Current and future costs of cancer, heart disease and stroke attributable to obesity in Australia - a comparison of two birth cohorts

The obesity epidemic appears set to worsen the morbidity and mortality from leading causes of death in Australia -ischaemic heart disease, stroke and obesity-related cancers. The aim of this study was to compare hospital separations, deaths and direct health costs for middle-aged adults (45 to 54 years) in 2004/05 with those attaining age 45 to 54 years in 2024/25 who were born into an obesogenic environment. Using data from National Health Surveys, prevalence of obesity in 2004/05 was calculated for those born in 1950/51-59/60 and four scenarios were considered to project rates in 2024/25 for those born in 1970/71-79/80: an age-cohort model; a linear trend model; a steady state where rates increase to equal those of the older birth cohort at the same age; and a best case where rates remain at 2004/05 levels. Population attributable fractions were calculated by gender and disease using relative risks of disease from the literature, and applied to hospital separations, deaths, and direct health system costs data to estimate the proportion of each attributable to obesity. In 2024/25 the projected number of hospitalizations of 45 to 54 year olds due to the diseases of interest could be more than halved, over 200 lives rescued and $51.5 million (in 2004/05 dollars) saved if further gains in obesity in the younger birth cohort are halted. Instead, if the worst case scenario is realized there will be a more than doubling in costs (in 2004/05 dollars) compared with those born in 1950/51-59/60

Temporal associations between national outbreaks of meningococcal serogroup W and C disease in the Netherlands and England: an observational cohort study

Background: Since 2009, the incidence of meningococcal serogroup W disease has increased rapidly in the UK because of a single strain (the so-called original UK strain) belonging to the hypervirulent sequence type-11 clonal complex (cc11), with a variant outbreak strain (the so-called 2013 strain) emerging in 2013. Subsequently, the Netherlands has had an increase in the incidence of meningococcal serogroup W disease. We assessed the temporal and phylogenetic associations between the serogroup W outbreaks in the Netherlands and England, and the historical serogroup C outbreaks in both countries. Methods: For this observational cohort study, we used national surveillance data for meningococcal serogroup W and serogroup C disease in the Netherlands and England for the epidemiological years (July to June) 1992–93 to 2015–16. We also did whole genome sequencing and core genome multilocus sequence typing (1546 loci) on serogroup W disease isolates from both countries for surveillance years 2008–09 to 2015–16. We used Poisson regression to compare the annual relative increase in the incidence of serogroup W and serogroup C between both countries. Findings: In the Netherlands, the incidence of meningococcal serogroup W disease increased substantially in 2015–16 compared with 2014–15, with an incidence rate ratio of 5·2 (95% CI 2·0–13·5) and 11% case fatality. In England, the incidence increased substantially in 2012–13 compared with 2011–12, with an incidence rate ratio of 1·8 (1·2–2·8). The relative increase in the Netherlands from 2014–15 to 2015–16 was 418% (95% CI 99–1248), which was significantly higher than the annual relative increase of 79% (61–99) per year in England from 2011–12 to 2014–15 (p=0·03). Cases due to meningococcal serogroup W cc11 (MenW:cc11) emerged in 2012–13 in the Netherlands. Of 29 MenW:cc11 cases found up to 2015–16, 26 (90%) were caused by the 2013 strain. For both the current serogroup W outbreak and the historical serogroup C outbreak, the increase in incidence started several years later in the Netherlands than in England, the rate of increase was higher in the Netherlands, and age distributions were similar in both countries. Interpretation: Given the historical similarities of meningococcal serogroup W with meningococcal serogroup C emergence, the rapid expansion of the MenW:cc11 2013 strain in the Netherlands, its high case fatality, and the availability of a safe and effective vaccine, urgent consideration is needed for public health interventions in the Netherlands and other affected countries to prevent further serogroup W cases and deaths. Funding: National Institute for Public Health and the Environment (Netherlands), Academic Medical Center (Netherlands), and Public Health England

Circulation Study From Birth to 22 Years of Age Fetal, Infant, and Childhood Growth and Adult Blood Pressure: A Longitudinal Fetal, Infant, and Childhood Growth and Adult Blood Pressure A Longitudinal Study From Birth to 22 Years of Age

Background-People who are small at birth tend to have higher blood pressure in later life. However, it is not clear whether it is fetal growth restriction or the accelerated postnatal growth that often follows it that leads to higher blood pressure. Methods and Results-We studied blood pressure in 346 British men and women aged 22 years whose size had been measured at birth and for the first 10 years of life. Their childhood growth was characterized using a conditional method that, free from the effect of regression to the mean, estimated catch-up growth. People who had been small at birth but who gained weight rapidly during early childhood (1 to 5 years) had the highest adult blood pressures. Systolic pressure increased by 1.3 mm Hg (95% CI, 0.3 to 2.3) for every standard deviation score decrease in birth weight and, independently, increased by 1.6 mm Hg (95% CI, 0.6 to 2.7) for every standard deviation score increase in early childhood weight gain. Adjustment for adult body mass index attenuated the effect of early childhood weight gain but not of birth weight. Relationships were smaller for diastolic pressure. Weight gain in the first year of life did not influence adult blood pressure. Conclusions-Part of the risk of adult hypertension is set in fetal life. Accelerated weight gain in early childhood adds to this risk, which is partly mediated through the prediction of adult fatness. The primary prevention of hypertension may depend on strategies that promote fetal growth and reduce childhood obesity