Gender differences in response to an opportunistic brief intervention for obesity in primary care: Data from the BWeL trial

Weight loss programmes appeal mainly to women, prompting calls for gender-specific programmes. In the United Kingdom, general practitioners (GPs) refer nine times as many women as men to community weight loss programmes. GPs endorsement and offering programmes systematically could reduce this imbalance. In this trial, consecutively attending patients in primary care with obesity were invited and 1882 were enrolled and randomized to one of two opportunistic 30-second interventions to support weight loss given by GPs in consultations unrelated to weight. In the support arm, clinicians endorsed and offered referral to a weight loss programme and, in the advice arm, advised that weight loss would improve health. Generalized linear mixed effects models examined whether gender moderated the intervention. Men took effective weight loss action less often in both arms (support: 41.6% vs 60.7%; advice: 12.1% vs 18.3%; odds ratio (OR) = 0.38, 95% confidence interval (CI), 0.27, 0.52, P < .001) but there was no evidence that the relative effect differed by gender (interaction P = .32). In the support arm, men accepted referral and attended referral less often, 69.3% vs 82.4%; OR = 0.48, 95% CI, 0.35, 0.66, P < .001 and 30.4% vs 47.6%; OR = 0.48, 95% CI, 0.36, 0.63, P < .001, respectively. Nevertheless, the gender balance in attending weight loss programmes closed to 1.6:1. Men and women attended the same number of sessions (9.7 vs 9.1 sessions, P = .16) and there was no evidence weight loss differed by gender (6.05 kg men vs 4.37 kg women, P = .39). Clinician-delivered opportunistic 30-second interventions benefits men and women equally and reduce most of the gender imbalance in attending weight loss programmes

Behavioural sleep problems in children with attention-deficit/hyperactivity disorder (ADHD): protocol for a prospective cohort study

Introduction Children with attention-deficit/hyperactivity disorder (ADHD) commonly experience behavioural sleep problems, yet these difficulties are not routinely assessed and managed in this group. Presenting with similar symptoms to ADHD itself, sleep problems are complex in children with ADHD and their aetiology is likely to be multifactorial. Common internalising and externalising comorbidities have been associated with sleep problems in children with ADHD; however, this relationship is yet to be fully elucidated. Furthermore, limited longitudinal data exist on sleep problems in children with ADHD, thus their persistence and impact remain unknown. In a diverse sample of children with ADHD, this study aims to: (1) quantify the relationship between sleep problems and internalising and externalising comorbidities; (2) examine sleep problem trajectories and risk factors; and (3) examine the longitudinal associations between sleep problems and child and family functioning over a 12-month period.Methods and analysis A prospective cohort study of 400 children with ADHD (150 with no/mild sleep problems, 250 with moderate/severe sleep problems) recruited from paediatric practices across Victoria, Australia. The children\u27s parents and teacher provide data at baseline and 6-month and 12-month post enrolment.Key measures Parent report of child\u27s sleep problem severity (no, mild, moderate, severe); specific sleep domain scores assessed using the Child Sleep Habits Questionnaire; internalising and externalising comorbidities assessed by the Anxiety Disorders Interview Schedule for Children IV/Parent version.Analyses Multiple variable logistic and linear regression models examining the associations between key measures, adjusted for confounders identified a priori.Ethics and dissemination Ethics approval has been granted. Findings will contribute to our understanding of behavioural sleep problems in children with ADHD. Clinically, they could improve the assessment and management of sleep problems in this group. We will seek to publish in leading paediatric journals, present at conferences and inform Australian paediatricians through the Australian Paediatric Research Network.<br /

Associations of retinal microvascular caliber with large arterial function and structure: A population-based study of 11 to 12 year-olds and midlife adults

Objective We examined associations between retinal microvascular and large arterial phenotypes to explore relationships between the micro- and macro-vasculature in childhood and midlife. Methods Participants were 1288 children (11-12 years, 50.9% female) and 1264 adults (mean age 44 years, 87.6% female) in a cross-sectional population-based study. Exposures were retinal arteriolar and venular caliber quantified from retinal images. Outcomes included arterial function (pulse wave velocity; carotid arterial elasticity) and structure (carotid intima-media thickness). Multivariable regression models were performed adjusting for age, sex, and family socioeconomic position. Results In children, one standard deviation wider arteriolar caliber was associated with slower pulse wave velocity (-0.15 SD, 95% CI -0.21, -0.09) and higher elasticity (0.13 SD, 95% CI 0.06, 0.20); per SD wider venular caliber was associated with faster pulse wave velocity (0.09 SD, 95% CI 0.03, 0.15) and lower elasticity (-0.07 SD, 95% CI -0.13, -0.01). The size of adult associations was approximately double. Wider arteriolar caliber was associated with smaller carotid intima-media thickness (-0.09 SD, 95% CI -0.16, -0.03) in adults but not children. Venular caliber and carotid intima-media thickness showed little evidence of association. Conclusions Narrower retinal arterioles and wider venules are associated with large arterial function as early as mid-childhood. Associations strengthen by midlife and also extend to arterial structure, although effect sizes remain small.</p

Inflammatory diet and preclinical cardiovascular phenotypes in 11–12 year-olds and mid-life adults: A cross-sectional population-based study

Background and aims: Pro-inflammatory diet may be a modifiable risk factor for cardiovascular disease. We examine associations of two inflammatory diet scores with preclinical cardiovascular phenotypes at two life course stages.Methods: Participants: 1771 children (49% girls) aged 11–12 years and 1793 parents (87% mothers, mean age 43.7 (standard deviation 5.2) years) in the Child Health CheckPoint Study. Measures: 23 items in the Australian National Secondary Students' Diet and Activity (NaSSDA) survey were used to derive two inflammatory diet scores based on: 1) published evidence of associations with C-reactive protein (literature-derived score), and 2) empirical associations with CheckPoint's inflammatory biomarker (glycoprotein acetyls, GlycA-derived score). Cardiovascular phenotypes assessed vascular structure (carotid intima-media thickness, retinal vessel calibre) and function (pulse wave velocity, blood pressure). Analyses: Linear regression models were conducted, adjusted for age, sex, socioeconomic position and child pubertal status, plus a sensitivity analysis also including BMI (z-score for children).Results: In adults, both inflammatory diet scores showed small associations with adverse cardiovascular function and microvascular structure. Per standard deviation higher GlycA-derived diet score, pulse wave velocity was 0.17  m/s faster (95% CI 0.11 to 0.22), mean arterial pressure was 1.85  mmHg (1.34–2.37) higher, and retinal arteriolar calibre was 1.29 μm narrower (−2.10 to −0.49). Adding BMI to models attenuated associations towards null. There was little evidence of associations in children.Conclusions: Our findings support cumulative adverse effects of a pro-inflammatory diet on preclinical cardiovascular phenotypes across the life course. Associations evident by mid-life were not present in childhood, when preventive measures should be instituted.</p

Early clinical markers of overweight/obesity onset and resolution by adolescence

Objectives: We examined how combinations of clinical indicators at various ages predict overweight/obesity development, as well as resolution, by 10–11 and 14–15 years of age.Methods: Data were derived from Birth (N = 3469) and Kinder (N = 3276) cohorts of the Longitudinal Study of Australian Children, followed from ages 2–3 and 4–5 years, respectively. Every two years, 25 potential obesity-relevant clinical indicators were quantified. Overweight/obesity was defined using International Obesity Taskforce cutpoints at 10–11 years and 14–15 years.Results: In both cohorts, three factors predicted both development and resolution of overweight/obesity in multivariable models. Among normal weight children, increased odds of developing overweight/obesity were associated with higher child (odd ratio (OR) 1.67–3.35 across different study waves) and maternal (OR 1.05–1.09) BMI, and inversely with higher maternal education (OR 0.60–0.62, when assessed at age 2–7 years). Lower odds of resolving existing overweight/obesity were related with higher child (OR 0.51–0.79) and maternal (OR 0.89–0.95) BMI, and inversely with higher maternal education (OR 1.62–1.92, when assessed at age 2–5 years). The prevalence of overweight/obesity at the age of 14–15 years was 13% among children with none of these risk factors at age 6–7 years, compared with 71% among those with all 3 risk factors (P Conclusions: From early childhood onwards, child and maternal BMI and maternal education predict overweight/obesity onset and resolution by adolescence. A simple risk score, easily available to child health clinicians, could help target treatment or prevention.</p

Screening and brief intervention for obesity in primary care:cost-effectiveness analysis in the BWeL trial

This paper is closed access until 31 July 2019.Background: The Brief Intervention for Weight Loss Trial enrolled 1882 consecutively attending primary care patients who were obese and participants were randomised to physicians opportunistically endorsing, offering, and facilitating a referral to a weight loss programme (support) or recommending weight loss (advice). After one year, the support group lost 1.4 kg more (95%CI 0.9 to 2.0): 2.4 kg versus 1.0 kg. We use a cohort simulation to predict effects on disease incidence, quality of life, and healthcare costs over 20 years. Methods: Randomly sampling from the trial population, we created a virtual cohort of 20 million adults and assigned baseline morbidity. We applied the weight loss observed in the trial and assumed weight regain over four years. Using epidemiological data, we assigned the incidence of 12 weight-related diseases depending on baseline disease status, age, gender, body mass index. From a healthcare perspective, we calculated the quality adjusted life years (QALYs) accruing and calculated the incremental difference between trial arms in costs expended in delivering the intervention and healthcare costs accruing. We discounted future costs and benefits at 1.5% over 20 years. Results: Compared with advice, the support intervention reduced the cumulative incidence of weight-related disease by 722/100,000 people, 0.33% of all weight-related disease. The incremental cost of support over advice was £2.01million/100,000. However, the support intervention reduced health service costs by £5.86 million/100,000 leading to a net saving of £3.85 million/100,000. The support intervention produced 992 QALYs/100,000 people relative to advice. Conclusions: A brief intervention in which physicians opportunistically endorse, offer, and facilitate a referral to a behavioural weight management service to patients with a BMI of at least 30 kg/m2 reduces healthcare costs and improves health more than advising weight loss

Do body mass index and waist-to-height ratio over the preceding decade predict retinal microvasculature in 11-12 year olds and midlife adults?

Background/objectives Microvascular changes may contribute to obesity-associated cardiovascular disease. We examined whether body mass index (BMI) and waist-to-height ratio (WHtR) (1) at multiple earlier time points and (2) decade-long trajectories predicted retinal microvascular parameters in mid-childhood/adulthood. Methods Participants/design: 1288 11-12 year olds (51% girls) and 1264 parents (87% mothers) in the population-based Child Health CheckPoint (CheckPoint) module within the Longitudinal Study of Australian Children (LSAC). LSAC exposure measures: biennial BMI z-score and WHtR for children at five time points from age 2-3 to 10-11 years and self-reported parent BMI at six time points from child age 0-1 years to 10-11 years. CheckPoint outcome measures: retinal arteriolar and venular caliber. Analyses: BMI/WHtR trajectories were identified by group-based trajectory modeling; linear regression models estimated associations between BMI/WHtR at each time point/trajectories and later retinal vascular caliber, adjusted for age, sex, and family socioeconomic status. Results In time point analyses, higher child BMI/WHtR from age 4 to 5 years was associated with narrower arteriolar caliber at the age of 11-12 years, but not venular caliber. For example, each standard deviation higher in BMI z-score at 4-5 years was associated with narrower arteriolar caliber at 11-12 years (standardized mean difference (SMD): -0.05, 95% confidence interval (CI): -0.10 to 0.01); by 10-11 years, associations had doubled to -0.10 (95% CI: -0.16 to -0.05). In adults, these finding were similar, except the magnitude of BMI and arteriolar associations were similar across all time points (SMD: -0.11 to -0.13). In child and adult BMI trajectory analyses, less favorable trajectories predicted narrower arteriolar (p-trend 0.1), caliber. Compared with those in the average BMI trajectory, SMDs in arterial caliber for children and adults in the highest trajectory were -0.25 (95% CI: -0.44 to -0.07) and -0.42 (95% CI: -0.73 to -0.10), respectively. Venular caliber showed late associations with child WHtR, but not with BMI in children or adults. Conclusions Associations of decade-long high BMI trajectories with narrowed retinal arteriolar caliber emerge in children, and are clearly evident by midlife. Adiposity appears to exert its early adverse life course impacts on the microcirculation more via arteriolar than venular mechanisms.</div

Exposure to adversity and inflammatory outcomes in mid and late childhood

Background We aimed to estimate the association between exposure to adversity and inflammatory markers in mid (4 years) and late (11-12 years) childhood, and whether effects differ by type and timing of exposure. Methods Data sources: Barwon Infant Study (BIS; N = 510 analyzed) and Longitudinal Study of Australian Children (LSAC; N = 1156 analyzed). Exposures: Adversity indicators assessed from 0 to 4 (BIS) and 0-11 years (LSAC): parent legal problems, mental illness and substance abuse, anger in parenting responses, separation/divorce, unsafe neighborhood, and family member death; a count of adversities; and, in LSAC only, early (0-3), middle (4-7), or later (10-11) initial exposure. Outcomes: Inflammation quantified by high sensitivity C-reactive protein (hsCRP, Log (ug/ml)) and glycoprotein acetyls (GlycA, Log (umol/L)). Analyses: Linear regression was used to estimate relative change in inflammatory markers, adjusted for sociodemographic characteristics, with exposure to adversity. Outcomes were log-transformed. Results Evidence of an association between adversity and hsCRP was weak and inconsistent (e.g., 3+ versus no adversity: BIS: 12% higher, 95%CI -49.4, 147.8; LSAC 4.6% lower, 95%CI: −36.6, 48.3). A small positive association between adversity and GlycA levels was observed at both 4 years (e.g., 3+ versus no adversity: 3.3% higher, 95%CI -3.0, 9.9) and 11-12 years (3.2% higher, 95%CI 0.8, 5.8). In LSAC, we did not find evidence that inflammatory outcomes differed by initial timing of adversity exposure. Conclusions Small positive associations between adversity and inflammation were consistently observed for GlycA, across two cohorts with differing ages. Further work is needed to understand mechanisms, clinical relevance, and to identify opportunities for early intervention.Meredith O'Connor and Sarah Arnup were supported by the Melbourne Children's LifeCourse initiative, funded by a Royal Children's Hospital Foundation Grant (2018-984). Anne-Louise Ponsonby is supported by a National Health and Medical Research Council (NHMRC) Fellowship (1110200). Peter Sly is sup- ported by an NHMRC Fellowship (APP1102590). Naomi Priest is sup- ported by an NHMRC Career Development Fellowship (APP1123677). Kate Lycett is supported by an NHMRC Early Career Fellowship (APP1091124) and Honorary National Heart Foundation Postdoctoral Fellowship (101239). Sharon Goldfeld is supported by an NHMRC Career Development Fellowship (1082922). David Burgner is supported by an NHMRC Investigator Grant (1175744)