Determining pathways of effect between correlates and outcomes of transport-related physical activity at differing timepoints across the lifecourse: A structural equation modelling approach.

Transport-related physical activity levels differ across the lifecourse; however, the nature of these differences is poorly understood. This study examined the relationship between correlates of transport-related physical activity and how they differ in strength, pathway, and direction across the lifecourse. Structural Equation Modelling assessed relationships between correlates (e.g., age, smoking, education) and transport-related physical activity (assessed via the International Physical Activity Questionnaire) at four timepoints of the Australian Childhood Determinants of Adult Health study: childhood (7-15y; n = 6302), early-adulthood (26-36y; n = 2700), early/mid-adulthood (31-41y; n = 1649), and mid-adulthood (36-49y; n = 1794). Several pathways were consistent across the lifecourse. Self-rated health directly associated with transport-related physical activity across all timepoints. During adulthood greater body mass index and smoking frequency were indirectly associated with lower levels of transport-related physical activity via self-rated health; similarly, lower educated adults, who smoked more frequently, and had poorer health, had lower transport-related physical activity. Urban residence was directly associated with greater transport-related physical activity in childhood and early-adulthood; having more children in early/mid- and mid-adulthood was directly associated with less transport-related physical activity. This is the first study to report pathways of direct and indirect association between correlates and transport-related physical activity at key lifecourse stages. The pathways highlighted can inform policy and practice to aid in the development of age-specific lifecourse interventions.

Sex differences in the association between stroke risk factors and pre-clinical predictors of stroke in the childhood determinants of Adult Health study.

BACKGROUND AND AIMS: It is unclear why blood pressure (BP), metabolic markers and smoking increase stroke incidence in women more than men. We examined these associations with carotid artery structure and function in a prospective cohort study. METHODS: Participants in the Australian Childhood Determinants of Adult Health study at ages 26-36 years (2004-06) were followed-up at 39-49 years (2014-19). Baseline risk factors included smoking, fasting glucose, insulin, systolic and diastolic BP. Carotid artery plaques, intima-media thickness [IMT], lumen diameter and carotid distensibility [CD] were assessed at follow up. Log binomial and linear regression with risk factor × sex interactions predicted carotid measures. Sex-stratified models adjusting for confounders were fitted when significant interactions were identified. RESULTS: Among 779 participants (50% women), there were significant risk factor × sex interactions with baseline smoking, systolic BP and glucose associated with carotid measures in women only. Current smoking was associated with incidence of plaques (RRunadjusted 1.97 95% CI 1.4, 3.39), which reduced when adjusted for sociodemographics, depression, and diet (RRadjusted 1.82 95% CI 0.90, 3.66). Greater systolic BP was associated with lower CD adjusted for sociodemographics (ßadjusted -0.166 95% CI -0.233, -0.098) and hypertension with greater lumen diameter (ßunadjusted 0.131 95% CI 0.037, 0.225), which decreased when adjusted for sociodemographics, body composition and insulin (ßadjusted 0.063 95% CI -0.052, 0.178). Greater glucose (ßunadjusted -0.212 95% CI -0.397, -0.028) was associated with lower CD, which decreased when adjusted for sociodemographics, BP, depression and polycystic ovary syndrome (ßadjusted -0.023 95% CI -0.249, 0.201). CONCLUSIONS: Smoking, SBP and glucose affect carotid structure and function more in women than men with some of this risk due to co-occurring risk factors.

Distinct patterns of adult transport-related physical activity (TRPA) behaviour exist independent of the TRPA behaviours of childhood: the childhood determinants of adult health study.

BACKGROUND: Transport-related physical activity (TRPA) is recognised as a potential means of increasing total physical activity participation that may yield substantial health benefits. Public health campaigns focusing on promoting TRPA from a young age aim to develop life-long healthy habits. However, few studies have examined how TRPA changes across the lifecourse and whether childhood TRPA levels influence those observed later in life. METHODS: Using the Australian Childhood Determinants of Adult Health study (baseline, 1985), latent class growth mixture modelling with adjustment for time-varying covariates was performed using four timepoints (ranging from 7 to 49 years) to assess behavioural patterns and retention of TRPA across the lifecourse. As child and adult adjusted TRPA measures could not be harmonised, trajectories of adult TRPA (n = 702) were instead identified, and log-binomial regression analysis was performed to determine whether childhood levels of TRPA (high/medium/low) influenced these trajectories. RESULTS: Two stable groups of adult TRPA trajectories were identified: persistently low (n = 520; 74.2%), and increasingly high TRPA (n = 181; 25.8%). There was no significant relationship between childhood TRPA levels and patterns in adulthood (relative risk of high childhood TRPA yielding high adult TRPA trajectory membership = 1.06; 95% confidence interval = 0.95-1.09). CONCLUSION: This study found childhood TRPA levels were not associated with TRPA patterns in adulthood. These findings suggest that while TRPA in childhood may have health, social, and environmental benefits, it does not appear to impact adult TRPA directly. Therefore, further intervention is required beyond childhood to promote the implementation of healthy TRPA behaviours into adulthood.

Area-level and individual-level socio-economic differences in health-related quality of life trajectories: Results from a 10-year longitudinal stroke study.

BACKGROUND: We examined area-level (aSES) and individual-level (iSES) socio-economic status on trajectories of HRQoL to 10 years following stroke. METHODS: Participants with strokes between 1/5/1996 and 30/4/1999 completed the Assessment of Quality of Life instrument (AQoL, range: -0.04 [worse than death] to 0 [death] to 1 [full health]) at ≥one of 3month, 6-month, 1-year, 2-year, 3-year, 4-year, 5-year, 7-year and 10-year interviews after stroke. Sociodemographic and health information were collected at baseline. We derived aSES from postcode using the Australian Socio-Economic Indexes For Area (2006) (categories: high, medium, low), and iSES from lifetime occupation (categories: non-manual, manual). Multivariable linear mixed effects modelling was used to estimate trajectories of HRQoL over 10 years, by aSES and iSES, adjusting for age, sex, cardiovascular disease, smoking, diabetes, stroke severity, stroke type, and the time influence on age and health conditions. RESULTS: Of 1,686 participants enrolled, we excluded 239 with 'possible' stroke and 284 with missing iSES. Among the remaining 1,163 participants, 1,123 (96.6%) had AQoL assessed at ≥3 timepoints. In multivariable analysis, over time, people in the medium aSES group had mean 0.02 (95% CI -0.06, 0.02) greater reduction in AQoL score, and people in the low aSES group had mean 0.04 (95% CI, -0.07, -0.001) greater reduction, than those in the high aSES group. Manual workers had an average 0.04 (95% CI, -0.07, -0.01) greater reduction in AQoL score over time than non-manual workers. CONCLUSIONS: Over time, HRQoL declines in all people with stroke, declining most rapidly in lower SES groups.

A Pilot Randomised Trial Investigating the Effects of Including Efficacy Messaging on Tobacco Warning Labels.

INTRODUCTION: Smokers can respond defensively to health risk communication such as on-pack warning labels, potentially reducing their effectiveness. Theory suggests that risk perception together with self-efficacy reduces defensive responses and predicts target behaviors. Currently, tobacco warning labels globally predominantly target risk and do not explicitly consider efficacy. AIMS: This study explores the effectiveness of combining Australian tobacco warning labels with efficacy content to increase quitting intentions. METHODS: RCT in 83 smokers over 3 weeks. After a seven-day baseline phase (smoking from usual tobacco packaging), participants were randomized to one of two adhesive labels groups for the remaining 14 days: Standard health warning labels (HWLs) featuring enhanced efficacy messages (experimental group) or unmodified standard HWLs (control group). Participants attached these labels to their tobacco packaging and recorded their cognitions and smoking behavior once daily using Smartphones. Multilevel structural equation modeling was used to test theorized effects of the labels on self-efficacy, risk perception, and intentions to quit. RESULTS: There was no effect of exposure to efficacy messages on either self-efficacy, risk perceptions, or intentions to quit. However, self-efficacy and risk perceptions were positively associated with quitting intentions at the within-person level. CONCLUSIONS: The predictive relationships between self-efficacy, risk perception, and intention to quit were supported, however, supplementing standard warning labels with efficacy messages had no effect on these cognitions. Whether this is due to conditioned avoidance of HWLS, characteristics of the messages, or limitations imposed by format are unclear. IMPLICATIONS: Self-efficacy and risk perception predict intentions to quit smoking. Adding efficacy content to tobacco health warnings may have the potential to bolster these cognitions but more research is required to determine the contexts in which this would be effective and who would be likely to benefit. The time course by which exposure to efficacy content might influence cessation self-efficacy and downstream quitting intentions also needs to be investigated.

Association of Onset-to-Treatment Time With Discharge Destination, Mortality, and Complications Among Patients With Aneurysmal Subarachnoid Hemorrhage.

Importance: Rapid access to specialized care is recommended to improve outcomes after aneurysmal subarachnoid hemorrhage (SAH), but understanding of the optimal onset-to-treatment time for aneurysmal SAH is limited. Objective: To assess the optimal onset-to-treatment time for aneurysmal SAH that maximized patient outcomes after surgery. Design, Setting, and Participants: This cohort study assessed 575 retrospectively identified cases of first-ever aneurysmal SAH occurring within the referral networks of 2 major tertiary Australian hospitals from January 1, 2010, to December 31, 2016. Individual factors, prehospital factors, and hospital factors were extracted from the digital medical records of eligible cases. Data analysis was performed from March 1, 2020, to August 31, 2021. Exposures: Main exposure was onset-to-treatment time (time between symptom onset and aneurysm surgical treatment in hours) derived from medical records. Main Outcomes and Measures: Clinical characteristics, complications, and discharge destination were extracted from medical records and 12-month survival obtained from data linkage. The associations of onset-to-treatment time (in hours) with (1) discharge destination of survivors (home vs rehabilitation), (2) 12-month survival, and (3) neurologic complications (rebleed, delayed cerebral ischemia, meningitis, seizure, hydrocephalus, and delayed cerebral injury) were investigated using natural cubic splines in multivariable Cox proportional hazards and logistic regression models. Results: Of the 575 patients with aneurysmal SAH, 482 patients (mean [SD] age, 55.0 [14.5] years; 337 [69.9%] female) who received endovascular coiling or neurosurgical clipping were studied. A nonlinear association of treatment delay was found with the odds of being discharged home vs rehabilitation (effective df = 3.83 in the generalized additive model, χ2 test P = .002 for the 4-df cubic spline), with a similar nonlinear association remaining significant after adjustment for sex, treatment modality, severity, Charlson Comorbidity Index, history of hypertension, and hospital transfer (likelihood ratio test: df = 3, deviance = 9.57, χ2 test P = .02). Both unadjusted and adjusted cox regression models showed a nonlinear association between time to treatment and 12-month mortality with the lowest hazard of death with receipt of treatment at 12.5 hours after symptom onset, although the nonlinear term became nonsignificant upon adjustment. The odds of being discharged home were higher with treatment before 20 hours after onset, with the probability of being discharged home compared with rehabilitation or other hospital increased by approximately 10% when treatment was received within the first 12.5 hours after symptom onset and increased by an additional 5% from 12.5 to 20 hours. Time to treatment was not associated with any complications. Conclusions and Relevance: This cohort study found evidence that more favorable outcomes (discharge home and survival at 12 months) were achieved when surgical treatment occurred at approximately 12.5 hours. These findings provide more clarity around optimal timelines of treatment with people with aneurysmal SAH; however, additional studies are needed to confirm the findings.

Reliability and Validity of a Life Course Passive Smoke Exposure Questionnaire in an Australian Cohort From Childhood to Adulthood.

OBJECTIVES: Life course exposure to passive smoke may predict health, but there are few validated measures. We tested the reliability and validity of a retrospective life course passive smoking questionnaire. METHODS: Participants from the third follow-up of the Childhood Determinants of Adult Health study (2014-2019, ages 36-49 years) retrospectively reported mother/father/other household member smoking when living at home during childhood, including duration (years) and smoking location (never/sometimes/always inside house). The severity of exposure index (SEI; sum of mother/father/other years smoked multiplied by smoking location), cumulative years of exposure (CYE; sum of mother/father/other years), and total household smokers (THS) were derived. The reliability of retrospective passive smoking reports was examined with intraclass correlation coefficients (ICCs) using household smoking reported 34 years earlier in 1985 by participants when aged 7-15 years. Construct validity was examined by correlating retrospective passive smoking with participants' smoking in adulthood and lung function in childhood and adulthood. RESULTS: Among 2082 participants (mean±standard deviation [SD], 45.0±2.5 years; 55.2% females), THS ranged from 0 to 5 (mean± SD, 0.9±1.0), CYE ranged from 0 to 106 (mean±SD, 10.5±13.9), and SEI ranged from 0 to 318 (mean±SD, 24.4±36.0). Retrospective measures showed moderate agreement with total household smokers reported in childhood (ICC, 0.58 to 0.62). The retrospective measures were weakly but significantly (p<0.05) correlated with participants' smoking (r=0.13 to 0.15) and lung function (r= -0.05 to -0.06). CONCLUSIONS: The retrospective passive smoking questionnaire showed reasonable reliability and validity. This measure may be useful for epidemiological studies.

Association of Non-High-Density Lipoprotein Cholesterol Measured in Adolescence, Young Adulthood, and Mid-Adulthood With Coronary Artery Calcification Measured in Mid-Adulthood.

Importance: Elevated non-high-density lipoprotein cholesterol (non-HDL-C) is associated with the presence of coronary artery calcification (CAC), a marker of heart disease in adulthood. However, the relative importance of non-HDL-C levels at specific life stages for CAC remains unclear. Objective: To identify the relative association of non-HDL-C measured at distinct life stages (adolescence, young adulthood, mid-adulthood) with the presence of CAC measured in mid-adulthood. Design, Setting, and Participants: The Cardiovascular Risk in Young Finns Study is a population-based prospective cohort study that started in 1980 with follow-up over 28 years. Participants from 3 population centers (Kuopio, Tampere, and Turku in Finland) represent a convenience sample drawn from the 3 oldest cohorts at baseline (aged 12-18 years in 1980). Data were collected from September 1980 to August 2008. Analysis began February 2020. Exposures: Non-HDL-C levels were measured at 3 life stages including adolescence (aged 12-18 years), young adulthood (aged 21-30 years), and mid-adulthood (aged 33-45 years). Main Outcomes and Measures: In 2008, CAC was determined from computed tomography and dichotomized as 0 (no CAC, Agatston score = 0) and 1 (presence of CAC, Agatston score ≥1) for analysis. Using a bayesian relevant life course exposure model, the relative association was determined between non-HDL-C at each life stage and the presence of CAC in mid-adulthood. Results: Of 589 participants, 327 (56%) were female. In a model adjusted for year of birth, sex, body mass index, systolic blood pressure, blood glucose level, smoking status, lipid-lowering and antihypertensive medication use, and family history of heart disease, cumulative exposure to non-HDL-C across all life stages was associated with CAC (odds ratio [OR], 1.50; 95% credible interval [CrI], 1.14-1.92). At each life stage, non-HDL-C was associated with CAC and exposure to non-HDL-C during adolescence had the strongest association (adolescence: OR, 1.16; 95% CrI, 1.01-1.46; young adulthood: OR, 1.14; 95% CrI, 1.01-1.43; mid-adulthood: OR, 1.12; 95% CrI, 1.01-1.34). Conclusions and Relevance: These data suggest that elevated non-HDL-C levels at all life stages are associated with coronary atherosclerosis in mid-adulthood. However, adolescent non-HDL-C levels showed the strongest association with the presence of CAC in mid-adulthood, and greater awareness of the importance of elevated non-HDL-C in adolescence is needed.

Prediction of Adult Dyslipidemia Using Genetic and Childhood Clinical Risk Factors: The Cardiovascular Risk in Young Finns Study.

BACKGROUND: Dyslipidemia is a major modifiable risk factor for cardiovascular disease. We examined whether the addition of novel single-nucleotide polymorphisms for blood lipid levels enhances the prediction of adult dyslipidemia in comparison to childhood lipid measures. METHODS AND RESULTS: Two thousand four hundred and twenty-two participants of the Cardiovascular Risk in Young Finns Study who had participated in 2 surveys held during childhood (in 1980 when aged 3-18 years and in 1986) and at least once in a follow-up study in adulthood (2001, 2007, and 2011) were included. We examined whether inclusion of a lipid-specific weighted genetic risk score based on 58 single-nucleotide polymorphisms for low-density lipoprotein cholesterol, 71 single-nucleotide polymorphisms for high-density lipoprotein cholesterol, and 40 single-nucleotide polymorphisms for triglycerides improved the prediction of adult dyslipidemia compared with clinical childhood risk factors. Adjusting for age, sex, body mass index, physical activity, and smoking in childhood, childhood lipid levels, and weighted genetic risk scores were associated with an increased risk of adult dyslipidemia for all lipids. Risk assessment based on 2 childhood lipid measures and the lipid-specific weighted genetic risk scores improved the accuracy of predicting adult dyslipidemia compared with the approach using only childhood lipid measures for low-density lipoprotein cholesterol (area under the receiver-operating characteristic curve 0.806 versus 0.811; P=0.01) and triglycerides (area under the receiver-operating characteristic curve 0.740 versus area under the receiver-operating characteristic curve 0.758; P<0.01). The overall net reclassification improvement and integrated discrimination improvement were significant for all outcomes. CONCLUSIONS: The inclusion of weighted genetic risk scores to lipid-screening programs in childhood could modestly improve the identification of those at highest risk of dyslipidemia in adulthood.