Cohort Profile: The National Longitudinal Study of Adolescent to Adult Health (Add Health).
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ABSTRACT:
SUBMITTER: Harris KM
PROVIDER: S-EPMC6857761 | biostudies-literature | 2019 Oct
REPOSITORIES: biostudies-literature
Publications
Cohort Profile: The National Longitudinal Study of Adolescent to Adult Health (Add Health).
Harris Kathleen Mullan KM Halpern Carolyn Tucker CT Whitsel Eric A EA Hussey Jon M JM Killeya-Jones Ley A LA Tabor Joyce J Dean Sarah C SC
International journal of epidemiology 20191001 5
Similar Datasets
Project description:Add Health (National Longitudinal Study of Adolescent to Adult Health)
| PRJNA384882 | ENA
Project description:Here we provide a detailed description of the genome-wide information available on the National Longitudinal Study of Adolescent to Adult Health (Add Health) sibling pair subsample (Harris et al. in Twin Res Hum Genet 16:391-398, 2013). A total of 2,020 samples were genotyped (including duplicates) arising from 1946 Add Health individuals from the sibling pairs subsample. After various steps for quality control (QC) and quality assurance (QA), we have high quality genome-wide data available on 1,888 individuals. In this report, we first highlight the QC and QA steps that were taken to prune the data of poorly performing samples and genetic markers. We further estimate the pairwise biological relationships using genome-wide data and compare those estimates to the assumed relationships in Add Health. Additionally, using genome-wide data from known regional reference populations from Europe, West Africa, North and South America, Japan and China, we estimate the relative genetic ancestry of the respondents. Finally, rather than conducting a traditional cross-sectional genome-wide association study (GWAS) of body mass index (BMI), we opted to utilize the extensive publicly available genome-wide information to conduct a weighted GWAS of longitudinal BMI while accounting for both family and ethnic variation.
| S-EPMC4289640 | biostudies-literature
Project description:This article describes the design and phenotype and genotype data available for sibling pairs with varying genetic relatedness in the National Longitudinal Study of Adolescent Health (Add Health). Add Health is a nationally representative longitudinal study of over 20,000 adolescents in the United States in 1994-1995 who have been followed for 15 years into adulthood. The Add Health design included oversamples of more than 3,000 pairs of individuals with varying genetic resemblance, ranging from monozygotic twins, dizygotic twins, full siblings, half siblings, and unrelated siblings who were raised in the same household. Add Health sibling pairs are therefore nationally representative and followed longitudinally from early adolescence into adulthood with four in-home interviews during the period 1994-2009. Add Health has collected rich longitudinal social, behavioral, environmental, and biological data, as well as buccal cell DNA from all sample members, including sibling pairs. Add Health has an enlightened dissemination policy and to date has released phenotype and genotype data to more than 10,000 researchers in the scientific community.
| S-EPMC3574787 | biostudies-literature
Project description:BackgroundAir pollution exposure is associated with cardiovascular morbidity and mortality. Although exposure to air pollution early in life may represent a critical window for development of cardiovascular disease risk factors, few studies have examined associations of long-term air pollution exposure with markers of cardiovascular and metabolic health in young adults.ObjectivesBy combining health data from the National Longitudinal Study of Adolescent to Adult Health (Add Health) with air pollution data from the Fused Air Quality Surface using Downscaling (FAQSD) archive, we: (1) calculated multi-year estimates of exposure to ozone (O3) and particulate matter with an aerodynamic diameter ≤ 2.5 µm (PM2.5) for Add Health participants; and (2) estimated associations between air pollution exposures and multiple markers of cardiometabolic health.MethodsAdd Health is a nationally representative longitudinal cohort study of over 20,000 adolescents aged 12-19 in the United States (US) in 1994-95 (Wave I). Participants have been followed through adolescence and into adulthood with five in-home interviews. Estimated daily concentrations of O3 and PM2.5 at census tracts were obtained from the FAQSD archive and used to generate tract-level annual averages of O3 and PM2.5 concentrations. We estimated associations between average O3 and PM2.5 exposures from 2002 to 2007 and markers of cardiometabolic health measured at Wave IV (2008-09), including hypertension, hyperlipidemia, body mass index (BMI), diabetes, C-reactive protein, and metabolic syndrome.ResultsThe final sample size was 11,259 individual participants. The average age of participants at Wave IV was 28.4 years (range: 24-34 years). In models adjusting for age, race/ethnicity, and sex, long-term O3 exposure (2002-07) was associated with elevated odds of hypertension, with an odds ratio (OR) of 1.015 (95% confidence interval [CI]: 1.011, 1.029); obesity (1.022 [1.004, 1.040]); diabetes (1.032 [1.009,1.054]); and metabolic syndrome (1.028 [1.014, 1.041]); PM2.5 exposure (2002-07) was associated with elevated odds of hypertension (1.022 [1.001, 1.045]).ConclusionFindings suggest that long-term ambient air pollution exposure, particularly O3 exposure, is associated with cardiometabolic health in early adulthood.
| S-EPMC10664021 | biostudies-literature
Project description:Hearing loss is a major public problem with a heritability of up to 70%. Catechol-O-methyltransferase (COMT) encodes an enzyme that is highly expressed in sensory hair cells of the inner ear. The association between COMT and hearing loss has not been reported previously in nationally representative population-based studies. A regression linear model was used to estimate associations between the allele/genotype of COMT and self-reported hearing loss based on 13,403 individuals from Wave IV of the Add Health study, a nationally representative sample of multiethnic U.S. young adults. The inverse variance-weighted effect magnitude was estimated using a genetic meta-analysis model. The "A" allele frequency of rs6480 (a missense variant in COMT) was 0.44. The prevalence of hearing loss was 7.9% for individuals with the "A" allele and 6.5% for those with the "G" allele. The "A" allele was significantly associated with increased hearing loss (p = 0.01). The prevalence of hearing loss was 6.0%, 7.2%, and 8.7% for individuals with GG, AG, and AA genotypes, respectively, which was consistent with a genetic additive model. The genotypic association model showed that rs4680 was significantly associated with increased hearing loss (p = 0.006). A missense variant of rs4680 in COMT was significantly associated with increased hearing loss among young adults in a multi-racial/ethnic U.S. population-based cohort.
| S-EPMC9687786 | biostudies-literature
Project description:BackgroundThe low transcriptionally efficient short-allele of the 5HTTLPR serotonin transporter polymorphism has been implicated to moderate the relationship between the experience of stressful life events (SLEs) and depression. Despite numerous attempts at replicating this observation, results remain inconclusive.MethodsWe examined this relationship in young-adult Non-Hispanic white males and females between the ages of 22 and 26 (n = 4724) participating in the National Longitudinal Study of Adolescent to Adult Health (Add Health) with follow-up information every six years since 1995.ResultsLinear and logistic regression models, corrected for multiple testing, indicated that carriers of one or more of the S-alleles were more sensitive to stress than those with two L-alleles and at a higher risk for depression. This relationship behaved in a dose-response manner such that the risk for depression was greatest among those who reported experiencing higher numbers of SLEs. In post-hoc analyses we were not able to replicate an interaction effect for suicide ideation but did find suggestive evidence that the effects of SLEs and 5HTTLPR on suicide ideation differed for males and females. There were no effects of childhood maltreatment.DiscussionOur results provide partial support for the original hypothesis that 5-HTTLPR genotype interacts with the experience of stressful life events in the etiology of depression during young adulthood. However, even with this large sample, and a carefully constructed a priori analysis plan, the results were still not definitive. For the purposes of replication, characterizing the 5HTTLPR in other large data sets with extensive environmental and depression measures is needed.
| S-EPMC4777542 | biostudies-literature
Project description:<p>The National Longitudinal Study of Adolescent to Adult Health [Add Health] is an ongoing longitudinal study of a nationally representative U.S. cohort of more than 20,000 adolescents in grades 7-12 (aged 12-19 years) in 1994 followed into adulthood with five interviews/surveys in 1995, 1996, 2001-02, 2008, and 2016-18. Add Health was designed to understand how social environments and behaviors in adolescence are linked to health and achievement outcomes in young adulthood. Add Health contains unprecedented environmental, behavioral, psychosocial, biological, and genetic data from early adolescence and into adulthood on a large, nationally representative cohort with unprecedented racial, ethnic, socioeconomic, and geographic diversity. Add Health has a large, multidisciplinary user base of over 50,000 researchers around the world who have published over 3,400 research articles. Add Health is housed at the Carolina Population Center of the University of North Carolina at Chapel Hill. Add Health datasets are distributed according to a tiered data disclosure plan designed to protect the data from the risk of direct and indirect disclosure of respondent identity.</p> <p>Add Health's large sample size, population diversity and rich longitudinal data base of psychosocial, physical, and contextual data will permit investigation of an exceptionally broad range of phenotypes with known genetic variation. Prospective longitudinal measures are available to document change over time in each of these phenotypes, as well as change in the social environment and life experiences, making the Add Health sample ideal for understanding genetic linkages with health and behavior across the life course.</p> <p>The original design of Add Health included important features for understanding biological processes in health and developmental trajectories across the life course of young people, including an embedded genetic sample with more than 3,000 pairs of adolescents with varying biological resemblance (e.g., twins, full sibs, half sibs, and adolescents who grew up in the same household but have no biological relationship), testing of saliva and urine for sexually transmitted infections and HIV, and biomarkers of cardiovascular health, metabolic processes, immune function, renal function, and inflammation. Add Health therefore has critical objective indicators of health status and disease markers in young adulthood, well before chronic illness or its complications emerge in later adulthood. Because DNA has been collected on the full sample at Wave IV, it is possible to link genetic profiles with social, behavioral, and biological measures over time from adolescence into adulthood. </p> <p>Add Health sampled the multiple environments in which young people live their lives, including the family, peers, school, neighborhood, community, and relationship dyads, and provides independent and direct measurement of these environments over time. Add Health contains extensive longitudinal information on health-related behavior, including life histories of physical activity, involvement in risk behavior, substance use, sexual behavior, civic engagement, education, and multiple indicators of health status based on self-report (e.g., general health, chronic illness), direct measurement (e.g., overweight status and obesity), and biomarkers. No other data resource with this expanse of genotype and phenotype data on a large nationally representative longitudinal sample with race, ethnic, socioeconomic, and geographic diversity exists. </p> <p>A complete reference guide on study design and accomplishments can be found on the Add Health website: <a href="http://www.cpc.unc.edu/projects/addhealth/data/guides/DesignPaperWIIV.pdf">Design Paper</a>: <b>The Add Health Study: Design and Accomplishments Kathleen Mullan Harris Carolina Population Center University of North Carolina at Chapel Hill 2013</b> </p>
| phs001367 | dbGaP
Project description:BackgroundAdolescence is a sensitive period for weight gain and risky health behaviors, such as smoking. Genome-wide association studies (GWAS) have identified loci contributing to adult body mass index (BMI). Evidence suggests that many of these loci have a larger influence on adolescent BMI. However, few studies have examined interactions between smoking and obesity susceptibility loci on BMI. This study investigates the interaction of current smoking and established BMI SNPs on adolescent BMI. Using data from the National Longitudinal Study of Adolescent to Adult Health, a nationally-representative, prospective cohort of the US school-based population in grades 7 to 12 (12-20 years of age) in 1994-95 who have been followed into adulthood (Wave II 1996; ages 12-21, Wave III; ages 18-27), we assessed (in 2014) interactions of 40 BMI-related SNPs and smoking status with percent of the CDC/NCHS 2000 median BMI (%MBMI) in European Americans (n = 5075), African Americans (n = 1744) and Hispanic Americans (n = 1294).ResultsTwo SNPs showed nominal significance for interaction (p < 0.05) between smoking and genotype with %MBMI in European Americans (EA) (rs2112347 (POC5): β = 1.98 (0.06, 3.90), p = 0.04 and near rs571312 (MC4R): β 2.15 (-0.03, 4.33) p = 0.05); and one SNP showed a significant interaction effect after stringent correction for multiple testing in Hispanic Americans (HA) (rs1514175 (TNNI3K): β 8.46 (4.32, 12.60), p = 5.9E-05). Stratifying by sex, these interactions suggest a stronger effect in female smokers.ConclusionsOur study highlights potentially important sex differences in obesity risk by smoking status in adolescents, with those who may be most likely to initiate smoking (i.e., adolescent females), being at greatest risk for exacerbating genetic obesity susceptibility.
| S-EPMC4634717 | biostudies-literature
Project description:Humans tend to form social relationships with others who resemble them. Whether this sorting of like with like arises from historical patterns of migration, meso-level social structures in modern society, or individual-level selection of similar peers remains unsettled. Recent research has evaluated the possibility that unobserved genotypes may play an important role in the creation of homophilous relationships. We extend this work by using data from 5,500 adolescents from the National Longitudinal Study of Adolescent to Adult Health (Add Health) to examine genetic similarities among pairs of friends. Although there is some evidence that friends have correlated genotypes, both at the whole-genome level as well as at trait-associated loci (via polygenic scores), further analysis suggests that meso-level forces, such as school assignment, are a principal source of genetic similarity between friends. We also observe apparent social-genetic effects in which polygenic scores of an individual's friends and schoolmates predict the individual's own educational attainment. In contrast, an individual's height is unassociated with the height genetics of peers.
| S-EPMC5789914 | biostudies-literature
Project description:Recent studies have begun to uncover the genetic architecture of educational attainment. We build on this work using genome-wide data from siblings in the National Longitudinal Study of Adolescent to Adult Health (Add Health). We measure the genetic predisposition of siblings to educational attainment using polygenic scores. We then test how polygenic scores are related to social environments and educational outcomes. In Add Health, genetic predisposition to educational attainment is patterned across the social environment. Participants with higher polygenic scores were more likely to grow up in socially advantaged families. Even so, the previously published genetic associations appear to be causal. Among pairs of siblings, the sibling with the higher polygenic score typically went on to complete more years of schooling as compared to their lower-scored co-sibling. We found subtle differences between sibling fixed effect estimates of the genetic effect versus those based on unrelated individuals.
| S-EPMC5291340 | biostudies-literature