OBJECTIVE To review and critically appraise published and preprint reports of prediction models for diagnosing coronavirus disease 2019 (covid-19) in patients with suspected infection, for prognosis of patients with covid-19, and for detecting people in the general population at increased risk of becoming infected with covid-19 or being admitted to hospital with the disease. DESIGNLiving systematic review and critical appraisal. DATA SOURCESPubMed and Embase through Ovid, Arxiv, medRxiv, and bioRxiv up to 7 April 2020.Cite this as: BMJ 2020;369:m1328 http://dx.
SummaryBackgroundFast weight gain and linear growth in children in low-income and middle-income countries are associated with enhanced survival and improved cognitive development, but might increase risk of obesity and related adult cardiometabolic diseases. We investigated how linear growth and relative weight gain during infancy and childhood are related to health and human capital outcomes in young adults.MethodsWe used data from five prospective birth cohort studies from Brazil, Guatemala, India, the Philippines, and South Africa. We investigated body-mass index, systolic and diastolic blood pressure, plasma glucose concentration, height, years of attained schooling, and related categorical indicators of adverse outcomes in young adults. With linear and logistic regression models, we assessed how these outcomes relate to birthweight and to statistically independent measures representing linear growth and weight gain independent of linear growth (relative weight gain) in three age periods: 0–2 years, 2 years to mid-childhood, and mid-childhood to adulthood.FindingsWe obtained data for 8362 participants who had at least one adult outcome of interest. A higher birthweight was consistently associated with an adult body-mass index of greater than 25 kg/m2 (odds ratio 1·28, 95% CI 1·21–1·35) and a reduced likelihood of short adult stature (0·49, 0·44–0·54) and of not completing secondary school (0·82, 0·78–0·87). Faster linear growth was strongly associated with a reduced risk of short adult stature (age 2 years: 0·23, 0·20–0·52; mid-childhood: 0·39, 0·36–0·43) and of not completing secondary school (age 2 years: 0·74, 0·67–0·78; mid-childhood: 0·87, 0·83–0·92), but did raise the likelihood of overweight (age 2 years: 1·24, 1·17–1·31; mid-childhood: 1·12, 1·06–1·18) and elevated blood pressure (age 2 years: 1·12, 1·06–1·19; mid-childhood: 1·07, 1·01–1·13). Faster relative weight gain was associated with an increased risk of adult overweight (age 2 years: 1·51, 1·43–1·60; mid-childhood: 1·76, 1·69–1·91) and elevated blood pressure (age 2 years: 1·07, 1·01–1·13; mid-childhood: 1·22, 1·15–1·30). Linear growth and relative weight gain were not associated with dysglycaemia, but a higher birthweight was associated with decreased risk of the disorder (0·89, 0·81–0·98).InterpretationInterventions in countries of low and middle income to increase birthweight and linear growth during the first 2 years of life are likely to result in substantial gains in height and schooling and give some protection from adult chronic disease risk factors, with few adverse trade-offs.FundingWellcome Trust and Bill & Melinda Gates Foundation.
The rapid urbanization of the developing world has important consequences for human health. Although several authorities have called for better research on the relationships between urbanicity and health, most researchers still use a poor measurement of urbanicity, the urban-rural dichotomy. Our goal was to construct a scale of urbanicity using community level data from the Cebu Longitudinal Health and Nutrition Survey. We used established scale development methods to validate the new measure and tested its performance against the dichotomy. The new scale illustrated misclassification by the urban-rural dichotomy, and was able to detect differences in urbanicity, both between communities and across time, that were not apparent before. Furthermore, using a continuous measure of urbanicity allowed for better illustrations of the relationships between urbanicity and health. The new scale is a better measure of urbanicity than the traditionally used urban-rural dichotomy.
Background: Promoting catch-up growth in malnourished children has health benefits, but recent evidence suggests that accelerated child weight gain increases adult chronic disease risk.Objective: We aimed to determine how birth weight (BW) and weight gain to midchildhood relate to blood pressure (BP) in young adults.Design: We pooled data from birth cohorts in Brazil, Guatemala, India, the Philippines, and South Africa. We used conditional weight (CW), a residual of current weight regressed on prior weights, to represent deviations from expected weight gain from 0 to 12, 12 to 24, 24 to 48 mo, and 48 mo to adulthood. Adult BP and risk of prehypertension or hypertension (P/HTN) were modeled before and after adjustment for adult body mass index (BMI) and height. Interactions of CWs with small size-for-gestational age (SGA) at birth were tested.Results: Higher CWs were associated with increased BP and odds of P/HTN, with coefficients proportional to the contribution of each CW to adult BMI. Adjusted for adult height and BMI, no child CW was associated with adult BP, but 1 SD of BW was related to a 0.5-mm Hg lower systolic BP and a 9% lower odds of P/HTN. BW and CW associations with systolic BP and P/HTN were not different between adults born SGA and those with normal BW, but higher CW at 48 mo was associated with higher diastolic BP in those born SGA.Conclusions: Greater weight gain at any age relates to elevated adult BP, but faster weight gains in infancy and young childhood do not pose a higher risk than do gains at other ages.
ObjectiveTo investigate associations between adverse childhood experiences (ACEs) and later-life depressive symptoms; and to explore whether perceived social support (PSS) moderates these.MethodWe analysed baseline data from the Mitchelstown (Ireland) 2010–2011 cohort of 2047 men and women aged 50–69 years. Self-reported measures included ACEs (Centre for Disease Control ACE questionnaire), PSS (Oslo Social Support Scale) and depressive symptoms (CES-D). The primary exposure was self-report of at least one ACE. We also investigated the effects of ACE exposure by ACE scores and ACE subtypes abuse, neglect and household dysfunction. Associations between each of these exposures and depressive symptoms were estimated using logistic regression, adjusted for socio-demographic factors. We tested whether the estimated associations varied across levels of PSS (poor, moderate and strong).Results23.7% of participants reported at least one ACE (95% CI 21.9% to 25.6%). ACE exposures (overall, subtype or ACE scores) were associated with a higher odds of depressive symptoms, but only among individuals with poor PSS. Exposure to any ACE (vs none) was associated with almost three times the odds of depressive symptoms (adjusted OR 2.85; 95% CI 1.64 to 4.95) among individuals reporting poor PSS, while among those reporting moderate and strong PSS, the adjusted ORs were 2.21 (95% CI 1.52 to 3.22) and 1.39 (95% CI 0.85 to 2.29), respectively. This pattern of results was similar when exposures were based on ACE subtype and ACE scores, though the interaction was clearly strongest among those reporting abuse.ConclusionsACEs are common among older adults in Ireland and are associated with higher odds of later-life depressive symptoms, particularly among those with poor PSS. Interventions that enhance social support, or possibly perceptions of social support, may help reduce the burden of depression in older populations with ACE exposure, particularly in those reporting abuse.
Over the past 20 years a large and varied body of research has attempted to make the case for the developmental origins of elevated adult blood pressure (BP). Experimental animal research has identified plausible biological mechanisms through which fetal nutritional insufficiency may affect adult BP. The majority of human epidemiologic studies demonstrate an inverse association of birth weight (the most commonly used marker of fetal nutrition) with adult BP and higher risk of hypertension among individuals with lower weight at birth. The most adverse BP outcomes occur among individuals who were small at birth but relatively large as adults, a finding that suggests a role for postnatal growth. We critically review the literature on proposed mechanisms and epidemiologic evidence for developmental origins of adult BP and hypertension, considering associations with birth weight, maternal nutrition during pregnancy, child growth patterns, and infant feeding.
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