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Schools implementing Positive Behavioral Interventions and Supports (PBIS) with fidelity demonstrate a wealth of student and school benefits. At the same time, there exists limited research from an inclusive innovation perspective: examining whether schools and communities have equitable access to PBIS based on sociodemographic school and community variables. This article presents the results of an ex post facto research design examining PBIS implementation and access across sociodemographic school and community variables from an inclusive innovation lens, examining data from schools ( N = 489) in the state of Georgia. The significant interaction effects revealed that between both PBIS and non-PBIS schools, those located in suburban areas had significantly higher median household incomes compared with rural and urban schools. Additional findings included the following: PBIS rural schools had higher household incomes and lower percentages of free/reduced-price lunch than non-PBIS schools in rural communities, and PBIS schools included significantly higher proportions of students who identified as White compared with non-PBIS schools.

LifeMatters is a 10-session life skills program implemented with youth that uses mental skills training and games to meet the three basic psychological needs of relatedness, autonomy, and competenc...

Glycosuria is a condition where glucose is detected in urine at higher concentrations than normal (i.e. not detectable). Glycosuria at some point during pregnancy has an estimated prevalence of 50% and is associated with adverse outcomes in both mothers and offspring. Little is currently known about the genetic contribution to this trait or the extent to which it overlaps with other seemingly related traits, e.g. diabetes. We performed a genome-wide association study (GWAS) for self-reported glycosuria in pregnant mothers from the Avon Longitudinal Study of Parents and Children (cases/controls = 1249/5140). We identified two loci, one of which (lead SNP = rs13337037; chromosome 16; odds ratio of glycosuria per effect allele: 1.42; 95% CI: 1.30, 1.56; P = 1.97 × 10−13) was then validated using an obstetric measure of glycosuria measured in the same cohort (227/6639). We performed a secondary GWAS in the 1986 Northern Finland Birth Cohort (NFBC1986; 747/2991) using midwife-reported glycosuria and offspring genotype as a proxy for maternal genotype. The combined results revealed evidence for a consistent effect on glycosuria at the chromosome 16 locus. In follow-up analyses, we saw little evidence of shared genetic underpinnings with the exception of urinary albumin-to-creatinine ratio (Rg = 0.64; SE = 0.22; P = 0.0042), a biomarker of kidney disease. In conclusion, we identified a genetic association with self-reported glycosuria during pregnancy, with the lead SNP located 15kB upstream of SLC5A2, a target of antidiabetic drugs. The lack of strong genetic correlation with seemingly related traits such as type 2 diabetes suggests different genetic risk factors exist for glycosuria during pregnancy.

We conducted genome-wide association study (GWAS) meta-analyses of relative caloric intake from fat, protein, carbohydrates and sugar in over 235,000 individuals. We identified 21 approximately independent lead SNPs. Relative protein intake exhibits the strongest relationships with poor health, including positive genetic associations with obesity, type 2 diabetes, and heart disease (rg ≈ 0.15 – 0.5). Relative carbohydrate and sugar intake have negative genetic correlations with waist circumference, waist-hip ratio, and neighborhood poverty (|rg| ≈ 0.1 – 0.3). Overall, our results show that the relative intake of each macronutrient has a distinct genetic architecture and pattern of genetic correlations suggestive of health implications beyond caloric content.

Calls to integrate social justice principles and training into programs pre- paring practitioners in various mental health fields are now well established within the professional literature (Bemak, Chung, Talleyrand, Jones, & Daquin, 2011). Counselors are increasingly expected to operate from a social justice orientation to promote wellness for their clients and students (AmericanCounselingAssociation, �2014). �T odothis, �counselorsmusthave� the ability to (a) recognize discrimination and oppression across the micro- and macrosystems in which people live; (b) understand the impact that discrimination and oppression have on the development and well-being of clients; and (c) intervene competently across multiple contexts to promote justice, equity, and access with and on behalf of students and clients (Lewis, Arnold, House, & Toporek, 2002; Sue, Arredondo, & McDavis, 1992; Toporek, Lewis, & Crethar, 2009). Attention to these skills requires counselor train- ing programs to change the way that counselors are prepared (Odegard & Vereen, �2010; �T oporeketal., �2009). In response to the call for social justice counselor education, scholars have articulated and endorsed specific advocacy competencies (Ratts, Toporek, & Lewis, 2010), written and published texts to promote social justice advo- cacy in counseling students (e.g., Chung & Bemak, 2012; Ratts & Pedersen, 2014), �andpublishedmanuscriptsthatillustratehowgraduatetraining� programs can incorporate social justice initiatives (e.g., Ali, Liu, Mahmood, & Arguello, 2008; Bemak et al., 2011). Despite increased attention in this area, few studies have provided evaluative data on the effectiveness of social justice training practices (e.g., teaching strategies) in counseling preparation programs; most of the work in this area is theoretical (Manis, 2012; Murray, Pope, �& �Rowell, �2010; �Nilsson �& �Schmidt, �2005; �Odegard �& �V ereen, �2010).

Aims: Alcohol problems (AP) contribute substantially to the global disease burden. Twin and family studies suggest that AP are genetically influenced, although few studies have identified variants or genes that are robustly associated with risk. This study identifies genetic and genomic influences on AP during young adulthood, which is often when drinking habits are established. Design: We conducted a genome-wide association study of AP. We further conducted gene-based tests, gene ontology analyses and functional genomic enrichment analyses to assess genomic factors beyond single variants that are relevant to AP. Setting: The Avon Longitudinal Study of Parents and Children, a large population-based study of a UK birth cohort. Participants: Genetic and phenotypical data were available for 4304 participants. Measurements: The AP phenotype was a factor score derived from items from the Alcohol Use Disorders Identification Test, symptoms of DSM-IV alcohol dependence, and three additional problem-related items. Findings: One variant met genome-wide significance criteria. Four out of 22880 genes subjected to gene-based analyses survived a stringent significance threshold (q

BackgroundIt has been suggested that greater maternal adiposity during pregnancy affects lifelong risk of offspring fatness via intra-uterine mechanisms. Our aim was to use Mendelian randomizationto investigate the causal effect of intra-uterine exposure to greater maternal body mass index (BMI) on offspring BMI and fat mass from childhood to early adulthood.Methods and FindingsWe used maternal genetic variants as instrumental variables to test the causal effect of maternal BMI in pregnancy on offspring fatness (BMI and dual-energy X-ray absorptiometry (DXA) determined fat mass index (FMI)) in a Mendelian randomization approach. This was investigated, with repeat measurements, from age 7 to 18 in the Avon Longitudinal Study of Parents and Children (ALSPAC; N = 2,521 to 3,720 for different ages). We then sought to replicate findings with results for BMI at age 6 in Generation R (N = 2,337 for replication sample; N= 6,057 for total pooled sample).In confounder adjusted multivariable regression in ALSPAC, a 1 SD (equivalent of 3.7 kg/m2) increase in maternal BMI was associated with a 0.25 SD (95% confidence interval (CI) = 0.21, 0.29) increase in offspring BMI at age 7, with similar results at later ages and when FMI was used as the outcome.A weighted genetic risk score was generated from 32 genetic variants robustly associated with BMI (minimum F-statistic = 45 in ALSPAC). The Mendelian randomization results using this genetic risk score as an instrumental variable in ALSPAC were close to the null at all ages (e.g. 0.04 SD (95% CI -0.21, 0.30) at age 7 and 0.03 SD (95% CI -0.26, 0.32) at age 18 per SD increase in maternal BMI), which was similar when a 97 variant generic risk score was used in ALSPAC.When findings from age 7 in A 52 LSPAC were meta-analysed with those from age 6 in Generation R, the pooled confounder adjusted multivariable regression association was 0.22 SD (95%CI: 0.19, 0.25) per SD increase in maternal BMI and the pooled Mendelian randomization effect (pooling the 97 variant score results from ALSPAC with the 32 variant score results from Generation R) was 0.05 SD (95%CI: -0.11, 0.21) per SD increase in maternal BMI (p-value for difference between the two results = 0.05). A number of sensitivity analyses exploring violation of the Mendelian randomization results supported our main findings. However, power was limited for some of the sensitivity tests and further studies with relevant data on maternal, offspring (and paternal) genotype are required to obtain more precise (and unbiased) causal estimates.ConclusionsOur findings provide little evidence to support a strong causal intrauterine effect of incrementally greater maternal BMI resulting in greater offspring adiposity.

The world has changed dramatically in the past 150 years, so much so that the common artifacts of the 21st century would make life hardly recognizable to someone from the early 1900s. In contrast to the great advances that have been seen in technology, health care, and engineering, the educational system in the United States has changed very little since the early 1900s (Heckman & Monterra, 2009). Grounded in the segmented, linear, and time-bound paradigm of the industrial revolution, many public schools operate similar to a factory (U.S. Department of Education, n.d.), where students are raw products that are run through the assembly line of education, exposed to different teachers who work independently to add their piece to the developing student before moving that student along to the next stop on the assembly line (Ayers, 2009). These schools-as-factories have a clear vision of what the final products should look like, and this final product is assessed and evaluated in an attempt to ensure that all graduates meet the same standards. Students who do not match these standards or who do not move through the process on time are deemed to be deficient and are eventually discarded (or allowed to discard themselves) from the system. The industrial model of education has grown stale and, too often, discourages innovation, collaboration, and shared leadership (U.S. Department of Education, n.d.). This approach, which values linear processes over cyclical processes, efficiency over quality, and uniformity over uniqueness, leads to an undemocratic system that asks a group of unique individuals to engage in a process that will attempt to make them more uniform and closer to a standardized vision of a "good student" and graduate (Angus, Mirel, & Vinovskis, 1988). As William Ayers (2009) put it, the message to the students is, "You are not important or unique; be only malleable and productive in terms established by a higher authority" (p. 390). One danger inherent in the industrial model of education is the number of students who do not fit the model's vision of a successful student. In an ever-changing world where people from different backgrounds must work together and where new technology is being introduced at incredible rates, the concept of a standardized learner is simply no longer relevant. Schools and school systems that operate under the belief that learning should take place in ordered, time-bound chunks and that knowledge remains static through time will not produce the graduates and, therefore, the workers and community members that an increasingly multicultural and technology-driven world demands (Angus et al., 1988; U.S. Department of Education, n.d.). Moreover, at a time when student alienation from schools is a serious problem (Schulz & Rubel, 2011; Sciarra & Ambrosino, 2011), educators who internalize the industrial model's vision of a successful student and place those expectations on their students may be exacerbating students' beliefs that school is not for them. In addition, counselors who cling to a rigid perspective of successful students rather than understanding the cultural values inherent in that vision are missing a key piece of being a culturally responsive counselor (Brown & Trusty, 2005; Locke, 2003); they are also more likely to participate in troublesome practices such as inequitable scheduling and advising (Holcomb-McCoy, 2007). What is needed is a new paradigm that appreciates diversity and is more responsive to the changes that characterize the 21st-century world. Because of their training in leadership, advocacy, and collaboration skills and their ability to think and work systemically, professional school counselors may be in a unique position to help initiate this change. In fact, professional school counseling has already started this process. Efforts to transform school counseling practice in order to address educational inequity and be more responsive to the needs of all students have taken root. …

The American Psychiatric Association estimates that 3 to 7 per cent of all school aged children are diagnosed with attention deficit hyperactivity disorder (ADHD). Even after correcting for general cognitive ability, numerous studies report a negative association between ADHD and educational achievement. With polygenic scores we examined whether genetic variants that have a positive influence on educational attainment have a protective effect against ADHD. The effect sizes from a large GWA meta-analysis of educational attainment in adults were used to calculate polygenic scores in an independent sample of 12-year-old children from the Netherlands Twin Register. Linear mixed models showed that the polygenic scores significantly predicted educational achievement, school performance, ADHD symptoms and attention problems in children. These results confirm the genetic overlap between ADHD and educational achievement, indicating that one way to gain insight into genetic variants responsible for variation in ADHD is to include data on educational achievement, which are available at a larger scale. (C) 2014 Wiley Periodicals, Inc.

Authors performed a content analysis of school counseling–related intervention research in 21 journals affiliated with the American Counseling Association and the American School Counselor Association across the 10-year span of 2006–2016. Results indicated that minimal school counseling intervention research articles were published ( N = 53) in these 21 journals during that time period and that most studies were quasi-experimental, single-group, pre-/posttest design with a fairly small N, raising questions about validity and generalizability of findings. We discuss implications for practice and future research.

Inclusive innovation is a research framework used to assess the degree to which innovations are accessible to and useful within communities experiencing high need. We describe the tenets of inclusive innovation research and outline how the model could be added to the current evidence-based school counseling research agenda to begin to answer questions of access and equity in the distribution of effective practices.

Allergic disease is very common and carries substantial public-health burdens. We conducted a meta-analysis of genome-wide associations with self-reported cat, dust-mite and pollen allergies in 53,862 individuals. We used generalized estimating equations to model shared and allergy-specific genetic effects. We identified 16 shared susceptibility loci with association P

The purpose of this study is to understand the experiences of secondary school counselors who develop and lead groups. The study explored participants’ perceptions and their motivations for leading groups. Findings from data analysis revealed four major themes. Unappreciated and Dismissed describes the way participants felt in response to the implicit and explicit messages received from colleagues as they planned and facilitated groups. Outside the Comfort Zone describes the participants’ feelings of vulnerability and/or inadequacy during group facilitation. Participants described Meaningful Relationships which developed through the groups. Finally, participants recounted Encouraging Feedback they received as a result of leading groups.

Author version made available in accordance with the publisher's policy., Refractive error is the most common eye disorder worldwide and is a prominent cause of blindness. Myopia affects over 30% of Western populations and up to 80% of Asians. The CREAM consortium conducted genome-wide meta-analyses, including 37,382 individuals from 27 studies of European ancestry and 8,376 from 5 Asian cohorts. We identified 16 new loci for refractive error in individuals of European ancestry, of which 8 were shared with Asians. Combined analysis identified 8 additional associated loci. The new loci include candidate genes with functions in neurotransmission (GRIA4), ion transport (KCNQ5), retinoic acid metabolism (RDH5), extracellular matrix remodeling (LAMA2 and BMP2) and eye development (SIX6 and PRSS56). We also confirmed previously reported associations with GJD2 and RASGRF1. Risk score analysis using associated SNPs showed a tenfold increased risk of myopia for individuals carrying the highest genetic load. Our results, based on a large meta-analysis across independent multiancestry studies, considerably advance understanding of the mechanisms involved in refractive error and myopia., Australian National Health and Medical Research Council.

Educational attainment is associated with many health outcomes, including longevity. It is also known to be substantially heritable. Here, we used data from three large genetic epidemiology cohort studies (Generation Scotland, n = ∼17,000; UK Biobank, n = ∼115,000; and the Estonian Biobank, n = ∼6,000) to test whether education-linked genetic variants can predict lifespan length. We did so by using cohort members' polygenic profile score for education to predict their parents' longevity. Across the three cohorts, meta-analysis showed that a 1 SD higher polygenic education score was associated with ∼2.7% lower mortality risk for both mothers (total n deaths = 79,702) and ∼2.4% lower risk for fathers (total n deaths = 97,630). On average, the parents of offspring in the upper third of the polygenic score distribution lived 0.55 y longer compared with those of offspring in the lower third. Overall, these results indicate that the genetic contributions to educational attainment are useful in the prediction of human longevity. Marioni RE, Ritchie SJ, Joshi PK, Hagenaars SP, Okbay A, Fischer K, Adams MJ, Hill WD, Davies G, Social Science Genetic Association Consortium, Nagy R, Amador C, Läll K, Metspalu A, Liewald DC, Campbell A, Wilson JF, Hayward C, Esko T, Porteous DJ, Proceedings of the National Academy of Sciences of the United States of America, 2016, vol. 113, no. 47, pp. 13366-13371, 2016 Refereed/Peer-reviewed

Background It has been suggested that greater maternal adiposity during pregnancy affects lifelong risk of offspring fatness via intrauterine mechanisms. Our aim was to use Mendelian randomisation (MR) to investigate the causal effect of intrauterine exposure to greater maternal body mass index (BMI) on offspring BMI and fat mass from childhood to early adulthood. Methods and Findings We used maternal genetic variants as instrumental variables (IVs) to test the causal effect of maternal BMI in pregnancy on offspring fatness (BMI and dual-energy X-ray absorptiometry [DXA] determined fat mass index [FMI]) in a MR approach. This was investigated, with repeat measurements, from ages 7 to 18 in the Avon Longitudinal Study of Parents and Children (ALSPAC; n = 2,521 to 3,720 for different ages). We then sought to replicate findings with results for BMI at age 6 in Generation R (n = 2,337 for replication sample; n = 6,057 for total pooled sample). In confounder-adjusted multivariable regression in ALSPAC, a 1 standard deviation (SD, equivalent of 3.7 kg/m2) increase in maternal BMI was associated with a 0.25 SD (95% CI 0.21–0.29) increase in offspring BMI at age 7, with similar results at later ages and when FMI was used as the outcome. A weighted genetic risk score was generated from 32 genetic variants robustly associated with BMI (minimum F-statistic = 45 in ALSPAC). The MR results using this genetic risk score as an IV in ALSPAC were close to the null at all ages (e.g., 0.04 SD (95% CI -0.21–0.30) at age 7 and 0.03 SD (95% CI -0.26–0.32) at age 18 per SD increase in maternal BMI), which was similar when a 97 variant generic risk score was used in ALSPAC. When findings from age 7 in ALSPAC were meta-analysed with those from age 6 in Generation R, the pooled confounder-adjusted multivariable regression association was 0.22 SD (95% CI 0.19–0.25) per SD increase in maternal BMI and the pooled MR effect (pooling the 97 variant score results from ALSPAC with the 32 variant score results from Generation R) was 0.05 SD (95%CI -0.11–0.21) per SD increase in maternal BMI (p-value for difference between the two results = 0.05). A number of sensitivity analyses exploring violation of the MR results supported our main findings. However, power was limited for some of the sensitivity tests and further studies with relevant data on maternal, offspring, and paternal genotype are required to obtain more precise (and unbiased) causal estimates. Conclusions Our findings provide little evidence to support a strong causal intrauterine effect of incrementally greater maternal BMI resulting in greater offspring adiposity., Using a Mendelian randomization approach, Rebecca Richmond and colleagues find limited evidence for a causal effect of maternal pregnancy adiposity on future offspring adiposity during childhood and adolescence., Author Summary Why Was This Study Done? Being overweight or obese in pregnancy causes babies to be born larger. Whether these babies go into childhood and adolescence more overweight as a result of their mothers being overweight in pregnancy has not been fully established. We wanted to investigate whether genetically elevated body mass index (BMI) of mothers in pregnancy was causally associated with higher levels of fatness in their offspring in childhood and adolescence, over and above the association expected given genetic transmission of BMI-associated variants. What Did the Researchers Do and Find? We used information on 6,057 mother–child pairs from two prospective birth cohort studies, the Avon Longitudinal Study of Parents and Children (ALSPAC) and the Generation R study to assess this. Our findings provide little evidence to support the long-term impact of maternal BMI in pregnancy on the child’s risk of fatness in childhood and adolescence. Rather, most of the association between a mother’s BMI in pregnancy and her child’s fatness is explained by genetic transmission of BMI-associated variants. What Do These Findings Mean? These findings suggest that public health interventions directed at all family members and at different stages of the life course are likely to be important and are potentially more likely to halt the obesity epidemic than a focus on maternal overweight and obesity status in pregnancy. Although we found no large effects of being overweight or obese in pregnancy on offspring’s risk of fatness in later life, further studies with relevant data are required to determine whether there might be smaller effects that our study was unable to detect.

Contains fulltext : 167137.pdf (Publisher’s version ) (Closed access) Educational attainment is strongly influenced by social and other environmental factors, but genetic factors are estimated to account for at least 20% of the variation across individuals. Here we report the results of a genome-wide association study (GWAS) for educational attainment that extends our earlier discovery sample of 101,069 individuals to 293,723 individuals, and a replication study in an independent sample of 111,349 individuals from the UK Biobank. We identify 74 genome-wide significant loci associated with the number of years of schooling completed. Single-nucleotide polymorphisms associated with educational attainment are disproportionately found in genomic regions regulating gene expression in the fetal brain. Candidate genes are preferentially expressed in neural tissue, especially during the prenatal period, and enriched for biological pathways involved in neural development. Our findings demonstrate that, even for a behavioural phenotype that is mostly environmentally determined, a well-powered GWAS identifies replicable associated genetic variants that suggest biologically relevant pathways. Because educational attainment is measured in large numbers of individuals, it will continue to be useful as a proxy phenotype in efforts to characterize the genetic influences of related phenotypes, including cognition and neuropsychiatric diseases.

Craniofacial morphology is highly heritable, but little is known about which genetic variants influence normal facial variation in the general population. We aimed to identify genetic variants associated with normal facial variation in a population-based cohort of 15-year-olds from the Avon Longitudinal Study of Parents and Children. 3D high-resolution images were obtained with two laser scanners, these were merged and aligned, and 22 landmarks were identified and their x, y, and z coordinates used to generate 54 3D distances reflecting facial features. 14 principal components (PCs) were also generated from the landmark locations. We carried out genome-wide association analyses of these distances and PCs in 2,185 adolescents and attempted to replicate any significant associations in a further 1,622 participants. In the discovery analysis no associations were observed with the PCs, but we identified four associations with the distances, and one of these, the association between rs7559271 in PAX3 and the nasion to midendocanthion distance (n-men), was replicated (p = 4 × 10(-7)). In a combined analysis, each G allele of rs7559271 was associated with an increase in n-men distance of 0.39 mm (p = 4 × 10(-16)), explaining 1.3% of the variance. Independent associations were observed in both the z (nasion prominence) and y (nasion height) dimensions (p = 9 × 10(-9) and p = 9 × 10(-10), respectively), suggesting that the locus primarily influences growth in the yz plane. Rare variants in PAX3 are known to cause Waardenburg syndrome, which involves deafness, pigmentary abnormalities, and facial characteristics including a broad nasal bridge. Our findings show that common variants within this gene also influence normal craniofacial development.

This article describes a cohort model of school counselor preparation designed to enhance graduate student commitment to social justice. Foundational principles of group work are used as the vehicle for understanding self in context and for integrating the tenets associated with social justice advocacy. Key components related to program mission, admissions processes, and course sequence are discussed. Recommendations for other counselor education programs are also identified.

This qualitative study explored the experiences of new school counselors in establishing themselves as leaders in their schools. Specifically, it focused on factors this population perceives as promoting or impeding their role as leaders. We interviewed 12 participants in their first through third year as school counselors. Four themes emerged from the data including intrapersonal factors, sociocultural factors, systemic factors, and interactive factors. We discuss implications for counselor educators, district supervisors, and school counselors.

If the full impact of the transformation of the school counseling profession is to be enacted, it is incumbent upon school counselor educators to model the same skills and professional mindset that are expected of practicing school counselors. Specifically, school counselor educators can serve as leaders within their educational communities in order to promote systemic change that will remove barriers to student success. The notion of school counselor educators as educational leaders represents a philosophical and behavioral congruence that churns the professional ecosystem, from the professor to the practitioner to the P-12 student. This article outlines the role that school counselor educators can play in modeling leadership and other essential skills for the profession.

This article describes three creative arts exercises designed to promote belonging, connectedness, and wellness among adolescents with and without disabilities. The scenarios are multifaceted and based on utilization of creative visual and performing arts. Creative outlets may help groups be more effective and meaningful for participants, particularly creative adolescents, adolescents with various learning styles, and those with learning differences.

Recent changes in the field of school counseling have called for professional school counselors to provide evidence of the effect their work has on the academic success of their students. This article presents the findings of a multi faceted action research intervention designed to help students at risk for retention. Findings indicate that students participating in the intervention did improve their grades. Implications for school counselors wanting to lead such programs are discussed.

Aims To estimate associations between smoking initiation, smoking persistence and smoking heaviness and caffeine consumption in two population‐based samples from the Netherlands and the United Kingdom. Design Observational study employing data on self‐reported smoking behaviour and caffeine consumption. Setting Adults from the general population in the Netherlands and the United Kingdom. Participants Participants from the Netherlands Twin Register [NTR: n = 21 939, mean age 40.8, standard deviation (SD) = 16.9, 62.6% female] and the Avon Longitudinal Study of Parents and Children (ALSPAC: n = 9086, mean age 33.2, SD = 4.7, 100% female). Measurements Smoking initiation (ever versus never smoking), smoking persistence (current versus former smoking), smoking heaviness (number of cigarettes smoked) and caffeine consumption in mg per day through coffee, tea, cola and energy drinks. Findings After correction for age, gender (NTR), education and social class (ALSPAC), smoking initiation was associated with consuming on average 52.8 [95% confidence interval (CI) = 45.6–60.0; NTR] and 59.5 (95% CI = 51.8–67.2; ALSPAC) mg more caffeine per day. Smoking persistence was also associated with consuming more caffeine [+57.9 (95% CI = 45.2–70.5) and +83.2 (95% CI = 70.2–96.3) mg, respectively]. Each additional cigarette smoked per day was associated with 3.7 (95% CI = 1.9–5.5; NTR) and 8.4 (95% CI = 6.9–10.0; ALSPAC) mg higher daily caffeine consumption in current smokers. Smoking was associated positively with coffee consumption and less strongly with cola and energy drinks. For tea, associations were positive in ALSPAC and negative in NTR. Conclusions There appears to be a positive association between smoking and caffeine consumption in the Netherlands and the United Kingdom.

A large number of genetic loci are associated with adult body mass index. However, the genetics of childhood body mass index are largely unknown. We performed a meta-analysis of genome-wide association studies of childhood body mass index, using sex- and age-adjusted standard deviation scores. We included 35 668 children from 20 studies in the discovery phase and 11 873 children from 13 studies in the replication phase. In total, 15 loci reached genome-wide significance (P-value < 5 × 10−8) in the joint discovery and replication analysis, of which 12 are previously identified loci in or close to ADCY3, GNPDA2, TMEM18, SEC16B, FAIM2, FTO, TFAP2B, TNNI3K, MC4R, GPR61, LMX1B and OLFM4 associated with adult body mass index or childhood obesity. We identified three novel loci: rs13253111 near ELP3, rs8092503 near RAB27B and rs13387838 near ADAM23. Per additional risk allele, body mass index increased 0.04 Standard Deviation Score (SDS) [Standard Error (SE) 0.007], 0.05 SDS (SE 0.008) and 0.14 SDS (SE 0.025), for rs13253111, rs8092503 and rs13387838, respectively. A genetic risk score combining all 15 SNPs showed that each additional average risk allele was associated with a 0.073 SDS (SE 0.011, P-value = 3.12 × 10−10) increase in childhood body mass index in a population of 1955 children. This risk score explained 2% of the variance in childhood body mass index. This study highlights the shared genetic background between childhood and adult body mass index and adds three novel loci. These loci likely represent age-related differences in strength of the associations with body mass index. Refereed/Peer-reviewed

Purpose Studies in relatives have generally yielded high heritability estimates for refractive error: twins 75–90%, families 15–70%. However, because related individuals often share a common environment, these estimates are inflated (via misallocation of unique/common environment variance). We calculated a lower-bound heritability estimate for refractive error free from such bias. Methods Between the ages 7 and 15 years, participants in the Avon Longitudinal Study of Parents and Children (ALSPAC) underwent non-cycloplegic autorefraction at regular research clinics. At each age, an estimate of the variance in refractive error explained by single nucleotide polymorphism (SNP) genetic variants was calculated using genome-wide complex trait analysis (GCTA) using high-density genome-wide SNP genotype information (minimum N at each age=3,404). Results The variance in refractive error explained by the SNPs (“SNP heritability”) was stable over childhood: Across age 7–15 years, SNP heritability averaged 0.28 (SE=0.08, p

Mendelian randomization (MR), the use of genetic variants as instrumental variables (IVs) to test causal effects, is increasingly used in aetiological epidemiology. Few of the methodological developments in MR have considered the specific situation of using genetic IVs to test the causal effect of exposures in pregnant women on postnatal offspring outcomes. In this paper we describe specific ways in which the IV assumptions might be violated when MR is used to test such intrauterine effects. We highlight the importance of considering the extent to which there is overlap between genetic variants in offspring that influence the offspring outcome of interest overlap with genetic variants used as IVs in their mothers. Where there is such overlap, and particularly if it generates a strong association of maternal genetic IVs with offspring outcome via the offspring genotype, the exclusion restriction assumption of instrumental variable analyses will be violated and the causal effect estimate biased. Simple adjustment for offspring genotype might suffice in some circumstances but might also introduce further bias via the father’s genotype. We recommend a set of analyses that ought to be considered when MR is used to address research questions concerned with intrauterine effects on post-natal offspring outcomes, and provide details of how these can be undertaken and interpreted. These additional analyses include the use of genetic data from offspring and fathers, examining associations using maternal non-transmitted alleles, and using simulated data in sensitivity analyses (for which we provide code). We explore the extent to which new methods that have been developed for exploring violation of the exclusion restriction assumption in the two-sample setting (MR-Egger and median based methods) might be used when exploring intrauterine effects in one-sample MR. We provide a list of recommendations that researchers should use when applying MR to test the effects of intrauterine exposures on postnatal offspring outcomes and use an illustrative example with real data to demonstrate how our recommended analysis steps and approaches can be applied and appropriately interpreted.

While numerous scholars in the fields of counseling and psychology have called for the implementation of social justice counselor education and training, there remains concern that both multiculturalism and social justice are only embraced superficially and may not truly be enacted in counseling and psychology training programs. Often, counseling and psychology education programs include multiculturalism, diversity, and even social justice in their mission statements, but they fail to offer their students the depth and breadth of training experiences required to actually provide such an education. For instance, most programs have one course that addresses multiculturalism, but this concept is only occasionally mentioned in other courses and social justice is rarely discussed at all. This gives the false impression that counseling and psychology education programs are addressing diversity, when in actuality these programs are not preparing students to practice in ways that attend to the unique experiences of the diverse clients they will serve or to address to the complex ways in which social injustice manifests in the lives of clients, particularly those from marginalized social groups. Further, since multiculturalism and social justice have become popularized in the counseling and psychology lexicon, we now see regular attempts within counseling and psychology education programs to actualize these concepts, but in ways that are often superficial and simply reinforce the status quo.

Alcohol problems (AP) contribute substantially to the global disease burden. Twin and family studies suggest that AP are genetically influenced, although few studies have identified variants or genes that are robustly associated with risk. This study identifies genetic and genomic influences on AP during young adulthood, which is often when drinking habits are established.We conducted a genome-wide association study of AP. We further conducted gene-based tests, gene ontology analyses and functional genomic enrichment analyses to assess genomic factors beyond single variants that are relevant to AP.The Avon Longitudinal Study of Parents and Children, a large population-based study of a UK birth cohort.Genetic and phenotypical data were available for 4304 participants.The AP phenotype was a factor score derived from items from the Alcohol Use Disorders Identification Test, symptoms of DSM-IV alcohol dependence, and three additional problem-related items.One variant met genome-wide significance criteria. Four out of 22,880 genes subjected to gene-based analyses survived a stringent significance threshold (q0.05); none of these have been implicated previously in alcohol-related phenotypes. Several biologically plausible gene ontologies were statistically over-represented among implicated single nucleotide polymorphisms (SNPs). SNPs on the Illumina 550 K SNP chip accounted for ~5% of the phenotypical variance in AP.Genetic and genomic factors appear to play a role in alcohol problems in young adults. Genes involved in nervous system-related processes, such as signal transduction and neurogenesis, potentially contribute to liability to alcohol problems, as do genes expressed in non-brain tissues.

Genome-wide association study results have yielded evidence for the association of common genetic variants with crude measures of completed educational attainment in adults. Whilst informative, these results do not inform as to the mechanism of these effects or their presence at earlier ages and where educational performance is more routinely and more precisely assessed. Single nucleotide polymorphisms exhibiting genome-wide significant associations with adult educational attainment were combined to derive an unweighted allele score in 5,979 and 6,145 young participants from the Avon Longitudinal Study of Parents and Children with key stage 3 national curriculum test results (SATS results) available at age 13 to 14 years in English and mathematics respectively. Standardised (z-scored) results for English and mathematics showed an expected relationship with sex, with girls exhibiting an advantage over boys in English (0.433 SD (95%CI 0.395, 0.470), p10(-10)) with more similar results (though in the opposite direction) in mathematics (0.042 SD (95%CI 0.004, 0.080), p = 0.030). Each additional adult educational attainment increasing allele was associated with 0.041 SD (95%CI 0.020, 0.063), p = 1.79×10(-04) and 0.028 SD (95%CI 0.007, 0.050), p = 0.01 increases in standardised SATS score for English and mathematics respectively. Educational attainment is a complex multifactorial behavioural trait which has not had heritable contributions to it fully characterised. We were able to apply the results from a large study of adult educational attainment to a study of child exam performance marking events in the process of learning rather than realised adult end product. Our results support evidence for common, small genetic contributions to educational attainment, but also emphasise the likely lifecourse nature of this genetic effect. Results here also, by an alternative route, suggest that existing methods for child examination are able to recognise early life variation likely to be related to ultimate educational attainment.

Migraine is a debilitating neurological disorder affecting around 1 in 7 people worldwide, but its molecular mechanisms remain poorly understood. Some debate exists over whether migraine is a disease of vascular dysfunction or a result of neuronal dysfunction with secondary vascular changes. Genome-wide association (GWA) studies have thus far identified 13 independent loci associated with migraine. To identify new susceptibility loci, we performed the largest genetic study of migraine to date, comprising 59,674 cases and 316,078 controls from 22 GWA studies. We identified 44 independent single nucleotide polymorphisms (SNPs) significantly associated with migraine risk (P < 5 × 10−8) that map to 38 distinct genomic loci, including 28 loci not previously reported and the first locus identified on chromosome X. In subsequent computational analyses, the identified loci showed enrichment for genes expressed in vascular and smooth muscle tissues, consistent with a predominant theory of migraine that highlights vascular etiologies.

Myopia is the most common human eye disorder and it results from complex genetic and environmental causes. The rapidly increasing prevalence of myopia poses a major public health challenge. Here, the CREAM consortium performs a joint meta-analysis to test single-nucleotide polymorphism (SNP) main effects and SNP × education interaction effects on refractive error in 40,036 adults from 25 studies of European ancestry and 10,315 adults from 9 studies of Asian ancestry. In European ancestry individuals, we identify six novel loci (FAM150B-ACP1, LINC00340, FBN1, DIS3L-MAP2K1, ARID2-SNAT1 and SLC14A2) associated with refractive error. In Asian populations, three genome-wide significant loci AREG, GABRR1 and PDE10A also exhibit strong interactions with education (P, This report by the Consortium for Refractive Error and Myopia uses gene-environment-wide interaction study (GEWIS) to identify genetic loci that affect environmental influence in myopia development, and identifies ethnic specific genetic loci that attribute to eye refractive errors.

Purpose Corneal curvature is a key determinant of the refractive power of the eye. Variants in two genes, FKBP12-rapamycin complex-associated protein 1 (FRAP1) on chromosome 1p36.2 and platelet-derived growth factor receptor alpha (PDGFRA) on chromosome 4q12, have shown genome-wide significant association with normal variation in corneal curvature in a study of subjects of Asian origin. Variants at the PDGFRA locus have also shown genome-wide significant association with corneal astigmatism. Whether these variants influence other ocular parameters such as axial length has yet to be reported. We performed a genome-wide association study for corneal curvature in white European subjects from a population-based birth cohort, with the aim of replicating and extending the above findings. Methods White European children participating in the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort were examined at age about 15.5 years (95% confidence interval=15.45 to 15.48 years). Radius of corneal curvature and axial eye length were measured with an IOLmaster. DNA samples were genotyped with Illumina HumanHap550 arrays and untyped variants imputed using MACH, with CEU individuals from HapMap release 22, Phase II NCBI B36, Single Nucleotide Polymorphism database 126 as the reference panel. Association between corneal curvature and single nucleotide polymorphism (SNP) genotype was tested, genome-wide, using mach2qtl, with sex as a covariate (n=2023; 46.6% male). Results The variant exhibiting the strongest evidence for association with corneal curvature (rs6554163; p=2.8×10−6) was located in the same linkage disequilibrium block as the previously discovered PDGFRA variants. Meta-analysis of the current and prior findings enhanced the evidence for association (rs17084051, p=4.5×10−14). rs6554163 genotype predicted 1.0% of variation in corneal curvature. In addition, these PDGFRA variants were associated with axial eye length, predicting 0.6% of the normal trait variation (p=5.3×10−4). Each copy of the minor allele of variants at the locus also increased the risk of corneal astigmatism in this white European cohort (odds ratio [OR]=1.24, 95% confidence interval=1.07–1.45; p=0.006). Conclusion As in Asians, variants at the PDGFRA locus influence corneal curvature (and corneal astigmatism). However, rather than affecting corneal curvature in isolation, this locus influences the size of the eye while maintaining its scaling.

Birth weight within the normal range is associated with a variety of adult-onset diseases, but the mechanisms behind these associations are poorly understood1. Previous genome-wide association studies of birth weight identified a variant in the ADCY5 gene associated both with birth weight and type 2 diabetes and a second variant, near CCNL1, with no obvious link to adult traits2. In an expanded genome-wide association meta-analysis and follow-up study of birth weight (of up to 69,308 individuals of European descent from 43 studies), we have now extended the number of loci associated at genome-wide significance to 7, accounting for a similar proportion of variance as maternal smoking. Five of the loci are known to be associated with other phenotypes: ADCY5 and CDKAL1 with type 2 diabetes, ADRB1 with adult blood pressure and HMGA2 and LCORL with adult height. Our findings highlight genetic links between fetal growth and postnatal growth and metabolism. Major funding for the research in this paper is provided by the Academy of Finland (project grants 126925, 121584, 124282, 129378 (Salve), 117787 (Gendi), 41071 (Skidi), 209072, 129255, 104781, 120315, 129269, 1114194, 206374, 251360, 139900/24300796, Center of Excellence in Complex Disease Genetics and SALVE) and Biocentrum Helsinki; Arthritis Research UK; the Augustinus Foundation; the Biobanking and Biomolecular Resources Research Infrastructure (BBMRI-NL); the Biomedical Research Council, Singapore (BMRC 06/1/21/19/466); BIF: Boehringer Ingelheim Fonds (travel grant to A.T.); the British Heart Foundation; the C.G. Sundell Foundation; the Canadian Institutes of Health Research (grant MOP-82893); Cancer Research UK; the Chief Scientist Office of the Scottish Government; the Children’s Hospital of Philadelphia (Institute Development Award); Conselleria de Sanitat Generalitat Valenciana; the Copenhagen Graduate School of Health Sciences; the Cotswold Foundation (Research Development Award); the Curtin University and Women and Infants Research Foundation; the Danish Health Insurance Societies (Health Fund); the Danish Medical Research Council; the Danish National Research Foundation; the Danish Pediatric Asthma Centre; the Danish Pharmacists’ Fund; the Danish Strategic Research Council; the Darlington Trust; the Department of Health and Social Services in Northern Ireland; Deutsche Forschungsgemeinschaft (DFG); Diabetes Hilfs- und Forschungsfonds Deutschland (DHFD; travel grant to M. Stumvoll); Diabetes UK (grants RD08/0003704 and RD08/0003692); the Dunhill Medical Trust; the Dutch Asthma Foundation (grants 3.4.01.26, 3.2.06.022, 3.4.09.081 and 3.2.10.085CO); the Dutch Ministry of the Environment (EFRE): Europäische Fonds für Regionale Entwicklung (LIFE Child Obesity); the Egmont Foundation; the Else Kröner-Fresenius Foundation; the Emil Aaltonen Foundation (T.L.); the ENGAGE project and grant agreement HEALTH-F4-2007-201413; the Erasmus Medical Center; Erasmus University, Rotterdam; the European Commission (EURO-BLCS, Beta-JUDO, Framework 5 award QLG1-CT-2000-01643, GABRIEL (Integrated Program LSH-2004-1.2.5-1 contract 018996), framework programme 6 EUROSPAN project (contract LSHG-CT-2006-018947), Sixth Research, Technological Development (RTD) Framework Programme (Contract FOOD-CT-2005-007034) and Seventh Framework Programme (FP7/2007-2013)); the European Research Council (ERC Advanced; 230374); the European Science Foundation (ESF; EU/QLRT-2001-01254); the Exeter NHS Research and Development; Faculty of Biology and Medicine of Lausanne; the Finnish Foundation of Cardiovascular Research; the Finnish Cultural Foundation; the Finnish Innovation Fund Sitra; the Finnish Ministry of Education and Culture; the Finnish Ministry of Social Affairs and Health; the Finnish Social Insurance Institution; the Foundation for Paediatric Research; Fundació La Marató de TV3; Fundación Roger Torné; Generalitat de Catalunya–Interminesterial Council for Research and Technological Innovation (CIRIT; 1999SGR) 00241; the German Diabetes Association (A.T.); the German Bundesministerium fuer Forschung und Technology (grants 01 AK 803 A-H and 01 IG 07015 G); the German Research Foundation for the Clinical Research Group Atherobesity KFO 152 (KO3512/1 to A.K.); GlaxoSmithKline; the Hagedorn Research Institute; Instituto de Salud Carlos III (CB06/02/0041, FIS PI041436, PI081151, PI041705 and PS09/00432 and FIS-FEDER 03/1615, 04/1509, 04/1112, 04/1931, 05/1079, 05/1052, 06/1213, 07/0314 and 09/02647); the Interdisciplinary Centre for Clinical Research at the University of Leipzig (B27 to A.T. and M. Stumvoll); the Integrated Research and Treatment Centre (IFB) Adiposity Diseases; the Jackstädt-Foundation; the Juho Vainio Foundation; the Juvenile Diabetes Research Foundation International (JDRF); Kuopio, Tampere and Turku University Hospital Medical Funds (grant 5031343 to T.A. Lakka and grant 9M048 to T.L.); The Lundbeck Foundation; the Lundbeck Foundation Centre of Applied Medical Genomics for Personalized Disease Prediction, Prevention and Care (LuCAMP); the March of Dimes Birth Defects Foundation (6-FY09-507); the MRC, UK (grants 74882, G0000934, G0601653, G0500539, G0600705, G0601261, G0600331, PrevMetSyn/SALVE PS0476 and MC-A760-5QX00); the Munich Center of Health Sciences (MC Health); the National Health and Medical Research Council of Australia (grants 403981 and 003209); the US National Human Genome Research Institute; the US National Institute of Allergy and Infectious Diseases; the US National Institute of Child Health and Human Development; the US National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); the US National Institutes of Health (grants U01DK062418, U01HG004423, U01HG004446, U01HG004438, R01DK075787, 1R01HD056465-01A, R01D0042157-01A, DK078150, TW05596, HL085144, HD054501, RR20649, ES10126, DK56350 and Biomedical Research Centers funding); the Netherlands Bioinformatics Centre (NBIC) BioAssist (RK/2008.024); a National Heart, Lung, and Blood Institute (NHLBI) grant 5R01HL087679-02 through the STAMPEED program (1RL1MH083268-01); the NIH Genetic Association Information Network (GAIN); the NIH/National Institute of Mental Health (NIMH) (5R01MH63706:02 and MH081802); the Rutgers University Cell and DNA Repository cooperative agreement (NIMH U24 MH068457-06); the Novo Nordisk Foundation Center for Basic Metabolic Research; the Center for Medical Systems Biology (CMSB; NWO Genomics); the Netherlands Organization for Scientific Research (NWO: Social Sciences (MaGW) and the Netherlands Organization for Health Research and Development (ZonMw) (Middelgroot-911-09-032, Spinozapremie 56-464-14192, 904-61-090, 904-61-193, 480-04-004, 400-05-717, Addiction-31160008, 985-10-002, 40-0056-98-9032 and 912-03-031); the Paavo Nurmi Foundation; the Peninsula NIHR Clinical Research Facility; the Pharmacy Foundation of 1991; the PhD School of Molecular Metabolism University of Southern Denmark; the Raine Medical Research Foundation; the Royal Society; the Sigrid Juselius Foundation; South West NHS Research and Development; the Spanish Ministry of Science and Innovation (SAF2008-00357), Turku University Hospital; the Swiss National Science Foundation (33CSCO-122661); the Tampere Tuberculosis Foundation; the Telethon Institute for Child Health Research; the Turku University Foundation; the US Centers for Disease Control and Prevention; University Hospital Oulu, Biocenter, the University of Oulu (75617); the University of Bristol; the University of Potsdam; the University of Southampton; the University of Western Australia (UWA); the VU Institute for Health and Care Research (EMGO+) and the Neuroscience Campus Amsterdam (NCA); the Wellcome Trust (grants GR069224, WT088806, 068545/Z/02, 076467, 085301, 090532, 083270, 083948, 085541/Z/08/Z, WT089549 and WT083431MA); and the Yrjö Jahnsson Foundation.

Purpose Three previous studies have tested for an association between high myopia and polymorphisms in the open angle glaucoma gene, myocilin (MYOC), all in subjects of Chinese ethnicity. In two of the studies, a significant association was found while in the third, there was no association. We sought to investigate the association between high myopia and polymorphisms in MYOC in subjects of European ethnicity. Methods Subjects were recruited from two sites, Cardiff University in the UK and Duke University in the United States. The Cardiff University cohort was comprised of 164 families with high myopia (604 subjects) plus 112 unrelated, highly myopic cases and 114 emmetropic controls. The Duke University cohort was comprised of 87 families with high myopia (362 subjects) plus 59 unrelated, highly myopic cases. Subject DNA was genotyped with a panel of MYOC single nucleotide polymorphisms (SNPs) including those found previously associated with high myopia. The Cardiff cohort was also genotyped for two flanking microsatellite markers analyzed in prior studies. Association between high myopia and MYOC polymorphisms was assessed using the Unphased program. Results Since there was no evidence of heterogeneity in genotype frequencies between families and singleton samples or between cohorts, both subject groups (families and unrelated subjects) from both recruitment sites were analyzed jointly for those SNPs genotyped in common. Two variants showed significant association before correction for multiple testing. These two variants were rs16864720 (p=0.043) and NGA17 (p=0.026). However, there was no significant association after Bonferroni correction. The estimated relative risk (RR) conferred by each of the MYOC variants was low (RR

Purpose: Mandel et al recently reported that season of birth and daylight hours (photoperiod) at birth were associated with moderate and high levels of myopia in Israeli conscripts. We sought to investigate whether these associations were evident in subjects from the United Kingdom (UK). Design: Retrospective cross-sectional study. Participants: The study population comprised 74,459 subjects aged 18 to 100 years attending UK optometry practices for an eye examination. Methods: Data comprising non-cycloplegic spectacle prescription, sex, date of birth, and date of eye examination were collected from UK optometry practices. The average refractive error in fellow eyes was used to classify the degree of myopia in diopters (D) for each subject as follows: absent (??0.75 D), low (?0.75 to ?2.99 D), moderate (?3.00 to ?5.99 D), or high (??6.00 D). The average monthly hours of daylight for London, UK, were classified into 1 of 4 “photoperiod categories,” following Mandel et al. The odds ratio (OR) for each level of severity of myopia was calculated using multivariate logistic regression with age, sex, and either season of birth or photoperiod category as risk factors. Main Outcome Measures: The OR for season of birth and photoperiod category as potential risk factors for myopia. Results: Season of birth was significantly associated with the presence of high myopia: Subjects born in summer or autumn were more likely to be highly myopic compared with those born in winter (summer OR ? 1.17; 95% confidence interval [CI], 1.05–1.30; P ? 0.006; autumn OR ? 1.16; 95% CI, 1.04–1.30; P ? 0.007). However, season of birth was not a significant risk factor for low or moderate myopia. Photoperiod category was weakly associated with low myopia (OR ? 0.94; 95% CI, 0.89–0.99; P ? 0.019), but with a direction of effect opposite to that observed by Mandel et al. Conclusions: As in Israel, a disproportionate number of UK high myopes were born in summer or autumn rather than in winter. However, unlike the situation in Israel, this association does not seem to be related to daylight hours during the postnatal period, implicating alternative physiologic influences that vary with season, such as birth weight.

Stature at a particular age can be considered the cumulative result of growth during a number of preceding growth trajectory periods. We investigated whether height and weight growth trajectories from birth to age 10 years were related to refractive error at ages 11 and 15 years, and eye size at age 15 years.Prospective analysis in a birth cohort.Children participating in the Avon Longitudinal Study of Parents and Children (ALSPAC) U.K. birth cohort (minimum N = 2676).Growth trajectories between birth and 10 years were modeled from a series of height and weight measurements (N = 6815). Refractive error was assessed by noncycloplegic autorefraction at ages 11 and 15 years (minimum N = 4737). Axial length (AXL) and radius of corneal curvature were measured with an IOLMaster (Carl Zeiss Meditec, Welwyn Garden City, U.K.) at age 15 years (minimum N = 2676). Growth trajectories and an allelic score for 180 genetic variants associated with adult height were tested for association with refractive error and eye size.Noncycloplegic autorefraction at ages 11 and 15 years, and AXL and corneal curvature at age 15 years.Height growth trajectory during the linear phase between 2.5 and 10 years was negatively associated with refractive error at 11 and 15 years (P0.001), but explained0.5% of intersubject variation. Height and weight growth trajectories, especially shortly after birth, were positively associated with AXL and corneal curvature (P0.001), predicting 1% to 5% of trait variation. Height growth after 2.5 years was not associated with corneal curvature, whereas the association with AXL continued up to 10 years. The height allelic score was associated with corneal curvature (P = 0.03) but not with refractive error or AXL.Up to the age of 10 years, shared growth mechanisms contribute to scaling of eye and body size but minimally to the development of myopia.The author(s) have no proprietary or commercial interest in any materials discussed in this article.

Leadership is a vital skill called for by the school counseling profession. However, limited research has been done to examine how leadership is characterized by practicing school counselors. The purpose of the exploratory study in this article was to assess leadership practices of school counselors, and to analyze the relationships among demographics, experience, training, work setting, and leadership practices. Results presented are part of a larger study. Findings revealed that age, experience, size of school population, and professional licensure predicted leadership practices of school counselors.

Studies in relatives have generally yielded high heritability estimates for refractive error: twins 75–90%, families 15–70%. However, because related individuals often share a common environment, these estimates are inflated (via misallocation of unique/common environment variance). We calculated a lower-bound heritability estimate for refractive error free from such bias. Between the ages 7 and 15 years, participants in the Avon Longitudinal Study of Parents and Children (ALSPAC) underwent non-cycloplegic autorefraction at regular research clinics. At each age, an estimate of the variance in refractive error explained by single nucleotide polymorphism (SNP) genetic variants was calculated using genome-wide complex trait analysis (GCTA) using high-density genome-wide SNP genotype information (minimum N at each age=3,404). The variance in refractive error explained by the SNPs (“SNP heritability”) was stable over childhood: Across age 7–15 years, SNP heritability averaged 0.28 (SE=0.08, p

Background Thirty-two common variants associated with body mass index (BMI) have been identified in genome-wide association studies, explaining ∼1.45% of BMI variation in general population cohorts. We performed a genome-wide association study in a sample of young adults enriched for extremely overweight individuals. We aimed to identify new loci associated with BMI and to ascertain whether using an extreme sampling design would identify the variants known to be associated with BMI in general populations. Methodology/Principal Findings From two large Danish cohorts we selected all extremely overweight young men and women (n = 2,633), and equal numbers of population-based controls (n = 2,740, drawn randomly from the same populations as the extremes, representing ∼212,000 individuals). We followed up novel (at the time of the study) association signals (p