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Much is still unknown about the transition to adulthood for youth with autism spectrum disorder (ASD), including what preparation activities best support positive adult outcomes. Parents play a crucial role in the transition planning and preparation process, yet the existing literature lacks detailed information about parent perceptions about transition preparation activities. To examine family transition preparation activities, we conducted a ten-month study of the transition preparation process of 15 families of youth with ASD across an academic year. Youth were ages 14-17 and 93% male. We collected data on transition preparation activity time spent and parent satisfaction over twenty data collection points. We used multi-level modeling to determine longitudinal trajectories of parent-reported preparation for the transition to adulthood based on endorsed transition preparation activities. Findings from this preliminary study revealed that discussions about the future were the most commonly endorsed activities, while social activities were most associated with increased parental perception of transition preparation over time. This study expands understanding of various transition preparation activities engaged in by families of youth with ASD during high school, though research with a larger and more diverse sample is needed to extend findings.

Background Genetic influence on DNA methylation is potentially an important mechanism affecting individual differences in humans. We use next-generation sequencing to assay blood DNA methylation at approximately 4.5 million loci, each comprising 2.9 CpGs on average, in 697 normal subjects. Methylation measures at each locus are tested for association with approximately 4.5 million single nucleotide polymorphisms (SNPs) to exhaustively screen for methylation quantitative trait loci (meQTLs). Results Using stringent false discovery rate control, 15 % of methylation sites show genetic influence. Most meQTLs are local, where the associated SNP and methylation site are in close genomic proximity. Distant meQTLs and those spanning different chromosomes are less common. Most local meQTLs encompass common SNPs that alter CpG sites (CpG-SNPs). Local meQTLs encompassing CpG-SNPs are enriched in regions of inactive chromatin in blood cells. In contrast, local meQTLs lacking CpG-SNPs are enriched in regions of active chromatin and transcription factor binding sites. Of 393 local meQTLs that overlap disease-associated regions from genome-wide studies, a high percentage encompass common CpG-SNPs. These meQTLs overlap active enhancers, differentiating them from CpG-SNP meQTLs in inactive chromatin. Conclusions Genetic influence on the human blood methylome is common, involves several heterogeneous processes and is predominantly dependent on local sequence context at the meQTL site. Most meQTLs involve CpG-SNPs, while sequence-dependent effects on chromatin binding are also important in regions of active chromatin. An abundance of local meQTLs resulting from methylation of CpG-SNPs in inactive chromatin suggests that many meQTLs lack functional consequence. Integrating meQTL and Roadmap Epigenomics data could assist fine-mapping efforts.

We assess change in bleeding, cramping, and IUD satisfaction among new copper (Cu) IUD users during the first six months of use, and evaluate the impact of bleeding and cramping on method satisfaction. We recruited 77 women ages 18-45 for this prospective longitudinal observational cohort study. Eligible women reported regular menses, had no exposure to hormonal contraception in the last three months, and desired a Cu IUD for contraception. We collected data prospectively for 180 days following IUD insertion. Monthly, participants reported bleeding scores using the validated pictorial blood loss assessment chart (PBAC), IUD satisfaction using a five-point Likert scale, and cramping using a six-level ordinal scale. We used multiple imputation to address nonrandom attrition. Structural equation models for count and ordered outcomes were used to model bleeding, cramping, and IUD satisfaction growth curves over the six monthly repeated assessments. Bleeding significantly decreased (approximately 23%) over the course of the study from an estimated PBAC = 195 at one month post-insertion to PBAC = 151 at six months (t = -2.38, p<0.05). Additionally, IUD satisfaction improved over time (t = 2.65, p<0.01), increasing from between \"Neutral\" and \"Satisfied\" to \"Satisfied\" over the six month study. Cramping decreased notably over the six month study from between biweekly and weekly, to once or twice a month (t = -4.38, p<0.001). Finally, bleeding, but not cramping, was associated with IUD satisfaction across the study (t = -2.31, p<0.05) and at study end (t = -2.81, p<0.01). New Cu IUD users reported decreasing bleeding and cramping, and increasing IUD satisfaction, over the first six months. Method satisfaction was negatively associated with bleeding.

It is well established that immigrant adolescents have lower smoking rates than their native-born counterparts. Although smoking rates among immigrants have been theorized to increase with U.S. acculturation, this hypothesis has seldom been tested using longitudinal data spanning multiple developmental stages. The authors address this limitation using data from the National Longitudinal Study of Adolescent to Adult Health to model age-based smoking trajectories by gender and nativity status among Asian Americans (ages 10–33 years), adjusting for a range of control covariates. Trajectory analyses indicate that the gap between immigrants and natives generally increases as individuals age, but this process varies by gender, with immigrant women exhibiting a significantly less steep smoking growth trajectory (b = −.011, p < .001) compared with native-born men (and all other nativity-gender combinations), whereas immigrant men show no significant smoking trajectory slope difference compared with native men. In summary, results suggest a gendered acculturation process for smoking behavior among Asian Americans.

Neurocognitive deficits are a core feature of schizophrenia and, therefore, represent potentially critical outcome variables for assessing antipsychotic treatment response. We performed genome-wide association studies (GWAS) with 492K single nucleotide polymorphisms (SNPs) in a sample of 738 patients with schizophrenia from the Clinical Antipsychotic Trials of Intervention Effectiveness study. Outcome variables consisted of a neurocognitive battery administered at multiple time points over an 18-month period, measuring processing speed, verbal memory, vigilance, reasoning, and working memory domains. Genetic mediation of improvements in each of these five domains plus a composite neurocognitive measure was assessed for each of five antipsychotics (olanzapine, perphenazine, quetiapine, risperidone, and ziprasidone). Six SNPs achieved genome-wide significance using a pre-specified threshold that ensures, on average, only 1 in 10 findings is a false discovery. These six SNPs were located within, or in close proximity to, genes EHF , SLC26A9 , DRD2 , GPR137B , CHST8 , and IL1A . The more robust findings, that is those significant across multiple neurocognitive domains and having adjacent SNPs showing evidence for association, were rs286913 at the EHF gene ( p -value 6.99 × 10 −8 , q -value 0.034, mediating the effects of ziprasidone on vigilance), rs11240594 at SLC26A9 ( p -value 1.4 × 10 −7 , q -value 0.068, mediating the effects of olanzapine on processing speed), and rs11677416 at IL1A ( p -value 6.67 × 10 −7 , q -value 0.081, mediating the effects of olanzapine on working memory). This study has generated several novel candidate genes for antipsychotic response. However, our findings will require replication and functional validation. To facilitate replication efforts, we provide all GWAS p -values for download.

Racism drives population health inequities by shaping the unequal distribution of key social determinants of health, such as socioeconomic resources and exposure to stressors. Research on interrelationships among race, socioeconomic resources, stressors, and health has proceeded along two lines that have largely remained separate: one examining differential effects of socioeconomic resources and stressors on health across racialized groups (moderation processes), and the other examining the role of socioeconomic resources and stressors in contributing to racial inequities in health (mediation processes). We conceptually and analytically integrate these areas using race theory and a novel moderated mediation approach to path analysis to formally quantify the extent to which an array of socioeconomic resources and stressors—collectively and individually—mediate racialized health inequities among a sample of older adults from the Health and Retirement Study. Our results yield theoretical contributions by showing how the socioeconomic status–health gradient and stress processes are racialized (24% of associations examined varied by race), substantive contributions by quantifying the extent of moderated mediation of racial inequities (approximately 70%) and the relative importance of various social factors, and methodological contributions by showing how commonly used simple mediation approaches that ignore racialized moderation processes overestimate—by between 5% and 30%—the collective roles of socioeconomic status and stressors in accounting for racial inequities in health.

Objectives Little is known about maternal and infant health among sexual minority women (SMW), despite the large body of research documenting their multiple preconception risk factors. This study used data from the 2006–2015 National Survey of Family Growth (NSFG) to investigate sexual orientation inequities in pregnancy and birth outcomes, including miscarriage, stillbirth, preterm birth, and birth weight. Methods Women reported 19,955 study eligible pregnancies and 15,996 singleton live births. Sexual orientation was measured using self-reported identity and histories of same-sex sexual experiences (heterosexual-WSM [women who only report sex with men]; heterosexual-WSW [women who report sex with women]; bisexual, and lesbian). Logistic regression models were used that adjusted for several maternal characteristics. Results Compared to heterosexual-WSM, heterosexual-WSW (OR 1.25, 95% CI 1.00–1.58) and bisexual and lesbian women (OR 1.77, 95% CI 1.34–2.35) were more likely to report miscarriage, and bisexual and lesbian women were more likely to report a pregnancy ending in stillbirth (OR 2.85, 95% CI 1.40–5.83). Lesbian women were more likely to report low birth weight infants (OR 2.64, 95% CI 1.38–5.07) and bisexual and lesbian women were more likely to report very preterm births (OR 1.84, 95% CI 1.11–3.04) compared to heterosexual-WSM. Conclusions for Practice This study documents significant sexual orientation inequities in pregnancy and birth outcomes. More research is needed to understand the mechanisms that underlie disparate outcomes and to develop interventions to improve sexual minority women’s maternal and infant health.

Genetic liability to substance use disorders can be parsed into loci that confer general or substance-specific addiction risk. We report a multivariate genome-wide association meta-analysis that disaggregates general and substance-specific loci for published summary statistics of problematic alcohol use, problematic tobacco use, cannabis use disorder, and opioid use disorder in a sample of individuals of European descent and African descent. Nineteen independent SNPs were genome-wide significant ( < 5e-8) for the general addiction risk factor ( ), which showed high polygenicity. Across ancestries, was significant (among other genes), suggesting dopamine regulation as a cross-substance vulnerability. An polygenic risk score was associated with substance use disorders, psychopathologies, somatic conditions, and environments associated with the onset of addictions. Substance-specific loci (9 for alcohol, 32 for tobacco, 5 for cannabis, 1 for opioids) included metabolic and receptor genes. These findings provide insight into genetic risk loci for substance use disorders that could be leveraged as treatment targets.

Decades of fetal programming research indicates that we may be able to map the origins of many physical, psychological, and medical variations and morbidities before the birth of the child. While great strides have been made in identifying associations between prenatal insults, such as undernutrition or psychosocial stress, and negative developmental outcomes, far less is known about how adaptive responses to adversity regulate the developing phenotype to match stressful conditions. As the application of epigenetic methods to human behavior has exploded in the last decade, research has begun to shed light on the role of epigenetic mechanisms in explaining how prenatal conditions shape later susceptibilities to mental and physical health problems. In this review, we describe and attempt to integrate two dominant fetal programming models: the cumulative stress model (a disease-focused approach) and the match–mismatch model (an evolutionary–developmental approach). In conjunction with biological sensitivity to context theory, we employ these two models to generate new hypotheses regarding epigenetic mechanisms through which prenatal and postnatal experiences program child stress reactivity and, in turn, promote development of adaptive versus maladaptive phenotypic outcomes. We conclude by outlining priority questions and future directions for the fetal programming field.

Racial-ethnic disparities in static levels of health are well documented. Less is known about racialethnic differences in age trajectories of health. The few studies on this topic have examined only single health outcomes and focused on black-white disparities. This study extends prior research by using a life course perspective, panel data from the Health and Retirement Study, and multilevel growth curve models to investigate racial-ethnic differences in the trajectories of serious conditions and functional limitations among blacks, Mexican Americans, and whites. We test three hypotheses on the nature of racialethnic disparities in health across the life course (aging-as-leveler, persistent inequality, and cumulative disadvantage). Results controlling for mortality selection reveal that support for the hypotheses varies by health outcome, racial-ethnic group, and life stage. Controlling for childhood socioeconomic status, adult social and economic resources, and health behaviors reduces but does not eliminate racial-ethnic disparities in health trajectories.