To estimate the impact of osteoporosis fractures on health-related quality of life (HRQOL) in postmenopausal women.
To compare the impact on HRQOL of different osteoporotic fractures, 600 consecutive ...women 55-75 years old with a new fracture (inclusion fracture) were invited by mail. After exclusions by preset criteria (high-energy fractures, ongoing osteoporosis treatment, or unwillingness to participate), 303 women were included, 171 (56%) of whom had a forearm, 37 (12%) proximal humerus, 40 (13%) hip, and 55 (18%) vertebral fracture, respectively, and all were investigated and treated according to the current local consensus program for osteoporosis. In addition, HRQOL was evaluated by the SF-36 questionnaire and compared with local, age-matched reference material. Examinations were performed 82 days (median) after the fracture and 2 years later.
HRQOL was significantly reduced at baseline regarding all SF-36 domains after vertebral fractures and most after hip fractures, but only regarding some domains after forearm and humerus fracture. After 2 years, improvements had occurred after all types of fractures, and after forearm or humerus fracture, HRQOL was completely normalized in all domains. However, 2 years after hip fracture, HRQOL was still below normal regarding physical function, role-physical and social function, while after vertebral fracture, scores were still significantly lower for all domains, physical as well as mental. Patients with one or more previous fractures before the inclusion fracture had lower HRQOL at baseline and after 2 years, compared with those with no previous fracture. Patients with osteoporosis (T-score <-2.5 in hip or spine) had lower HRQOL than those with normal BMD.
Vertebral and hip fractures have a considerably greater and more prolonged impact on HRQOL than forearm and humerus fractures. The number of fractures was inversely correlated to HRQOL. These differences should be taken into account when making priorities in health care programs.
Maternal polycystic ovary syndrome (PCOS) has been proposed as a model for investigating the role of prenatal androgen exposure in the development of neuropsychiatric disorders. However, women with ...PCOS are at higher risk of developing psychiatric conditions and previous studies are likely confounded by genetic influences.
A Swedish nationwide register-based cohort study was conducted to disentangle the influence of prenatal androgen exposure from familial confounding in the association between maternal PCOS and offspring attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorders (ASD), and Tourette's disorder and chronic tic disorders (TD/CTD). PCOS-exposed offspring (n = 21 280) were compared with unrelated PCOS-unexposed offspring (n = 200 816) and PCOS-unexposed cousins (n = 17 295). Associations were estimated with stratified Cox regression models.
PCOS-exposed offspring had increased risk of being diagnosed with ADHD, ASD, and TD/CTD compared with unrelated PCOS-unexposed offspring. Associations were stronger in girls for ADHD and ASD but not TD/CTD ADHD: adjusted hazard ratio (aHR) = 1.61 (95% confidence interval (CI) 1.31-1.99), ASD: aHR = 2.02 (95% CI 1.45-2.82) than boys ADHD: aHR = 1.37 (95% CI 1.19-1.57), ASD: aHR = 1.46 (95% CI 1.21-1.76). For ADHD and ASD, aHRs for girls were stronger when compared with PCOS-unexposed cousins, but slightly attenuated for boys.
Estimates were similar when accounting for familial confounding (i.e. genetics and environmental factors shared by cousins) and stronger in girls for ADHD and ASD, potentially indicating a differential influence of prenatal androgen exposure v. genetic factors. These results strengthen evidence for a potential causal influence of prenatal androgen exposure on the development of male-predominant neuropsychiatric disorders in female offspring of women with PCOS.
Abstract
Background
Previous studies are inconclusive concerning the association between maternal pre-pregnancy overweight/obesity and risk of attention-deficit/hyperactivity disorder (ADHD) in ...offspring. We therefore conducted a systematic review and meta-analysis to clarify this association. To address the variation in confounding adjustment between studies, especially inadequate adjustment of unmeasured familial confounding in most studies, we further performed cousin and sibling comparisons in a nationwide population-based cohort in Sweden.
Methods
We searched PubMed, Embase and PsycINFO during 1975–2018. We used random-effects models to calculate pooled risk ratios (RRs) with 95% confidence interval. In the population-based study, Cox proportional hazard models were used to calculate the unadjusted hazard ratios (HRs) and HRs adjusted for all confounders identified in previous studies. Stratified Cox models were applied to data on full cousins and full siblings to further control for unmeasured familial confounding.
Results
Eight cohorts with a total of 784 804 mother–child pairs were included in the meta-analysis. Maternal overweight RRoverweight = 1.31 (1.25–1.38), I2 = 6.80% and obesity RRobesity = 1.92 (1.84–2.00), I2 = 0.00% were both associated with an increased risk of ADHD in offspring. In the population-based cohort of 971 501 individuals born between 1992 and 2004, unadjusted Cox models revealed similar associations HRoverweight = 1.30 (1.28–1.34), HRobesity = 1.92 (1.87–1.98). These associations gradually attenuated towards the null when adjusted for measured confounders HRoverweight = 1.21 (1.19–1.25), HRobesity = 1.60 (1.55–1.65), unmeasured factors shared by cousins HRoverweight = 1.10 (0.98–1.23), HRobesity = 1.44 (1.22–1.70) and unmeasured factors shared by siblings HRoverweight = 1.01 (0.92–1.11), HRobesity = 1.10 (0.94–1.27).
Conclusion
Pre-pregnancy overweight/obesity is associated with an increased risk of ADHD in offspring. The observed association is largely due to unmeasured familial confounding.
Autism and autistic traits onset in childhood but persist into adulthood. Little is known about how genetic and environmental factors influence autism and autistic traits into adulthood. We aimed to ...determine age effects on the heritability of clinically diagnosed autism and the etiological stability of autistic traits from childhood to adulthood using twin methods.
From 23,849 twin pairs in the Swedish Twin Register born between 1959 and 2010, we identified 485 individuals (1.01%, 31.5% female) with a clinical autism diagnosis. We estimated and compared the relative contribution of genetic, shared, and nonshared environmental influences to autism in childhood and adulthood. We further used multivariate twin analysis with four measurement points among 1,348 twin pairs in the longitudinal Twin Study of Child and Adolescent Development to assess the phenotypic and etiological stability of autistic traits - measured with three scales from the Child Behavior Checklist - from childhood to adulthood.
Autism heritability was comparable from childhood, (96% 95% CI, 76-99%) to adulthood (87% 67-96%). Autistic traits were moderately stable (phenotypic correlation = 0.35-0.61) from childhood to adulthood, and their heritability varied between 52 and 71%. We observed stable as well as newly emerging genetic influences on autistic traits from ages 8-9 to 19-20, and unique nonshared environmental influences at each age.
Genetic factors are important for autism and autistic traits in adulthood and separate genetic studies in adults are warranted.
Background
Prenatal exposure to maternal adverse life events has been associated with offspring ADHD, but the role of familial confounding is unclear. We aimed to clarify if adverse life events ...during pregnancy are related to ADHD symptoms in offspring, taking shared familial factors into account.
Method
Data were collected on 34,751 children (including 6,427 siblings) participating in the population‐based Norwegian Mother and Child Cohort Study. During pregnancy, mothers reported whether they had experienced specific life events. We assessed ADHD symptoms in five‐year‐old children with the Conners’ Parent Rating Scale–Revised: short form. We modeled the associations between life events and mean ADHD scores with ordinary linear regression in the full cohort, and with fixed‐effect linear regression in sibling comparisons to adjust for familial confounding.
Results
Children exposed to adverse life events had higher ADHD scores at age 5, with the strongest effect observed for financial problems (mean differences 0.10 95% CI: 0.09, 0.11 in adjusted model), and the weakest for having lost someone close (0.02 95% CI 0.01, 0.04 in adjusted model). Comparing exposure‐discordant siblings resulted in attenuated estimates that were no longer statistically significant (e.g. mean difference for financial problems −0.03 95% CI −0.07, 0.02). ADHD scores increased if the mother had experienced the event as painful or difficult, and with the number of events, whereas sibling‐comparison analyses resulted in estimates attenuated toward the null.
Conclusions
These results suggest that the association between adverse life events during pregnancy and offspring ADHD symptoms is largely explained by familial factors.
In the latest edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), obsessive-compulsive disorder (OCD) included a new "tic-related" specifier. However, strong evidence ...supporting tic-related OCD as a distinct subtype of OCD is lacking. This study investigated whether, at the population level, tic-related OCD has a stronger familial load than non-tic-related OCD. From a cohort of individuals born in Sweden between 1967 and 2007 (n = 4,085,367; 1257 with tic-related OCD and 20,975 with non-tic-related OCD), we identified all twins, full siblings, maternal and paternal half siblings, and cousins. Sex- and birth year-adjusted hazard ratios (aHR) were calculated to estimate the risk of OCD in relatives of individuals with OCD with and without comorbid tics, compared with relatives of unaffected individuals. We found that OCD is a familial disorder, regardless of comorbid tic disorder status. However, the risk of OCD in relatives of individuals with tic-related OCD was considerably greater than the risk of OCD in relatives of individuals with non-tic-related OCD (e.g., risk for full siblings: aHR = 10.63 95% CI, 7.92-14.27 and aHR = 4.52 95% CI, 4.06-5.02, respectively; p value for the difference < 0.0001). These differences remained when the groups were matched by age at first OCD diagnosis and after various sensitivity analyses. The observed familial patterns of OCD in relation to tics were not seen in relation to other neuropsychiatric comorbidities. Tic-related OCD is a particularly familial subtype of OCD. The results have important implications for ongoing gene-searching efforts.
Aim
Neonatal jaundice is associated with higher risk of attention deficit hyperactivity disorder (ADHD), but it is unclear if the association is influenced by genetic and other familial factors. In ...this large population‐based study, we investigated the association between neonatal jaundice and ADHD while adjusting for familial factors.
Methods
We linked several Swedish registers to identify all singleton births without congenital malformations between 1992 and 2000 (n = 814 420, including 384 290 full siblings) and followed them up until 2009. We calculated hazard ratios (HRs) for the association between neonatal jaundice and ADHD, adjusting for pregnancy, delivery and neonatal characteristics including prematurity, and parental age and education. We repeated the analyses among siblings to adjust for shared familial factors.
Results
At a population level, children treated for neonatal jaundice had an increased risk of ADHD (adjusted HR (aHR): 1.13, 95% CI: 1.05‐1.22). In the sibling comparisons, there was no clear association between neonatal jaundice and ADHD (aHR: 1.03, 95% CI: 0.82‐1.29).
Conclusion
We found no evidence of an independent association between neonatal jaundice and ADHD within siblings in this large population‐based study, suggesting that the association is probably influenced by shared familial factors, such as parental genetic and/or lifestyle effects.
This study shows the use of dual-polarized L-band Synthetic Aperture Radar (SAR) data acquired by the Advanced Land Observing Satellite (ALOS) Phased Array type L-band Synthetic Aperture Radar sensor ...(PALSAR) system for differentiation between primary forest and new deforestation fronts. Results showed that the new deforested areas are not unequivocally detected in either of the single bands individually. Although most of the recent deforestation appears brighter than mature forests in the HH band, the identification of new deforestation using only this band depends on the stage of the clearing process. Then, the contribution of the HV band through a normalized difference index (NDI) is important for detection of the new deforested fronts. Results indicate that the method can be used as the basis for an operational programme to monitor deforestation in the Brazilian Amazônia.
Background
Many psychiatric disorders show gender differences in prevalence. Recent studies suggest that female patients diagnosed with anxiety and depression carry more genetic risks related to ...attention-deficit hyperactivity disorder (ADHD) compared with affected males.
Aims
In this register-based study, we aimed to test whether female patients who received clinical diagnoses of anxiety, depressive, bipolar and eating disorders are at higher familial risk for ADHD and other neurodevelopmental disorders, compared with diagnosed male patients.
Method
We analysed data from a record-linkage of several Swedish national registers, including 151 025 sibling pairs from 103 941 unique index individuals diagnosed with anxiety, depressive, bipolar or eating disorders, as well as data from 646 948 cousin pairs. We compared the likelihood of having a relative diagnosed with ADHD/neurodevelopmental disorders in index males and females.
Results
Female patients with anxiety disorders were more likely than affected males to have a brother with ADHD (odd ratio (OR) = 1.13, 95% CI 1.05–1.22). Results for broader neurodevelopmental disorders were similar and were driven by ADHD diagnoses. Follow-up analyses revealed similar point estimates for several categories of anxiety disorders, with the strongest effect observed for agoraphobia (OR = 1.64, 95% CI 1.12–2.39). No significant associations were found in individuals with depressive, bipolar or eating disorders, or in cousins.
Conclusions
These results provide modest support for the possibility that familial/genetic risks for ADHD may show gender-specific phenotypic expression. Alternatively, there could be gender-specific biases in diagnoses of anxiety and ADHD. These factors could play a small role in the observed gender differences in prevalence of ADHD and anxiety.
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