Global Effect of Modifiable Risk Factors on Cardiovascular Disease and Mortality.

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.).

Role of Polyunsaturated Fat in Modifying Cardiovascular Risk Associated With Family History of Cardiovascular Disease: Pooled De Novo Results From 15 Observational Studies.

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 40 885 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.

Sustained Hypothetical Interventions on Midlife Alcohol Consumption in Relation to All-Cause and Cancer Mortality: The Australian Longitudinal Study on Women's Health.

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.

Ultra-processed foods and incident cardiovascular disease and hypertension in middle-aged women.

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.

Methylation scores for smoking, alcohol consumption and body mass index and risk of seven types of cancer.

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.

High cereal fibre but not total fibre is associated with a lower risk of type 2 diabetes: Evidence from the Melbourne Collaborative Cohort Study.

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.

The Relationship Between Psychological Distress and Physical Activity Is Non-linear and Differs by Domain: a Cross-Sectional Study.

BACKGROUND: There is increasing evidence for the relationship between physical activity (PA), sedentary behaviour and mental health. Limited data exists on sex-specific associations. We aimed to identify associations between PA dose and domain and television time with psychological distress, including sex-stratified models. METHODS: A total of 22,176 adults from the Melbourne Collaborative Cohort Study follow-up 2 cohort (2003-2007) participated in this cross-sectional study. Occupational, household, transport, leisure PA, hours watching television and psychological distress were assessed. Restricted cubic splines were used to examine the relationships between PA domains, television viewing time and psychological distress. RESULTS: The relationships between PA and psychological distress were non-linear (p < 0.05) and differed by PA domain. There were dose-dependent, inverse associations between distress with transport (B[95% CI] = -0.39[-0.49, -0.30]) and leisure PA (B[95% CI] = -0.35[-0.46, -0.25]). The effect estimates for transport and leisure PA with distress were larger for women. For household domain, a U-shaped curve with an elongated tail was seen. Median PA was associated with lower distress compared with lower quantities (B[95% CI] = -0.12[-0.22, -0.03]); however, this association was not evident with increasing household PA. There were no clear associations between occupational PA and distress. Higher television viewing was associated with higher distress (B[95% CI] = 0.16[0.02, 0.30]). CONCLUSIONS: Increasing PA and reducing television viewing may contribute to reduced psychological distress, particularly in women. Future interventions should incorporate leisure and transport PA and decrease television viewing to assess the impact on mental health.

Gut microbiome composition is similar between pregnant women with excess body fat with healthy and less healthy dietary intake patterns.

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.

Quality of low-carbohydrate diets among Australian post-partum women: Cross-sectional analysis of a national population-based cohort study.

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.

Alcohol intake trajectories during the life course and risk of alcohol-related cancer: A prospective cohort study.

We examined associations between sex-specific alcohol intake trajectories and alcohol-related cancer risk using data from 22 756 women and 15 701 men aged 40 to 69 years at baseline in the Melbourne Collaborative Cohort Study. Alcohol intake for 10-year periods from age 20 until the decade encompassing recruitment, calculated using recalled beverage-specific frequency and quantity, was used to estimate group-based sex-specific intake trajectories. Hazard ratios (HR) and 95% confidence intervals (CI) were estimated for primary invasive alcohol-related cancer (upper aerodigestive tract, breast, liver and colorectum). Three distinct alcohol intake trajectories for women (lifetime abstention, stable light, increasing moderate) and six for men (lifetime abstention, stable light, stable moderate, increasing heavy, early decreasing heavy, late decreasing heavy) were identified. 2303 incident alcohol-related cancers were diagnosed during 485 525 person-years in women and 789 during 303 218 person-years in men. For men, compared with lifetime abstention, heavy intake (mean ≥ 60 g/day) at age 20 to 39 followed by either an early (from age 40 to 49) (early decreasing heavy; HR = 1.75, 95% CI: 1.25-2.44) or late decrease (from age 60 to 69) (late decreasing heavy; HR = 1.94, 95% CI: 1.28-2.93), and moderate intake (mean <60 g/day) at age 20 to 39 increasing to heavy intake in middle-age (increasing heavy; HR = 1.45, 95% CI: 1.06-1.97) were associated with increased risk of alcohol-related cancer. For women, compared with lifetime abstention, increasing intake from age 20 (increasing moderate) was associated with increased alcohol-related cancer risk (HR = 1.25, 95% CI: 1.06-1.48). Similar associations were observed for colorectal (men) and breast cancer. Heavy drinking during early adulthood might increase cancer risk later in life.

Television viewing time and all-cause mortality: interactions with BMI, physical activity, smoking, and dietary factors.

BACKGROUND: Higher levels of time spent sitting (sedentary behavior) contribute to adverse health outcomes, including earlier death. This effect may be modified by other lifestyle factors. We examined the association of television viewing (TV), a common leisure-time sedentary behavior, with all-cause mortality, and whether this is modified by body mass index (BMI), physical activity, smoking, alcohol intake, soft drink consumption, or diet-associated inflammation. METHODS: Using data from participants in the Melbourne Collaborative Cohort Study, flexible parametric survival models assessed the time-dependent association of self-reported TV time (three categories: < 2 h/day, 2-3 h/day, > 3 h/day) with all-cause mortality. Interaction terms were fitted to test whether there was effect modification of TV time by the other risk factors. RESULTS: From 19,570 participants, 4,417 deaths were reported over a median follow up of 14.5 years. More TV time was associated with earlier mortality; however, this relationship diminished with increasing age. The hazard ratio (HR) and 95% confidence interval (95% CI) for > 3 h/day compared with < 2 h/day of TV time was 1.34 (1.16, 1.55) at 70 years, 1.14 (1.04, 1.23) at 80 years, and 0.95 (0.84, 1.06) at 90 years. The TV time/mortality relationship was more evident in participants who were physically inactive (compared with active; p for interaction < 0.01) or had a higher dietary inflammatory index score (compared with a lower score; p for interaction = 0.03). No interactions were detected between TV time and BMI, smoking, alcohol intake, nor soft-drink consumption (all p for interaction > 0.16). CONCLUSIONS: The relationship between TV time and all-cause mortality may change with age. It may also be more pronounced in those who are otherwise inactive or who have a pro-inflammatory diet.

Diet and risk of Barrett's oesophagus: Melbourne collaborative cohort study.

Barrett's oesophagus (BE) is the precursor of oesophageal adenocarcinoma, which has become the most common type of oesophageal cancer in many Western populations. Existing evidence on diet and risk of BE predominantly comes from case-control studies, which are subject to recall bias in measurement of diet. We aimed to investigate the potential effect of diet, including macronutrients, carotenoids, food groups, specific food items, beverages and dietary scores, on risk of BE in over 20 000 participants of the Melbourne Collaborative Cohort Study. Diet at baseline (1990-1994) was measured using a food frequency questionnaire. The outcome was BE diagnosed between baseline and follow-up (2007-2010). Logistic regression models were used to estimate OR and 95 % CI for diet in relation to risk of BE. Intakes of leafy vegetables and fruit were inversely associated with risk of BE (highest v. lowest quartile: OR = 0·59; CI: 0·38, 0·94; P-trend = 0·02 and OR = 0·58; CI: 0·37, 0·93; P-trend = 0·02 respectively), as were dietary fibre and carotenoids. Stronger associations were observed for food than the nutrients found in them. Positive associations were observed for discretionary food (OR = 1·54; CI: 0·97, 2·44; P-trend = 0·04) and total fat intake (OR per 10 g/d = 1·11; CI: 1·00, 1·23), the association for fat was less robust in sensitivity analyses. No association was observed for meat, protein, dairy products or diet scores. Diet is a potential modifiable risk factor for BE. Public health and clinical guidelines that incorporate dietary recommendations could contribute to reduction in risk of BE and, thereby, oesophageal adenocarcinoma.

Demographic and lifestyle risk factors for gastroesophageal reflux disease and Barrett's esophagus in Australia.

We examined demographic and lifestyle risk factors for incidence of gastroesophageal reflux disease (GERD) and Barrett's esophagus (BE) in an Australian cohort of 20,975 participants aged 40-63 at recruitment (1990-1994). Information on GERD and BE was collected between 2007 and 2010. GERD symptoms were defined as self-reported heartburn or acid regurgitation. BE was defined as endoscopically confirmed columnar-lined esophagus. Risk factors for developing GERD symptoms, BE diagnosis, age at symptom onset, and age at BE diagnosis were quantified using regression. During a mean follow-up of 15.8 years, risk of GERD symptoms was 7.5% (n = 1,318) for daily, 7.5% (n = 1,333) for 2-6 days/week, and 4.3% (n = 751) for 1 day/week. There were 210 (1.0%) endoscopically diagnosed BE cases, of whom 141 had histologically confirmed esophageal intestinal metaplasia. Female sex, younger age, lower socioeconomic position (SEP) and educational attainment, and former smoking were associated with higher GERD risk. Male sex and smoking were associated with earlier GERD symptom onset. Men, older participants, those with higher SEP, and former smokers were at higher BE risk. There was some evidence higher SEP was associated with earlier BE diagnosis. GERD and BE had different demographic risk factors but shared similar lifestyle factors. Earlier GERD symptom onset for men and smokers might have contributed to higher BE risk. The SEP patterns observed for GERD and BE suggest potential inequity in access to care. These findings would be important in the development of clinical risk prediction models for early detection of BE.

Prediagnosis alcohol intake and metachronous cancer risk in cancer survivors: A prospective cohort study.

Alcohol consumption is a known cause of cancer, but its role in the etiology of second primary (metachronous) cancer is uncertain. Associations between alcohol intake up until study enrollment (prediagnosis) and risk of metachronous cancer were estimated using 9435 participants in the Melbourne Collaborative Cohort Study who were diagnosed with their first invasive cancer after enrollment (1990-1994). Follow-up was from date of first invasive cancer until diagnosis of metachronous cancer, death or censor date (February 2018), whichever came first. Alcohol intake for 10-year periods from age 20 until decade encompassing baseline using recalled beverage-specific frequency and quantity was used to calculate baseline and lifetime intakes, and group-based intake trajectories. We estimated hazard ratios (HRs) and 95% confidence intervals (CIs), adjusted for potential confounders. After a mean follow-up of 7 years, 1512 metachronous cancers were identified. A 10 g/d increment in prediagnosis lifetime alcohol intake (HR = 1.03, 95% CI = 1.00-1.06; Pvalue = .02) and an intake of ≥60 g/d (HR = 1.32, 95% CI = 1.01-1.73) were associated with increased metachronous cancer risk. We observed positive associations (per 10 g/d increment) for metachronous colorectal (HR = 1.07, 95% CI = 1.00-1.14), upper aero-digestive tract (UADT) (HR = 1.16, 95% CI = 1.00-1.34) and kidney cancer (HR = 1.24, 95% CI = 1.10-1.39). Although these findings were partly explained by effects of smoking, the association for kidney cancer remained unchanged when current smokers or obese individuals were excluded. Alcohol intake trajectories over the life course confirmed associations with metachronous cancer risk. Prediagnosis long-term alcohol intake, and particularly heavy drinking, may increase the risk of metachronous cancer, particularly of the colorectum, UADT and kidney.

Lifetime alcohol intake, drinking patterns over time and risk of stomach cancer: A pooled analysis of data from two prospective cohort studies.

Alcohol consumption is causally linked to several cancers but the evidence for stomach cancer is inconclusive. In our study, the association between long-term alcohol intake and risk of stomach cancer and its subtypes was evaluated. We performed a pooled analysis of data collected at baseline from 491 714 participants in the European Prospective Investigation into Cancer and Nutrition and the Melbourne Collaborative Cohort Study. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated for incident stomach cancer in relation to lifetime alcohol intake and group-based life course intake trajectories, adjusted for potential confounders including Helicobacter pylori infection. In all, 1225 incident stomach cancers (78% noncardia) were diagnosed over 7 094 637 person-years; 984 in 382 957 study participants with lifetime alcohol intake data (5 455 507 person-years). Although lifetime alcohol intake was not associated with overall stomach cancer risk, we observed a weak positive association with noncardia cancer (HR = 1.03, 95% CI: 1.00-1.06 per 10 g/d increment), with a HR of 1.50 (95% CI: 1.08-2.09) for ≥60 g/d compared to 0.1 to 4.9 g/d. A weak inverse association with cardia cancer (HR = 0.93, 95% CI: 0.87-1.00) was also observed. HRs of 1.48 (95% CI: 1.10-1.99) for noncardia and 0.51 (95% CI: 0.26-1.03) for cardia cancer were observed for a life course trajectory characterized by heavy decreasing intake compared to light stable intake (Phomogeneity = .02). These associations did not differ appreciably by smoking or H pylori infection status. Limiting alcohol use during lifetime, particularly avoiding heavy use during early adulthood, might help prevent noncardia stomach cancer. Heterogeneous associations observed for cardia and noncardia cancers may indicate etiologic differences.

Weight gain and lifestyle factors in women with and without polycystic ovary syndrome.

STUDY QUESTION: Do extrinsic factors including lifestyle, psychosocial factors and healthcare professional engagement independently contribute to weight gain in women with and without polycystic ovary syndrome (PCOS)? SUMMARY ANSWER: Women with PCOS had a higher rate of weight gain than women without PCOS which was most marked in those with unhealthy lifestyles. WHAT IS KNOWN ALREADY: Women with PCOS have a higher prevalence of overweight/obesity and greater weight gain than women without PCOS. The association of lifestyle factors with weight change in PCOS is not known. STUDY DESIGN, SIZE, DURATION: The study was a population-based observational study with data collected from seven surveys over 19 years (N = 14 127; Survey 1) involving women with and without PCOS. PARTICIPANTS/MATERIALS, SETTING, METHODS: We used data from the 1973-1978 birth cohort of the Australian Longitudinal Study on Women's Health. MAIN RESULTS AND THE ROLE OF CHANCE: Women with PCOS gained more weight annually (0.26 kg/year; 95% CI 0.12, 0.39; P < 0.0001) and over 19 years (4.62 kg; 95% CI 3.04, 6.21; P < 0.0001) than women without PCOS (adjusted analyses). For all women, there were positive associations between weight gain and energy intake, sitting time and stress; inverse associations with fibre intake and physical activity (PA); and no associations with diet quality, glycaemic index, healthcare utilization, depression or anxiety. There were interactions between lifestyle factors (energy intake P = 0.006, glycaemic index P = 0.025, sitting time P = 0.041 and PA P = 0.021), PCOS status and time such that weight gain varied between women with and without PCOS according to these factors. LIMITATIONS, REASONS FOR CAUTION: The limitations of this study include the use of self-reported measures such as diet, PA, sitting time, psychological factors and health care utilization. WIDER IMPLICATIONS OF THE FINDINGS: While women with PCOS are more prone to weight gain, lifestyle factors have a more profound impact on weight gain in women with PCOS than without PCOS. These study findings have implications for understanding the mechanisms of weight gain in women with PCOS. They also highlight the importance of early lifestyle intervention as soon as PCOS is diagnosed to address modifiable extrinsic factors and prevent excess weight gain and worsening of the clinical features of PCOS. STUDY FUNDING/COMPETING INTEREST(S): M.A.A. is funded by the Monash International Tuition Scholarship and Monash Graduate Scholarship and L.J.M. is funded by a National Heart Foundation Future Leader Fellowship. The authors declared no conflict of interest. TRIAL REGISTRATION NUMBER: N/A.

Inflammation-Related Marker Profiling of Dietary Patterns and All-cause Mortality in the Melbourne Collaborative Cohort Study.

BACKGROUND: Nutritional epidemiology research using self-reported dietary intake is prone to measurement error. Objective methods are being explored to overcome this limitation. OBJECTIVES: We aimed to examine 1) the association between plasma markers related to inflammation and derive marker scores for dietary patterns [Mediterranean dietary score (MDS), energy-adjusted Dietary Inflammatory Index (E-DIITM), Alternative Healthy Eating Index 2010 (AHEI)] and 2) the associations of these marker scores with mortality. METHODS: Weighted marker scores were derived from the cross-sectional association between 30 plasma markers and each dietary score (assessed using food-frequency questionnaires) using linear regression for 770 participants in the Melbourne Collaborative Cohort Study (aged 50-82 y). Prospective associations between marker scores and mortality (n = 249 deaths) were assessed using Cox regression (median follow-up: 14.4 y). RESULTS: The MDS, E-DII, and AHEI were associated (P < 0.05) with 9, 14, and 11 plasma markers, respectively. Healthier diets (higher MDS and AHEI, and lower anti-inflammatory, E-DII) were associated with lower concentrations of kynurenines, neopterin, IFN-γ, cytokines, and C-reactive protein. Five of 6 markers common to the 3 dietary scores were components of the kynurenine pathway. The 3 dietary-based marker scores were highly correlated (Spearman ρ: -0.74, -0.82, and 0.93). Inverse associations (for 1-SD increment) were observed with all-cause mortality for the MDS marker score (HR: 0.84; 95% CI: 0.72-0.98) and the AHEI marker score (HR: 0.76; 95% CI: 0.66-0.89), whereas a positive association was observed with the E-DII marker score (HR: 1.18; 95% CI: 1.01-1.39). The same magnitude of effect was not observed for the respective dietary patterns. CONCLUSIONS: Markers involved in inflammation-related processes are associated with dietary quality, including a substantial overlap between markers associated with the MDS, the E-DII, and the AHEI, especially kynurenines. Unfavorable marker scores, reflecting poorer-quality diets, were associated with increased mortality.

Sleep disturbances may influence lifestyle behaviours in women with self-reported polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is associated with a higher prevalence of sleep disturbances and obesity. Treatment of PCOS includes modifying lifestyle behaviours associated with weight management. However, poor sleep in the non-PCOS population has been associated with poorer lifestyle behaviours. The aim was to investigate whether sleep disturbance confounds or modifies the association between lifestyle factors and PCOS. This was a cross-sectional analysis from the Australian Longitudinal Study on Women's Health cohort aged 31-36 years in 2009 were analysed (n 6067, 464 PCOS, 5603 non-PCOS). Self-reported data were collected on PCOS, anthropometry, validated modified version of the Active Australia Physical Activity survey, validated FFQ and sleep disturbances through latent class analysis. Women with PCOS had greater adverse sleep symptoms including severe tiredness (P = 0·001), difficulty sleeping (P < 0·001) and restless sleep (P < 0·001), compared with women without PCOS. Women with PCOS also had higher energy consumption (6911 (sd 2453) v. 6654 (sd 2215) kJ, P = 0·017), fibre intake (19·8 (sd 7·8) v. 18·9 (sd 6·9) g, P = 0·012) and diet quality (dietary guidelines index (DGI)) (88·1 (sd 11·6) v. 86·7 (sd 11·1), P = 0·008), lower glycaemic index (50·2 (sd 4·0) v. 50·7 (sd 3·9), P = 0·021) and increased sedentary behaviour (6·3 (sd 2·8) v. 5·9 (sd 2·8) h, P = 0·009). There was a significant interaction between PCOS and sleep disturbances for DGI (P = 0·035), therefore only for women who had adequate sleep was PCOS associated with a higher DGI. For women with poorer sleep, there was no association between PCOS and DGI. The association between PCOS and improved diet quality may only be maintained if women can obtain enough good quality sleep.

BMI trajectory and subsequent risk of type 2 diabetes among middle-aged women.

BACKGROUND AND AIMS: Little is known about how weight trajectories among women during menopausal transition and beyond may be related to risk of type 2 diabetes mellitus (T2DM). The aim of this study was to examine associations between body mass index (BMI) trajectories over 20 years, age of obesity onset, cumulative obese-years and incidence of T2DM among middle-aged women. METHODS AND RESULTS: 12,302 women enrolled in the Australian Longitudinal Study on Women's Health (ALSWH) were surveyed in 1996 (Survey 1, age 45-50), 1998 and then every three years to 2016. Self-reported weight and height were collected for up to eight time points. Incident diabetes was assessed via validated self-report of physician-diagnosed diabetes. Growth mixture models were used to identify distinct BMI trajectories. A total of 1380 (11.2%) women newly developed T2DM over an average 16 years of follow-up. Seven distinct BMI trajectories were identified with differential risk of developing T2DM. Initial BMI was positively associated with T2DM risk. We also observed that risk of T2DM was positively associated with rapid weight increase, early age of obesity onset and greater obese-years. CONCLUSION: Slowing down weight increases, delaying the onset of obesity, or reducing cumulative exposure to obesity may substantially lower the risk of developing T2DM.

Diet scores and prediction of general and abdominal obesity in the Melbourne collaborative cohort study.

OBJECTIVE: To ascertain which of the Alternative Healthy Eating Index (AHEI) 2010, Dietary Inflammatory Index (DII®) and Mediterranean Diet Score (MDS) best predicted BMI and waist-to-hip circumference ratio (WHR). DESIGN: Body size was measured at baseline (1990-1994) and in 2003-2007. Diet was assessed at baseline using a FFQ, along with age, sex, socio-economic status, smoking, alcohol drinking, physical activity and country of birth. Regression coefficients and 95 % CI for the association of baseline dietary scores with follow-up BMI and WHR were generated using multivariable linear regression, adjusting for baseline body size, confounders and energy intake. SETTING: Population-based cohort in Melbourne, Australia. PARTICIPANTS: Included were data from 11 030 men and 16 774 women aged 40-69 years at baseline. RESULTS: Median (IQR) follow-up was 11·6 (10·7-12·8) years. BMI and WHR at follow-up were associated with baseline DII® (Q5 v. Q1 (BMI 0·41, 95 % CI 0·21, 0·61) and WHR 0·009, 95 % CI 0·006, 0·013)) and AHEI (Q5 v. Q1 (BMI -0·51, 95 % CI -0·68, -0·35) and WHR -0·011, 95 % CI -0·013, -0·008)). WHR, but not BMI, at follow-up was associated with baseline MDS (Group 3 most Mediterranean v. G1 (BMI -0·05, 95 % CI -0·23, 0·13) and WHR -0·004, 95 % CI -0·007, -0·001)). Based on Akaike's Information Criterion and Bayesian Information Criterion statistics, AHEI was a stronger predictor of body size than the other diet scores. CONCLUSIONS: Poor quality or pro-inflammatory diets predicted overall and central obesity. The AHEI may provide the best way to assess the obesogenic potential of diet.