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Qualitative food frequency questionnaires (Q-FFQ) omit portion size information from dietary assessment. This restricts researchers to consumption frequency data, limiting investigations of dietary composition (i.e., energy-adjusted intakes) and misreporting. To support such researchers, we provide an instructive example of Q-FFQ energy intake estimation that derives typical portion size information from a reference survey population and evaluates misreporting. A sample of 1,919 Childhood Determinants of Adult Health Study (CDAH) participants aged 26-36 years completed a 127-item Q-FFQ. We assumed sex-specific portion sizes for Q-FFQ items using 24-h dietary recall data from the 2011-2012 Australian National Nutrition and Physical Activity Survey (NNPAS) and compiled energy density values primarily using the Australian Food Composition Database. Total energy intake estimation was daily equivalent frequency × portion size (g) × energy density (kJ/g) for each Q-FFQ item, summed. We benchmarked energy intake estimates against a weighted sample of age-matched NNPAS respondents (n = 1,383). Median (interquartile range) energy intake was 9,400 (7,580-11,969) kJ/day in CDAH and 9,055 (6,916-11,825) kJ/day in weighted NNPAS. Median energy intake to basal metabolic rate ratios were 1.43 (1.15-1.78) in CDAH and 1.35 (1.03-1.74) in weighted NNPAS, indicating notable underreporting in both samples, with increased levels of underreporting among the overweight and obese. Using the Goldberg and predicted total energy expenditure methods for classifying misreporting, 65 and 41% of CDAH participants had acceptable/plausible energy intake estimates, respectively. Excluding suspected CDAH misreporters improved the plausibility of energy intake estimates, concordant with expected body weight associations. This process can assist researchers wanting an estimate of energy intake from a Q-FFQ and to evaluate misreporting, broadening the scope of diet-disease investigations that depend on

BACKGROUND: Dietary patterns and their association with subsequent clinical course have not been well studied in early multiple sclerosis (MS). OBJECTIVES: To describe dietary patterns in people in 5 years following first clinical demyelination and assess associations with MS conversion and relapse. METHODS: This study included baseline food frequency questionnaire dietary intake (entry to the Ausimmune Study) and 5-year follow-up; iterated principal factor analysis was applied. MS conversion and relapse risks were assessed by Cox proportional hazards models, adjusted for age, sex, study site, education, body mass index (BMI), smoking and omega-3 supplement use. RESULTS: In cases with a first clinical diagnosis of central nervous system (CNS) demyelination, we identified three major dietary patterns, 'Prudent', 'High-Vegetable' and 'Mixed', explaining 43%, 37% and 24% of diet variance in dietary intake, respectively. Fruits, vegetables, fish, wholegrains and nuts loaded highly on the Prudent pattern, starchy vegetables and legumes on the High-Vegetable pattern, and meats and alcohol on the Mixed pattern. Diet factor scores were not associated with MS conversion risk. Those with baseline Prudent scores above the median had significantly lower relapse risk (adjusted hazard ratio = 0.54, 95% confidence interval (CI) 0.37, 0.81) with some evidence of a plateau effect. CONCLUSION: Prudent diet factor score above the median was prospectively associated with lower relapse risk in the 5 years following the first clinical demyelinating event.

PURPOSE: To investigate the relationship between time spent outdoors, at particular ages in childhood and adolescence, and myopia status in young adulthood using serum 25-hydroxyvitamin D [25(OH)D] concentration as a biomarker of time spent outdoors. METHODS: Participants of the Raine Study Generation 2 cohort had 25(OH)D concentrations measured at the 6-, 14-, 17- and 20-year follow-ups. Participants underwent cycloplegic autorefraction at age 20 years, and myopia was defined as a mean spherical equivalent -0.50 dioptres or more myopic. Logistic regression was used to analyse the association between risk of myopia at age 20 years and age-specific 25(OH)D concentrations. Linear mixed-effects models were used to analyse trajectory of 25(OH)D concentrations from 6 to 20 years. RESULTS: After adjusting for sex, race, parental myopia, body mass index and studying status, myopia at 20 years was associated with lower 25(OH)D concentration at 20 years (per 10 nmol/L decrease, odds ratio (aOR)=1.10, 95% CI: 1.02, 1.18) and a low vitamin D status [25(OH)D < 50 nmol/L] at 17 years (aOR = 1.71, 95% CI: 1.06, 2.76) and 20 years (aOR = 1.71, 95% CI: 1.14, 2.56), compared to those without low vitamin D status. There were no associations between 25(OH)D at younger ages and myopia. Individuals who were myopic at 20 years had a 25(OH)D concentration trajectory that declined, relative to non-myopic peers, with increasing age. Differences in 25(OH)D trajectory between individuals with and without myopia were greater among non-Caucasians compared to Caucasians. CONCLUSIONS: Myopia in young adulthood was most strongly associated with recent 25(OH)D concentrations, a marker of time spent outdoors.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

PURPOSE: Potential links may exist between vitamin A intake and myopia via various pathways. In this study, we examined the association between dietary vitamin A intake during adolescence and myopia in early adulthood. METHODS: We performed a prospective analysis utilizing data collected from participants of the Raine Study Gen2. Dietary vitamin A intake, determined via food frequency questionnaires completed at ages 14, 17, and 20 years, was compared with ophthalmic measurements collected at year 20. Low vitamin A levels were defined as <600 µg/day. Regression models were used to adjust for ocular sun exposure level, educational level, and parental myopia as potential confounders. RESULTS: A total of 642 subjects were analyzed. Although those with adequate vitamin A intakes were less likely to be myopic (P = 0.03), this association became insignificant when adjusted for potential confounding factors in logistic regression modeling (odds ratio, 0.59; 95% confidence interval, 0.98-2.52; P = 0.06). CONCLUSIONS: There were no significant associations between total vitamin A intakes during adolescence and year 20 refractive errors after adjustment for confounders. Replication of this finding and further investigations are essential to rule out the suggestion that sufficient vitamin A intake during adolescence is associated with lower risk of myopia in early adulthood. TRANSLATIONAL RELEVANCE: Our findings are not definitive that ingesting foods high in vitamin A during childhood and adolescence does not have a role for preventing myopia in early adulthood.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Background: Several studies have shown effects of current and maternal smoking during pregnancy on DNA methylation of CpG sites in newborns and later in life. Here, we hypothesized that there are long-term and persistent epigenetic effects following maternal smoking during pregnancy on adolescent offspring DNA methylation, independent of paternal and postnatal smoke exposure. Furthermore, we explored the association between DNA methylation and cardiometabolic risk factors at 17 years of age. Materials and Methods: DNA methylation was measured using the Illumina HumanMethylation450K BeadChip in whole blood from 995 participants attending the 17-year follow-up of the Raine Study. Linear mixed effects models were used to identify differential methylated CpGs, adjusting for parental smoking during pregnancy, and paternal, passive, and adolescent smoke exposure. Additional models examined the association between DNA methylation and paternal, adolescent, and passive smoking over the life course. Offspring CpGs identified were analyzed against cardiometabolic risk factors (blood pressure, triacylglycerols (TG), high-density lipoproteins cholesterol (HDL-C), and body mass index). Results: We identified 23 CpGs (genome-wide p level: 1.06 × 10-7) that were associated with maternal smoking during pregnancy, including associated genes AHRR (cancer development), FTO (obesity), CNTNAP2 (developmental processes), CYP1A1 (detoxification), MYO1G (cell signalling), and FRMD4A (nicotine dependence). A sensitivity analysis showed a dose-dependent relationship between maternal smoking and offspring methylation. These results changed little following adjustment for paternal, passive, or offspring smoking, and there were no CpGs identified that associated with these variables. Two of the 23 identified CpGs [cg00253568 (FTO) and cg00213123 (CYP1A1)] were associated with either TG (male and female), diastolic blood pressure (female only), or HDL-C (male only), after Bonferroni correction. D

Dietary guidelines recommend removing visible fat from meat, choosing low-fat options and cooking with oil instead of butter. This study examined cross-sectional associations between fat-related eating behaviors and a continuous metabolic syndrome (cMetSyn) score among young adults. During 2004⁻2006, 2071 participants aged 26⁻36 years reported how often they trimmed fat from meat, consumed low-fat dairy products and used different types of fat for cooking. A fasting blood sample was collected. Blood pressure, weight and height were measured. To create the cMetSyn score, sex-specific principal component analysis was applied to normalized risk factors of the harmonized definition of metabolic syndrome. Higher score indicates higher risk. For each behavior, differences in mean cMetSyn score were calculated using linear regression adjusted for confounders. Analyses were stratified by weight status (Body mass index (BMI) < 25 kg/m² or ≥25 kg/m²). Mean cMetSyn score was positively associated with consumption of low-fat oily dressing (PTrend = 0.013) among participants who were healthy weight and frequency of using canola/sunflower oil for cooking (PTrend = 0.008) among participants who were overweight/obese. Trimming fat from meat, cooking with olive oil, cooking with butter, and consuming low-fat dairy products were not associated with cMetSyn score. Among young adults, following fat-related dietary recommendations tended to not be associated with metabolic risk.

BACKGROUND AND AIMS: Non-alcoholic fatty liver disease (NAFLD) and polycystic ovary syndrome (PCOS) share risk associations of adiposity and insulin resistance. We examined the impact of a PCOS diagnosis on the metabolic phenotype of adolescent girls with NAFLD and compared this to girls without PCOS or NAFLD and to age-matched boys. METHODS: Community-based adolescents from the Raine Cohort participated in assessments for NAFLD (572 girls and 592 boys) and PCOS (244 girls). One hundred and ninety-nine girls attended both assessments. RESULTS: Amongst the 199 girls, PCOS was diagnosed in 16.1% and NAFLD in 18.6%. NAFLD was diagnosed in 10.1% of the boys. NAFLD was more prevalent in girls with PCOS than girls without PCOS (37.5% vs 15.1%, P = 0.003). Girls with NAFLD plus PCOS had greater adiposity (waist circumference, body mass index, suprailiac skinfold thickness [SST], serum androgens, high-sensitivity C-reactive protein, ferritin, homeostasis model assessment for insulin resistance (HOMA-IR), and lower serum sex hormone binding globulin levels than girls with NAFLD without a PCOS diagnosis (all P < 0.05). Girls with NAFLD plus PCOS had similar adiposity, HOMA-IR, and adiponectin levels to boys with NAFLD, but more adiposity, serum leptin and HOMA-IR than both girls and boys without NAFLD. PCOS (odds ratios 2.99, 95% confidence intervals 1.01-8.82, P = 0.048) and SST (odds ratios 1.14, 95% confidence intervals 1.08-1.20, P < 0.001) independently predicted NAFLD in adolescent girls, however, serum androgens and HOMA-IR levels did not. CONCLUSIONS: Adolescent girls with NAFLD plus PCOS have a similar metabolic phenotype to boys with NAFLD. Increasing SST and pre-existing PCOS independently predict NAFLD in adolescent girls.

Background: Dietary changes may epigenetically modify fetal gene expression during critical periods of development to potentially influence disease susceptibility. This study examined whether maternal and/or fetal folate status in pregnancy is associated with infant allergic outcomes. Methods: Pregnant women (n = 628) were recruited in the last trimester of pregnancy. Folate status determined by both food frequency questionnaires and folate levels in maternal and cord blood serum was examined in relation to infant allergic outcomes at 1 year of age (n = 484). Results: Infants who developed allergic disease (namely eczema) did not show any differences in cord blood or maternal folate levels compared with children without disease. Although maternal folate intake from foods was also not different, folate derived from supplements was higher (P = 0.017) in children with subsequent eczema. Furthermore, infants exposed to >500 μg folic acid/day as a supplement in utero were more likely to develop eczema than those taking <200 μg/day (OR [odds ratio] = 1.85; 95% CI 1.14–3.02;P = 0.013), remaining significant after adjustment for maternal allergy and other confounders. There was a nonlinear relationship between cord blood folate and sensitization, with folate levels <50 nmol/l (OR = 3.02; 95% CI 1.16–7.87; P = 0.024) and >75 nmol/l (OR = 3.59; 95% CI 1.40–9.20; P = 0.008) associated with greater sensitization risk than levels between 50 and 75 nmol/l. Conclusion: Fetal levels between 50 and 75 nmol/l appeared optimal for minimizing sensitization. While folate taken as a supplement in higher doses during the third trimester was associated with eczema, there was no effect on other allergic outcomes including sensitization. Further studies are needed to determine the significance of this.

OBJECTIVE: In light of the obesity epidemic, we aimed to characterize novel childhood adiposity trajectories from birth to age 14 years and to determine their relation to adolescent insulin resistance. RESEARCH DESIGN AND METHODS: A total of 1,197 Australian children with cardiovascular/metabolic profiling at age 14 years were studied serially from birth to age 14 years. Semiparametric mixture modeling was applied to anthropometric data over eight time points to generate adiposity trajectories of z scores (weight-for-height and BMI). Fasting insulin and homeostasis model assessment of insulin resistance (HOMA-IR) were compared at age 14 years between adiposity trajectories. RESULTS: Seven adiposity trajectories were identified. Three (two rising and one chronic high adiposity) trajectories comprised 32% of the population and were associated with significantly higher fasting insulin and HOMA-IR compared with a reference trajectory group (with longitudinal adiposity z scores of approximately zero). There was a significant sex by trajectory group interaction (P < 0.001). Girls within a rising trajectory from low to moderate adiposity did not show increased insulin resistance. Maternal obesity, excessive weight gain during pregnancy, and gestational diabetes were more prevalent in the chronic high adiposity trajectory. CONCLUSIONS: A range of childhood adiposity trajectories exist. The greatest insulin resistance at age 14 years is seen in those with increasing trajectories regardless of birth weight and in high birth weight infants whose adiposity remains high. Public health professionals should urgently target both excessive weight gain in early childhood across all birth weights and maternal obesity and excessive weight gain during pregnancy.

OBJECTIVE: The purpose of this study was to investigate relationships between inflammatory markers and components of a metabolic syndrome cluster in adolescents. RESEARCH DESIGN AND METHODS: This was a cross-sectional analysis of an Australian childhood cohort (n = 1,377) aged 14 years. Cluster analysis defined a "high-risk" group similar to adults with metabolic syndrome. Relevant measures were anthropometry, fasting insulin, glucose, lipids, inflammatory markers, liver function, and blood pressure. RESULTS: Of the children, 29% fell into a high-risk metabolic cluster group compared with 2% by a pediatric metabolic syndrome definition. Relative to the "low-risk" cluster, they had higher BMI (95% CI 19.5-19.8 vs. 24.5-25.4), waist circumference (centimeters) (95% CI 71.0-71.8 vs. 83.4-85.8), insulin (units per liter) (95% CI 1.7-1.8 vs. 3.5-3.9), homeostasis model assessment (95% CI 1.7-1.8 vs. 3.5-3.9), systolic blood pressure (millimeters of mercury) (95% CI 110.8-112.1 vs. 116.7-118.9), and triglycerides (millimoles per liter) (95% CI 0.78-0.80 vs. 1.25-1.35) and lower HDL cholesterol (millimoles per liter) (95% CI 1.44-1.48 vs. 1.20-1.26). Inflammatory and liver function markers were higher in the high-risk group: C-reactive protein (CRP) (P < 0.001), uric acid (P < 0.001), alanine aminotransferase (ALT) (P < 0.001), and gamma-glutamyl transferase (GGT) (P < 0.001). The highest CRP, GGT, and ALT levels were restricted to overweight children in the high-risk group. CONCLUSIONS: Cluster analysis revealed a strikingly high proportion of 14 year olds at risk of cardiovascular disease-related metabolic disorders. Adiposity and the metabolic syndrome cluster are synergistic in the pathogenesis of inflammation. Systemic and liver inflammation in the high-risk cluster is likely to predict diabetes, cardiovascular disease, and nonalcoholic fatty liver disease.

Objective: Dietary intake during adolescence contributes to lifelong eating habits and the development of early risk factors for disease in adulthood. Few studies have examined the dietary patterns of adolescents and the social and environmental factors that may affect them during this life stage. The present study describes dietary patterns in a cohort of adolescents and examines their associations with socio-economic factors, as well as parental and adolescent risk factor behaviours. Design: A semi-quantitative FFQ was used to assess study adolescents’ usual dietary intake over the previous year. Information was collected on family functioning and various socio-economic and risk factor variables via questionnaire. Adolescents visited the study clinic for anthropometric measurements. Setting: The Western Australian Pregnancy Cohort Study (Raine Study), Perth, Western Australia. Subjects: Adolescents (n 1631) aged 14 years from a pregnancy cohort study. Results: Factor analysis identified two distinct dietary patterns that differed predominantly in fat and sugar intakes. The ‘Western’ pattern consisted of high intakes of take-away foods, soft drinks, confectionery, French fries, refined grains, full-fat dairy products and processed meats. The ‘healthy’ pattern included high intakes of whole grains, fruit, vegetables, legumes and fish. ANOVA showed that the ‘Western’ dietary pattern was positively associated with greater television viewing and having a parent who smoked, and was inversely associated with family income. The ‘healthy’ pattern was positively associated with female gender, greater maternal education, better family functioning and being in a two-parent family, and was inversely associated with television viewing. Conclusions: The study suggests that both lifestyle factors and family psycho-social environment are related to dietary patterns in Australian adolescents.

The aim of this study was to examine prospectively the relation between duration of breast feeding and cognitive outcomes. A cohort study of 2860 children enrolled before birth provided data from 2393 term infants of English-speaking mothers. Of these, complete infant feeding data in the first year of life and verbal cognitive IQ (Peabody Picture Vocabulary Test - PPVT-R) were available for 1450 children at 6 years, and a performance subtest (Perceptual organisation WISC - Block Design) for 1375 children at 8 years. Full breast feeding was categorised as none,> 0 to < 4 months, 4-6 months and> 6 months. Associations between breast-feeding duration and PPVT-R at 6 years and Block Design at 8 years were estimated before and after adjustment for gender, gestational age, maternal age, maternal education, parental smoking and the presence of older siblings. The early cessation of full breast feeding was associated with reduced verbal IQ and the performance subtest. In unadjusted analysis, mean standardised PPVT-R scores were 6.44 points greater (P < 0.0001) in children fully breast fed for> 6 months compared with those never breast fed. After adjustment, mean PPVT-R scores were 3.56 points higher in children fully breast fed for> 6 months compared with those children never breast fed (P = 0.003). Similarly, Block Design scores were higher in those fully breast fed for> 6 months compared with those never breast fed in unadjusted (P = 0.001) but not adjusted analyses (P = 0.223). Interactions between maternal education (four levels) and breast feeding demonstrated a positive association of maternal education on verbal IQ (F = 2.64; P = 0.005) in children breast fed for longer but not on performance (F = 0.74; P = 0.67). The early introduction of milk other than breast milk was associated with reduced verbal IQ after adjustment for social and perinatal confounders. Although these effects were interacting with maternal education, they may act through undefined mechanisms in