-analysis suggested that increased screen time is associated with an increased risk of MetS among children and adolescents. Public health strategies may target unhealthy screen-based related behaviors to halt the development of MetS among children and adolescents.
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Síndrome Metabólico , Adolescente , Estudios de Casos y Controles , Niño , Estudios Transversales , Humanos , Síndrome Metabólico/diagnóstico , Síndrome Metabólico/epidemiología , Síndrome Metabólico/prevención & control , Estudios Observacionales como Asunto , Tiempo de PantallaRESUMEN
Higher milk intake has been associated with a lower stroke risk, but not with risk of CHD. Residual confounding or reverse causation cannot be excluded. Therefore, we estimated the causal association of milk consumption with stroke and CHD risk through instrumental variable (IV) and gene-outcome analyses. IV analysis included 29 328 participants (4611 stroke; 9828 CHD) of the European Prospective Investigation into Cancer and Nutrition (EPIC)-CVD (eight European countries) and European Prospective Investigation into Cancer and Nutrition-Netherlands (EPIC-NL) case-cohort studies. rs4988235, a lactase persistence (LP) SNP which enables digestion of lactose in adulthood was used as genetic instrument. Intake of milk was first regressed on rs4988235 in a linear regression model. Next, associations of genetically predicted milk consumption with stroke and CHD were estimated using Prentice-weighted Cox regression. Gene-outcome analysis included 777 024 participants (50 804 cases) from MEGASTROKE (including EPIC-CVD), UK Biobank and EPIC-NL for stroke, and 483 966 participants (61 612 cases) from CARDIoGRAM, UK Biobank, EPIC-CVD and EPIC-NL for CHD. In IV analyses, each additional LP allele was associated with a higher intake of milk in EPIC-CVD (ß = 13·7 g/d; 95 % CI 8·4, 19·1) and EPIC-NL (36·8 g/d; 95 % CI 20·0, 53·5). Genetically predicted milk intake was not associated with stroke (HR per 25 g/d 1·05; 95 % CI 0·94, 1·16) or CHD (1·02; 95 % CI 0·96, 1·08). In gene-outcome analyses, there was no association of rs4988235 with risk of stroke (OR 1·02; 95 % CI 0·99, 1·05) or CHD (OR 0·99; 95 % CI 0·95, 1·03). Current Mendelian randomisation analysis does not provide evidence for a causal inverse relationship between milk consumption and stroke or CHD risk.
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Enfermedades Cardiovasculares , Neoplasias , Accidente Cerebrovascular , Humanos , Adulto , Animales , Leche , Estudios Prospectivos , Factores de Riesgo , Enfermedades Cardiovasculares/complicaciones , Accidente Cerebrovascular/etiología , Neoplasias/complicaciones , Pueblo EuropeoRESUMEN
PURPOSE: Advanced glycation end products (AGEs) can be formed in foods by the reaction of reducing sugars with proteins, and have been shown to induce insulin resistance and obesity in experimental studies. We examined the association between dietary AGEs intake and changes in body weight in adults over an average of 5 years of follow-up. METHODS: A total of 255,170 participants aged 25-70 years were recruited in ten European countries (1992-2000) in the PANACEA study (Physical Activity, Nutrition, Alcohol, Cessation of smoking, Eating out of home in relation to Anthropometry), a sub-cohort of the EPIC (European Prospective Investigation into Cancer and Nutrition). Body weight was measured at recruitment and self-reported between 2 and 11 years later depending on the study center. A reference database for AGEs was used containing UPLC-MS/MS-measured Nε-(carboxymethyl)-lysine (CML), Nε-(1-carboxyethyl)-lysine (CEL), and Nδ-(5-hydro-5-methyl-4-imidazolon-2-yl)-ornithine (MG-H1) in 200 common European foods. This reference database was matched to foods and decomposed recipes obtained from country-specific validated dietary questionnaires in EPIC and intake levels of CEL, CML, and MG-H1 were estimated. Associations between dietary AGEs intake and body weight change were estimated separately for each of the three AGEs using multilevel mixed linear regression models with center as random effect and dietary AGEs intake and relevant confounders as fixed effects. RESULTS: A one-SD increment in CEL intake was associated with 0.111 kg (95% CI 0.087-0.135) additional weight gain over 5 years. The corresponding additional weight gain for CML and MG-H1 was 0.065 kg (0.041-0.089) and 0.034 kg (0.012, 0.057), respectively. The top six food groups contributing to AGEs intake, with varying proportions across the AGEs, were cereals/cereal products, meat/processed meat, cakes/biscuits, dairy, sugar and confectionary, and fish/shellfish. CONCLUSION: In this study of European adults, higher intakes of AGEs were associated with marginally greater weight gain over an average of 5 years of follow-up.
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Peso Corporal , Dieta , Productos Finales de Glicación Avanzada , Adulto , Cromatografía Liquida , Europa (Continente) , Humanos , Estudios Prospectivos , Espectrometría de Masas en TándemRESUMEN
BACKGROUND: Adiposity has been associated with elevated risk of urinary incontinence in epidemiological studies; however, the strength of the association has differed between studies. OBJECTIVES: To conduct a systematic literature review and dose-response meta-analysis of prospective studies on adiposity and risk of urinary incontinence. SEARCH STRATEGY: We searched PubMed and Embase databases up to 19 July 2017. SELECTION CRITERIA: Prospective cohort studies were included. DATA COLLECTION AND ANALYSIS: Data were extracted by one reviewer and checked for accuracy by a second reviewer. Summary relative risks (RRs) and 95% confidence intervals (CIs) were calculated using random effects models. MAIN RESULTS: Twenty-four prospective studies were included. The summary RR per 5 kg/m2 increment in body mass index (BMI) was 1.20 (95% CI 1.16-1.25, I2 = 62%, n = 11) for population-based studies and 1.19 (95% CI 1.08-1.30, I2 = 87.1%, n = 8) for pregnancy-based studies, 1.18 (95% CI 1.14-1.22, I2 = 0%, n = 2) per 10 cm increase in waist circumference and 1.34 (95% CI 1.11-1.62, I2 = 90%, n = 2) per 10 kg of weight gain. Although the test for nonlinearity was significant for BMI, P = 0.04, the association was approximately linear. For subtypes of urinary incontinence the summary RR per 5 BMI units was 1.45 (95% CI 1.25-1.68, I2 = 85%, n = 3) for frequent incontinence, 1.52 (95% CI 1.37-1.68, I2 = 34%, n = 4) for severe incontinence, 1.33 (95% CI 1.26-1.41, I2 = 0%, n = 8) for stress incontinence, 1.26 (95% CI 1.14-1.40, I2 = 70%, n = 7) for urge incontinence, and 1.52 (95% CI 1.36-1.69, I2 = 0%, n = 3) for mixed incontinence. CONCLUSION: These results suggest excess weight may increase risk of urinary incontinence. TWEETABLE ABSTRACT: Overweight and obesity increase the risk of urinary incontinence.
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Obesidad Abdominal/complicaciones , Incontinencia Urinaria/etiología , Índice de Masa Corporal , Femenino , Humanos , Estudios Prospectivos , Factores de Riesgo , Aumento de PesoRESUMEN
BACKGROUND: To summarise the evidence on the associations between body mass index (BMI) and BMI in early adulthood, height, waist circumference (WC) and waist-to-hip ratio (WHR), and risk of lympho-haematopoietic cancers. METHOD: We conducted a meta-analysis of prospective studies and identified relevant studies published up to December 2017 by searching PubMed. A random-effects model was used to calculate dose-response summary relative risks (RRs). RESULTS: Our findings showed BMI, and BMI in early adulthood (aged 18-21 years) is associated with the risk of Hodgkin's and non-Hodgkin's lymphoma (HL and NHL), diffuse large beta-cell lymphoma (DLBCL), Leukaemia including acute and chronic myeloid lymphoma (AML and CML), and chronic lymphocytic leukaemia (CLL) and multiple myeloma (MM). The summary RR per 5 kg/m2 increase in BMI were 1.12 [95% confidence interval (CI): 1.05-1.20] for HL, 1.05 (95% CI: 1.03-1.08) for NHL, 1.11 (95% CI: 1.05-1.16) for DLBCL, 1.06 (95% CI: 1.03-1.09) for ML, 1.09 (95% CI: 1.03-1.15) for leukaemia, 1.13 (95% CI: 1.04-1.24) for AML, 1.13 (95% CI: 1.05-1.22) for CML and 1.04 (95% CI: 1.00-1.09) for CLL, and were1.12 (95% CI: 1.05-1.19) for NHL, 1.22 (95% CI: 1.09-1.37) for DLBCL, and 1.19 (95% CI: 1.03-1.38) for FL for BMI in early adulthood analysis. Results on mortality showed a 15%, 16% and 17% increased risk of NHL, MM and leukaemia, respectively. Greater height increased the risk of NHL by 7%, DLBCL by 10%, FL by 9%, MM by 5% and Leukaemia by 7%. WHR was associated with increased risk of DLBCL by 12%. No association was found between higher WC and risk of MM. CONCLUSION: Our results revealed that general adiposity in adulthood and early adulthood, and greater height may increase the risk of almost all types of lympho-haematopoietic cancers and this adds to a growing body of evidence linking body fatness to several types of cancers.
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Tamaño Corporal , Leucemia/epidemiología , Linfoma/epidemiología , Mieloma Múltiple/epidemiología , Obesidad/epidemiología , Adiposidad , Índice de Masa Corporal , Humanos , Medición de Riesgo , Factores de RiesgoRESUMEN
BACKGROUND AND AIM: The strength of the association between diabetes and risk of heart failure has differed between previous studies and the available studies have not been summarized in a meta-analysis. We therefore quantified the association between diabetes and blood glucose and heart failure in a systematic review and meta-analysis. METHODS AND RESULTS: PubMed and Embase databases were searched up to May 3rd 2018. Prospective studies on diabetes mellitus or blood glucose and heart failure risk were included. A random effects model was used to calculate summary relative risks (RRs) and 95% confidence intervals (CIs). Seventy seven studies were included. Among the population-based prospective studies, the summary RR for individuals with diabetes vs. no diabetes was 2.06 (95% CIs: 1.73-2.46, I2 = 99.8%, n = 30 studies, 401495 cases, 21416780 participants). The summary RR was 1.23 (95% CI: 1.15-1.32, I2 = 78.2%, n = 10, 5344 cases, 91758 participants) per 20 mg/dl increase in blood glucose and there was evidence of a J-shaped association with nadir around 90 mg/dl and increased risk even within the pre-diabetic blood glucose range. Among the patient-based studies the summary RR was 1.69 (95% CI: 1.57-1.81, I2 = 85.5%, pheterogeneity<0.0001) for diabetes vs. no diabetes (n = 41, 100284 cases and >613925 participants) and 1.25 (95% CI: 0.89-1.75, I2 = 95.6%, pheterogeneity<0.0001) per 20 mg/dl increase in blood glucose (1016 cases, 34309 participants, n = 2). In the analyses of diabetes and heart failure there was low or no heterogeneity among the population-based studies that adjusted for alcohol intake and physical activity and among the patient-based studies there was no heterogeneity among studies with ≥10 years follow-up. CONCLUSIONS: These results suggest that individuals with diabetes are at an increased risk of developing heart failure and there is evidence of increased risk even within the pre-diabetic range of blood glucose.
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Glucemia/metabolismo , Diabetes Mellitus/sangre , Diabetes Mellitus/epidemiología , Insuficiencia Cardíaca/sangre , Insuficiencia Cardíaca/epidemiología , Biomarcadores/sangre , Diabetes Mellitus/diagnóstico , Diabetes Mellitus/terapia , Insuficiencia Cardíaca/diagnóstico , Insuficiencia Cardíaca/prevención & control , Humanos , Pronóstico , Estudios Prospectivos , Medición de Riesgo , Factores de RiesgoRESUMEN
BACKGROUND: Although diabetes mellitus is an established risk factor for myocardial infarction and stroke, data on the association with sudden cardiac death are less extensive and the findings have not been entirely consistent. We therefore conducted a systematic review and meta-analysis of prospective studies on diabetes mellitus and risk of sudden cardiac death. METHODS AND RESULTS: PubMed and Embase databases were searched up to July 18th 2017. Prospective studies that reported adjusted relative risk (RR) estimates and 95% confidence intervals (CIs) for the association between a diabetes diagnosis or pre-diabetes and risk of sudden cardiac death were included. Summary RRs were estimated by use of a random effects model. Nineteen population-based prospective studies (11 publications) (3610 cases, 249,225 participants) and 10 patient-based prospective studies (2713 cases, 55,098 participants) were included. The summary RR for diabetes patients vs. persons without diabetes was 2.02 (95% CI: 1.81-2.25, I2 = 0%, pheterogeneity = 0.91) in the population-based studies. The summary RR was 1.23 (95% CI: 1.05-1.44, I2 = 6%, pheterogeneity = 0.34) for the association between pre-diabetes and sudden cardiac death (n = 3 studies, 1000 sudden cardiac deaths, 18,360 participants). In the patient-based studies, the summary RR of sudden cardiac death for diabetes patients vs. patients without diabetes was 1.75 (95% CI: 1.51-2.03, I2 = 39%, pheterogeneity = 0.10) for all patients combined, 1.63 (95% CI: 1.36-1.97, I2 = 39%, n = 5) for coronary heart disease patients, and 1.85 (95% CI: 1.48-2.33, I2 = 0%, n = 3) for heart failure patients. CONCLUSIONS: These results suggest that diabetes patients are at an increased risk of sudden cardiac death both in the general population and among different patient groups.
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Muerte Súbita Cardíaca/epidemiología , Diabetes Mellitus/mortalidad , Adulto , Anciano , Diabetes Mellitus/diagnóstico , Medicina Basada en la Evidencia , Femenino , Humanos , Masculino , Persona de Mediana Edad , Pronóstico , Estudios Prospectivos , Medición de Riesgo , Factores de Riesgo , Adulto JovenRESUMEN
AIM: This systematic review and meta-analysis aimed to clarify whether tobacco smoking is associated with an increased risk of diverticular disease. METHOD: The PubMed and Embase databases were searched for studies of smoking and diverticular disease up to 19 February 2016. Prospective studies that reported adjusted relative risk (RR) estimates and 95% confidence intervals (CIs) of diverticular disease associated with current or previous smoking were included. Summary RRs were estimated using a random effects model. RESULTS: We identified five prospective studies which comprised 6076 cases of incident diverticular disease (diverticulosis and diverticulitis) among 385 291 participants and three studies with 1118 cases of complications related to diverticular disease (abscess or perforation) among 292 965. The summary RR for incident diverticular disease was 1.36 (95% CI 1.15-1.61, I2 = 84%, n = 4) for current smokers, 1.17 (95% CI 1.05-1.31, I2 = 49%, n = 4) for former smokers and 1.29 (95% CI 1.16-1.44, I2 = 62%, n = 5) for ever smokers. The summary RR was 1.11 (95% CI 0.99-1.25, I2 = 82%, n = 4) per 10 cigarettes per day. Although there was some indication of nonlinearity there was a dose-dependent positive association with increasing number of cigarettes smoked per day. There was some evidence that smoking also increases the risk of complications of diverticular disease, but the number of studies was small. CONCLUSION: The current meta-analysis provides evidence that tobacco smoking is associated with an increased incidence of diverticular disease and related complications.
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Enfermedades Diverticulares/etiología , Fumar Tabaco/efectos adversos , Adulto , Anciano , Anciano de 80 o más Años , Enfermedades Diverticulares/epidemiología , Diverticulitis/etiología , Divertículo/etiología , Femenino , Humanos , Incidencia , Masculino , Persona de Mediana Edad , Estudios Prospectivos , Factores de RiesgoRESUMEN
BACKGROUND AND AIM: Epidemiological studies have reported increased risk of cardiovascular disease, cancer and all-cause mortality with greater resting heart rate, however, the evidence is not consistent. Differences by gender, adjustment for confounding factors, as well as the potential impact of subclinical disease are not clear. A previous meta-analysis missed a large number of studies, and data for atrial fibrillation have not been summarized before. We therefore aimed to clarify these associations in a systematic review and meta-analysis of prospective studies. METHODS AND RESULTS: PubMed and Embase were searched up to 29 March 2017. Summary RRs and 95% confidence intervals (CIs) were calculated using random effects models. Eighty seven studies were included. The summary RR per 10 beats per minute increase in resting heart rate was 1.07 (95% CI: 1.05-1.10, I2 = 61.9%, n = 31) for coronary heart disease, 1.09 (95% CI: 1.00-1.18, I2 = 62.3%, n = 5) for sudden cardiac death, 1.18 (95% CI: 1.10-1.27, I2 = 74.5%, n = 8) for heart failure, 0.97 (95% CI: 0.92-1.02, I2 = 91.4%, n = 9) for atrial fibrillation, 1.06 (95% CI: 1.02-1.10, I2 = 59.5%, n = 16) for total stroke, 1.15 (95% CI: 1.11-1.18, I2 = 84.3%, n = 35) for cardiovascular disease, 1.14 (95% CI: 1.06-1.23, I2 = 90.2%, n = 12) for total cancer, and 1.17 (95% CI: 1.14-1.19, I2 = 94.0%, n = 48) for all-cause mortality. There was a positive dose-response relationship for all outcomes except for atrial fibrillation for which there was a J-shaped association. CONCLUSION: This meta-analysis found an increased risk of coronary heart disease, sudden cardiac death, heart failure, atrial fibrillation, stroke, cardiovascular disease, total cancer and all-cause mortality with greater resting heart rate.
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Enfermedades Cardiovasculares/mortalidad , Enfermedades Cardiovasculares/fisiopatología , Frecuencia Cardíaca , Neoplasias/mortalidad , Neoplasias/fisiopatología , Enfermedades Cardiovasculares/diagnóstico , Causas de Muerte , Humanos , Neoplasias/diagnóstico , Dinámicas no Lineales , Oportunidad Relativa , Pronóstico , Estudios Prospectivos , Medición de Riesgo , Factores de RiesgoRESUMEN
BACKGROUND: Physical activity has been inconsistently associated with risk of preterm birth, and the strength of the association and the shape of the dose-response relationship needs clarification. OBJECTIVES: To conduct a systematic review and dose-response meta-analysis to clarify the association between physical activity and risk of preterm birth. SEARCH STRATEGY: PubMed, Embase and Ovid databases were searched for relevant studies up to 9 February 2017. SELECTION CRITERIA: Studies with a prospective cohort, case-cohort, nested case-control or randomized study design were included. DATA COLLECTION AND ANALYSIS: Data were extracted by one reviewer and checked for accuracy by a second reviewer. Summary relative risks (RRs) were estimated using a random effects model. MAIN RESULTS: Forty-one studies (43 publications) including 20 randomized trials and 21 cohort studies were included. The summary RR for high versus low activity was 0.87 [95% confidence interval (CI): 0.70-1.06, I2 = 17%, n = 5] for physical activity before pregnancy, and it was 0.86 (95% CI: 0.78-0.95, I2 = 0%, n = 30) for early pregnancy physical activity. The summary RR for a 3 hours per week increment in leisure-time activity was 0.90 (95% CI: 0.85-0.95, I2 = 0%, n = 5). There was evidence of a nonlinear association between physical activity and preterm birth, Pnonlinearity < 0.0001, with the lowest risk observed at 2-4 hours per week of activity. CONCLUSION: This meta-analysis suggests that higher leisure-time activity is associated with reduced risk of preterm birth. Further randomized controlled trials with sufficient frequency and duration of activity to reduce the risk and with larger sample sizes are needed to conclusively demonstrate an association. TWEETABLE ABSTRACT: Physically active compared with inactive women have an 10-14% reduction in the risk of preterm birth.
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Ejercicio Físico/fisiología , Nacimiento Prematuro/etiología , Fenómenos Fisiologicos de la Nutrición Prenatal , Femenino , Humanos , Embarazo , Nacimiento Prematuro/epidemiología , Atención Prenatal/métodos , Factores de RiesgoRESUMEN
BACKGROUND: Colorectal adenomas are known as precursors for the majority of colorectal carcinomas. While weight gain during adulthood has been identified as a risk factor for colorectal cancer, the association is less clear for colorectal adenomas. We conducted a systematic review and meta-analysis to quantify the evidence on this association. METHODS: We searched Medline up to September 2016 to identify observational (prospective, cross-sectional and retrospective) studies on weight gain during adulthood and colorectal adenoma occurrence and recurrence. We conducted meta-analysis on high weight gain versus stable weight, linear and non-linear dose-response meta-analyses to analyze the association. Summary odds ratios (OR) and 95% confidence intervals (95% CI) were estimated using a random effects model. RESULTS: For colorectal adenoma occurrence, the summary OR was 1.39 (95% CI: 1.17-1.65; I2: 43%, N = 9 studies, cases = 5507) comparing high (midpoint: 17.4 kg) versus stable weight gain during adulthood and with each 5 kg weight gain the odds increased by 7% (2%-11%; I2: 65%, N = 7 studies). Although there was indication of non-linearity (Pnon-linearity < 0.001) there was an increased odds of colorectal adenoma throughout the whole range of weight gain. Three studies were identified investigating the association between weight gain and colorectal adenoma recurrence and data were limited to draw firm conclusions. CONCLUSIONS: Even a small amount of adult weight gain was related to a higher odds of colorectal adenoma occurrence. Our findings add to the benefits of weight control in adulthood regarding colorectal adenoma occurrence, which might be relevant for early prevention of colorectal cancer.
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Adenoma/fisiopatología , Neoplasias Colorrectales/fisiopatología , Aumento de Peso , Adulto , Femenino , Humanos , Masculino , Persona de Mediana EdadRESUMEN
BACKGROUND: Lung cancer is the most common cause of cancer death. Fruits and vegetables containing carotenoids and other antioxidants have been hypothesized to decrease lung cancer risk. As part of the World Cancer Research Fund International Continuous Update Project, we conducted a systematic review and meta-analysis of prospective studies. METHODS: We searched PubMed and several databases up to December 2014 for prospective studies. We conducted meta-analyses comparing the highest and lowest intakes and dose-response meta-analyses to estimate summary relative risks (RRs) and 95% confidence intervals (CIs), and examine possible non-linear associations. We combined results from the Pooling Project with the studies we identified to increase the statistical power of our analysis. RESULTS: When comparing the highest with the lowest intakes, the summary RR estimates were 0.86 [95% CI 0.78-0.94; n (studies) = 18] for fruits and vegetables, 0.92 (95% CI 0.87-0.97; n = 25) for vegetables and 0.82 (95% CI 0.76-0.89; n = 29) for fruits. The association with fruit and vegetable intake was marginally significant in current smokers and inverse but not significant in former or never smokers. Significant inverse dose-response associations were observed for each 100 g/day increase: for fruits and vegetables [RR: 0.96; 95% CI 0.94-0.98, I(2) = 64%, n = 14, N (cases) = 9609], vegetables (RR: 0.94; 95% CI 0.89-0.98, I(2) = 48%, n = 20, N = 12 563) and fruits (RR: 0.92; 95% CI 0.89-0.95, I(2) = 57%, n = 23, N = 14 506). Our results were consistent among the different types of fruits and vegetables. The strength of the association differed across locations. There was evidence of a non-linear relationship (P < 0.01) between fruit and vegetable intake and lung cancer risk showing that no further benefit is obtained when increasing consumption above â¼400 g per day. CONCLUSIONS: Eliminating tobacco smoking is the best strategy to prevent lung cancer. Although residual confounding by smoking cannot be ruled out, the current evidence from prospective studies is consistent with a protective role of fruit and vegetables in lung cancer aetiology.
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Frutas , Neoplasias Pulmonares/prevención & control , Verduras , Dieta , Humanos , Estudios Prospectivos , Factores de RiesgoRESUMEN
Evidence suggests that egg intake may be implicated in the aetiology of sex hormone-related cancers. However, dose-response relationships between egg intake and such cancers are unclear. Thus, we conducted a dose-response meta-analysis to summarise the dose-response relationships between egg consumption and the risk of breast, prostate and gynaecological cancers. A literature search was performed using PubMed and Embase up to April 2015 to identify relevant prospective observational studies. Summary relative risk (RR) and 95% CI were estimated using a random-effects model. For breast cancer, the linear dose-response meta-analysis found a non-significantly increased risk (RR for an increase of 5 eggs consumed/week: 1·05, 95% CI 0·99, 1·11, n 16,023 cases). Evidence for non-linearity was not statistically significant (P non-linearity= 0·50, n 15,415 cases) but consuming ≥ 5 eggs/week was significantly associated with an increased risk of breast cancer compared with no egg consumption, with the summary RR being 1·04 (95% CI 1·01, 1·07) for consuming 5 eggs/week and 1·09 (95% CI 1·03, 1·15) for consuming about 9 eggs/week. For other cancers investigated, the summary RR for an increase of 5 eggs consumed/week was 1·09 (95% CI 0·96, 1·24, n 2636 cases) for ovarian cancer; 1·47 (95% CI 1·01, 2·14, n 609 cases) for fatal prostate cancer, with evidence of small-study effects (P Egger= 0·04). No evidence was found for an association with the risk of total prostate cancer. While our conclusion was tempered by the potential for publication bias and confounding, high egg intake may be associated with a modestly elevated risk of breast cancer, and a positive association between egg intake and ovarian and fatal prostate cancers cannot be ruled out.
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Neoplasias de la Mama/epidemiología , Dieta , Huevos/efectos adversos , Neoplasias Ováricas/epidemiología , Neoplasias de la Próstata/epidemiología , Colesterol/efectos adversos , Colina/efectos adversos , Bases de Datos Factuales , Relación Dosis-Respuesta a Droga , Femenino , Humanos , Masculino , Estudios Observacionales como Asunto , Factores de RiesgoRESUMEN
BACKGROUND: High resting heart rate has been associated with increased risk of type 2 diabetes in several studies, but the available data are not consistent and it is unclear if there is a dose-response relationship between resting heart rate and type 2 diabetes risk. We aimed to clarify this association by conducting a systematic review and meta-analysis of published studies. METHODS AND RESULTS: PubMed, Embase and Ovid Medline databases were searched for prospective studies published up until October 11th, 2013. Summary relative risks were estimated using a random effects model. Ten cohort studies with >5628 cases and 119,915 participants were included. The summary RR for high vs. low resting heart rate was 1.83 (95% CI: 1.28-2.60, I(2) = 88%, n = 7), and in the dose-response analysis the summary RR was 1.20 (95% CI: 1.07-1.34, I(2) = 93%, n = 9) for an increase of 10 beats per minute. The heterogeneity was to a large degree explained by two studies. There was evidence of nonlinear associations between resting heart rate (pnonlinearity < 0.0001) and risk of type 2 diabetes. CONCLUSION: The current meta-analysis indicates a strong positive association between high resting heart rate and the risk of type 2 diabetes. As a non-invasive marker of type 2 diabetes risk, resting heart rate may have potential in the clinical setting, especially for interventions aimed at lowering the risk of type 2 diabetes. Additional studies are needed to clarify the mechanisms that may be responsible for the assoiation between resting heart rate and type 2 diabetes.
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Diabetes Mellitus Tipo 2/etiología , Frecuencia Cardíaca , Descanso , Diabetes Mellitus Tipo 2/diagnóstico , Diabetes Mellitus Tipo 2/fisiopatología , Humanos , Dinámicas no Lineales , Valor Predictivo de las Pruebas , Pronóstico , Medición de Riesgo , Factores de RiesgoRESUMEN
BACKGROUND: Greater body mass index (BMI) has been convincingly related to increased endometrial cancer risk, however, whether adiposity earlier in life or abdominal fatness is an independent risk factor and whether weight gain or greater height increases the risk is not clear. METHODS: As part of the Continuous Update Project of the World Cancer Research Fund International, we conducted a systematic review and meta-analysis of prospective studies of the association between anthropometric measures and endometrial cancer risk and searched PubMed and several other databases up to February 2015. Summary relative risks (RRs) were calculated using a random-effects model. RESULTS: Thirty prospective studies of BMI and endometrial cancer risk with 22 320 cases among 6 445 402 participants were included. The summary RR for a 5-unit increment was 1.54 [95% confidence interval (CI) 1.47-1.61, I(2) = 81%]. Although the test for non-linearity was significant, Pnon-linearity < 0.0001, and the curve was steeper within the overweight and obese BMI ranges, there was evidence of increased risk even within the high normal BMI range. The summary RR was 1.45 (95% CI 1.28-1.64, I(2) = 76%) per 5 BMI units for BMI in young adulthood, 1.18 (95% CI 1.14-1.23, I(2) = 67%) per 5 kg increase of weight, and 1.16 (95% CI 1.12-1.20, I(2) = 51%) per 5 kg of weight gained between young adulthood and study baseline, 1.27 (95% CI 1.17-1.39, I(2) = 71%) per 10 cm increase in waist circumference, 1.21 (95% CI 1.13-1.29, I(2) = 0%) per 0.1-unit increment in waist-to-hip ratio and 1.30 (95% CI 1.19-1.41, I(2) = 0%) per 10-cm increase in hips circumference. The summary RR was 1.15 (95% CI 1.09-1.22, I(2) = 61%) for a 10-cm increase in height. CONCLUSIONS: All measures of adiposity were associated with increased risk of endometrial cancer, and in addition increasing height was associated with increased risk.
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Neoplasias Endometriales/epidemiología , Obesidad Abdominal/epidemiología , Circunferencia de la Cintura , Relación Cintura-Cadera , Antropometría , Índice de Masa Corporal , Femenino , Humanos , Obesidad/epidemiología , Sobrepeso/epidemiología , Factores de Riesgo , Índice de Severidad de la Enfermedad , Factores de TiempoRESUMEN
BACKGROUND: Positive association between obesity and survival after breast cancer was demonstrated in previous meta-analyses of published data, but only the results for the comparison of obese versus non-obese was summarised. METHODS: We systematically searched in MEDLINE and EMBASE for follow-up studies of breast cancer survivors with body mass index (BMI) before and after diagnosis, and total and cause-specific mortality until June 2013, as part of the World Cancer Research Fund Continuous Update Project. Random-effects meta-analyses were conducted to explore the magnitude and the shape of the associations. RESULTS: Eighty-two studies, including 213 075 breast cancer survivors with 41 477 deaths (23 182 from breast cancer) were identified. For BMI before diagnosis, compared with normal weight women, the summary relative risks (RRs) of total mortality were 1.41 [95% confidence interval (CI) 1.29-1.53] for obese (BMI >30.0), 1.07 (95 CI 1.02-1.12) for overweight (BMI 25.0-<30.0) and 1.10 (95% CI 0.92-1.31) for underweight (BMI <18.5) women. For obese women, the summary RRs were 1.75 (95% CI 1.26-2.41) for pre-menopausal and 1.34 (95% CI 1.18-1.53) for post-menopausal breast cancer. For each 5 kg/m(2) increment of BMI before, <12 months after, and ≥12 months after diagnosis, increased risks of 17%, 11%, and 8% for total mortality, and 18%, 14%, and 29% for breast cancer mortality were observed, respectively. CONCLUSIONS: Obesity is associated with poorer overall and breast cancer survival in pre- and post-menopausal breast cancer, regardless of when BMI is ascertained. Being overweight is also related to a higher risk of mortality. Randomised clinical trials are needed to test interventions for weight loss and maintenance on survival in women with breast cancer.
Asunto(s)
Índice de Masa Corporal , Neoplasias de la Mama/epidemiología , Obesidad/epidemiología , Neoplasias de la Mama/patología , Femenino , Estudios de Seguimiento , Humanos , MEDLINE , Obesidad/complicaciones , Pronóstico , Ensayos Clínicos Controlados Aleatorios como Asunto , Factores de Riesgo , SobrevivientesRESUMEN
BACKGROUND AND AIMS: Breastfeeding has been associated with reduced risk of maternal type 2 diabetes in some cohort studies, but the evidence from published studies have differed with regard to the strength of the association. To clarify this association we conducted a systematic review and dose-response meta-analysis of breastfeeding and maternal risk of type 2 diabetes. METHODS AND RESULTS: We conducted a systematic review and dose-response meta-analysis of prospective studies of breastfeeding and maternal risk of type 2 diabetes. We searched the PubMed, Embase and Ovid databases up to September 19th 2013. Summary relative risks were estimated using a random effects model. Six cohort studies including 10,842 cases among 273,961 participants were included in the meta-analysis. The summary RR for the highest duration of breastfeeding vs. the lowest was 0.68 (95% CI: 0.57-0.82, I(2) = 75%, p heterogeneity = 0.001, n = 6). The summary RR for a three month increase in the duration of breastfeeding per child was 0.89 (95% CI: 0.77-1.04, I(2) = 93%, p heterogeneity < 0.0001, n = 3) and the summary RR for a one year increase in the total duration of breastfeeding was 0.91 (95% CI: 0.86-0.96, I(2) = 81%, p heterogeneity = 0.001, n = 4). There was little difference in the summary estimates whether or not BMI had been adjusted for. The inverse associations appeared to be nonlinear, p nonlinearity < 0.0001 for both analyses, and in both analyses the reduction in risk was steeper when increasing breastfeeding from low levels. CONCLUSION: This meta-analysis suggests that there is a statistically significant inverse association between breastfeeding and maternal risk of type 2 diabetes.
Asunto(s)
Lactancia Materna , Diabetes Mellitus Tipo 2/epidemiología , Femenino , Humanos , Embarazo , Factores de RiesgoRESUMEN
Evidence for an association between fruit and vegetable intake and breast cancer risk is inconclusive. To clarify the association, we conducted a systematic review and meta-analysis of the evidence from prospective studies. We searched PubMed for prospective studies of fruit and vegetable intake and breast cancer risk until April 30, 2011. We included fifteen prospective studies that reported relative risk estimates and 95 % confidence intervals (CIs) of breast cancer associated with fruit and vegetable intake. Random effects models were used to estimate summary relative risks. The summary relative risk (RR) for the highest versus the lowest intake was 0.89 (95 % CI: 0.80-0.99, I (2) = 0 %) for fruits and vegetables combined, 0.92 (95 % CI: 0.86-0.98, I (2) = 9 %) for fruits, and 0.99 (95 % CI: 0.92-1.06, I (2) = 20 %) for vegetables. In dose-response analyses, the summary RR per 200 g/day was 0.96 (95 % CI: 0.93-1.00, I (2) = 2 %) for fruits and vegetables combined, 0.94 (95 % CI: 0.89-1.00, I (2) = 39 %) for fruits, and 1.00 (95 % CI: 0.95-1.06, I (2) = 17 %) for vegetables. In this meta-analysis of prospective studies, high intake of fruits, and fruits and vegetables combined, but not vegetables, is associated with a weak reduction in risk of breast cancer.
Asunto(s)
Neoplasias de la Mama/epidemiología , Frutas , Verduras , Neoplasias de la Mama/etiología , Dieta , Femenino , Frutas/efectos adversos , Humanos , Estudios Prospectivos , Factores de Riesgo , Verduras/efectos adversosRESUMEN
BACKGROUND: Dietary carbohydrates, glycemic load and glycemic index have been hypothesized to influence pancreatic cancer risk, but epidemiological studies have been inconsistent. We conducted a systematic review and meta-analysis of prospective studies to clarify these results. METHODS: PubMed and several other databases were searched for prospective studies of intake of carbohydrates, glycemic index and glycemic load and pancreatic cancer up to September 2011. Summary relative risks were estimated using a random effects model. RESULTS: Ten cohort studies (13 publications) were included in the meta-analysis. The summary relative risk (RR) per 10 glycemic index units was 1.02 [95% confidence interval (CI): 0.93-1.12, I(2) = 0%], per 50 glycemic load units was 1.03 (95% CI: 0.93-1.14, I(2) = 10%), per 100 g/day of total carbohydrates was 0.97 (95% CI: 0.81-1.16, I(2) = 35%), and per 25 g/day of sucrose intake was 1.05 (95% CI: 0.85-1.23, I(2) = 53%). A positive association was observed with fructose intake, summary RR = 1.22 (95% CI: 1.08-1.37, I(2) = 0%) per 25 g/day. CONCLUSIONS: This meta-analysis does not support an association between diets high in glycemic index, glycemic load, total carbohydrates or sucrose and pancreatic cancer risk. The finding of an increased risk with fructose intake warrants further investigation in studies with better adjustment for confounding and in non-American populations.