Your browser doesn't support javascript.
Mostrar: 20 | 50 | 100
Resultados 1 - 16 de 16
Filtrar
Mais filtros










Intervalo de ano de publicação
1.
PLoS Med ; 16(8): e1002893, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31390370

RESUMO

BACKGROUND: Various risk factors have been associated with epithelial ovarian cancer risk in observational epidemiological studies. However, the causal nature of the risk factors reported, and thus their suitability as effective intervention targets, is unclear given the susceptibility of conventional observational designs to residual confounding and reverse causation. Mendelian randomization (MR) uses genetic variants as proxies for risk factors to strengthen causal inference in observational studies. We used MR to evaluate the association of 12 previously reported risk factors (reproductive, anthropometric, clinical, lifestyle, and molecular factors) with risk of invasive epithelial ovarian cancer, invasive epithelial ovarian cancer histotypes, and low malignant potential tumours. METHODS AND FINDINGS: Genetic instruments to proxy 12 risk factors were constructed by identifying single nucleotide polymorphisms (SNPs) that were robustly (P < 5 × 10-8) and independently associated with each respective risk factor in previously reported genome-wide association studies. These risk factors included genetic liability to 3 factors (endometriosis, polycystic ovary syndrome, type 2 diabetes) scaled to reflect a 50% higher odds liability to disease. We obtained summary statistics for the association of these SNPs with risk of overall and histotype-specific invasive epithelial ovarian cancer (22,406 cases; 40,941 controls) and low malignant potential tumours (3,103 cases; 40,941 controls) from the Ovarian Cancer Association Consortium (OCAC). The OCAC dataset comprises 63 genotyping project/case-control sets with participants of European ancestry recruited from 14 countries (US, Australia, Belarus, Germany, Belgium, Denmark, Finland, Norway, Canada, Poland, UK, Spain, Netherlands, and Sweden). SNPs were combined into multi-allelic inverse-variance-weighted fixed or random effects models to generate effect estimates and 95% confidence intervals (CIs). Three complementary sensitivity analyses were performed to examine violations of MR assumptions: MR-Egger regression and weighted median and mode estimators. A Bonferroni-corrected P value threshold was used to establish strong evidence (P < 0.0042) and suggestive evidence (0.0042 < P < 0.05) for associations. In MR analyses, there was strong or suggestive evidence that 2 of the 12 risk factors were associated with invasive epithelial ovarian cancer and 8 of the 12 were associated with 1 or more invasive epithelial ovarian cancer histotypes. There was strong evidence that genetic liability to endometriosis was associated with an increased risk of invasive epithelial ovarian cancer (odds ratio [OR] per 50% higher odds liability: 1.10, 95% CI 1.06-1.15; P = 6.94 × 10-7) and suggestive evidence that lifetime smoking exposure was associated with an increased risk of invasive epithelial ovarian cancer (OR per unit increase in smoking score: 1.36, 95% CI 1.04-1.78; P = 0.02). In analyses examining histotypes and low malignant potential tumours, the strongest associations found were between height and clear cell carcinoma (OR per SD increase: 1.36, 95% CI 1.15-1.61; P = 0.0003); age at natural menopause and endometrioid carcinoma (OR per year later onset: 1.09, 95% CI 1.02-1.16; P = 0.007); and genetic liability to polycystic ovary syndrome and endometrioid carcinoma (OR per 50% higher odds liability: 0.89, 95% CI 0.82-0.96; P = 0.002). There was little evidence for an association of genetic liability to type 2 diabetes, parity, or circulating levels of 25-hydroxyvitamin D and sex hormone binding globulin with ovarian cancer or its subtypes. The primary limitations of this analysis include the modest statistical power for analyses of risk factors in relation to some less common ovarian cancer histotypes (low grade serous, mucinous, and clear cell carcinomas), the inability to directly examine the association of some ovarian cancer risk factors that did not have robust genetic variants available to serve as proxies (e.g., oral contraceptive use, hormone replacement therapy), and the assumption of linear relationships between risk factors and ovarian cancer risk. CONCLUSIONS: Our comprehensive examination of possible aetiological drivers of ovarian carcinogenesis using germline genetic variants to proxy risk factors supports a role for few of these factors in invasive epithelial ovarian cancer overall and suggests distinct aetiologies across histotypes. The identification of novel risk factors remains an important priority for the prevention of epithelial ovarian cancer.

2.
Thorax ; 74(7): 633-642, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-30936389

RESUMO

INTRODUCTION: Males have a higher prevalence of asthma in childhood, whereas females have a higher prevalence in adolescence and adulthood. The 'adolescent switch' observed between sexes during puberty has been hypothesised to be due to fluctuating sex hormones. Robust evidence of the involvement of sex hormones in asthma could lead to development of therapeutic interventions. METHODS: We combine observational evidence using longitudinal data on sex hormone-binding globulin (SHBG), total and bioavailable testosterone and asthma from a subset of males (n=512) in the Avon Longitudinal Study of Parents and Children, and genetic evidence of SHBG and asthma using two-sample Mendelian randomisation (MR), a method of causal inference. We meta-analysed two-sample MR results across two large data sets, the Trans-National Asthma Genetics Consortium genome-wide association study of asthma and UK Biobank (over 460 000 individuals combined). RESULTS: Observational evidence indicated weak evidence of a protective effect of increased circulating testosterone on asthma in males in adolescence, but no strong pattern of association with SHBG. Genetic evidence using two-sample MR indicated a protective effect of increased SHBG, with an OR for asthma of 0.86 (95% CI 0.74 to 1.00) for the inverse-variance weighted approach and an OR of 0.83 (95% CI 0.72 to 0.96) for the weighted median estimator, per unit increase in natural log SHBG. A sex-stratified sensitivity analysis suggested the protective effect of SHBG was mostly evident in females. CONCLUSION: We report the first suggestive evidence of a protective effect of genetically elevated SHBG on asthma, which may provide a biological explanation behind the observed asthma sex discordance. Further work is required to disentangle the downstream effects of SHBG on asthma and the molecular pathways involved.

4.
Cancer Causes Control ; 29(11): 1073-1080, 2018 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-30306355

RESUMO

PURPOSE: Observational studies suggest that dietary and serum calcium are risk factors for prostate cancer. However, such studies suffer from residual confounding (due to unmeasured or imprecisely measured confounders), undermining causal inference. Mendelian randomization uses randomly assigned (hence unconfounded and pre-disease onset) germline genetic variation to proxy for phenotypes and strengthen causal inference in observational studies. We tested the hypothesis that serum calcium is associated with an increased risk of overall and advanced prostate cancer. METHODS: A genetic instrument was constructed using five single-nucleotide polymorphisms robustly associated with serum calcium in a genome-wide association study (n ≤ 61,079). This instrument was then used to test the effect of a 0.5 mg/dL increase (1 standard deviation, SD) in serum calcium on risk of prostate cancer in 72,729 men in the PRACTICAL (Prostate Cancer Association Group to Investigate Cancer Associated Alterations in the Genome) Consortium (44,825 cases, 27,904 controls) and risk of advanced prostate cancer in 33,498 men (6,263 cases, 27,235 controls). RESULTS: We found weak evidence for a protective effect of serum calcium on prostate cancer risk (odds ratio [OR] per 0.5 mg/dL increase in calcium: 0.83, 95% CI 0.63-1.08; p = 0.12). We did not find strong evidence for an effect of serum calcium on advanced prostate cancer (OR per 0.5 mg/dL increase in calcium: 0.98, 95% CI 0.57-1.70; p = 0.93). CONCLUSIONS: Our Mendelian randomization analysis does not support the hypothesis that serum calcium increases risk of overall or advanced prostate cancer.


Assuntos
Cálcio na Dieta/sangue , Cálcio/sangue , Análise da Randomização Mendeliana , Neoplasias da Próstata/sangue , Neoplasias da Próstata/epidemiologia , Cálcio na Dieta/efeitos adversos , Variação Genética , Estudo de Associação Genômica Ampla , Humanos , Masculino , Razão de Chances , Fenótipo , Polimorfismo de Nucleotídeo Único , Neoplasias da Próstata/etiologia , Neoplasias da Próstata/genética , Fatores de Risco
5.
Cancer Epidemiol Biomarkers Prev ; 27(9): 995-1010, 2018 09.
Artigo em Inglês | MEDLINE | ID: mdl-29941659

RESUMO

Observational epidemiologic studies are prone to confounding, measurement error, and reverse causation, undermining robust causal inference. Mendelian randomization (MR) uses genetic variants to proxy modifiable exposures to generate more reliable estimates of the causal effects of these exposures on diseases and their outcomes. MR has seen widespread adoption within cardio-metabolic epidemiology, but also holds much promise for identifying possible interventions for cancer prevention and treatment. However, some methodologic challenges in the implementation of MR are particularly pertinent when applying this method to cancer etiology and prognosis, including reverse causation arising from disease latency and selection bias in studies of cancer progression. These issues must be carefully considered to ensure appropriate design, analysis, and interpretation of such studies. In this review, we provide an overview of the key principles and assumptions of MR, focusing on applications of this method to the study of cancer etiology and prognosis. We summarize recent studies in the cancer literature that have adopted a MR framework to highlight strengths of this approach compared with conventional epidemiological studies. Finally, limitations of MR and recent methodologic developments to address them are discussed, along with the translational opportunities they present to inform public health and clinical interventions in cancer. Cancer Epidemiol Biomarkers Prev; 27(9); 995-1010. ©2018 AACR.


Assuntos
Análise da Randomização Mendeliana/métodos , Neoplasias/epidemiologia , Neoplasias/genética , Causalidade , Estudos Epidemiológicos , Humanos , Prognóstico
6.
J Natl Cancer Inst ; 110(9): 1035-1038, 2018 09 01.
Artigo em Inglês | MEDLINE | ID: mdl-29788239

RESUMO

In the Selenium and Vitamin E Cancer Prevention Trial (SELECT), selenium supplementation (causing a median 114 µg/L increase in circulating selenium) did not lower overall prostate cancer risk, but increased risk of high-grade prostate cancer and type 2 diabetes. Mendelian randomization analysis uses genetic variants to proxy modifiable risk factors and can strengthen causal inference in observational studies. We constructed a genetic instrument comprising 11 single nucleotide polymorphisms robustly (P < 5 × 10-8) associated with circulating selenium in genome-wide association studies. In a Mendelian randomization analysis of 72 729 men in the PRACTICAL Consortium (44 825 case subjects, 27 904 control subjects), 114 µg/L higher genetically elevated circulating selenium was not associated with prostate cancer (odds ratio [OR] = 1.01, 95% confidence interval [CI] = 0.89 to 1.13). In concordance with findings from SELECT, selenium was weakly associated with advanced (including high-grade) prostate cancer (OR = 1.21, 95% CI = 0.98 to 1.49) and type 2 diabetes (OR = 1.18, 95% CI = 0.97 to 1.43; in a type 2 diabetes genome-wide association study meta-analysis with up to 49 266 case subjects and 249 906 control subjects). Our Mendelian randomization analyses do not support a role for selenium supplementation in prostate cancer prevention and suggest that supplementation could have adverse effects on risks of advanced prostate cancer and type 2 diabetes.


Assuntos
Neoplasias da Próstata/epidemiologia , Neoplasias da Próstata/etiologia , Selênio/efeitos adversos , Diabetes Mellitus Tipo 2/epidemiologia , Diabetes Mellitus Tipo 2/etiologia , Predisposição Genética para Doença , Humanos , Masculino , Análise da Randomização Mendeliana , Razão de Chances , Polimorfismo de Nucleotídeo Único , Neoplasias da Próstata/patologia , Medição de Risco , Fatores de Risco , Selênio/sangue
7.
Elife ; 72018 05 30.
Artigo em Inglês | MEDLINE | ID: mdl-29846171

RESUMO

Results from genome-wide association studies (GWAS) can be used to infer causal relationships between phenotypes, using a strategy known as 2-sample Mendelian randomization (2SMR) and bypassing the need for individual-level data. However, 2SMR methods are evolving rapidly and GWAS results are often insufficiently curated, undermining efficient implementation of the approach. We therefore developed MR-Base (http://www.mrbase.org): a platform that integrates a curated database of complete GWAS results (no restrictions according to statistical significance) with an application programming interface, web app and R packages that automate 2SMR. The software includes several sensitivity analyses for assessing the impact of horizontal pleiotropy and other violations of assumptions. The database currently comprises 11 billion single nucleotide polymorphism-trait associations from 1673 GWAS and is updated on a regular basis. Integrating data with software ensures more rigorous application of hypothesis-driven analyses and allows millions of potential causal relationships to be efficiently evaluated in phenome-wide association studies.


Assuntos
Análise da Randomização Mendeliana , LDL-Colesterol/metabolismo , Doença das Coronárias/etiologia , Bases de Dados Genéticas , Pleiotropia Genética , Estudo de Associação Genômica Ampla , Humanos , Modelos Genéticos , Fenótipo , Polimorfismo de Nucleotídeo Único/genética
8.
Sao Paulo Med J ; 135(3): 266-269, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-28746662

RESUMO

CONTEXT AND OBJECTIVE:: It has been reported that earlier age at first childbirth may increase the risk of adult-onset diabetes among postmenopausal women, a novel finding with important public health implications. To date, however, no known studies have attempted to replicate this finding. We aimed to test the hypothesis that age at first childbirth is associated with the risk of adult-onset diabetes among postmenopausal women. DESIGN AND SETTING:: Cross-sectional analysis using baseline data from 2919 middle-aged and elderly postmenopausal women in the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil). METHODS:: Age at first childbirth was determined from self-reporting and newly diagnosed diabetes through a 2-hour 75-g oral glucose tolerance test and/or glycated hemoglobin. Logistic regression was performed to examine associations between age at first childbirth and newly diagnosed diabetes among postmenopausal women. RESULTS:: We did not find any association between age at first childbirth and diabetes, either when minimally adjusted for age, race and study center (odds ratio, OR [95% confidence interval, CI]: ≤ 19 years: 1.15 [0.82-1.59], 20-24 years: 0.90 [0.66-1.23] and ≥ 30 years: 0.86 [0.63-1.17] versus 25-29 years; P = 0.36) or when fully adjusted for childhood and adult factors (OR [95% CI]: ≤ 19 years: 0.95 [0.67-1.34], 20-24 years: 0.78 [0.56-1.07] and ≥ 30 years: 0.84 [0.61-1.16] versus 25-29 years; P = 0.40). CONCLUSION:: Our current analysis does not support the existence of an association between age at first childbirth and adult-onset diabetes among postmenopausal women, which had been reported previously.


Assuntos
Diabetes Mellitus/fisiopatologia , Idade Materna , Pós-Menopausa/fisiologia , Adulto , Idade de Início , Idoso , Glicemia/análise , Brasil , Estudos Transversais , Diabetes Mellitus/diagnóstico , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Razão de Chances , Estudos Prospectivos , Fatores de Risco , Estatísticas não Paramétricas , Fatores de Tempo
9.
Säo Paulo med. j ; 135(3): 266-269, May-June 2017. tab
Artigo em Inglês | LILACS-Express | ID: biblio-1043427

RESUMO

ABSTRACT CONTEXT AND OBJECTIVE: It has been reported that earlier age at first childbirth may increase the risk of adult-onset diabetes among postmenopausal women, a novel finding with important public health implications. To date, however, no known studies have attempted to replicate this finding. We aimed to test the hypothesis that age at first childbirth is associated with the risk of adult-onset diabetes among postmenopausal women. DESIGN AND SETTING: Cross-sectional analysis using baseline data from 2919 middle-aged and elderly postmenopausal women in the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil). METHODS: Age at first childbirth was determined from self-reporting and newly diagnosed diabetes through a 2-hour 75-g oral glucose tolerance test and/or glycated hemoglobin. Logistic regression was performed to examine associations between age at first childbirth and newly diagnosed diabetes among postmenopausal women. RESULTS: We did not find any association between age at first childbirth and diabetes, either when minimally adjusted for age, race and study center (odds ratio, OR [95% confidence interval, CI]: ≤ 19 years: 1.15 [0.82-1.59], 20-24 years: 0.90 [0.66-1.23] and ≥ 30 years: 0.86 [0.63-1.17] versus 25-29 years; P = 0.36) or when fully adjusted for childhood and adult factors (OR [95% CI]: ≤ 19 years: 0.95 [0.67-1.34], 20-24 years: 0.78 [0.56-1.07] and ≥ 30 years: 0.84 [0.61-1.16] versus 25-29 years; P = 0.40). CONCLUSION: Our current analysis does not support the existence of an association between age at first childbirth and adult-onset diabetes among postmenopausal women, which had been reported previously.


RESUMO CONTEXTO E OBJETIVO: Foi relatado que idade mais precoce no primeiro parto pode aumentar o risco do diabetes de início adulto entre mulheres na menopausa, um novo achado com implicações de saúde pública importantes. Até então, no entanto, nenhum estudo conhecido tentou replicar esta descoberta. Objetivou-se testar a hipótese de que a idade no primeiro parto está associada ao risco de diabetes de início na vida adulta em mulheres pós-menopáusicas. DESENHO DE ESTUDO E LOCAL: Análise transversal utilizando dados de base de 2.919 mulheres pós-menopáusicas de meia-idade e idosas no Estudo Longitudinal de Saúde do Adulto (ELSA-Brasil). MÉTODOS: A idade no primeiro parto foi determinada por autorrelato e diabetes recentemente diagnosticado por um teste de tolerância à glicose oral de 2 horas com 75 g e/ou hemoglobina glicada. A regressão logística foi realizada para examinar associações entre idade no primeiro parto e diabetes recentemente diagnosticada entre mulheres pós-menopáusicas. RESULTADOS: Não encontramos associação entre idade no primeiro parto e diabetes, quando ajustados minimamente para idade, raça e centro de estudo (odds ratio, OR [intervalo de confiança, IC 95%]: ≤ 19 anos: 1,15 [0,82-1,59], 20-24 anos: 0,90 [0,66-1,23], ≥ 30 anos: 0,86 [0,63-1,17] versus 25-29 anos, P = 0,36) ou quando totalmente ajustados para fatores infantis e adultos (OR [IC 95%]: ≤ 19 anos: 0,95 [0,67-1,34], 20-24 anos: 0,78 [0,56-1,07], ≥ 30 anos: 0,84 [0,61-1,16] versus 25-29 anos, P = 0,40). CONCLUSÃO: Nossa análise atual não apoia uma associação entre a idade no primeiro parto e o diabetes de início na vida adulta entre mulheres pós-menopáusicas, como relatado anteriormente.

11.
Sci Rep ; 6: 37032, 2016 11 15.
Artigo em Inglês | MEDLINE | ID: mdl-27845438

RESUMO

Emerging evidence suggests sex differences in the early origins of adult metabolic disease, but this has been little investigated in developing countries. We investigated sex-specific associations between low birth weight (LBW; <2.5 kg) and adult-onset diabetes in 12,525 participants from the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil). Diabetes was defined by self-reported information and laboratory measurements. In confounder-adjusted analyses, LBW (vs. 2.5-4 kg) was associated with higher prevalence of diabetes in women (Prevalence Ratio (PR) 1.54, 95% CI: 1.32-1.79), not in men (PR 1.06, 95% CI: 0.91-1.25; Pheterogeneity = 0.003). The association was stronger among participants with maternal diabetes (PR 1.60, 95% CI: 1.35-1.91), than those without (PR 1.15, 95% CI: 0.99-1.32; Pheterogeneity = 0.03). When jointly stratified by sex and maternal diabetes, the association was observed for women with (PR 1.77, 95% CI: 1.37-2.29) and without (PR 1.45, 95% CI: 1.20-1.75) maternal diabetes. In contrast, in men, LBW was associated with diabetes in participants with maternal diabetes (PR 1.45, 95% CI: 1.15-1.83), but not in those without (PR 0.92, 95% CI: 0.74-1.14). These sex-specific findings extended to continuous measures of glucose homeostasis. LBW was associated with higher diabetes prevalence in Brazilian women, and in men with maternal diabetes, suggesting sex-specific intrauterine effects on adult metabolic health.


Assuntos
Glicemia/metabolismo , Diabetes Mellitus/sangue , Diabetes Mellitus/epidemiologia , Homeostase , Recém-Nascido de Baixo Peso/sangue , Caracteres Sexuais , Adulto , Idade de Início , Idoso , Brasil/epidemiologia , Feminino , Humanos , Recém-Nascido , Estudos Longitudinais , Masculino , Pessoa de Meia-Idade , Prevalência
12.
Sci Rep ; 6: 17714, 2016 Jan 27.
Artigo em Inglês | MEDLINE | ID: mdl-26813008

RESUMO

An emerging body of evidence has implicated plasminogen activator inhibitor-1 (PAI-1) in the development of type 2 diabetes (T2D), though findings have not always been consistent. We systematically reviewed epidemiological studies examining the association of PAI-1 with T2D. EMBASE, PubMed, Web of Science, and the Cochrane Library were searched to identify studies for inclusion. Fifty-two studies (44 cross-sectional with 47 unique analytical comparisons and 8 prospective) were included. In pooled random-effects analyses of prospective studies, a comparison of the top third vs. bottom third of baseline PAI-1 values generated a RR of T2D of 1.67 (95% CI 1.28-2.18) with moderate heterogeneity (I(2) = 38%). Additionally, of 47 cross-sectional comparisons, 34(72%) reported significantly elevated PAI-1 among diabetes cases versus controls, 2(4%) reported significantly elevated PAI-1 among controls, and 11(24%) reported null effects. Results from pooled analyses of prospective studies did not differ substantially by study design, length of follow-up, adjustment for various putative confounding factors, or study quality, and were robust to sensitivity analyses. Findings from this systematic review of the available epidemiological literature support a link between PAI-1 and T2D, independent of established diabetes risk factors. Given the moderate size of the association and heterogeneity across studies, future prospective studies are warranted.


Assuntos
Diabetes Mellitus Tipo 2/etiologia , Diabetes Mellitus Tipo 2/metabolismo , Inibidor 1 de Ativador de Plasminogênio/metabolismo , Estudos Transversais , Diabetes Mellitus Tipo 2/epidemiologia , Humanos , Razão de Chances , Estudos Prospectivos
13.
J Nutr ; 146(2): 290-7, 2016 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-26661840

RESUMO

BACKGROUND: Recent animal studies suggest that artificially sweetened beverage (ASB) consumption increases diabetes risk. OBJECTIVE: We examined the relation of ASB intake with newly diagnosed diabetes and measures of glucose homeostasis in a large Brazilian cohort of adults. METHODS: We used cross-sectional data from 12,884 participants from the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil). ASB use was assessed by questionnaire and newly diagnosed diabetes by a 2-h 75-g oral glucose tolerance test and/or glycated hemoglobin. Logistic and linear regression analyses were performed to examine the association of ASB consumption with diabetes and continuous measures of glucose homeostasis, respectively. RESULTS: Although ASB consumption was not associated with diabetes in logistic regression analyses after adjustment for body mass index (BMI; in kg/m(2)) overall, the association varied across BMI categories (P-interaction = 0.04). Among those with a BMI <25, we found a 15% increase in the adjusted odds of diabetes for each increase in the frequency of ASB consumption per day (P = 0.001); compared with nonusers, ASB users presented monotonic increases in the adjusted ORs (95% CIs) of diabetes with increased frequency of consumption: 1.03 (0.60, 1.77), 1.43 (0.93, 2.20), 1.62 (1.08, 2.44), and 2.51 (1.40, 4.50) for infrequent, 1-2, 3-4, and >4 times/d, respectively. In linear regression analyses, among normal-weight individuals, greater ASB consumption was also associated with increased fasting glucose concentrations (P = 0.01) and poorer ß-cell function (P = 0.009). No such associations were seen for those with BMI ≥25. In fact, in overweight or obese participants, greater ASB consumption was significantly associated with improved indexes of insulin resistance and 2-h postload glucose. CONCLUSIONS: Normal-weight, but not excess-weight, individuals with greater ASB consumption presented diabetes more frequently and had higher fasting glucose and poorer ß-cell function.


Assuntos
Bebidas/efeitos adversos , Glicemia/metabolismo , Índice de Massa Corporal , Diabetes Mellitus Tipo 2/etiologia , Comportamento Alimentar , Obesidade/complicações , Edulcorantes/efeitos adversos , Adulto , Idoso , Brasil , Estudos Transversais , Diabetes Mellitus Tipo 2/sangue , Dieta , Feminino , Teste de Tolerância a Glucose , Hemoglobina A Glicada/metabolismo , Humanos , Resistência à Insulina , Modelos Logísticos , Estudos Longitudinais , Masculino , Pessoa de Meia-Idade , Obesidade/sangue , Sobrepeso , Valores de Referência , Ganho de Peso
14.
PLoS One ; 10(5): e0126469, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-25978631

RESUMO

INTRODUCTION: Observational studies have reported fairly consistent inverse associations between coffee consumption and risk of type 2 diabetes, but this association has been little investigated with regard to lesser degrees of hyperglycemia and other alterations in glucose homeostasis. Additionally, the association between coffee consumption and diabetes has been rarely investigated in South American populations. We examined the cross-sectional relationships of coffee intake with newly diagnosed diabetes and measures of glucose homeostasis, insulin sensitivity, and insulin secretion, in a large Brazilian cohort of middle-aged and elderly individuals. METHODS: We used baseline data from 12,586 participants of the Longitudinal Study of Adult Health (ELSA-Brasil). Logistic regression analyses were performed to examine associations between coffee consumption and newly diagnosed diabetes. Analysis of covariance was used to assess coffee intake in relation to two-hour glucose from an oral glucose tolerance test, fasting glucose, glycated hemoglobin, fasting and -2-hour postload insulin and measures of insulin sensitivity. RESULTS: We found an inverse association between coffee consumption and newly diagnosed diabetes, after adjusting for multiple covariates [23% and 26% lower odds of diabetes for those consuming coffee 2-3 and >3 times per day, respectively, compared to those reporting never or almost never consuming coffee, (p = .02)]. An inverse association was also found for 2-hour postload glucose [Never/almost never: 7.57 mmol/L, ≤1 time/day: 7.48 mmol/L, 2-3 times/day: 7.22 mmol/L, >3 times/day: 7.12 mol/L, p<0.0001] but not with fasting glucose concentrations (p = 0.07). Coffee was additionally associated with 2-hour postload insulin [Never/almost never: 287.2 pmol/L, ≤1 time/day: 280.1 pmol/L, 2-3 times/day: 275.3 pmol/L, >3 times/day: 262.2 pmol/L, p = 0.0005) but not with fasting insulin concentrations (p = .58). CONCLUSION: Our present study provides further evidence of a protective effect of coffee on risk of adult-onset diabetes. This effect appears to act primarily, if not exclusively, through postprandial, as opposed to fasting, glucose homeostasis.


Assuntos
Café , Diabetes Mellitus Tipo 2/epidemiologia , Glucose/metabolismo , Brasil/epidemiologia , Estudos Transversais , Diabetes Mellitus Tipo 2/prevenção & controle , Feminino , Teste de Tolerância a Glucose , Hemoglobina A Glicada/análise , Homeostase/efeitos dos fármacos , Humanos , Hiperglicemia/epidemiologia , Insulina/sangue , Estudos Longitudinais , Masculino , Pessoa de Meia-Idade
15.
Nutr Rev ; 73(4): 236-46, 2015 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-26024546

RESUMO

CONTEXT: Tea has been proposed as an antihypertensive agent for individuals with elevated blood pressure, yet the evidence for this has not been systematically reviewed to date. OBJECTIVE: The aim of this review was to evaluate the effects of tea on blood pressure in individuals within the prehypertensive and hypertensive blood pressure ranges. DATA SOURCES: The CENTRAL, PubMed, Embase, and Web of Science databases were searched for all relevant studies published from 1946 to September 27, 2013. STUDY SELECTION: The selection criteria included randomized controlled trials of adults whose blood pressure was within hypertensive or prehypertensive ranges and in which the applied intervention was green or black tea; controls consisting of placebo, minimal tea intervention, or no intervention; and a follow-up period of at least 2 months. DATA EXTRACTION: Two reviewers independently extracted data on participants, interventions, comparators, outcomes, and study design. Mean differences (MDs) and 95% confidence intervals (95%CIs) were pooled to generate summary effect estimates. RESULTS: Meta-analyses of 10 trials (834 participants) showed statistically significant reductions in systolic blood pressure (MD -2.36 mmHg, 95%CI -4.20 to -0.52) and diastolic blood pressure (MD -1.77 mmHg, 95%CI -3.03 to -0.52) with tea consumption. CONCLUSIONS: Consumption of green or black tea can reduce blood pressure in individuals within prehypertensive and hypertensive ranges, although further investigation with studies of longer duration and stronger methodological quality is warranted to confirm these findings.


Assuntos
Anti-Hipertensivos/uso terapêutico , Pressão Sanguínea/efeitos dos fármacos , Camellia sinensis , Hipertensão/prevenção & controle , Fitoterapia , Extratos Vegetais/uso terapêutico , Prevenção Secundária , Anti-Hipertensivos/farmacologia , Humanos , Extratos Vegetais/farmacologia , Ensaios Clínicos Controlados Aleatórios como Assunto , Chá
16.
J Can Dent Assoc ; 75(10): 707, 2009 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-20003754

RESUMO

OBJECTIVE: To compare levels of water fluoridation in urban and rural distribution systems in Ontario. METHODS: A random sample of 17 urban and 17 rural municipalities was taken from a list of 445 municipalities. The Ontario Ministry of the Environment (MOE) website was used to identify the water treatment plants that supply these municipalities, and water quality reports published by each of these distribution systems for 2007 were collected. For municipal distribution systems without published reports, staff were contacted directly. RESULTS: Far more urban distribution systems (82%) fluoridate their water compared with rural systems (18%). Most urban water suppliers (14 of 17) meet the 2000 MOE fluoride level standard of 0.5-0.8 mg/L, a range that includes the recently adopted Health Canada standard of 0.7 +/- 0.1 mg/L. Only 3 of 17 rural distributors artificially fluoridate their water and 11 of 16 supply suboptimal levels of fluoride. CONCLUSION: Most Ontarians who live in rural areas receive levels of fluoride that are outside MOE standards. Urban water distribution systems that regulate their fluoride content are compliant with the range recommended in 2000. The communal water supplies of some rural residents of southwestern Ontario contain levels of natural fluoride that are well above the standard for artificially fluoridated water.


Assuntos
Cariostáticos/análise , Fluoretos/análise , População Rural , População Urbana , Abastecimento de Água/análise , Fluoretação/estatística & dados numéricos , Humanos , Ontário , Purificação da Água
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA