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• We used data from a clinical sample and two nationally-representative birth cohorts to study how social isolation and loneliness are associated with markers of inflammation at different stages of the lifespan. • Childhood social isolation was longitudinally associated with elevated levels of soluble urokinase plasminogen activator receptor (suPAR), which is thought to be a marker of systemic chronic inflammation. • Social isolation was more consistently associated with suPAR than with C-reactive protein or interleukin-6. • Loneliness in mid-adulthood, but not early adulthood, was also associated with elevated suPAR. Social isolation and loneliness have been associated with poor health and increased risk for mortality, and inflammation might explain this link. We used data from the Danish TRIAGE Study of acutely admitted medical patients (N = 6,144, mean age 60 years), and from two population-representative birth cohorts: the New Zealand Dunedin Longitudinal Study (N = 881, age 45) and the UK Environmental Risk (E-Risk) Longitudinal Twin Study (N = 1448, age 18), to investigate associations of social isolation with three markers of systemic inflammation: C-reactive protein (CRP), interleukin-6 (IL-6), and a newer inflammation marker, soluble urokinase plasminogen activator receptor (suPAR), which is thought to index systemic chronic inflammation. In the TRIAGE Study, socially isolated patients (those living alone) had significantly higher median levels of suPAR (but not CRP or IL-6) compared with patients not living by themselves. Social isolation prospectively measured in childhood was longitudinally associated with higher CRP, IL-6, and suPAR levels in adulthood (at age 45 in the Dunedin Study and age 18 in the E-Risk Study), but only suPAR remained associated after controlling for covariates. Dunedin Study participants who reported loneliness at age 38 or age 45 had elevated suPAR at age 45. In contrast, E-Risk Study participants reporting loneliness at age 18 did not show any elevated markers of inflammation. In conclusion, social isolation was robustly associated with increased inflammation in adulthood, both in medical patients and in the general population. It was associated in particular with systemic chronic inflammation, evident from the consistently stronger associations with suPAR than other inflammation biomarkers. [ABSTRACT FROM AUTHOR]

The present study examined patterns of stability and change in loneliness across adolescence. Data were drawn from the Environmental Risk (E-Risk) Longitudinal Twin Study, a UK population-representative cohort of 2,232 individuals born in 1994 and 1995. Loneliness was assessed when participants were aged 12 and 18. Loneliness showed modest stability across these ages (r =.25). Behavioral genetic modeling indicated that stability in loneliness was explained largely by genetic influences (66%), while change was explained by nonshared environmental effects (58%). Individuals who reported loneliness at both ages were broadly similar to individuals who only reported it at age 18, with both groups at elevated risk of mental health problems, physical health risk behaviors, and education and employment difficulties. Individuals who were lonely only at age 12 generally fared better; however, they were still more likely to finish school with lower qualifications. Positive family influences in childhood predicted reduced risk of loneliness at age 12, while negative peer experiences increased the risk. Together, the findings show that while early adolescent loneliness does not appear to exert a cumulative burden when it persists, it is nonetheless a risk for a range of concomitant impairments, some of which can endure. [ABSTRACT FROM AUTHOR]

Purpose: Social isolation has been shown to have negative effects on mental health outcomes though little is known about trajectories across the life course. We examined the relationship between trajectory groups and selected mental health outcomes in mid-adulthood. Methods: We previously created a typology of social isolation based on onset during the life course and persistence into adulthood, using group-based trajectory analysis of longitudinal data from a New Zealand birth cohort. The typology comprises four groups: 'never-isolated', 'adult-only', 'child-only', and 'persistent (child–adult) isolation'. We undertook logistic regression analyses of three mental health outcomes with trajectory group as the predictor, adjusting for sex and a range of familial and child-behavioural factors. Results: Lifetime suicide attempt, and depression and suicide ideation in mid-adulthood were each associated with adult-only but not child-only social isolation. Depression in mid-adulthood was also associated with persistent child–adult social isolation. Conclusion: Although our findings are associational and not causal, they indicate that interrupting persistent social isolation may help to prevent adult depression whereas halting adult social isolation may ameliorate both depression and suicide outcomes. [ABSTRACT FROM AUTHOR]

Depression is a serious mental health condition and is the leading cause of disability worldwide. Previous research has demonstrated that work stress may contribute to the development of depression through psychophysiological pathways. The present study assessed associations of work stress – in terms of the effort-reward imbalance (ERI) model measuring unrewarding work – with major depressive episode (MDE). Data were from the Mid-life in the United States study, a national, population-based sample of U.S. workers with 9-year follow-up prospective cohort design. The cross-sectional sample at baseline had 2204 workers, and the prospective sample had 1591 workers at follow-up (78.7% follow-up rate). Multivariable Bayesian logistic regression and Poisson regression were applied for examining cross-sectional and prospective associations, respectively. ERI was assessed by a validated 17-item scale at baseline, and MDE in the past 12 months was assessed by the Composite International Diagnostic Interview Short Form at both baseline and follow-up. It was found that ERI at baseline was associated with higher odds of prevalent MDE in the cross-sectional sample (OR = 1.47, HPD interval [1.26–1.69]), and with higher risk of MDE at follow-up in the prospective sample (RR = 1.29, HPD interval [1.01–1.60]). In both cross-sectional and prospective analyses, strongest associations were observed among workers with the highest quartile of ERI, after adjusting for demographic, socioeconomic, lifestyle, and other psychosocial factors. The stable and robust findings strengthen and extend previous findings that unrewarding work is a risk factor of mental health. If confirmed by further evidence, intervention targeting work stress reduction is warranted. • Prior research suggested potential linkage between experiencing unrewarding work and depression. • Effort-reward imbalance at work was associated with depression in a national sample of U.S. workers. • Results were stable and robust both cross-sectionally and prospectively. • Unrewarding work may be a potential target for work stress reduction. [ABSTRACT FROM AUTHOR]

Hypertension is a key driver of cardiovascular diseases. However, how stressors contribute to the development of hypertension remains unclear. The objective of this study was to examine prospective associations of adverse childhood experiences (ACEs) and adulthood psychosocial disadvantages (APDs) with incident hypertension. Data were from the Mid-life in the United States (MIDUS) study, a national, population-based, prospective cohort study. ACEs were examined via retrospective reports, and APDs including work stress and social isolation were assessed using survey measures. Incident hypertension was defined based on self-reported physician diagnosis. Baseline data were collected in 1995, with follow-up in 2004–2006 and 2013–2014. Cox proportional hazards regression was applied to assess prospective associations of ACEs and APDs with incident hypertension in 2568 workers free from hypertension at baseline. After adjustment for covariates, baseline APDs were associated with increased incident hypertension (aHR and 95% CI = 1.48 [1.09, 2.01]) during a 20-year follow-up, whereas ACEs showed null associations. Moreover, a moderating effect by ACEs was observed—the effect of APDs on risk of hypertension was stronger when ACEs were present (aHR and 95% CI = 1.83 [1.17, 2.86]). These findings underscore the importance of psychosocial stressors as nontraditional risk factors of cardiometabolic disorders. [ABSTRACT FROM AUTHOR]

The opioid crisis in the United States (U.S.) is widespread and increasing in severity, and psychosocial exposures have been identified as potential risk factors. We examined associations of employment status with opioid misuse in a large, nationally representative, population-based sample in the U.S. Data were from the 2019 National Survey of Drug Use and Health (NSDUH), an annual cross-sectional survey. The association of employment status with opioid misuse in 40,143 participants was examined by multivariable logistic regression, adjusting for age, sex, race/ethnicity, marital status, household income, educational attainment, medical insurance status, physical health conditions and depression. Analyses were weighted to represent a nationally representative sample of adults in the U.S. In NSDUH 2019, 3.82% of American individuals reported past-year opioid misuse. After taking relevant variables into account, compared to workers who were employed with normal working hours (35–40 h/week), those who were currently unemployed had higher odds of opioid misuse (fully adjusted odds ratio and 95% confidence interval were 1.40 [1.09, 1.79]). Compared to workers employed with normal working hours, those who were in school/training or retired had lower odds of opioid misuse. Short or long working hours were not associated with opioid misuse. Government and employer policy interventions may benefit from emphasizing stable employment as a major social determinant of health in the context of the opioid crisis. • The opioid crisis in the U.S. is widespread and increasing in severity. • Unemployment was significantly associated with opioid misuse. • Short or long working hours were not associated with opioid misuse. • Stable employment may be a major social determinant against opioid crisis. [ABSTRACT FROM AUTHOR]

The present study used a longitudinal and discordant twin design to explore in depth the developmental associations between victimization and loneliness from mid-childhood to young adulthood. The data were drawn from the Environmental Risk (E-Risk) Longitudinal Twin Study, a birth cohort of 2,232 individuals born in England and Wales during 1994–1995. Diverse forms of victimization were considered, differing across context, perpetrator, and timing of exposure. The results indicated that exposure to different forms of victimization was associated with loneliness in a dose–response manner. In childhood, bullying victimization was uniquely associated with loneliness, over and above concurrent psychopathology, social isolation, and genetic risk. Moreover, childhood bullying victimization continued to predict loneliness in young adulthood, even in the absence of ongoing victimization. Within-twin pair analyses further indicated that this longitudinal association was explained by genetic confounds. In adolescence, varied forms of victimization were correlated with young adult loneliness, with maltreatment, neglect, and cybervictimization remaining robust to controls for genetic confounds. These findings indicate that vulnerability to loneliness in victimized young people varies according to the specific form of victimization in question, and also to the developmental period in which it was experienced. [ABSTRACT FROM AUTHOR]

OBJECTIVES: Job strain is positively associated with incident hypertension, while increasing leisure-time physical activity (LTPA) can reduce incident hypertension. However, the joint associations of job strain and LTPA with incident hypertension among United States workers have yet to be investigated. This study examined the independent and joint associations of job strain and LTPA with incident hypertension. METHODS: This prospective cohort study (n=1,160) utilized data from the population-based Midlife in the United States study. The associations of job strain and LTPA at baseline with incident hypertension during follow-up were examined using Cox proportional hazards models. High job strain was derived from a combination of high job demands and low job control, and high LTPA was defined as engagement in moderate or vigorous LTPA at least once per week. RESULTS: During 9,218 person-years of follow-up, the hypertension incidence rate was 30.6 (95% confidence interval [CI], 27.3 to 34.3) per 1,000 person-years. High job strain was associated with a higher risk for hypertension than low job strain (adjusted hazard ratio [aHR], 1.29; 95% CI, 1.00 to 1.67). High LTPA was associated with lower hypertension risk than low LTPA (aHR, 0.77; 95% CI, 0.60 to 0.98). Hypertension risk was higher among workers with high job strain and low LTPA than among those with low job strain and high LTPA (aHR, 1.70; 95% CI, 1.18 to 2.43). CONCLUSIONS: Job strain and LTPA showed positive and inverse associations, respectively, with incident hypertension. The combination of high job strain and low LTPA was associated with the highest risk for hypertension. [ABSTRACT FROM AUTHOR]

The present study used quantitative and qualitative methods to explore how lonely young people are seen from others' perspectives, in terms of their personality, behavior, and life circumstances. Data were drawn from the Environmental Risk Longitudinal Twin Study, a cohort of 2,232 individuals born in the U.K. in the mid-1990s. When participants were aged 18, they provided self-reports of loneliness, and informant ratings of loneliness were provided by interviewers, as well as participants' parents and siblings. Interviewers further provided Big Five personality ratings and detailed written notes in which they documented their perceptions of the participants and their reflections on the content of the interview. In the quantitative section of the article, regression analyses were used to examine the perceptibility of loneliness and how participants' loneliness related to their perceived personality traits. The informant ratings of participants' loneliness showed good agreement with self-reports. Furthermore, loneliness was associated with lower perceived conscientiousness, agreeableness, and extroversion and higher perceived neuroticism. Within-twin pair analyses indicated that these associations were partly explained by common underlying genetic influences. In the qualitative section of the study, the loneliest 5% of study participants (N = 108) were selected, and thematic analysis was applied to the study interviewers' notes about those participants. Three themes were identified and named: "uncomfortable in own skin," "clustering of risk," and "difficulties accessing social resources." These results add depth to the current conceptualization of loneliness and emphasize the complexity and intersectional nature of the circumstances severely lonely young adults live in. [ABSTRACT FROM AUTHOR]

Supplemental Digital Content is available in the text Objective: We examined associations of negative employment changes during the COVID-19 pandemic with mental health in a national sample of U.S. workers, and whether the associations differed by race. Methods: Data were from the Health, Ethnicity, and Pandemic Study, a cross-sectional survey. The effects of negative employment changes on psychological distress in 1510 workers were examined via linear regression, and stratified analyses were conducted across racial subgroups. Results: After adjustment for covariates, compared to workers with no change in employment, those who experienced permanent job loss had the highest psychological distress (β and 95% CI = 3.27 [1.89, 4.65]). Permanent job loss had the greatest effect on psychological distress in Blacks and Asians. Conclusion: Negative employment changes related to the pandemic may have deleterious impacts on workers' mental health, with disproportionate effects on racial minorities. [ABSTRACT FROM AUTHOR]

In this study, we investigated associations between the characteristics of the neighborhoods in which young adults live and their feelings of loneliness, using data from different sources. Participants were drawn from the Environmental Risk Longitudinal Twin Study. Loneliness was measured via self-reports at ages 12 and 18 years and also by interviewer ratings at age 18. Neighborhood characteristics were assessed between the ages of 12 and 18 via government data, systematic social observations, a resident survey, and participants' self-reports. Greater loneliness was associated with perceptions of lower collective efficacy and greater neighborhood disorder but not with more objective measures of neighborhood characteristics. Lonelier individuals perceived the collective efficacy of their neighborhoods to be lower than did their less lonely siblings who lived at the same address. These findings suggest that feelings of loneliness are associated with negatively biased perceptions of neighborhood characteristics, which may have implications for lonely individuals' likelihood of escaping loneliness. [ABSTRACT FROM AUTHOR]

Background: The aim of this study was to build a detailed, integrative profile of the correlates of young adults' feelings of loneliness, in terms of their current health and functioning and their childhood experiences and circumstances. Methods: Data were drawn from the Environmental Risk Longitudinal Twin Study, a birth cohort of 2232 individuals born in England and Wales in 1994 and 1995. Loneliness was measured when participants were aged 18. Regression analyses were used to test concurrent associations between loneliness and health and functioning in young adulthood. Longitudinal analyses were conducted to examine childhood factors associated with young adult loneliness. Results: Lonelier young adults were more likely to experience mental health problems, to engage in physical health risk behaviours, and to use more negative strategies to cope with stress. They were less confident in their employment prospects and were more likely to be out of work. Lonelier young adults were, as children, more likely to have had mental health difficulties and to have experienced bullying and social isolation. Loneliness was evenly distributed across genders and socioeconomic backgrounds. Conclusions: Young adults' experience of loneliness co-occurs with a diverse range of problems, with potential implications for health in later life. The findings underscore the importance of early intervention to prevent lonely young adults from being trapped in loneliness as they age. [ABSTRACT FROM AUTHOR]

How does literacy develop in children's early years, and what programs or practices promote adequate literacy for all children? These are the questions Catherine Snow and Timothy Matthews tackle in this article. Fundamental literacy skills can be grouped into two categories, Snow and Matthews write. The first category is constrained skills, which are readily teachable because they're finite: for example, the 26 letters of the alphabet, or a set of 20 to 30 common spelling rules. These skills have a ceiling; young children can and do achieve perfect performance. As they grow older, though, children need to understand words rarely encountered in spoken language and to integrate new information they encounter with relevant background information. Vocabulary and background knowledge are examples of unconstrained skills-- large domains of knowledge acquired gradually through experience. Unconstrained skills are particularly important for children's long-term literacy success (that is, success in outcomes measured after third grade). Compared to constrained skills, they're also more strongly predicted by children's social class or their parents' education, and more difficult to teach in the classroom. And because of their open-ended nature, unconstrained skills are also much harder to test for. Snow and Matthews write that a drop in literacy scores we see as US children move from elementary to middle school suggests that our schools may be focusing too much on constrained skills--and too little on unconstrained ones--in the early grades. The authors review promising programs and practices for enhancing both constrained and unconstrained skills, ranging from comprehensive school-improvement programs to efforts to improve curricula and teachers' professional development--although they note that vast differences in programs' scope, cost, targets, and theories of change make comparing them difficult. Another challenge is that it's hard to maintain quality and consistency when implementing complex programs over time. Snow and Matthews suggest that to improve young children's success with literacy, it might be better to introduce and evaluate promising practices that can be mixed and matched, rather than complex programs that are implemented as a package. [ABSTRACT FROM AUTHOR]

Purpose: To investigate the association between social isolation and loneliness, how they relate to depression, and whether these associations are explained by genetic influences.Methods: We used data from the age-18 wave of the Environmental Risk Longitudinal Twin Study, a birth cohort of 1116 same-sex twin pairs born in England and Wales in 1994 and 1995. Participants reported on their levels of social isolation, loneliness and depressive symptoms. We conducted regression analyses to test the differential associations of isolation and loneliness with depression. Using the twin study design, we estimated the proportion of variance in each construct and their covariance that was accounted for by genetic and environmental factors.Results: Social isolation and loneliness were moderately correlated (r = 0.39), reflecting the separateness of these constructs, and both were associated with depression. When entered simultaneously in a regression analysis, loneliness was more robustly associated with depression. We observed similar degrees of genetic influence on social isolation (40 %) and loneliness (38 %), and a smaller genetic influence on depressive symptoms (29 %), with the remaining variance accounted for by the non-shared environment. Genetic correlations of 0.65 between isolation and loneliness and 0.63 between loneliness and depression indicated a strong role of genetic influences in the co-occurrence of these phenotypes.Conclusions: Socially isolated young adults do not necessarily experience loneliness. However, those who are lonely are often depressed, partly because the same genes influence loneliness and depression. Interventions should not only aim at increasing social connections but also focus on subjective feelings of loneliness. [ABSTRACT FROM AUTHOR]

R2781 --> 761.15 --> Hypobaric hypoxia (HH) experienced at high altitude initiates a series of physiological adaptations to maintain homeostasis. One such adaptation is the activation of the Epo gene which encodes the glycoprotein hormone erythropoietin (EPO). Increased circulating EPO levels defend against HH by facilitating blood O2 transport through increasing red blood cell production. HH also increases blood pressure (BP) through activation of the sympathetic nervous system and the ensuing elevation of circulating catecholamine levels. The present study examined the role of sympathetic nerve activation in HH‐evoked Epo gene activation and elevated circulating levels of EPO. Studies were performed on adult, male wild‐type (WT) mice treated with 18 hours of HH (0.4 atmospheres), simulating low O2 condition experienced at high altitude. Our results showed increased renal Epo gene abundance and elevated plasma EPO levels. Remarkably, these responses were either markedly attenuated or absent in mice with selective ablation of adrenal medulla as well as after treatment with propranolol, a non‐selective beta‐adrenergic receptor blocker. Moreover, infusion of epinephrine alone activated renal Epo gene and elevated plasma EPO levels. These results suggest that sympathetic nerve activation and the ensuing increase in plasma epinephrine contribute to Epo gene activation by HH. [ABSTRACT FROM AUTHOR]

Objective We tested whether children who are socially isolated early in their schooling develop mental health problems in early adolescence, taking into account their mental health and family risk at school entry. Method We used data from the Environmental Risk (E-Risk) Longitudinal Twin Study, a birth cohort of 2,232 children born in England and Wales in 1994 and 1995. We measured social isolation using mothers' and teachers' reports at ages 5 and 12 years. We assessed mental health symptoms via mothers' and teachers' ratings at age 5 and self-report measures at age 12. We collected mother-reported information about the family environment when children were 5 years old. We conducted regression analyses to test concurrent and longitudinal associations between early family factors, social isolation, and mental health difficulties. Results At both primary and secondary school, children who were socially isolated experienced greater mental health difficulties. Children with behavioral problems or attention-deficit/hyperactivity disorder (ADHD) symptoms at age 5 years had an elevated risk of becoming more socially isolated at age 12. However, children who were isolated at age 5 did not have greater mental health symptoms at age 12, over and above pre-existing difficulties. Conclusion Although social isolation and mental health problems co-occur in childhood, early isolation does not predict worse mental health problems later on. However, children who exhibit problematic behaviors may struggle to cope with the social challenges that accompany their progression through the early school years. [ABSTRACT FROM AUTHOR]

Background: Studies assessing sex differences in the associations of psychosocial strain with depression have shown mixed and inconsistent results. Our objective was to examine prospective associations of job strain and family strain with risk of major depressive episode (MDE) among United States workers, as well as assess potential effect modification by sex.Methods: Using data from the nationally representative and population-based Mid-life in the United States (MIDUS) study with a prospective cohort design and a 9-year follow-up period, the effects of job strain and family strain at baseline on risk of MDE within the 12 months prior to the follow-up assessment were examined in 1581 workers (805 men, 776 women) who were free from MDE within the 12 months prior to the baseline survey, by multivariate Poisson regression analysis.Results: After adjustment for relevant covariates, there was evidence for effect modification by sex for the association between job strain and MDE but not for the association between family strain and MDE. Indeed, high job strain was prospectively associated with the risk of MDE (RR and 95% CI = 2.14 [1.14, 4.03]) in men but not in women. Moreover, high family strain was prospectively associated with a higher risk of MDE (RR and 95% CI = 1.57 [1.05, 2.37]) in the whole sample.Conclusion: Family strain was associated with risk of MDE regardless of the sex of a person. In contrast, high job strain may involve an increased risk of developing MDE only in men but not in women. [ABSTRACT FROM AUTHOR]

Background: Older brain age – as estimated from structural MRI data – is known to be associated with detrimental mental and physical health outcomes in older adults. Social isolation, which has similar detrimental effects on health, may be associated with accelerated brain aging though little is known about how different trajectories of social isolation across the life course moderate this association. We examined the associations between social isolation trajectories from age 5 to age 38 and brain age assessed at age 45. Methods: We previously created a typology of social isolation based on onset during the life course and persistence into adulthood, using group-based trajectory analysis of longitudinal data from a New Zealand birth cohort. The typology comprises four groups: 'never-isolated', 'adult-only', 'child-only', and persistent 'child-adult' isolation. A brain age gap estimate (brainAGE) – the difference between predicted age from structural MRI date and chronological age – was derived at age 45. We undertook analyses of brainAGE with trajectory group as the predictor, adjusting for sex, family socio-economic status, and a range of familial and child-behavioral factors. Results: Older brain age in mid-adulthood was associated with trajectories of social isolation after adjustment for family and child confounders, particularly for the 'adult-only' group compared to the 'never-isolated' group. Conclusions: Although our findings are associational, they indicate that preventing social isolation, particularly in mid-adulthood, may help to avert accelerated brain aging associated with negative health outcomes later in life. [ABSTRACT FROM AUTHOR]

Background To determine the short-term effects following corticosteroid injection into the shoulder. Methods Type-specific shoulder injection was administered, followed by physiotherapy 7 days to 10 days later. One hundred and sixteen adult patients were prospectively followed-up. The primary outcome was a visual analogue score (VAS) for pain. Scores were recorded immediately before injection, 30 minutes after, daily until day 7 and then at 6 weeks. Post injection pain was defined as an increase of 2 or more points in the VAS score after the injection. The secondary outcome was determined at 6 months as successful discharge or progression onto surgery. Results The VAS showed a significant reduction from the pre-injection score for all patients at day 1 and was maintained until week 6. Forty-one (35.3%) patients experienced post-injection pain. The mean duration of symptoms was 3.9 days. At 6 months, 81 (69.8%) patients were discharged successfully and, at a mean of 23.2 months, did not require re-referral; 29 (25%) had surgery; and six (5.2%) were referred for a spinal opinion. Conclusions One in three patients developed delayed post-injection pain. Flare phenomenon had no determinate effect on outcome. Patients’ pain response by 6 weeks is predictive of final outcome at 6 months and may help clinicians plan further treatment without delay. [ABSTRACT FROM AUTHOR]

Attention-deficit/hyperactivity disorder (ADHD) is associated with poor sleep quality, but there is more to learn about the longitudinal association and aetiology of this association. We investigated the following: (a) Is there an association between childhood ADHD and poor sleep quality in young adulthood? (b) Is this driven by the long-term effects of childhood ADHD or concurrent associations with ADHD in young adulthood? (c) To what extent do genetic and environmental influences explain the overlap between symptoms of ADHD and poor sleep quality? Participants were from the Environmental Risk Longitudinal Twin Study of 2,232 twin children born in the United Kingdom in 1994–1995. We ascertained ADHD diagnoses at ages 5, 7, 10, 12, and 18. We assessed sleep quality using the Pittsburgh Sleep Quality Index at age 18. We used regression models to examine longitudinal associations and bivariate twin modelling to test genetic and environmental influences. Children with ADHD had poorer sleep quality in young adulthood, but only if their ADHD persisted. Adults with ADHD had more sleep problems than those without ADHD, over and above psychiatric comorbidity and maternal insomnia. ADHD and sleep problems in young adulthood were associated because of genetic (55%) and nonshared environmental influences (45%). Should ADHD remit, children with ADHD do not appear to have an increased risk of later sleep problems. Good quality sleep is important for multiple areas of functioning, and a better understanding of why adults with ADHD have poorer sleep quality will further the goal of improving treatments. [ABSTRACT FROM AUTHOR]

The aim of this study was to disentangle pervasive from situational antisocial behaviors using multiple informants, and to investigate their genetic and environmental etiologies in preadolescence and across time. Antisocial behaviors were assessed in 2,232 twins from the Environmental Risk (E-Risk) Longitudinal Twin Study at ages 5 and 12. Pervasive antisocial behaviors were defined as behaviors that mothers, teachers, interviewers, and twins themselves agreed on. Results from a psychometric model indicated that the variation in children's pervasive antisocial behaviors was mostly accounted for by familial influences that originated in childhood, whereas situational behaviors were explained by newly emerging nonshared environmental and genetic influences. This study shows that children's pervasive and situational antisocial behaviors have distinct etiologies that could guide research and treatment. [ABSTRACT FROM AUTHOR]

Background Children with externalising problems are at risk of developing internalising problems as they grow older. The pathways underlying this developmental association remain to be elucidated. We tested two processes that could explain why some children with externalising problems develop internalising symptoms in preadolescence: a mediation model whereby the association between early externalising and later new internalising symptoms is explained by negative experiences; and a genetic model, whereby genes influence both problems. Methods We used data from the Environmental Risk (E-Risk) Study, a 1994-1995 birth cohort of 2,232 twins born in England and Wales. We assessed externalising and internalising problems using combined mothers' and teachers' ratings at age 5 and 12. We measured bullying victimisation, maternal dissatisfaction and academic difficulties between age 7 and 10 and used linear regression analyses to test the effects of these negative experiences on the association between early externalising and later internalising problems. We employed a Cholesky decomposition to examine the genetic influences on the association. Results Children with externalising problems at age 5 showed increased rates of new internalising problems at age 12 ( r = .24, p < .001). Negative experiences accounted for some of the association between early externalising and later internalising problems. Behavioural-genetic analyses indicated that genes influencing early externalising problems also affected later internalising problems. Conclusions Our findings highlight the role of genetic influences in explaining why some children with externalising problems develop internalising symptoms in preadolescence. Negative experiences also contribute to the association, possibly through gene-environment interplay. Mental health professionals should monitor the development of internalising symptoms in young children with externalising problems. [ABSTRACT FROM AUTHOR]

Purpose: Bullying behaviours and other conduct problems often co-occur. However, we do not yet know whether bullying behaviours are associated with early factors and later poor outcomes independently of conduct problems. While there are differing, specific interventions for bullying behaviours and for conduct problems, it is unclear if such specificity is justified given parallels between both behaviours. Methods: We used prospective data from the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally representative sample of 2232 children. Mothers and teachers reported on children's bullying behaviours and conduct problems at ages 7 and 10. We collected measures of risk factors, including temperament and family factors, when children were age 5. We assessed behavioural, emotional, educational and social problems when participants reached the ages of 12 and 18. Results: Bullying behaviours and conduct problems co-occurred in childhood. Our findings indicated that bullying behaviours and other conduct problems were independently associated with the same risk factors. Furthermore, they were associated with the same poor outcomes at both ages 12 and 18. Despite this, bullying behaviours were uniquely associated with behavioural, emotional, educational and social problems at age 18. Conclusions: Our findings suggest that anti-bullying programmes and interventions aimed at reducing conduct problems could benefit from greater integration. Furthermore, our study highlights the mental health problems children who bully may face in later years and the need to consider those in intervention plans. [ABSTRACT FROM AUTHOR]

The methionine-to-valine mutation in codon 184 (M184V) in reverse transcriptase (RT) of human immunodeficiency virus type 1 (HIV-1) or simian immunodeficiency virus (SIV) confers resistance to (-)-2'-deoxy3'-thiacytidine (3TC; lamivudine) and increased sensitivity to 9-[2-(phosphonomethoxy)propyl]adenine (PMPA; tenofovir). We have used the SIV model to evaluate the effect of the M184V mutation on the emergence of resistance to the combination of 3TC plus PMPA. A site-directed mutant of SIVmac239 containing M184V (SIVmac239-184V) was used to select for resistance to both 3TC and PMPA by serial passage in the presence of increasing concentrations of both drugs. Under these selection conditions, the M184V mutation reverted in the majority of the selections. Variants resistant to both drugs were found to have the lysine-to-arginine mutation at codon 65 (K65R), which has previously been associated with resistance to PMPA in both SIV and HIV. Similarly, in rhesus macaques infected with SIVmac239-184V for 46 weeks and treated daily with (-)-2'-deoxy-5-fluoro-3'-thiacytidine [(-)-FTC], there was no reversion of M184V, but this mutation reverted to 184 M in all three animals within 24 weeks of treatment with (-)-FTC and PMPA. Although the addition of PMPA to the (-)-FTC therapy induced a decrease in virus loads in plasma, these loads eventually returned to pre-PMPA levels in each case. All animals receiving this combination developed the K65R mutation. These results demonstrate that the combination of PMPA with 3TC or (-)-FTC selects for the K65R mutation and against the M184V mutation in SIV RT. [ABSTRACT FROM AUTHOR]

Chronic intermittent hypoxia (CIH) is a hallmark manifestation of obstructive sleep apnea (OSA), a widespread breathing disorder. CIH-treated rodents exhibit activation of the sympathetic nervous system and hypertension. Heightened carotid body (CB) activity has been implicated in CIH-induced hypertension. CB expresses high abundance of olfactory receptor (Olfr) 78, a G-protein coupled receptor. Olfr 78 null mice exhibit impaired CB sensory nerve response to acute hypoxia. Present study examined whether Olfr78 participates in CB-dependent activation of the sympathetic nervous system and hypertension in CIH-treated mice and in hemeoxygenase (HO)-2 null mice experiencing CIH as a consequence of naturally occurring OSA. CIH-treated wild-type (WT) mice showed hypertension, biomarkers of sympathetic nerve activation, and enhanced CB sensory nerve response to hypoxia and sensory long-term facilitation (sLTF), and these responses were absent in CIH-treated Olfr78 null mice. HO-2 null mice showed higher apnea index (AI) (58 ± 1.2 apneas/h) than WT mice (AI = 8 ± 0.8 apneas/h) and exhibited elevated blood pressure (BP), elevated plasma norepinephrine (NE) levels, and heightened CB sensory nerve response to hypoxia and sLTF. The magnitude of hypertension correlated with AI in HO-2 null mice. In contrast, HO-2/Olfr78 double null mice showed absence of elevated BP and plasma NE levels and augmented CB response to hypoxia and sLTF. These results demonstrate that Olfr78 participates in sympathetic nerve activation and hypertension and heightened CB activity in two murine models of CIH. [ABSTRACT FROM AUTHOR]

Background: Attention deficit/hyperactivity disorder (ADHD) is associated with emotional problems, and their co‐occurrence often leads to worse outcomes. We investigated the developmental associations between ADHD and emotional problems from childhood to early adolescence and examined the genetic and environmental contributions to their developmental link. We further tested whether this developmental association remained across the transition to young adulthood. Methods: We used data from the Environmental Risk (E‐Risk) Longitudinal Twin Study, a cohort of 2,232 British twins. In childhood, ADHD and emotional problems were assessed at ages 5, 7, 10 and 12 with mothers' and teachers' reports. At age 18, we used self‐reported symptoms according to DSM‐5 criteria for ADHD, and DSM‐IV for anxiety and depression. Results: Longitudinal analyses showed that earlier ADHD was associated with later emotional problems consistently across childhood. However, earlier emotional problems were not associated with later ADHD symptoms. The developmental association between ADHD and later emotional problems in childhood was entirely explained by common genetic factors. Consistent with results in childhood, earlier symptoms of ADHD were associated with later emotional problems during the transition to young adulthood. Conclusions: Our findings demonstrate that ADHD symptoms are predictors of the development of emotional problems, from childhood up to young adulthood, through shared genetic influences. Interventions targeting ADHD symptoms might prevent the development of emotional problems. Clinicians treating youth with ADHD must be aware of their risk for developing emotional problems and ought to assess, monitor and treat emotional problems alongside ADHD symptoms from childhood to adulthood. [ABSTRACT FROM AUTHOR]

This study tested implications of new genetic discoveries for understanding the association between parental investment and children's educational attainment. A novel design matched genetic data from 860 British mothers and their children with home-visit measures of parenting: the E-Risk Study. Three findings emerged. First, both mothers' and children's education-associated genetics, summarized in a genome-wide polygenic score, were associated with parenting-a gene-environment correlation. Second, accounting for genetic influences slightly reduced associations between parenting and children's attainment-indicating some genetic confounding. Third, mothers' genetics were associated with children's attainment over and above children's own genetics, via cognitively stimulating parenting-an environmentally mediated effect. Findings imply that, when interpreting parents' effects on children, environmentalists must consider genetic transmission, but geneticists must also consider environmental transmission. [ABSTRACT FROM AUTHOR]

Objective: Victimized adolescents have an increased risk of self-injurious thoughts and behaviors. However, poor understanding of causal and non-causal mechanisms underlying this observed risk limits the development of interventions to prevent premature death in adolescents. This study tested whether pre-existing family-wide and individual vulnerabilities account for victimized adolescents' increased risk of self-injurious thoughts and behaviors.Method: Participants were 2,232 British children followed from birth to 18 years of age as part of the Environmental Risk Longitudinal Twin Study. Adolescent victimization (maltreatment, neglect, sexual victimization, family violence, peer/sibling victimization, cyber victimization, and crime victimization) was assessed through interviews with participants and co-informant questionnaires at the 18-year assessment. Suicidal ideation, self-harm, and suicide attempt in adolescence were assessed through interviews with participants at 18 years.Results: Victimized adolescents had an increased risk of suicidal ideation (odds ratio [OR] 2.40, 95% CI 2.11-2.74), self-harm (OR 2.38, 95% CI 2.10-2.69), and suicide attempt (OR 3.14, 95% CI 2.54-3.88). Co-twin control and propensity score matching analyses showed that these associations were largely accounted for by pre-existing familial and individual vulnerabilities, respectively. Over and above their prior vulnerabilities, victimized adolescents still showed a modest increase in risk for suicidal ideation (OR 1.45, 95%CI 1.10-1.91) and self-harm (OR 1.50, 95% CI 1.18-1.91) but not for suicide attempt (OR 1.28, 95% CI 0.83-1.98).Conclusion: Risk for self-injurious thoughts and behaviors in victimized adolescents is explained only in part by the experience of victimization. Pre-existing vulnerabilities account for a large proportion of the risk. Therefore, effective interventions to prevent premature death in victimized adolescents should not only target the experience of victimization but also address pre-existing vulnerabilities. [ABSTRACT FROM AUTHOR]

Objective: Self-harm is associated with violent offending. However, little is known about young people who engage in "dual-harm" behavior. The authors investigated antecedents, clinical features, and life characteristics distinguishing dual-harming adolescents from those who self-harm only.Methods: Participants were from the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally representative U.K. cohort of 2,232 twins born in 1994 and 1995. Self-harm in adolescence was assessed through interviews at age 18. Violent offending was assessed using a computer questionnaire at age 18 and police records through age 22. Risk factors were assessed between ages 5 and 12. Adolescent mental health, victimization, personality functioning, and use of support services were measured at age 18.Results: Self-harm was associated with violent crime (odds ratio=3.50, 95% CI=2.61-4.70), even after accounting for familial risk factors. Dual harmers had been victims of violence from childhood and exhibited lower childhood self-control and lower childhood IQ than self-only harmers. Dual harmers experienced higher rates of concurrent psychotic symptoms and substance dependence. They also exhibited distinct personality styles characterized by resistance to change and by emotional and interpersonal lability. However, dual harmers were not more likely than self-only harmers to have contact with mental health services.Conclusions: Dual harmers have self-control difficulties and are immersed in violence from a young age. A treatment- rather than punishment-oriented approach is indicated to meet these individuals' needs. Connecting self-harming adolescents with delinquency-reduction programs and transdiagnostic approaches that target self-regulation may reduce harmful behaviors. Preventing childhood maltreatment and implementing strategies to reduce victimization exposure could mitigate risk for both internalized and externalized violence. [ABSTRACT FROM AUTHOR]

Experiencing multiple types of victimization (poly-victimization) during adolescence is associated with the onset of psychotic experiences (such as hearing voices, having visions, or being extremely paranoid). However, many poly-victimized adolescents will not develop such subclinical phenomena and the factors that protect them are unknown. This study investigated whether individual, family, or community-level characteristics were associated with an absence of psychotic experiences amongst poly-victimized adolescents. Participants were from the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally-representative cohort of 2232 UK-born twins. Exposure to seven different types of victimization between ages 12–18 was ascertained using a modified version of the Juvenile Victimization Questionnaire at age 18. Adolescents were also interviewed about psychotic experiences at age 18. Protective factors were measured at ages 12 and 18. We found that exposure to poly-victimization during adolescence was associated with age-18 psychotic experiences (OR = 4.62, 95% CI 3.59–5.94, P < 0.001), but more than a third of the poly-victimized adolescents reported having no psychotic experiences (40.1%). Greater social support was found to be protective against adolescent psychotic experiences even amongst those exposed to poly-victimization. Engaging in physical activity and greater neighborhood social cohesion were also associated with a reduced likelihood of age-18 psychotic experiences in the whole sample, with non-significant trends in the poly-victimized group. Increasing social support and promoting physical activity appear to be important areas for future research into the development of preventive interventions targeting adolescent psychotic experiences. This adds further weight to calls to increase the promotion of these factors on a public health scale. [ABSTRACT FROM AUTHOR]

Child maltreatment has consistently been found to be associated with attention deficit/hyperactivity disorder (ADHD). However, the robustness of this association and the direction of the link between maltreatment and ADHD remain unclear. We used data from the Environmental Risk (E-Risk) Longitudinal Twin Study, a cohort of 2232 British twins, to investigate the associations between exposure to abuse/neglect and ADHD in childhood and in young adulthood, and to test their robustness and specificity. We also aimed to test longitudinal associations between abuse/neglect and ADHD from childhood to young adulthood, controlling for confounders. Results indicated strong associations between abuse/neglect and ADHD in childhood and also in young adulthood. In childhood, the association was concentrated among children with comorbid conduct disorder. Longitudinal analyses showed that childhood ADHD predicted abuse/neglect in later years. This association was again concentrated among individuals with comorbid conduct disorder. Abuse/neglect in childhood was not associated with later ADHD in young adulthood after adjusting for childhood ADHD. Our study does not provide support of a causal link between child abuse/neglect and adult ADHD but highlights the possibility of a long-term effect of disruptive behaviors on the risk for experiencing abuse/neglect. These findings emphasize the need for clinicians treating people with ADHD, especially those with comorbid conduct disorder, to be aware of their increased risk for experiencing abuse/neglect. Interventions aimed at reducing risks of abuse/neglect should also focus on the environment of individuals with disruptive behaviors. [ABSTRACT FROM AUTHOR]

Objective Childhood victimization is an important risk factor for later immune-related disorders. Previous evidence has demonstrated that childhood victimization is associated with elevated levels of inflammation biomarkers measured decades after exposure. However, it is unclear whether this association is (1) already detectable in young people, (2) different in males and females, and (3) confounded by genetic liability to inflammation. Here we sought to address these questions. Method Participants were 2232 children followed from birth to age 18 years as part of the Environmental Risk (E-Risk) Longitudinal Twin Study. Childhood victimization was measured prospectively from birth to age 12 years. Inflammation was measured through C-reactive protein (CRP) levels in dried blood spots at age 18 years. Latent genetic liability for high inflammation levels was assessed through a twin-based method. Results Greater exposure to childhood victimization was associated with higher CRP levels at age 18 (serum-equivalent means were 0.65 in non-victimized Study members, 0.74 in those exposed to one victimization type, and 0.81 in those exposed to poly-victimization; p = 0.018). However, this association was driven by a significant association in females (serum-equivalent means were 0.75 in non-victimized females, 0.87 in those exposed to one type of victimization, and 1.19 in those exposed to poly-victimization; p = 0.010), while no significant association was observed in males (p = 0.19). Victimized females showed elevated CRP levels independent of latent genetic influence, as well as childhood socioeconomic status, and waist-hip ratio and body temperature at the time of CRP assessment. Conclusion Childhood victimization is associated with elevated CRP levels in young women, independent of latent genetic influences and other key risk factors. These results strengthen causal inference about the effects of childhood victimization on inflammation levels in females by accounting for potential genetic confounding. [ABSTRACT FROM AUTHOR]

In the present study, we used separate measures of parental monitoring and parental knowledge and compared their associations with youths' antisocial behavior during preadolescence, between the ages of 10 and 12. Parental monitoring and knowledge were reported by mothers, fathers, and youths taking part in the Environmental Risk (E-Risk) Longitudinal Twin Study that follows 1,116 families with twins. Information on youths' antisocial behavior was obtained from mothers as well as teachers. We report two main findings. First, longitudinal cross-lagged models revealed that greater parental monitoring did not predict less antisocial behavior later, once family characteristics were taken into account. Second, greater youth antisocial behavior predicted less parental knowledge later. This effect of youths' behavior on parents' knowledge was consistent across mothers', fathers', youths', and teachers' reports, and robust to controls for family confounders. The association was partially genetically mediated according to a Cholesky decomposition twin model; youths' genetically influenced antisocial behavior led to a decrease in parents' knowledge of youths' activities. These two findings question the assumption that greater parental monitoring can reduce preadolescents' antisocial behavior. They also indicate that parents' knowledge of their children's activities is influenced by youths' behavior. [ABSTRACT FROM AUTHOR]

We report the case of a middle-age lady who presented following minor trauma, with dominant-sided anterior elbow pain and swelling of 6 months in duration. She was assessed clinically, and underwent investigations, which confirmed features consistent with giant cell tumour (GCT) of distal biceps tendon sheath. She underwent uneventful en-bloc excisional surgery. She did not have radiotherapy. She is now 5 years postoperatively asymptomatic, with full function, and with no signs of recurrence. [ABSTRACT FROM AUTHOR]

The appearance of the optic disc is a key measure of disease status in idiopathic intracranial hypertension (IIH). The Frisén classification describes stages of optic disc swelling (grades 0-5). It is the only classification of papilloedema, and is used internationally in clinical and research practice. Despite this, there has been very limited evaluation of the scale. We assessed the inter-rater reproducibility and ability to discriminate optic disc changes over time using the Frisén classification compared with a system of ranking papilloedema severity in patients with IIH. Paired disc photographs (before and after treatment) were obtained from 47 patients with IIH (25 acute and 22 chronic). Six neuro-ophthalmologists blinded to patient identity, clinical information and chronology of the photographs reviewed the discs and allocated a Frisén grade and ranked the paired discs in order of papilloedema severity (disc ranking). A total of 188 optic disc photographs were reviewed. All six reviewers agreed in only three comparisons (1.6%) when using the Frisén classification, compared with 42 comparisons (45.2%) when using disc ranking. The probability of agreement between any two reviewers was 36.1% for Frisén grade and 70.0% for disc ranking. Disc ranking had significantly greater sensitivity for finding differences in degree of disc oedema, identifying a difference in 75.3% of paired photographs compared to 53.2% detected using the Frisén classification ( p < 0.001). This study demonstrated the limited reproducibility and discriminative ability of the Frisén classification in identifying changes in serial optic disc photographs in IIH. Simple optic disc ranking appears to be a more sensitive and reliable tool to monitor changes in optic disc appearance. The use of disc ranking in clinical practice and research studies is recommended to monitor alterations in optic disc appearance until alternative schemes, specific to IIH, have been developed. [ABSTRACT FROM AUTHOR]

The cause of idiopathic intracranial hypertension (IIH) remains unknown, and no consensus exists on how patients should be monitored and treated. Acetazolamide is a common treatment but has never been examined in a randomised controlled trial. The objectives of this pilot trial are to prospectively evaluate the use of acetazolamide, to explore various outcome measures and to inform the design of a definitive trial in IIH. Fifty patients were recruited from six centres over 23 months and randomised to receive acetazolamide ( n = 25) or no acetazolamide ( n = 25). Symptoms, body weight, visual function and health-related quality-of-life measures were recorded over a 12-month period. Recruited patients had typical features of mild IIH and most showed improvement, with 44% judged to have IIH in remission at the end of the trial. Difficulties with recruitment were highlighted as well as poor compliance with acetazolamide therapy (12 patients). A composite measure of IIH status was tested, and the strongest concordance with final disease status was seen with perimetry (Somers' D = 0.66) and optic disc appearance ( D = 0.59). Based on the study data, a sample size of 320 would be required to demonstrate a 20% treatment effect in a substantive trial. Clinical trials in IIH require pragmatic design to involve sufficiently large numbers of patients. Future studies should incorporate weighted composite scores to reflect the relative importance of common outcome measures in IIH. [ABSTRACT FROM AUTHOR]

Background: We reported previously on the emergence and clinical implications of simian immunodeficiency virus (SIVmac251) mutants with a K65R mutation in reverse transcriptase (RT), and the role of CD8+ cell-mediated immune responses in suppressing viremia during tenofovir therapy. Because of significant sequence differences between SIV and HIV-1 RT that affect drug susceptibilities and mutational patterns, it is unclear to what extent findings with SIV can be extrapolated to HIV-1 RT. Accordingly, to model HIV-1 RT responses, 12 macaques were inoculated with RT-SHIV, a chimeric SIV containing HIV-1 RT, and started on prolonged tenofovir therapy 5 months later. Results: The early virologic response to tenofovir correlated with baseline viral RNA levels and expression of the MHC class I allele Mamu-A*01. For all animals, sensitive real-time PCR assays detected the transient emergence of K70E RT mutants within 4 weeks of therapy, which were then replaced by K65R mutants within 12 weeks of therapy. For most animals, the occurrence of these mutations preceded a partial rebound of plasma viremia to levels that remained on average 10-fold below baseline values. One animal eventually suppressed K65R viremia to undetectable levels for more than 4 years; sequential experiments using CD8+ cell depletion and tenofovir interruption demonstrated that both CD8+ cells and continued tenofovir therapy were required for sustained suppression of viremia. Conclusion: This is the first evidence that tenofovir therapy can select directly for K70E viral mutants in vivo. The observations on the clinical implications of the K65R RT-SHIV mutants were consistent with those of SIVmac251, and suggest that for persons infected with K65R HIV-1 both immune-mediated and drug-dependent antiviral activities play a role in controlling viremia. These findings suggest also that even in the presence of K65R virus, continuation of tenofovir treatment as part of HAART may be beneficial, particularly when assisted by antiviral immune responses. [ABSTRACT FROM AUTHOR]

The Epstein-Barr virus (EBV) genome is highly methylated in latently infected cells. We recently reported that the EBV immediate-early (IE) protein BZLF1 (Z) preferentially binds to and activates transcription from the methylated form of the BRLF1 IE gene promoter (Rp). We now report that serine residue 186 in the Z DNA-binding domain plays an important role in the ability of Z to bind to and activate methylated Rp. A Z mutant containing an alanine residue at position 186 [Z(S186A)] was significantly defective in binding to methylated, as well as unmethylated, ZREs (Z-responsive elements) in Rp and was unable to activate lytic EBV gene transcription from the methylated or demethylated form of the viral genome. A Z mutant containing threonine at residue 186 [Z(S186T)] bound only to the methylated form of the ZRE-2 site in Rp and induced lytic EBV gene transcription from the methylated, but not demethylated, form of the viral genome. The defect in both of these mutants was primarily due to an inability to activate the Rp in the context of the viral genome. Finally, a Z mutant containing an aspartic acid at position 186 [Z (S186D)] did not bind to either the consensus AP-1 site or to the methylated or unmethylated Rp ZRE-2 site and did not induce lytic gene transcription. These results indicate that replacement of serine with threonine at residue 186 in the Z DNA-binding domain differentially affects its ability to reactivate the unmethylated, versus methylated, viral genome. [ABSTRACT FROM AUTHOR]

Objective: Borderline personality disorder in adolescence remains a controversial construct. We addressed concerns about the prognostic significance of adolescent borderline pathology by testing whether borderline symptoms at age 12 years predict functioning during the transition to adulthood, at age 18 years, in areas critical to life-course development.Method: We studied members of the Environmental Risk (E-Risk) Longitudinal Twin Study, which tracks the development of a birth cohort of 2,232 British twin children. At age 12, study members' borderline symptoms were measured using mothers' reports. At age 18, study members' personality, psychopathology, functional outcomes, and experiences of victimization were measured using self-reports, coinformant reports, and official records.Results: At age 18, study members who had more borderline symptoms at age 12 were more likely to have difficult personalities, to struggle with poor mental health, to experience poor functional outcomes, and to have become victims of violence. Reports of poor outcomes were corroborated by coinformants and official records. Borderline symptoms in study members at 12 years old predicted poor outcomes over and above other behavioral and emotional problems during adolescence. Twin analyses showed that borderline symptoms in 12-year-olds were influenced by familial risk, particularly genetic risk, which accounted for associations with most poor outcomes at age 18.Conclusion: Borderline symptoms in 12-year-olds signal risk for pervasive poor functioning during the transition to adulthood. This association is driven by genetic influences, suggesting that borderline symptoms and poor outcomes are manifestations of shared genetic risk. [ABSTRACT FROM AUTHOR]

The article offers information on a study which investigated the efficacy of weight loss in reducing intracranial pressure and treating patients with idiopathic intracranial hypertension. The study subjects, who were recruited in two hospitals in Great Britain, were 25 women with chronic active idiopathic and intracranial pressure. Outcome measures studied were reduction in intracranial pressure after the diet and papilloedema as measured by ultrasonography of the optic disc elevation and nerve sheath diameter. The research findings are presented.