Understanding heterogeneity in the effects of birth weight on adult cognition and wages.
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ABSTRACT:
SUBMITTER: Justin Cook C
PROVIDER: S-EPMC4417462 | biostudies-literature | 2015 May
REPOSITORIES: biostudies-literature
Publications
Understanding heterogeneity in the effects of birth weight on adult cognition and wages.
Justin Cook C C Fletcher Jason M JM
Journal of health economics 20150221
A large economics literature has shown long term impacts of birth weight on adult outcomes, including IQ and earnings that are often robust to sibling or twin fixed effects. We examine potential mechanisms underlying these effects by incorporating findings from the genetics and neuroscience literatures. We use a sample of siblings combined with an "orchids and dandelions hypothesis", where the IQ of genetic dandelions is not affected by in utero nutrition variation but genetic orchids thrive und ...[more]
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Project description:Birth weight is an important indicator of prenatal environment, and subtle variations of birth weight within the normal range have been associated with differential risk for cognitive and behavioral problems. Therefore, we aimed to determine if there are differences in birth weight between full-term children with uncomplicated new/recent-onset epilepsies and typically developing healthy controls. We further examined the relationships between birth weight and childhood/adolescent cognition, behavior, and academic achievement.One hundred eight children with new-onset/recent-onset epilepsy and 70 healthy controls underwent neuropsychological assessment. All participants were born full-term (>37 weeks) without birth complications. Parents were interviewed regarding their child's gestation, birth, and neurodevelopmental history.Birth weight of children with epilepsy was significantly lower than healthy controls (p = 0.023). Whereas birth weight (covaried with age, sex, handedness, and mother's education) was significantly associated with cognition in controls in multiple domains (intelligence, language, aspects of academic achievement), this relationship was absent in children with epilepsy. Birth weight was not associated with clinical epilepsy variables (age of onset, epilepsy syndrome) and was not predictive of a variety of other academic or psychiatric comorbidities of epilepsy.Although the origin of lower birth weight in children with epilepsy is unknown, these findings raise the possibility that abnormal prenatal environment may affect childhood-onset epilepsy. Furthermore, the positive relationship between birth weight and cognition evident in healthy controls was disrupted in children with epilepsy. However, birth weight was not related to academic and psychiatric comorbidities of childhood epilepsy. A PowerPoint slide summarizing this article is available for download in the Supporting Information section here.
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Project description:This paper studies the effects of minimum wages in Indonesia around the time of birth on child height-for-age Z scores (HAZ) up to five years of age. Using variations in annual fluctuations in real minimum wages in different Indonesian provinces, it finds that children exposed to increases in minimum wages in their birth years have higher HAZ in the first five years of their lives. The estimated impacts are based on difference-in-differences models with biological-mother fixed effects and year-of-birth fixed effects and are robust to inclusion of multiple time-varying factors. The impacts are prominent particularly among male children.
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Project description:ObjectivesAmong low-birth-weight infants, exposure to stress or undernutrition in utero may adversely affect cochlear development. As cochlear reserve declines, the risk of hearing loss may increase with age. While low birth weight is associated with a higher risk of neonatal hearing loss, our objective was to examine whether birth weight was associated with adult-onset, self-reported hearing loss in the Nurses' Health Studies (NHS) I and II (n = 113,130).DesignWe used Cox proportional hazards regression to prospectively examine whether birth weight, as well as gestational age at birth, is associated with adult-onset hearing loss. Participants reported their birth weight in 1992 in NHS I and 1991 in NHS II. Mothers of NHS II participants reported gestational age at birth in a substudy (n = 28,590). The primary outcome was adult-onset, self-reported moderate or greater hearing loss, based on questionnaires administered in 2012/2016 in NHS I and 2009/2013 in NHS II.ResultsOur results suggested a higher risk of hearing loss among those with birth weight <5.5 lbs compared with birth weight 7 to <8.5 lbs (pooled multivariable-adjusted hazard ratio 1.14, 95% confidence interval = 1.04-1.23; p trend = 0.01). Additionally, participants with gestational age at birth ≥42 weeks had a higher risk of hearing loss, compared with gestational age 38 to <42 weeks (multivariable-adjusted hazard ratio 1.33, 95% confidence interval = 1.06-1.65).ConclusionsBirth weight <5.5 lbs was independently associated with higher risk of self-reported, adult-onset hearing loss. In addition, gestational age at birth ≥42 weeks was also associated with higher risk.
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Project description:Birth weight (BW) has been shown to be influenced by both fetal and maternal factors and in observational studies is reproducibly associated with future risk of adult metabolic diseases including type 2 diabetes (T2D) and cardiovascular disease. These life-course associations have often been attributed to the impact of an adverse early life environment. Here, we performed a multi-ancestry genome-wide association study (GWAS) meta-analysis of BW in 153,781 individuals, identifying 60 loci where fetal genotype was associated with BW (P < 5 × 10-8). Overall, approximately 15% of variance in BW was captured by assays of fetal genetic variation. Using genetic association alone, we found strong inverse genetic correlations between BW and systolic blood pressure (Rg = -0.22, P = 5.5 × 10-13), T2D (Rg = -0.27, P = 1.1 × 10-6) and coronary artery disease (Rg = -0.30, P = 6.5 × 10-9). In addition, using large -cohort datasets, we demonstrated that genetic factors were the major contributor to the negative covariance between BW and future cardiometabolic risk. Pathway analyses indicated that the protein products of genes within BW-associated regions were enriched for diverse processes including insulin signalling, glucose homeostasis, glycogen biosynthesis and chromatin remodelling. There was also enrichment of associations with BW in known imprinted regions (P = 1.9 × 10-4). We demonstrate that life-course associations between early growth phenotypes and adult cardiometabolic disease are in part the result of shared genetic effects and identify some of the pathways through which these causal genetic effects are mediated.
| S-EPMC5164934 | biostudies-literature
Project description:We aimed to gain mechanistic insights into the impact of uteroplacental insufficiency upon hepatic cholestrol metabolism pathways in young adult offspring.Uterine artery ablation-induced low birth weight (LBW) and normal birth weight (NBW) male and female guinea pig offspring were fed a control diet from weaning until postnatal day 150. Analysis of whole hepatic transcriptome results identified that between LBW and NBW offspring livers, 51 (29 up-regulated and 22 down-regulated) and 31 (8 up-regulated and 23 down-regulated) genes were differentially expressed in males and females respectively (fold change| >= 2 and p-value < 0.05). KEGG pathway analysis of these differentially expressed genes revealed that “Cholesterol metabolism” was an enriched pathway in LBW males but not females (p<0.05).
2020-11-10 | GSE161124 | GEO
Project description:BackgroundEducational attainment is highly correlated with social inequalities in adult cognitive health; however, the nature of this correlation is in dispute. Recently, researchers have argued that educational inequalities are an artefact of selection by individual differences in prior cognitive ability, which both drives educational attainment and tracks across the rest of the life course. Although few would deny that educational attainment is at least partly determined by prior cognitive ability, a complementary, yet controversial, view is that education has a direct causal and lasting benefit on cognitive development.MethodsWe use observational data from three birth cohorts, with cognition measured in adolescence and adulthood. Ordinary least squares regression was used to model the relationship between adolescent cognition and adult fluid cognition and to test the sensitivity of our analyses to sample selection, projection and backdoor biases using propensity score matching.ResultsWe find that having a university education is correlated with higher fluid cognition in adulthood, after adjustment for adolescent cognition. We do not find that adolescent cognition, gender or parental social class consistently modify this effect; however, women benefited more in the 1946 sample from Great Britain.ConclusionsIn all three birth cohorts, substantial educational benefit remained after adjustment for adolescent cognition and parental social class, offsetting an effect equivalent of 0.5 to 1.5 standard deviations lower adolescent cognition. We also find that the likelihood of earning a university degree depends in part on adolescent cognition, gender and parental social class. We conclude that inequalities in adult cognition derive in part from educational experiences after adolescence.
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Project description:BackgroundAssociations between birth weight (BW) and adult lung function have been inconsistent and limited to early adulthood. We aimed to study this association in two population-based cohorts and explore if BW, adjusted for gestational age, predicts adult lung function. We also tested adult lung function impairment according to the mis-match hypothesis-small babies growing big as adults.MethodsWe included 3495 individuals (aged 46.4 ± 5.4 years) from the Malmo Preventive Project (MPP), Sweden, born between 1921 and 1949, and 1401 young to middle-aged individuals (aged 28.6 ± 6.7 years) from the Malmo Offspring Study (MOS) with complete data on BW and gestational age. Adult lung function (forced vital capacity [FVC], forced expiratory volume in one second [FEV1] and the FEV1/FVC-ratio) were analysed as level of impairment (z-score), using multiple linear and logistic regressions.ResultsBW (z-score) did not predict adult lung function in MPP, whereas BW was a significant (p = 0.003) predictor of FEV1 following full adjustment in MOS. For every additional unit increase in BW, children were 0.77 (95% CI 0.65-0.92) times less likely to have impaired adult lung function (FEV1). Moreover, adults born with lower BW (< 3510 g) showed improved lung function (FEV1 and FEV1/FVC in MOS and MPP, respectively) if they achieved higher adult body weight.ConclusionsAdults born with lower birth weight, adjusted for gestational age, are more likely to have impaired lung function, seen in a younger birth cohort. Postnatal growth pattern may, however, compensate for low birth weight and contribute to better adult lung function.
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Project description:BackgroundMost evidence about associations between birth weight and adult cancer risk comes from studies linking birth records to cancer registration data, where information on known risk factors for cancer is generally lacking. Here, we report on associations between birth weight and cause-specific cancer risk in a large cohort of UK women, and investigate how observed associations are affected by other factors.MethodsA total of 453 023 women, born in the 1930s and 1940s, reported their birth weight, maternal smoking, parental heights, age at menarche, adult height, adult smoking, and many other personal characteristics. They were followed for incident cancer. Using Cox regression, relative risks by birth weight were estimated for cancers with more than 1500 incident cases, adjusting for 17 potential confounding factors, individually and simultaneously.ResultsBirth weight reported in adulthood was strongly correlated with that recorded at birth (correlation coefficient = 0.78, P < 0.0001). Reported birth weight was associated with most of the potential confounding factors examined, the strongest association being with adult height. After 9.2 years follow-up per woman, 39 060 incident cancers were registered (4414 colorectal, 3175 lung, 1795 malignant melanoma, 14 542 breast, 2623 endometrial, 2009 ovarian, 1565 non-Hodgkin lymphoma, and 8937 other cancers). Associations with birth weight were null or weak and reduced after adjustment by adult height (P[trend] > 0.01 for every cancer, after adjustment). In contrast, adult height was strongly related to the risk of every cancer except lung cancer, after adjusting for birth weight and other factors (P[trend] < 0.0001 for most cancers). For lung cancer, adjusting for smoking reduced the association with birth weight. Meta-analyses were dominated by our findings.ConclusionBirth weight and adult height are correlated and likely to be markers of some aspect of growth that affects cancer risk in adulthood. However, birth weight adds little, if any, additional information to adult height as a predictor of cancer incidence in women.
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