The evidence examining the relationship between specific social factors and early childhood health and developmental outcomes has never been systematically collated or synthesized. This review aims to identify the key social factors operating at the household, neighborhood, and country levels that drive inequalities in child health and development. Medline and CHICOS (a European child-cohort inventory) were systematically searched to identify all European studies published within the past 10 y. 13,270 Medline articles and 77 European child cohorts were searched, identifying 201 studies from 32 European countries. Neighborhood deprivation, lower parental income/wealth, educational attainment, and occupational social class, higher parental job strain, parental unemployment, lack of housing tenure, and household material deprivation were identified as the key social factors associated with a wide range of adverse child health and developmental outcomes. Similar association trends were observed across most European countries, with only minor country-level differences. Multiple adverse social factors operating at both the household and neighborhood levels are independently associated with a range of adverse health and developmental outcomes throughout early childhood. The social gradient in health and developmental outcomes observed throughout the remaining life course may be partly explained by gradients initiated in early childhood.

Recent genome-wide association (GWA) studies have identified dozens of common variants associated with adult height. However, it is unknown how these variants influence height growth during childhood. We derived peak height velocity in infancy (PHV1) and puberty (PHV2) and timing of pubertal height growth spurt from parametric growth curves fitted to longitudinal height growth data to test their association with known height variants. The study consisted of N = 3,538 singletons from the prospective Northern Finland Birth Cohort 1966 with genotype data and frequent height measurements (on average 20 measurements per person) from 0–20 years. Twenty-six of the 48 variants tested associated with adult height (p<0.05, adjusted for sex and principal components) in this sample, all in the same direction as in previous GWA scans. Seven SNPs in or near the genes HHIP, DLEU7, UQCC, SF3B4/SV2A, LCORL, and HIST1H1D associated with PHV1 and five SNPs in or near SOCS2, SF3B4/SV2A, C17orf67, CABLES1, and DOT1L with PHV2 (p<0.05). We formally tested variants for interaction with age (infancy versus puberty) and found biologically meaningful evidence for an age-dependent effect for the SNP in SOCS2 (p = 0.0030) and for the SNP in HHIP (p = 0.045). We did not have similar prior evidence for the association between height variants and timing of pubertal height growth spurt as we had for PHVs, and none of the associations were statistically significant after correction for multiple testing. The fact that in this sample, less than half of the variants associated with adult height had a measurable effect on PHV1 or PHV2 is likely to reflect limited power to detect these associations in this dataset. Our study is the first genetic association analysis on longitudinal height growth in a prospective cohort from birth to adulthood and gives grounding for future research on the genetic regulation of human height during different periods of growth.

IMPORTANCE Longer-term mortality in individuals who have survived a traumatic brain injury (TBI) is not known. OBJECTIVES To examine the relationship between TBI and premature mortality, particularly by external causes, and determine the role of psychiatric comorbidity. DESIGN, SETTING, AND PATIENTS We studied all persons born in 1954 or later in Sweden who received inpatient and outpatient International Classification of Diseases-based diagnoses of TBI from 1969 to 2009 (n = 218 300). We compared mortality rates 6 months or more after TBI to general population controls matched on age and sex (n = 2 163 190) and to unaffected siblings of patients with TBI (n = 150 513). Furthermore, we specifically examined external causes of death (suicide, injury, or assault). We conducted sensitivity analyses to investigate whether mortality rates differed by sex, age at death, severity (including concussion), and different follow-up times after diagnosis. MAIN OUTCOMES AND MEASURES Adjusted odds ratios (AORs) of premature death by external causes in patients with TBI compared with general population controls. RESULTS Among those who survived 6 months after TBI, we found a 3-fold increased odds of mortality (AOR, 3.2; 95% CI, 3.0-3.4) compared with general population controls and an adjusted increased odds of mortality of 2.6 (95% CI, 2.3-2.8) compared with unaffected siblings. Risks of mortality from external causes were elevated, including for suicide (AOR, 3.3; 95% CI, 2.9-3.7), injuries (AOR, 4.3; 95% CI, 3.8-4.8), and assault (AOR, 3.9; 95% CI, 2.7-5.7). Among those with TBI, absolute rates of death were high in those with any psychiatric or substance abuse comorbidity (3.8% died prematurely) and those with solely substance abuse (6.2%) compared with those without comorbidity (0.5%). CONCLUSIONS AND RELEVANCE Traumatic brain injury is associated with substantially elevated risks of premature mortality, particularly for suicide, injuries, and assaults, even after adjustment for sociodemographic and familial factors. Current clinical guidelines may need revision to reduce mortality risks beyond the first few months after injury and address high rates of psychiatric comorbidity and substance abuse.

The authors examined associations between postnatal growth velocity through age 2 years and metabolic outcomes at age 31 years in a population-based birth-cohort study of 3,778 Finns (1966-1998). Approximately 8 height measurements and 9 weight measurements were obtained from birth to age 2 years. Peak height velocity (PHV) and peak weight velocity (PWV) in infancy were derived from parametric growth curves fitted to longitudinal height and weight growth data. Body mass index (BMI), waist circumference (WC), high density lipoprotein (HDL) cholesterol, triglycerides, glucose, systolic and diastolic blood pressure (BP), and the metabolic syndrome were measured at age 31 years. PHV was significantly positively associated with systolic and diastolic BP and WC in adulthood. For each 8-cm/year (2-standard-deviation) increase in PHV, WC increased by 1.60 cm (95% confidence interval: 0.73, 2.46), after adjustment for potential confounders, including birth weight. PWV was significantly associated with adulthood systolic BP, WC, and BMI. A 4-kg/year higher PWV was associated with a 1.87-cm (95% confidence interval: 1.08, 2.65) larger WC in adulthood, after adjustment for potential confounders. HDL cholesterol (direct), triglycerides (inverse), and metabolic syndrome (inverse) displayed associations with PWV only after BMI was accounted for. These results showed that growth during the immediate postnatal period is associated with adulthood obesity and BP. Lifestyle changes from early life might be important in reducing adulthood obesity and high-BP risk.