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AIMS: We aimed to assess the association of a low carbohydrate diet score (LCD) with the incidence of type 2 diabetes (T2D) using Melbourne Collaborative Cohort Study (MCCS) data. METHODS: Between 1990 and 1994, the MCCS recruited 41,513 people aged 40-69 years. The first and second follow-ups were conducted in 1995-1998 and 2003-2007, respectively. We analyzed data from 39,185 participants. LCD score was calculated at baseline as the percentage of energy from carbohydrate, fat, and protein. The higher the score the less percentage of carbohydrates contributed to energy intake. The association of LCD quintiles with the incidence of diabetes was assessed using modified Poisson regression, adjusted for lifestyle, obesity, socioeconomic and other confounders. Mediation of the association by adiposity (BMI) was assessed. RESULTS: LCD was positively associated with diabetes risk. Higher LCD score (p for trend = 0.001) was associated with increased risk of T2D. Quintile 5 (38 % energy from carbohydrates) versus quintile 1 (55 % energy from carbohydrates) showed a 20 % increased diabetes risk (incidence risk ratio (IRR) = 1.20 (95 % CI: 1.05-1.37)). A further adjustment for BMI (Body Mass Index) and WHR (Waist-to-Hip-Ratio) eliminated the association. Mediation analysis demonstrated that BMI mediated 76 % of the LCD & diabetes association. CONCLUSIONS: Consuming a low carbohydrate diet, reflected as a high LCD score, may increase the risk of T2D which is largely explained by obesity. Results highlight the need for further studies, including clinical trials investigating the effects of a low carbohydrate diet in T2D.
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Self-rated health (SRH) is a subjective indicator of overall health based on a single questionnaire item. Previous evidence found that it is a strong predictor of mortality, although the underlying mechanism is poorly understood. Epigenetic age is an objective, emerging biomarker of health, estimated using DNA methylation data at hundreds of sites across the genome. This study aimed to assess the overlap and interaction between SRH and epigenetic ageing in predicting mortality risk. We used DNA methylation data from 1059 participants in the Melbourne Collaborative Cohort Study (mean age: 69 years) to calculate three age-adjusted measures of epigenetic ageing: GrimAge, PhenoAge, and DunedinPACE. SRH was assessed using a five-category questionnaire item ("excellent, very good, good, fair, poor"). Cox models were used to assess the associations of SRH, epigenetic ageing, and their interaction, with all-cause mortality over up to 17 years of follow-up (Ndeaths = 345). The association of SRH with mortality per category increase was HR = 1.29; 95%CI: 1.14-1.46. The association was slightly attenuated after adjusting for all three epigenetic ageing measures (HR = 1.25, 95%CI: 1.10-1.41). A strong gradient was observed in the association of GrimAge (Pinteraction = 0.006) and DunedinPACE (Pinteraction = 0.002) with mortality across worsening SRH strata. For example, the association between DunedinPACE and mortality in participants with "excellent" SRH was HR = 1.02, 95%CI: 0.73-1.43 and for "fair/poor" HR = 1.72, 95%CI: 1.35-2.20. SRH and epigenetic ageing were synergistic risk factors of mortality in our study. These findings suggest that consideration of subjective and objective factors may improve general health assessment, which has implications for the ongoing development of molecular markers of ageing.
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Epigenetic age is an emerging marker of health that is highly predictive of disease and mortality risk. There is a lack of evidence on whether lifestyle changes are associated with changes in epigenetic aging. We used data from 1 041 participants in the Melbourne Collaborative Cohort Study with blood DNA methylation measures at baseline (1990-1994, mean age: 57.4 years) and follow-up (2003-2007, mean age: 68.8 years). The Alternative Healthy Eating Index-2010 (AHEI-2010), the Mediterranean Dietary Score, and the Dietary Inflammatory Index were used as measures of diet quality, and weight, waist circumference, and waist-to-hip ratio as measures of body size. Five age-adjusted epigenetic aging measures were considered: GrimAge, PhenoAge, PCGrimAge, PCPhenoAge, and DunedinPACE. Multivariable linear regression models including restricted cubic splines were used to assess the cross-sectional and longitudinal associations of body size and diet quality with epigenetic aging. Associations between weight and epigenetic aging cross-sectionally at both time points were positive and appeared greater for DunedinPACE (per SD: ß ~0.24) than for GrimAge and PhenoAge (ß ~0.10). The longitudinal associations with weight change were markedly nonlinear (U-shaped) with stable weight being associated with the lowest epigenetic aging at follow-up, except for DunedinPACE, for which only weight gain showed a positive association. We found negative, linear associations for AHEI-2010 both cross-sectionally and longitudinally. Other adiposity measures and dietary scores showed similar results. In middle-aged to older adults, declining diet quality and weight gain may increase epigenetic age, while the association for weight loss may require further investigation. Our study sheds light on the potential of weight management and dietary improvement in slowing aging processes.
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Envelhecimento , Dieta , Humanos , Idoso , Pessoa de Meia-Idade , Estudos de Coortes , Estudos Transversais , Índice de Massa Corporal , Envelhecimento/genética , Aumento de Peso , Circunferência da Cintura , Epigênese GenéticaRESUMO
BACKGROUND: We examined associations between adherence to adaptations of the 2018 World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) cancer prevention recommendations and total, exposure-related and site-specific cancer risk. METHODS: A total of 20,001 participants ages 40 to 69 years at enrollment into the Melbourne Collaborative Cohort Study in 1990 to 1994, who had diet, body size, and lifestyle reassessed in 2003 to 2007 ("baseline"), were followed-up through June 2021. We constructed diet and standardized lifestyle scores based on core WCRF/AICR recommendations on diet, alcohol intake, body size and physical activity, and additional scores incorporating weight change, sedentary behavior, and smoking. Associations with cancer risk were estimated using Cox regression, adjusting for confounders. RESULTS: During follow-up (mean = 16 years), 4,710 incident cancers were diagnosed. For highest quintile ("most adherent") of the standardized lifestyle score, compared with lowest ("least adherent"), a HR of 0.82 [95% confidence interval (CI): 0.74-0.92] was observed for total cancer. This association was stronger with smoking included in the score (HR = 0.74; 95% CI: 0.67-0.81). A higher score was associated with lower breast and prostate cancer risk for the standardized score, and with lung, stomach, rectal, and pancreatic cancer risk when the score included smoking. Our analyses identified alcohol use, waist circumference and smoking as key drivers of associations with total cancer risk. CONCLUSIONS: Adherence to WCRF/AICR cancer prevention recommendations is associated with lower cancer risk. IMPACT: With <0.2% of our sample fully adherent to the recommendations, the study emphasizes the vast potential for preventing cancer through modulation of lifestyle habits.
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Administração Financeira , Neoplasias Pancreáticas , Masculino , Humanos , Estados Unidos , Estudos de Coortes , Fatores de Risco , DietaRESUMO
BACKGROUND: It is unknown whether dietary intake of polyunsaturated fatty acids (PUFA) modifies the cardiovascular disease (CVD) risk associated with a family history of CVD. We assessed interactions between biomarkers of low PUFA intake and a family history in relation to long-term CVD risk in a large consortium. METHODS: Blood and tissue PUFA data from 40â 885 CVD-free adults were assessed. PUFA levels ≤25th percentile were considered to reflect low intake of linoleic, alpha-linolenic, and eicosapentaenoic/docosahexaenoic acids (EPA/DHA). Family history was defined as having ≥1 first-degree relative who experienced a CVD event. Relative risks with 95% CI of CVD were estimated using Cox regression and meta-analyzed. Interactions were assessed by analyzing product terms and calculating relative excess risk due to interaction. RESULTS: After multivariable adjustments, a significant interaction between low EPA/DHA and family history was observed (product term pooled RR, 1.09 [95% CI, 1.02-1.16]; P=0.01). The pooled relative risk of CVD associated with the combined exposure to low EPA/DHA, and family history was 1.41 (95% CI, 1.30-1.54), whereas it was 1.25 (95% CI, 1.16-1.33) for family history alone and 1.06 (95% CI, 0.98-1.14) for EPA/DHA alone, compared with those with neither exposure. The relative excess risk due to interaction results indicated no interactions. CONCLUSIONS: A significant interaction between biomarkers of low EPA/DHA intake, but not the other PUFA, and a family history was observed. This novel finding might suggest a need to emphasize the benefit of consuming oily fish for individuals with a family history of CVD.
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Doenças Cardiovasculares , Ácidos Graxos Ômega-3 , Animais , Doenças Cardiovasculares/diagnóstico , Doenças Cardiovasculares/epidemiologia , Doenças Cardiovasculares/genética , Fatores de Risco , Ácidos Docosa-Hexaenoicos , BiomarcadoresRESUMO
No randomized controlled trial has evaluated the effect of long-term alcohol interventions on mortality. Results reported in existing observational studies may be subject to selection bias and time-varying confounding. Using data from the Australian Longitudinal Study on Women's Health 1946-1951 birth cohort, collected regularly from 1996-2016, we estimated all-cause and cancer mortality had women been assigned various alcohol interventions (in categories ranging from 0 to >30 g/day ethanol, or reduced to ≤20 g/day if higher) at baseline, and had they maintained these levels of consumption. The cumulative risks for all-cause and cancer mortality were 5.6% (10,118 women followed for 20 years) and 2.9% (18 years), respectively. For all-cause and cancer mortality, baseline ethanol up to 30 g/day showed lower risk and >30 g/day showed higher risk relative to abstention. Had women sustainedly followed the interventions, a similar relationship was observed for all-cause mortality. However, the negative association observed for intakes ≤30 g/day and positive association for intakes >30 g/day was not evident for cancer mortality. Our findings suggest that all-cause mortality could have been lower than observed if this cohort of women had consumed some alcohol (no more than 30 g/day) rather than no consumption, but cancer mortality might not.
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Neoplasias , Saúde da Mulher , Feminino , Humanos , Consumo de Bebidas Alcoólicas/efeitos adversos , Consumo de Bebidas Alcoólicas/epidemiologia , Austrália/epidemiologia , Etanol , Estudos Longitudinais , Pessoa de Meia-IdadeRESUMO
PURPOSE: Ultra-processed food (UPF) intake has increased in recent decades, yet limited knowledge of long-term effects on cardiovascular health persists and sex-specific data is scant. We determined the association of UPF intake with incident cardiovascular disease (CVD) and/or hypertension in a population-based cohort of women. METHODS: In the Australian Longitudinal Study on Women's Health, women aged 50-55 years were prospectively followed (2001-2016). UPFs were identified using NOVA classification and contribution of these foods to total dietary intake by weight was estimated. Primary endpoint was incident CVD (self-reported heart disease/stroke). Secondary endpoints were self-reported hypertension, all-cause mortality, type 2 diabetes mellitus, and/or obesity. Logistic regression models assessed associations between UPF intake and incident CVD, adjusting for socio-demographic, medical comorbidities, and dietary variables. RESULTS: We included 10,006 women (mean age 52.5 ± 1.5; mean UPF intake 26.6 ± 10.2% of total dietary intake), with 1038 (10.8%) incident CVD, 471 (4.7%) deaths, and 4204 (43.8%) hypertension cases over 15 years of follow-up. In multivariable-adjusted models, the highest [mean 42.0% total dietary intake] versus the lowest [mean 14.2% total dietary intake] quintile of UPF intake was associated with higher incident hypertension [odds ratio (OR) 1.39, 95% confidence interval (CI) 1.10-1.74; p = 0.005] with a linear trend (ptrend = 0.02), but not incident CVD [OR 1.22, 95% CI 0.92-1.61; p = 0.16] or all-cause mortality (OR 0.80, 95% CI 0.54-1.20; p = 0.28). Similar results were found after multiple imputations for missing values. CONCLUSION: In women, higher UPF intake was associated with increased hypertension, but not incident CVD. These findings may support minimising UPFs within a healthy diet for women.
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Doenças Cardiovasculares , Diabetes Mellitus Tipo 2 , Hipertensão , Pessoa de Meia-Idade , Masculino , Humanos , Feminino , Doenças Cardiovasculares/epidemiologia , Estudos Longitudinais , Alimento Processado , Austrália/epidemiologia , Dieta , Hipertensão/epidemiologia , Manipulação de Alimentos , Fast Foods/efeitos adversosRESUMO
BACKGROUND: Cereal-derived polyphenols have demonstrated protective mechanisms in colorectal cancer (CRC) models; however, confirmation in human studies is lacking. Therefore, this study examined the association between cereal polyphenol intakes and CRC risk in the Melbourne Collaborative Cohort Study (MCCS), a prospective cohort study in Melbourne, Australia that recruited participants between 1990 and 1994 to investigate diet-disease relationships. METHODS: Using food frequency questionnaire diet data matched to polyphenol data, dietary intakes of alkylresorcinols, phenolic acids, lignans, and total polyphenols from cereals were estimated. Hazard ratios (HRs) and 95% confidence intervals for CRC risk were estimated for quintiles of intake with the lowest quintile as the comparison category, using multivariable adjusted Cox proportional hazards models with age as the time axis adjusted for sex, socio-economic status, alcohol consumption, fibre intake, country of birth, total energy intake, physical activity and smoking status. RESULTS: From 35,245 eligible adults, mean (SD) age 54.7 (8.6) years, mostly female (61%) and Australian-born (69%), there were 1394 incident cases of CRC (946 colon cancers and 448 rectal cancers). Results for total cereal polyphenol intake showed reduced HRs in Q2 (HR: 0.80; 95% CI, 0.68-0.95) and Q4 (HR: 0.75; 95% CI, 0.62-0.90), and similar for phenolic acids. Alkylresorcinol intake showed reduced HR in Q3 (HR: 0.80; 95% CI, 0.67-0.95) and Q4 (HR: 0.79; 95% CI, 0.66-0.95). CONCLUSIONS: Overall, the present study showed little evidence of association between intakes of cereal polyphenols and CRC risk. Future investigations may be useful to understand associations between cereal-derived polyphenols and additional cancers in different populations.
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BACKGROUND: Five modifiable risk factors are associated with cardiovascular disease and death from any cause. Studies using individual-level data to evaluate the regional and sex-specific prevalence of the risk factors and their effect on these outcomes are lacking. METHODS: We pooled and harmonized individual-level data from 112 cohort studies conducted in 34 countries and 8 geographic regions participating in the Global Cardiovascular Risk Consortium. We examined associations between the risk factors (body-mass index, systolic blood pressure, non-high-density lipoprotein cholesterol, current smoking, and diabetes) and incident cardiovascular disease and death from any cause using Cox regression analyses, stratified according to geographic region, age, and sex. Population-attributable fractions were estimated for the 10-year incidence of cardiovascular disease and 10-year all-cause mortality. RESULTS: Among 1,518,028 participants (54.1% of whom were women) with a median age of 54.4 years, regional variations in the prevalence of the five modifiable risk factors were noted. Incident cardiovascular disease occurred in 80,596 participants during a median follow-up of 7.3 years (maximum, 47.3), and 177,369 participants died during a median follow-up of 8.7 years (maximum, 47.6). For all five risk factors combined, the aggregate global population-attributable fraction of the 10-year incidence of cardiovascular disease was 57.2% (95% confidence interval [CI], 52.4 to 62.1) among women and 52.6% (95% CI, 49.0 to 56.1) among men, and the corresponding values for 10-year all-cause mortality were 22.2% (95% CI, 16.8 to 27.5) and 19.1% (95% CI, 14.6 to 23.6). CONCLUSIONS: Harmonized individual-level data from a global cohort showed that 57.2% and 52.6% of cases of incident cardiovascular disease among women and men, respectively, and 22.2% and 19.1% of deaths from any cause among women and men, respectively, may be attributable to five modifiable risk factors. (Funded by the German Center for Cardiovascular Research (DZHK); ClinicalTrials.gov number, NCT05466825.).
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Doenças Cardiovasculares , Fatores de Risco de Doenças Cardíacas , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Doenças Cardiovasculares/epidemiologia , Doenças Cardiovasculares/mortalidade , Diabetes Mellitus , Fatores de Risco , Fumar/efeitos adversos , InternacionalidadeRESUMO
Enhanced survival following a diagnosis of cancer has led to a steep rise in the number of individuals diagnosed with a second primary cancer. We examined the association between pre-cancer cigarette smoking and risk of second cancer in 9785 participants diagnosed with first invasive cancer after enrolment in the Melbourne Collaborative Cohort Study. Follow-up was from date of first invasive cancer until diagnosis of second primary invasive cancer, death, or 31 July 2019, whichever came first. Data on cigarette smoking was collected at enrolment (1990-94) along with information on other lifestyle factors including body size, alcohol intake and diet. We estimated hazard ratios (HR) and 95 % confidence intervals (CI) for incident second cancer with several smoking measures, adjusted for potential confounders. After a mean follow-up of 7.3 years, 1658 second cancers were identified. All measures of smoking were associated with increased risk of second cancer. We observed a 44 % higher risk of second cancer for smokers of ≥ 20 cigarettes/day (HR=1.44, 95 % CI: 1.18-1.76), compared with never smokers. We also observed dose-dependent associations with number of cigarettes smoked (HR=1.05 per 10 cigarettes/day, 95 % CI: 1.01-1.09) and duration of smoking (HR=1.07 per 10 years, 95 % CI: 1.03-1.10). The risk of second cancer increased by 4 % per 10 pack-years of smoking (HR=1.04, 95 % CI: 1.02-1.06; p < 0.001). There was suggestive evidence of stronger associations with number of cigarettes smoked and pack-years of smoking for women (pinteraction<0.05), particularly for the highest risk categories of both variables. These associations with pre-diagnostic smoking were markedly stronger for second cancers known to be smoking-related than for others (phomogeneity<0.001). Our findings for pre-diagnostic cigarette smoking indicated increased risk of second primary cancer for cancer sites considered smoking-related, highlighting the importance of assessing smoking habits in cancer survivors.
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Fumar Cigarros , Segunda Neoplasia Primária , Humanos , Feminino , Estudos de Coortes , Fumar Cigarros/efeitos adversos , Fumar Cigarros/epidemiologia , Fatores de Risco , Segunda Neoplasia Primária/epidemiologia , Segunda Neoplasia Primária/etiologia , Consumo de Bebidas AlcoólicasRESUMO
Cereal foods are consumed globally and are important sources of polyphenols with potential health benefits, yet dietary intakes are unclear. We aimed to calculate the dietary intakes of polyphenols from cereal foods in the Melbourne Collaborative Cohort Study (MCCS), and describe intakes by demographic and lifestyle factors. We estimated intakes of alkylresorcinols, lignans and phenolic acids in n = 39,892 eligible MCCS participants, using baseline dietary data (1990-1994) from a 121-item FFQ containing 17 cereal foods, matched to a polyphenol database developed from published literature and Phenol-Explorer Database. Intakes were estimated within groups according to lifestyle and demographic factors. The median (25th-75th percentile) intake of total polyphenols from cereal foods was 86.9 mg/day (51.4-155.8). The most consumed compounds were phenolic acids, with a median intake of 67.1 mg (39.5-118.8), followed by alkylresorcinols of 19.7 mg (10.8-34.6). Lignans made the smallest contribution of 0.50 mg (0.13-0.87). Higher polyphenol intakes were associated with higher relative socio-economic advantage and prudent lifestyles, including lower body mass index (BMI), non-smoking and higher physical activity scores. The findings based on polyphenol data specifically matched to the FFQ provide new information on intakes of cereal polyphenols, and how they might vary according to lifestyle and demographic factors.
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Lignanas , Polifenóis , Humanos , Polifenóis/análise , Grão Comestível/química , Estudos de Coortes , Flavonoides , Dieta , Ingestão de Alimentos , Estilo de Vida , DemografiaRESUMO
BACKGROUND: Few studies have tested longitudinal associations between ultra-processed food consumption and depressive outcomes. As such, further investigation and replication are necessary. The aim of this study is to examine associations of ultra-processed food intake with elevated psychological distress as an indicator of depression after 15 years. METHOD: Data from the Melbourne Collaborative Cohort Study (MCCS) were analysed (n = 23,299). We applied the NOVA food classification system to a food frequency questionnaire (FFQ) to determine ultra-processed food intake at baseline. We categorised energy-adjusted ultra-processed food consumption into quartiles by using the distribution of the dataset. Psychological distress was measured by the ten-item Kessler Psychological Distress Scale (K10). We fitted unadjusted and adjusted logistic regression models to assess the association of ultra-processed food consumption (exposure) with elevated psychological distress (outcome and defined as K10 ≥ 20). We fitted additional logistic regression models to determine whether these associations were modified by sex, age and body mass index. RESULTS: After adjusting for sociodemographic characteristics and lifestyle and health-related behaviours, participants with the highest relative intake of ultra-processed food were at increased odds of elevated psychological distress compared to participants with the lowest intake (aOR: 1.23; 95%CI: 1.10, 1.38, p for trend = 0.001). We found no evidence for an interaction of sex, age and body mass index with ultra-processed food intake. CONCLUSION: Higher ultra-processed food intake at baseline was associated with subsequent elevated psychological distress as an indicator of depression at follow-up. Further prospective and intervention studies are necessary to identify possible underlying pathways, specify the precise attributes of ultra-processed food that confer harm, and optimise nutrition-related and public health strategies for common mental disorders.
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Dieta , Ingestão de Energia , Humanos , Adulto , Estudos de Coortes , Alimento Processado , Depressão/epidemiologia , Fast FoodsRESUMO
AIM: The kynurenine pathway is increasingly recognised to play a role in inflammation and disease. We assessed the cross-sectional and longitudinal associations of adiposity measures (body mass index, waist-hip ratio, waist circumference and fat mass ratio) with plasma concentrations of kynurenine pathway metabolites and traditional markers of inflammation. METHODS: We used data from 970 Melbourne Collaborative Cohort Study participants who had plasma markers measured at baseline (median age 59 years) and follow-up (median age 70 years). Linear regression was used to assess cross-sectional and longitudinal associations between four adiposity measures and concentrations of i) nine kynurenine pathway metabolites; ii) two derived markers; iii) eight traditional inflammatory markers. RESULTS: Cross-sectionally, most kynurenine metabolites were strongly associated with adiposity measures at both time points; associations were generally stronger than for most inflammation markers except CRP (e.g. body mass index at baseline, quinolinic acid (per S.D. ß = 0.30, 95%CI: 0.24-0.36, P = 10-21), kynurenine (ß = 0.25, 95%CI: 0.19-0.31, P = 10-16) and CRP (ß = 0.31, 95%CI: 0.25-0.37, P = 10-24), and remained largely unchanged after adjustment for confounders. Longitudinally, changes in adiposity measures over approximately a decade were positively associated with changes in kynurenine metabolite concentrations (in particular for 3-hydroxyanthranilic acid, kynurenine and quinolinic acid), and more strongly so than for other markers of inflammation, including CRP. CONCLUSIONS: In middle-aged and older adults, plasma concentrations of kynurenine metabolites are strongly associated with adiposity, both cross-sectionally and longitudinally. Our study demonstrates that kynurenine metabolites may be valuable markers to monitor the adverse consequences of obesity.
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Cinurenina , Triptofano , Pessoa de Meia-Idade , Humanos , Idoso , Cinurenina/metabolismo , Triptofano/metabolismo , Estudos de Coortes , Adiposidade , Ácido Quinolínico , Estudos Transversais , Inflamação , Obesidade , BiomarcadoresRESUMO
Methylation marks of exposure to health risk factors may be useful markers of cancer risk as they might better capture current and past exposures than questionnaires, and reflect different individual responses to exposure. We used data from seven case-control studies nested within the Melbourne Collaborative Cohort Study of blood DNA methylation and risk of colorectal, gastric, kidney, lung, prostate and urothelial cancer, and B-cell lymphoma (N cases = 3123). Methylation scores (MS) for smoking, body mass index (BMI), and alcohol consumption were calculated based on published data as weighted averages of methylation values. Rate ratios (RR) and 95% confidence intervals for association with cancer risk were estimated using conditional logistic regression and expressed per SD increase of the MS, with and without adjustment for health-related confounders. The contribution of MS to discriminate cases from controls was evaluated using the area under the curve (AUC). After confounder adjustment, we observed: large associations (RR = 1.5-1.7) with lung cancer risk for smoking MS; moderate associations (RR = 1.2-1.3) with urothelial cancer risk for smoking MS and with mature B-cell neoplasm risk for BMI and alcohol MS; moderate to small associations (RR = 1.1-1.2) for BMI and alcohol MS with several cancer types and cancer overall. Generally small AUC increases were observed after inclusion of several MS in the same model (colorectal, gastric, kidney, urothelial cancers: +3%; lung cancer: +7%; B-cell neoplasms: +8%). Methylation scores for smoking, BMI and alcohol consumption show independent associations with cancer risk, and may provide some improvements in risk prediction.
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Neoplasias Colorretais , Neoplasias Pulmonares , Masculino , Humanos , Índice de Massa Corporal , Estudos de Coortes , Fumar/efeitos adversos , Fumar/genética , Fatores de Risco , Consumo de Bebidas Alcoólicas/efeitos adversos , Metilação de DNA , Neoplasias Pulmonares/etiologia , Neoplasias Pulmonares/genética , Neoplasias Colorretais/genéticaRESUMO
AIM: To assess the associations of total dietary fibre and fibre from different food sources (ie, cereal, fruit and vegetables) with the risk of diabetes. MATERIALS AND METHODS: The Melbourne Collaborative Cohort Study enrolled 41 513 participants aged 40 to 69 years from 1990 to 1994. The first and second follow-ups were conducted in 1994 to 1998 and 2003 to 2007, respectively. Self-reported diabetes incidence was recorded at both follow-ups. We analysed data from 39 185 participants, with a mean follow-up of 13.8 years. The relationships between dietary fibre intake (total, fruit, vegetable and cereal fibre) and the incidence of diabetes were assessed using modified Poisson regression, adjusted for dietary, lifestyle, obesity, socioeconomic and other possible confounders. Fibre intake was categorized into quintiles. RESULTS: At total of 1989 incident cases were identified over both follow-up surveys. Total fibre intake was not associated with diabetes risk. Higher intake of cereal fibre (P for trend = 0.003), but not fruit (P for trend = 0.3) and vegetable fibre (P for trend = 0.5), was protective against diabetes. For cereal fibre, quintile 5 versus quintile 1 showed a 25% reduction in diabetes risk (incidence risk ratio [IRR] 0.75, 95% confidence interval [CI] 0.63-0.88). For fruit fibre, only quintile 2 versus quintile 1 showed a 16% risk reduction (IRR 0.84, 95% CI 0.73-0.96). Adjustment for body mass index (BMI) and waist-to-hip ratio eliminated the association and mediation analysis showed that BMI mediated 36% of the relationship between fibre and diabetes. CONCLUSION: Intake of cereal fibre and, to a lesser extent, fruit fibre, may reduce the risk of diabetes, while total fibre showed no association. Our data suggest that specific recommendations regarding dietary fibre intake may be needed to prevent diabetes.
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Diabetes Mellitus Tipo 2 , Humanos , Estudos de Coortes , Diabetes Mellitus Tipo 2/epidemiologia , Diabetes Mellitus Tipo 2/prevenção & controle , Grão Comestível , Fatores de Risco , Estudos Prospectivos , Dieta , Verduras , Fibras na DietaRESUMO
Low-carbohydrate diets (LCDs) are popular among people attempting weight loss and recommended for pregnant women with gestational diabetes (GDM), but they may increase health risks if nutritionally inadequate. We aimed to describe the dietary intake of post-partum women according to their relative carbohydrate intake, overall, and among women attempting weight loss or diagnosed with GDM in their recent pregnancy. This cross-sectional population-based cohort study included 2093 post-partum women aged 25-36 years who participated in the Australian Longitudinal Study on Women's Health. Dietary intake was assessed using a validated food frequency questionnaire. Relative carbohydrate intake was determined using a previously developed LCD score. Data were weighted to account for oversampling of women from rural/remote areas. More than half of women (n[weighted] = 1362, 66.3%) were trying to lose weight, and 4.6% (n[weighted]=88) had GDM in their recent pregnancy. Women with the lowest relative carbohydrate intake (LCD score quartile 4) consumed 36.8% of total energy intake from carbohydrates, and had a lower intake of refined grains, whole grains, fruit and fruit juice, and a higher intake of red and processed meat, compared with women with the highest relative carbohydrate intake (quartile 1). Different food groups, both healthy and unhealthy, were restricted depending on whether women were attempting weight loss and had recent GDM. These findings may reflect a lack of knowledge among post-partum women on carbohydrates and dietary guidelines. Health professionals may have an important role in providing advice and support for post-partum women who wish to restrict their carbohydrate intake, to ensure optimal diet quality.
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Diabetes Gestacional , Dieta com Restrição de Carboidratos , Feminino , Humanos , Gravidez , Austrália , Carboidratos , Estudos de Coortes , Estudos Transversais , Dieta , Estudos Longitudinais , Período Pós-Parto , Redução de Peso , AdultoRESUMO
BACKGROUND: Dietary composition influences the composition of the gut microbiota in healthy adults. Little is known about the effect of dietary patterns on gut microbiota composition in pregnancy. This cross-sectional study aimed to investigate the associations between two diet quality scores adapted from the Australian Recommended Food Score (ARFS) and the Mediterranean Dietary Score (MDS) with the composition of the gut microbiota in pregnant women with excess body fat at 28 weeks' gestation. METHODS: Women from the Study of Probiotics IN Gestational diabetes (SPRING) who had completed a food frequency questionnaire (FFQ; n = 395) were classified according to tertiles of ARFS and the MDS. Higher dietary pattern scores in both the ARFS and the MDS represent better diet quality. Gut microbiota composition was assessed using 16S rRNA gene amplicon sequencing and analysed using MicrobiomeAnalyst in a subset of 196 women with faecal samples. RESULTS: No significant difference was found in alpha or beta diversity. A higher ARFS was associated with a higher abundance of Ruminococcus and lower abundance of Akkermansia, whereas a higher MDS was associated with a higher abundance of Ruminococcus and Butyricicoccus, though these changes disappeared after correction for multiple testing. CONCLUSION: These results suggest that dietary patterns defined by the ARFS and MDS were not associated with gut microbiota composition in pregnant women classified as overweight and obese at 28 weeks' gestation within this study.