High-density lipoprotein-cholesterol (HDL-C) levels are influenced by gender and by genetic and environmental factors. We aimed to assess the impact of passive smoking exposure since birth on HDL-C levels of nonsmoking adolescents at age 17 years and to determine whether there was a gender difference in the relationship between smoking exposure and HDL-C. A total of 804 nonsmoking adolescents with biochemical, anthropometric, and lifestyle data from a cohort of 1754 adolescents (mean age, 17 ± 0.25 y) of the Western Australian Pregnancy Cohort (Raine) Study had data of maternal smoking during pregnancy and smoking exposure in the household over 17 years. HDL-C was analyzed using multivariable linear regression, with adjustment for early-life, adiposity, and current lifestyle confounders. HDL-C levels were significantly lower in girls exposed to passive smoking compared to those not exposed (regression coefficient b = −0.09 [95% confidence interval, −0.15, −0.03]); this was not observed in boys (b = 0.02 [95% confidence interval, −0.04, 0.08]), with a significant sex interaction P = .009. The effects of passive smoking in girls persisted after adjusting for oral contraceptive use. This study has shown a gender difference in the relationship between passive smoking exposure since birth and HDL-C in late adolescence. Exposure to passive smoking in girls could have adverse consequences on their risk of cardiovascular disease in adulthood. These findings reinforce the need for future public health measures to reduce children's exposure to passive smoking.
Objective This study aimed to examine the association between age at menarche and a range of cardiovascular disease (CVD) risk factors at 17 and 20 years of age, and whether this was influenced by childhood body mass index (BMI). Methods Of the 1413 girls born in the Western Australian Pregnancy Cohort (Raine) Study, 846 had age at menarche recorded. Subsequently 557 underwent metabolic assessment at 17 years and 541 at 20 years. Associations between age at menarche and cardiovascular risk factors, and being in a high-risk metabolic cluster at 17 and 20 years, or having the metabolic syndrome at 20 years, were investigated by linear mixed effects and logistic regressions, respectively. Results Each year later of onset of menarche was associated with a 0.75 kg/m2 reduction in BMI (coefficient -0.75 [95%CI -1.06, -0.44]), and an approximate 30% reduction in the odds of being in the high-risk metabolic cluster at 17 years (OR = 0.73 [95%CI 0.57, 0.94]) and 20 years of age (OR = 0.68 [95%CI 0.52, 0.87]), and a 40% reduction in the odds of having the metabolic syndrome at 20 years (OR = 0.60 [95% CI 0.41, 0.88]). These data show earlier age at menarche was associated with increased BMI and odds of being in the high-risk metabolic cluster at 17 and 20 years, and increased odds of having the metabolic syndrome at 20 years. However, these associations were no longer statistically significant after adjustment for BMI at age 8 years. Current smoking, alcohol consumption, physical activity, socio-economic status, or hormonal contraceptives use did not affect these associations. Conclusions Earlier age at menarche may be indicative of a higher risk profile for CVD in young adulthood. Our findings suggest that targeted interventions to reduce BMI in girls who experience menarche at younger age may reduce CVD risk in the future.
C-reactive protein (CRP), smoking, and oral contraceptive (OC) use are associated with CVD risk in adults. This study examines the effect of smoking on high-sensitivity CRP (hs-CRP) levels, and the interactive effects of sex and OC use on this relationship in an adolescent cohort. A total of 1,050 adolescents (mean age 17 ± 0.25 years) from the Western Australian Pregnancy Cohort (Raine) Study had anthropometric, lifestyle, and metabolic measures recorded. The association between smoking status and log-transformed hs-CRP was analyzed using multivariable Tobit linear regression models, with adjustment for adiposity, lifestyle, and early-life confounders. A three-level variable (girls not using OCs, girls using OCs, and boys) was employed to assess the interactive effects of sex, OC use, and smoking. Smoking associated with higher hs-CRP levels in girls not using OCs (b = 0.571; P = 0.001), but not in girls using OCs (b = -0.117; P = 0.598) or in boys (b = 0.183; P = 0.2). OC use in nonsmoking girls was the strongest factor associated with higher hs-CRP levels (b = 1.189; P < 0.001). This study has demonstrated a more robust effect of smoking on hs-CRP levels in girls not using OCs compared with boys. The findings may explain why CVD risk conferred by smoking is higher in women than in men.
Objective: Animal studies have shown intrauterine androgen exposure leads to offspring adult cardiovascular dysfunction, including hypertension. In humans, androgens in umbilical cord blood at birth reflect the androgen environment in pregnancy. In a population-based sample studied from in utero, we aimed to explore the association between prenatal testosterone exposure and BP in young adulthood. Design and method: In the Raine Study cohort, data was available on umbilical cord blood androgens and on BP, anthropometric and socio-behavioural information in 387 participants at 20 years and 319 at 27 years. Total testosterone was measured using liquid chromatography-tandem mass spectrometry; free testosterone, by empirical method (Sartorius et al.); and sex hormone binding globulin, by ELISA. Bioavailable testosterone (BioT; nmol L) was calculated employing the formula: BioT = free testosterone + albumin-bound testosterone. We employed hierarchical linear mixed effects regression, with maximum likelihood estimation, to assess the association of BioT with blood pressure at 20 and 27 years adjusting for potential confounders. Results: Umbilical cord BioT levels were significantly higher in males than in females (0.14 [95%CI 0.13; 0.16] vs 0.08 [95%CI 0.07; 0.09] nM/L; p < 0.001). Mean systolic BP were 122.9 (95%CI 121.3; 124.6) and 110.5 (95%CI 109.1; 111.9) mmHg at 20 years, and 122.4 (95%CI 120.7; 124.1) and 111.2 (95%CI 109.8; 112.7) mmHg at 27 years, in males and females, respectively. Longitudinal regression models showed higher BioT levels were positively associated with systolic BP (coefficient: 16.1 [95% CI: 1.8; 30.4]; p = 0.027) at both 20 and 27 years, after adjusting for BMI, sex and hormone contraceptive use. This translates to a 1 mmHg increase in systolic BP for a 1 standard deviation increase in BioT. There was no difference in this association between sexes. Conclusions: To our knowledge, this is the first population-based study that shows testosterone in umbilical cord blood at birth is significantly associated with systolic BP in young adulthood. Our data support previous findings in animal studies of a causal relationship. The data suggest that higher testosterone levels in utero may increase the risk of hypertension later in life.
AimsLifestyle behaviours established during adolescence may adversely affect blood pressure (BP) and contribute to gender differences in cardiovascular risk in adulthood. We aimed to assess the association of health behaviours with BP in adolescents, using data from the Western Australian Pregnancy (Raine) Study.
Objective — To assess the impact of prenatal screening on the birth prevalence of three categories of structural congenital anomaly: abdominal wall defects (omphalocele and gastroschisis), renal agenesis/dysgenesis, and limb reduction defects. Setting — Glasgow, Scotland, United Kingdom. Methods — Data on the selected defects were obtained retrospectively from the population based Glasgow Register of Congenital Anomalies for the period 1980–91 inclusive. The register records all clinical or laboratory diagnoses of congenital anomaly in live births, stillbirths, and induced abortions occurring in women resident within the boundaries of the Greater Glasgow Health Board. The secular trends in the proportions of the defects diagnosed prenatally and terminated after screening, and in their prevalence at birth and during pregnancy, were examined. A total of 154845 births were surveyed: 309 cases were identified in the selected anomaly categories. Results — 83 cases of omphalocele/gastroschisis (5·4/10000 births), 92 cases of renal agenesis/dysgenesis (5·9/10000 births), and 134 cases of limb reduction defects (8·7/10000 births) were found. Marked increases occurred over the study period in the proportions of cases diagnosed prenatally but not in the proportions terminated. The greatest difference between the prevalence at birth and during pregnancy was found for omphalocele. There were no significant secular trends in the prevalence of the selected defects. Conclusions — Prenatal screening has made a limited epidemiological impact on the prevalence of these defects. It has been moderately (but inconsistently) effective in the avoidance of births of infants with omphalocele/gastroschisis and renal agenesis/dysgenesis but not of limb reduction defects. Future efforts should be directed towards improving the technical aspects of the ultrasonographic detection of fetal abnormalities and exploring in detail, locally, the reasons for the varying pattern of decision making about termination of pregnancy among prospective parents.
Background & Objectives: HDL-cholesterol (HDL-C) levels are dependent on gender and environmental factors. We aimed to assess the independent impact of maternal smoking during pregnancy and passive smoking exposure since birth on HDL-C levels of non-smoking adolescents at age 17 years. We also aimed to determine if there was a gender difference in the relationship between smoking exposure and HDL-C. Methods: Eight hundred and sixteen non-smoking adolescents from a cohort of 1220 adolescents (mean age of 17 ± 0.25 years) of the Western Australian Pregnancy Cohort (Raine) Study had data of maternal smoking during pregnancy and smoking exposure in the household over 17 years. HDL-C was analysed using multivariable linear regression, with adjustment for adiposity and lifestyle confounders. Differences in gender effects were assessed via interaction terms. Results: There was a significant reduction in the average HDL-C for girls exposed to passive smoking compared to unexposed girls (β = -0.09 [95%CI -0.15, -0.03]) that was not observed in boys (β = 0.02 [95%CI -0.04, 0.08], interaction p = 0.009). No additional detrimental effect was detected in those exposed to passive smoking from maternal smoking. There was no evidence found to indicate an effect of alcohol consumption on the passive smoking-HDL-C association. Conclusion: This study has shown a gender difference in the relationship between passive smoking and HDL-C in adolescents. Exposure to passive smoking in girls could have adverse consequences on their risk of cardiovascular disease in adulthood.
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