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Background Although neurodevelopmental disorders are demarcated as discrete entities in the Diagnostic Statistical Manual of mental disorders, empirical evidence indicates that there is a high degree of overlap among them. The first aim of this investigation was to explore if a single general factor could account for the large degree of observed overlap among neurodevelopmental problems, and explore whether this potential factor was primarily genetic or environmental in origin. The second aim was to explore whether there was systematic covariation, either genetic or environmental, over and above that contributed by the potential general factor, unique to each syndrome. Method Parents of all Swedish 9- and 12-year-old twin pairs born between 1992 and 2002 were targeted for interview regarding problems typical of autism spectrum disorders, ADHD and other neurodevelopmental conditions (response rate: 80 percent). Structural equation modeling was conducted on 6,595 pairs to examine the genetic and environmental structure of 53 neurodevelopmental problems. Results One general genetic factor accounted for a large proportion of the phenotypic covariation among the 53 symptoms. Three specific genetic subfactors identified 'impulsivity,' 'learning problems,' and 'tics and autism,' respectively. Three unique environment factors identified 'autism,' 'hyperactivity and impulsivity,' and 'inattention and learning problems,' respectively. Conclusion One general genetic factor was responsible for the wide-spread phenotypic overlap among all neurodevelopmental symptoms, highlighting the importance of addressing broad patient needs rather than specific diagnoses. The unique genetic factors may help guide diagnostic nomenclature, whereas the unique environmental factors may highlight that neurodevelopmental symptoms are responsive to change at the individual level and may provide clues into different mechanisms and treatments. Future research would benefit from assessing the general factor separately from specific factors to better understand observed overlap among neurodevelopmental problems. [ABSTRACT FROM AUTHOR]

Objectives To examine how body mass index ( BMI) and change in BMI are associated with mortality in old (70-79) and very old (≥80) individuals. Design Pooled data from three multidisciplinary prospective population-based studies: OCTO-twin, Gender, and NONA. Setting Sweden. Participants Eight hundred eighty-two individuals aged 70 to 95. Measurements BMI was calculated from measured height and weight as kg/m2. Information about survival status and time of death was obtained from the Swedish Civil Registration System. Results Mortality hazard was 20% lower for the overweight group than the normal-underweight group (relative risk ( RR) = 0.80, P = .011), and the mortality hazard for the obese group did not differ significantly from that of the normal-underweight group ( RR = 0.93, P = .603), independent of age, education, and multimorbidity. Furthermore, mortality hazard was 65% higher for the BMI loss group than for the BMI stable group ( RR = 1.65, P < .001) and 53% higher for the BMI gain group than for the BMI stable group ( RR = 1.53, P = .001). Age moderated the BMI change differences. That is, the higher mortality risks associated with BMI loss and gain were less severe in very old age. Conclusion Old persons who were overweight had a lower mortality risk than old persons who were of normal weight, even after controlling for weight change and multimorbidity. Persons who increased or decreased in BMI had a greater mortality risk than those who had a stable BMI, particularly those aged 70 to 79. This study lends further support to the belief that the World Health Organization guidelines for BMI are overly restrictive in old age. [ABSTRACT FROM AUTHOR]

Objective: Early maturing girls are at increased risk for disordered eating. However, it is unclear if the association between puberty and disordered eating continues throughout pubertal development and if a similar association is exhibited in boys. Method: Participants included 1340 same- and 624 opposite-sex twins from the Swedish Twin Study of Child and Adolescent Development. Pubertal development was assessed at age 13-14 with the pubertal development scale. General disordered eating, measured with the eating disorder inventory-2 (EDI) was assessed at age 16-17, and dieting and purging behaviors were assessed at both ages 16-17 and 19-20. We applied analysis of variance and logistic regression analyses to determine whether pubertal development in early-to-mid adolescence predicted eating disorder-related behaviors in late adolescence and young adulthood. Results: Pubertal development in early-to-mid adolescence was significantly associated with EDI scores and dieting in late adolescence. No significant association was observed between pubertal development and dieting and purging in young adulthood. Discussion: Complex combinations of cultural and biological influences likely converge during pubertal development increasing vulnerability to disordered eating. The impact of pubertal development on disordered eating appears to be limited to the adolescent period. © 2012 by Wiley Periodicals, Inc. (Int J Eat Disord 2012;45:819-826) [ABSTRACT FROM AUTHOR]

Objectives To examine job control, job demands, social support at work, and job strain (ratio of demands to control) in relation to risk of any dementia, Alzheimer's disease ( AD), and vascular dementia ( VaD). Design Cohort study. Setting The population-based Study of Dementia in Swedish Twins. Participants Two hundred fifty-seven people with dementia (167 AD, 46 VaD) and 9,849 without. Measurements Dementia diagnoses were based on telephone screening for cognitive impairment followed by in-person clinical examination. An established job exposure matrix was matched to main occupation categories to measure work characteristics. Results In generalized estimating equations (adjusted for the inclusion of complete twin pairs), lower job control was associated with greater risk of any dementia (odds ratio ( OR) = 1.17, 95% confidence interval ( CI) = 1.04-1.31) and VaD specifically ( OR = 1.39, 95% CI = 1.07-1.81). Lower social support at work was associated with greater risk of dementia ( OR = 1.15, 95% CI = 1.03-1.28), AD ( OR = 1.14, 95% CI = 1.00-1.31), and VaD ( OR = 1.28, 95% CI = 1.02-1.60). Greater job strain was associated with greater risk of VaD only ( OR = 1.28, 95% CI = 1.02-1.60), especially in combination with low social support ( OR = 1.35, 95% CI = 1.11-1.64). Age, sex, and education were controlled for. Work complexity, manual work, and vascular disease did not explain the results. No differences in work-related stress scores were observed in the 54 twin pairs discordant for dementia, although only two pairs included a twin with VaD. Conclusion Work-related stress, including low job control and low social support at work, may increase the risk of dementia, particularly VaD. Modification to work environment, including attention to social context and provision of meaningful roles for employees, may contribute to efforts to promote cognitive health. [ABSTRACT FROM AUTHOR]

Background: Although the clinical utility of categorically defined attention-deficit hyperactivity disorder (ADHD) is well established, there is also strong evidence supporting the notion of ADHD as an extreme of a continuous trait. Nevertheless, the question of whether the etiology is the same for different levels of DSM-IV ADHD symptoms remains to be investigated. The aim of this study was to assess genetic links between the extreme and the subthreshold range of ADHD symptoms. Method: Parents of all Swedish 9- and 12-year-old twins born between 1992 and 2000 were interviewed for DSM-IV ADHD symptoms and associated conditions. Two validated cutoff values were used for screening and assigning research diagnoses. Response rate was 80%. Twin methods were applied to investigate the extent to which ADHD is etiologically distinct from subthreshold variations in ADHD symptoms. Results: Extremes analyses indicated a strong genetic link between the extreme and the subthreshold variation, with almost identical group heritability estimates around .60 for the diagnostic (prevalence 1.78%) and screening (prevalence 9.75%) criteria of ADHD. Conclusion: A strong genetic link between the extreme and the subthreshold variation of DSM-IV based assessments of ADHD symptoms was found. The data suggest that ADHD is best viewed as the quantitative extreme of genetic and environmental factors operating dimensionally throughout the distribution of ADHD symptoms, indicating that the same etiologic factors are involved in the full range of symptoms of inattention, hyperactivity and impulsivity. [ABSTRACT FROM AUTHOR]

Previous studies have found inverse associations between intelligence quotient (IQ) and cigarette smoking, but the causal pathways linking IQ with smoking status and nicotine dependence (ND) are not well understood. The aim of this study was to explore the associations between IQ and ND using a genetically informative twin design to detect whether any association is because of shared genetic or environmental factors. A population-based twin cohort with IQ measured in adolescence and ND later in life, analysed by classical twin modeling based on linear structural equations. Swedish national registry data. A total of 5040 male twins born 1951-84. IQ was measured at military conscription at a mean age of 18 years. ND was self-reported at the ages of 22-57 years using the Fagerström Test for ND scale (FTND). Both cigarette smoking and Swedish snus use were analysed. Both IQ and ND showed moderate heritability (0.58 and 0.39, respectively). The heritability of ND was similar for cigarette smoking and snus use. The phenotypic correlation between IQ and ND was weak: −0.11 (−0.16, −0.06) for total ND. Bivariate analysis revealed that this correlation was mainly because of genetic factors, but still the genetic correlation between IQ and ND from cigarette smoking was only −0.24. Nicotine dependence, as measured by the Fagerström Test for Nicotine Dependence, shows moderate heritability in both smokers and snus users but is only weakly associated with intelligence quotient; common genetic factors underlying nicotine dependence and intelligence quotient probably account for little of the observed association between smoking and intelligence quotient. [ABSTRACT FROM AUTHOR]

Scand J Caring Sci; 2010; 24; 541–547 High sense of coherence in adolescence is a protective factor in the longitudinal development of ADHD symptoms The key feature of salutogenesis is that good health can be directly sustained by positive factors. The Sense of Coherence (SOC) scale was developed by Antonovsky as a measure related to the concept of salutogenesis including aspects of comprehensibility, manageability and meaningfulness. Aim: The aim was to investigate whether Sense of Coherence can serve as a salutogenetic factor modifying the long-term development of Attention Deficit Hyperactivity Disorder (ADHD) Symptoms. Subjects and methods: Twin study of Child and Adolescent Development (TCHAD) is a longitudinal study of all twin pairs born in Sweden between May 1985 and December 1986. The present project is a sub-sample of 312 individuals (135 boys and 177 girls). At 16 years of age, the young persons and their parents were interviewed with K-SADS especially symptoms of ADHD. The young person also completed the SOC questionnaire. At 21 years of age, the young person completed a questionnaire about symptoms of ADHD. Findings: Higher (worse) ADHD scores at 16 years of age were associated with higher (worse) ADHD scores at 21 years of age. However, this relationship was stronger for lower (worse) SOC. A higher (better) SOC at 16 years was associated with lower (better) ADHD at 21 years and this relationship was stronger for higher (worse) ADHD at 16 years. Conclusion: A high Sense of Coherence in adolescence was a protective factor for the long-term development of ADHD. [ABSTRACT FROM AUTHOR]