Search

Background: Understanding the origins of sex differences in cardiovascular diseases (CVD) may help with prevention. We examined sex differences in carotid artery IMT and plaques in adulthood including the contribution of childhood risk factors. Methods: Boys and girls aged 7-15 years old from the Australian Schools Health and Fitness Survey in 1985 were followed up in the Childhood Determinants of Adult Health study at ages 36-49 years between 2014-19. Sex differences in adult carotid IMT and plaques, identified with 2D ultrasound of left and right carotid arteries, were examined with linear and log binomial regression, respectively. Childhood sociodemographic, psychosocial, health-related behavioural and biomedical risk factors that might contribute to sex differences in carotid IMT/plaques were identified with purposeful model building. Results: Among 1,286 men and women with vascular measurements of carotid IMT (53% women, mean carotid IMT 0.63 mm ± 0.09 standard deviation) women had thinner carotid IMT measurements than men (β coefficients -0.053 95% CI -0.063, -0.043). Adjusting for age standardised waist circumference (WC), waist/hip ratio (WHR), waist/height ratio (WHtR) and systolic blood pressure (SBP) in childhood reduced the sex difference of carotid IMT in adulthood (see Figure), but a significant sex-difference in carotid IMT remained. Women had a 42% lower risk of plaques than men (Relative Risk 0.58 95% CI 0.42, 0.79). School achievement levels, endurance/power fitness and SBP in childhood partially explained the sex difference in the prevalence of plaques at adulthood (see Figure) as the sex difference decreased and became statistically insignificant. Conclusion: Various factors in childhood had contributed to thicker carotid IMT and higher prevalence of carotid plaques in men compared to women. These findings suggest that the origins of adult sex differences in CVD may begin in childhood. There may be benefits of sex-specific primary prevention programs starting in childhood.

Introduction: Prolonged childhood passive smoke exposure may affect adult cardiovascular health but there are few studies of cardiac function. Subclinical left ventricular dysfunction detected by global longitudinal strain (GLS) is predictive of the subsequent development of heart failure. We investigated the association of passive smoke exposure during childhood with GLS in adults. Methods: Data were from the Childhood Determinants of Adult Health (CDAH) study 34-year follow-up (2014-19). Three measures of passive smoking (severity of exposure index [SEI], cumulative years of exposure [CYE], total household smokers [THS]) were derived retrospectively from a validated questionnaire. GLS was measured in clinics using a Siemens Acuson SC2000 ultrasound machine and 4V1c transducer with speckle tracking analysis. Linear regression adjusted for confounding factors (age, gender, childhood socioeconomic position, childhood smoking, adult smoking status, parental education level) examined the association between childhood passive smoke exposure and GLS in adulthood. Results: Among 781 participants (mean age 45.2 ± 2.5 SD years, 52.6% females, 54.2% exposed to passive smoking), GLS showed a decrease (β adjusted -0.17% 95% CI -0.32%, -0.02%) per SD of SEI (range: 0-318, mean 24.2 ± 35.8 SD). CYE (range: 0-106, mean 10.4 ± 13.9 SD) was associated with a decrease in GLS (β adjusted -0.18% 95% CI -0.33%, -0.05%) per SD of exposure. For each THS in childhood (range: 0-5, mean 0.9 ± 1.0 SD), there was a decrease in GLS (β adjusted -0.20% 95% CI -0.36%, -0.05%). Conclusion: Childhood passive smoke exposure, independent of own smoking, was associated with a reduction in GLS, a measure of subclinical cardiac dysfunction. Each 1% decrease in GLS has been associated with 12% higher risk of cardiovascular morbidity and mortality in low-risk general population. There are potential long-term consequences to cardiac function from childhood passive smoke exposure.

Background: Understanding body mass index (BMI) trajectories across the lifecourse may help identify risk of overweight or obesity and strategic points for preventive interventions. We describe BMI trajectories from childhood to adulthood in four population-based cohorts established in the 1970s-80s and their sociodemographic correlates. Methods: Data were from 12,086 participants (45% male) from four cohorts established in Australia, Finland and the US. Participants had ≥3 measures of height and weight, including ≥1 in childhood (6-18 years, mean 9.7 to 11.1 years at first visit) and ≥1 in adulthood (mean 40.0 to 50.9 years at last visit). Latent Class Growth Mixture Modelling estimated BMI trajectory groups. Correlates (age, gender, race, parental education) of BMI trajectories were identified with log multinomial regression. Results: Mean BMI ranged from 17.8-18.3 kg/m 2 at first visit and 26.4-30.2 kg/m 2 at last visit. Six BMI trajectories (Figure) were identified in three cohorts: persistently normal (48-57% of participants), improving from high (1-2%), progressing to overweight (30-39%), progressing to obese (1-8%), late onset obese (2-6%), and progressing to severe obesity (1-3%). One cohort had a seventh group: greatly improving ( Conclusion: Similar BMI trajectories were identified across cohorts, countries and time, despite different BMI distributions. Females and black Americans were most likely to be of high BMI at the end of follow-up. Few participants (≤2%) improved from high BMI. A better understanding of the factors that influence the highest and improving BMI trajectories may help identify risk reduction strategies.