Oxidative stress, anti-oxidants and the cross-sectional and longitudinal association with depressive symptoms: results from the CARDIA study.

Depression may be accompanied by increased oxidative stress and decreased circulating anti-oxidants. This study examines the association between depressive symptoms, F2-isoprostanes and carotenoids in a US community sample. The study includes 3009 participants (mean age 40.3, 54.2% female) from CARDIA (Coronary Artery Risk Development in Young Adults). Cross-sectional analyses were performed on data from the year 15 examination (2000-2001) including subjects whose depressive symptoms were assessed with the Center for Epidemiologic Studies Depression Scale (CES-D) and had measurements of plasma F2-isoprostanes (gas chromatography/mass spectrometry) or serum carotenoids (high-performance liquid chromatography). Carotenoids zeaxanthin/lutein, ß-cryptoxanthin, lycopene, α-carotene, ß-carotene were standardized and summed. Longitudinal analyses were conducted using the data from other examinations at 5-year intervals. Cross-lagged analyses investigated whether CES-D predicted F2-isoprostanes or carotenoids at the following exam, and vice versa. Regression analyses were controlled for sociodemographics, health and lifestyle factors. F2-isoprostanes were higher in subjects with depressive symptoms (CES-D ⩾ 16) after adjustment for sociodemographics (55.7 vs 52.0 pg ml(-1); Cohen's d = 0.14, P < 0.001). There was no difference in F2-isoprostanes after further adjustment for health and lifestyle factors. Carotenoids were lower in those with CES-D scores ⩾ 16, even after adjustment for health and lifestyle factors (standardized sum 238.7 vs 244.0, Cohen's d = -0.16, P < 0.001). Longitudinal analyses confirmed that depression predicts subsequent F2-isoprostane and carotenoid levels. Neither F2-isoprostanes nor carotenoids predicted subsequent depression. In conclusion, depressive symptoms were cross-sectionally and longitudinally associated with increased F2-isoprostanes and decreased carotenoids. The association with F2-isoprostanes can largely be explained by lifestyle factors, but lower carotenoids were independently associated with depressive symptoms.

Diet quality and markers of endothelial function: the CARDIA study.

BACKGROUND AND AIM: Dietary patterns are associated cross-sectionally with cellular adhesion molecules (CAMs). We studied prospective associations of three dietary patterns with CAMs. METHODS AND RESULTS: In the Coronary Artery Risk Development in Young Adults (CARDIA) study, diet was assessed at years 0 (1985-86) and 7 (1992-93) examinations. Four circulating CAMs (E-selectin, P-selectin, soluble intercellular adhesion molecule 1 (sICAM-1), and vascular cellular adhesion molecule (VCAM)) were assayed at years 7 and 15 (2000-01). We created one index score "A Priori Diet Quality Score" and derived dietary patterns using principal components analysis (PCA). Multivariable linear regression models predicted year 15 CAMs from averaged (year 0/7) dietary patterns. The A Priori Diet Quality Score rated 46 food groups beneficial, neutral or adverse based on hypothesized health effects. We derived two PCA dietary patterns: "fruit and vegetables (FV)" (high intakes of fruit, vegetables, and whole grains) and "meat" (high intakes of red meat, refined grain, and butter). All dietary patterns were related to E-selectin and sICAM-1. P-selectin was not related to the FV dietary pattern. VCAM was only related to the A Priori Diet Quality Score. Strongest associations were for the meat dietary pattern with E-selectin (effect size 28% of an SD (+3.9/13.7 ng/mL)) and P-selectin (effect size 37% of an SD (+4.1/11.2 ng/mL)) and the A Priori Diet Quality Score with sICAM-1 (effect size 34% of an SD (-15.1/44.7 ng/mL)) and VCAM (effect size of 26% of an SD (-45.1/170.3 ng/mL)). CONCLUSION: This prospective analysis suggests that dietary patterns are associated with CAMs.

Higher parity is associated with an increased risk of type-II diabetes in Chinese women: the Singapore Chinese Health Study.

OBJECTIVE: The association between parity and type-II diabetes has been studied primarily in Western populations, and the findings have been inconsistent. Here, we examine whether parity was positively associated with incident type-II diabetes in Singaporean Chinese women. DESIGN: Prospective cohort study. SETTING: Singapore. POPULATION: A total of 25,021 Singaporean Chinese women aged 45-74 years from the Singapore Chinese Health Study who were free of cancer, heart disease, stroke, and diabetes at baseline (1993-1998). METHODS: Women were followed through 2004 for incident diabetes. Hazard ratios for type-II diabetes were computed across parity (of live births) categories and adjusted for baseline age, interview year, dialect, education, smoking, dietary pattern, physical activity, age at menarche, oral contraceptive use, menopausal status, hormone therapy use, and body mass index (BMI). MAIN OUTCOME MEASURE: Self-reported diabetes, as diagnosed by a doctor. RESULTS: Over an average of 5.7 person-years of follow-up, 1294 women were diagnosed with diabetes. Before and after multivariable adjustment there was a positive graded association between parity and type-II diabetes risk (P < 0.001). In the fully adjusted model, which included adult BMI, the risk of type-II diabetes increased by 31% (from -2 to 76%), 62% (from 22 to 116%), and 74% (from 29 to 133%) for women with one or two, three or four, and five or more live births, respectively, compared with women with no live births. Moreover, in a supplementary multivariate analysis in non-diabetic women we found a positive monotonic association between parity and glycated haemoglobin (HbA1c) (P = 0.01). CONCLUSIONS: Increased parity may be a risk factor for type-II diabetes in Chinese women. More research is needed on lifestyle and physiologic factors that may explain this association.

Stronger influence of maternal than paternal obesity on infant and early childhood body mass index: the Fels Longitudinal Study.

WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT: Excessive early childhood adiposity is a prevalent and increasing concern in many parts of the world. Parental obesity is one of the several factors previously associated with infant and early childhood weight, length and adiposity. Parental obesity represents a surrogate marker of the complex interplay among genetic, epigenetic and shared environmental factors, and is potentially modifiable. The relative contributions of maternal and paternal body mass index (BMI) to infant and early childhood growth, as well as the timing of such effects, have not been firmly established. WHAT THIS STUDY ADDS: Utilizing serial infant measurements and growth curve modelling, this is the largest study to fully characterize and formally compare associations between maternal and paternal BMI and offspring growth across the entire infancy and early childhood period. Maternal obesity is a stronger determinant of offspring BMI than paternal obesity at birth and from 2 to 3 years of age, suggesting that prevention efforts focused particularly on maternal lifestyle and BMI may be important in reducing excess infant BMI. The observation that maternal BMI effects are not constant, but rather present at birth, wane and re-emerge during late infancy, suggests that there is a window of opportunity in early infancy when targeted interventions on children of obese mothers may be most effective. BACKGROUND/OBJECTIVE: Parental obesity influences infant body size. To fully characterize their relative effects on infant adiposity, associations between maternal and paternal body mass index (BMI) category (normal: ≤25 kg m(-2) , overweight: 25 - <30 kg m(-2) , obese: ≥30 kg m(-2) ) and infant BMI were compared in Fels Longitudinal Study participants. METHODS: A median of 9 serial weight and length measures from birth to 3.5 years were obtained from 912 European American children born in 1928-2008. Using multivariable mixed effects regression, contributions of maternal vs. paternal BMI status to infant BMI growth curves were evaluated. Cubic spline models also included parental covariates, infant sex, age and birth variables, and interactions with child's age. RESULTS: Infant BMI curves were significantly different across the three maternal BMI categories (Poverall < 0.0001), and offspring of obese mothers had greater mean BMI at birth and between 1.5 and 3.5 years than those of over- and normal weight mothers (P ≤ 0.02). Average differences between offspring of obese and normal weight mothers were similar at birth (0.8 kg m(-2) , P = 0.0009) and between 2 and 3.5 years (0.7-0.8 kg m(-2) , P < 0.0001). Infants of obese fathers also had BMI growth curves distinct from those of normal weight fathers (P = 0.02). Infant BMI was more strongly associated with maternal than paternal obesity overall (P < 0.0001); significant differences were observed at birth (1.11 kg m(-2) , P = 0.006) and from 2 to 3 years (0.62 kg m(-2) , P3 years = 0.02). CONCLUSION: At birth and in later infancy, maternal BMI has a stronger influence on BMI growth than paternal BMI, suggesting weight control in reproductive age women may be of particular benefit for preventing excess infant BMI.