Depression, Neuroticism, and Urinary Incontinence in Premenopausal Women: A Nationwide Twin Study

2013 ◽  
Vol 16 (5) ◽  
pp. 977-984 ◽  
Author(s):  
Giorgio Tettamanti ◽  
Daniel Altman ◽  
Anastasia N. Iliadou ◽  
Rino Bellocco ◽  
Nancy L. Pedersen

Previous studies have found that major depression and neuroticism are positively associated with urinary incontinence (UI). However, the genetic contribution to these associations has never been investigated. In 2005, a total of 14,094 female twins born 1959–1985 in the Swedish Twin Registry participated in a comprehensive survey on common exposures and complex diseases. Structured questions provided information on UI, depressive symptoms, major depression, and neuroticism. A logistic regression model based on generalized estimating equations (GEE) was used to estimate odds ratios (ORs) with 95% confidence intervals (CIs). Environmental and genetic influences were assessed in co-twin control analyses and quantitative genetic analyses, which were also used to determine the proportion of the phenotypic correlation explained by familial factors. Major depression, depressive symptoms, and neuroticism were positively associated with all UI subtypes (overall, stress, urge, and mixed UI). In a trivariate Cholesky model with neuroticism, depressive symptoms (or depression), and UI a modest genetic correlation was found between indicators of depression and overall, or stress, UI. The majority of this correlation was independent from neuroticism. In contrast, the genetic factors shared between indicators of depression and urge or mixed UI were entirely in common with neuroticism. In conclusion, depression and neuroticism are associated with UI among premenopausal women: the associations are in part determined by genetic factors in common to the disorders.

2009 ◽  
Vol 66 (8) ◽  
pp. 857 ◽  
Author(s):  
Kenneth S. Kendler ◽  
Charles O. Gardner ◽  
Amy Fiske ◽  
Margaret Gatz

1999 ◽  
Vol 23 (2) ◽  
pp. 357-374 ◽  
Author(s):  
Birgitta Steffensson ◽  
Jan-Olov Larsson ◽  
Ingegärd Fried ◽  
Eman El-Sayed ◽  
Per-Anders Rydelius ◽  
...  

Attention deficit hyperactivity disorder (ADHD) has been shown to be substantially influenced by genetic factors. However it is still not known how these effects are mediated. The aim of this study is to evaluate whether genetic disposition for global maturity could be a mediator of the well-known findings of genetic factors for ADHD symptoms. A total of 1480 pairs of twins aged 8-9 years were identified through the population-based Swedish Twin Registry. A mailed questionnaire with items from DSM-III-R for ADHD and items concerning global maturity were completed by the parents. The results showed that global maturity mediated part of genetic effects for ADHD for both boys and girls. There were also genetic, shared environmental, as well as nonshared environmental effects unique to ADHD not in common with global maturity. Thus, there are at least two pathways through which genetic effects can influence ADHD: one through predisposition for maturational lag and one unique to ADHD, possibly mediated by personality. The results indicate that maturational lag could be of importance for treatment and prognosis of ADHD.


2007 ◽  
Vol 32 (7) ◽  
pp. 843-853 ◽  
Author(s):  
Elizabeth A. Young ◽  
Susan G. Kornstein ◽  
Anne T. Harvey ◽  
Stephen R. Wisniewski ◽  
Jennifer Barkin ◽  
...  

1998 ◽  
Vol 53A (6) ◽  
pp. M441-M446 ◽  
Author(s):  
B. Ljungquist ◽  
S. Berg ◽  
J. Lanke ◽  
G. E. McClearn ◽  
N. L. Pedersen

2013 ◽  
Vol 44 (7) ◽  
pp. 1439-1449 ◽  
Author(s):  
K. Bolhuis ◽  
T. A. McAdams ◽  
B. Monzani ◽  
A. M. Gregory ◽  
D. Mataix-Cols ◽  
...  

BackgroundDepression is commonly co-morbid with obsessive–compulsive disorder (OCD). However, it is unknown whether depression is a functional consequence of OCD or whether these disorders share a common genetic aetiology. This longitudinal twin study compared these two hypotheses.MethodData were drawn from a longitudinal sample of adolescent twins and siblings (n = 2651; Genesis 12–19 study) and from a cross-sectional sample of adult twins (n = 4920). The longitudinal phenotypic associations between OCD symptoms (OCS) and depressive symptoms were examined using a cross-lag model. Multivariate twin analyses were performed to explore the genetic and environmental contributions to the cross-sectional and longitudinal relationship between OCS and depressive symptoms.ResultsIn the longitudinal phenotypic analyses, OCS at time 1 (wave 2 of the Genesis 12–19 study) predicted depressive symptoms at time 2 (wave 3 of the Genesis 12–19 study) to a similar extent to which depressive symptoms at time 1 predicted OCS at time 2. Cross-sectional twin analyses in both samples indicated that common genetic factors explained 52–65% of the phenotypic correlation between OCS and depressive symptoms. The proportion of the phenotypic correlation due to common non-shared environmental factors was considerably smaller (35%). In the adolescent sample, the longitudinal association between OCS at time 1 and subsequent depressive symptoms was accounted for by the genetic association between OCS and depressive symptoms at time 1. There was no significant environmental association between OCS and later depressive symptoms.ConclusionsThe present findings show that OCS and depressive symptoms co-occur primarily due to shared genetic factors and suggest that genetic, rather than environmental, effects account for the longitudinal relationship between OCS and depressive symptoms.


2020 ◽  
Vol 23 (6) ◽  
pp. 338-344
Author(s):  
Moritz Herle ◽  
Juan J. Madrid-Valero ◽  
José J. Morosoli ◽  
Lucía Colodro-Conde ◽  
Juan Ordoñana

AbstractResearch has emphasized the genetic basis of individual differences in body mass index (BMI); however, genetic factors cannot explain the rapid rise of obesity. Eating behaviors have been stipulated to be the behavioral expression of genetic risk in an obesogenic environment. In this study, we decompose variation and covariation between three key eating behaviors and BMI in a sample of 698 participants, consisting of 167 monozygotic, 150 dizygotic complete same-sex female twins and 64 incomplete pairs from a population-based twin registry in the southeast of Spain, The Murcia Twin Registry. Phenotypes were emotional eating, uncontrolled eating and cognitive restraint, measured by the Three Factor Eating Questionnaire and objectively measured BMI. Variation in eating behaviors was driven by nonshared environmental factors (range: 56%−65%), whereas shared environmental and genetic factors were secondary. All three eating behaviors were correlated with BMI (r = .19–.25). Nonshared environmental factors explained the covariations (Emotional eating–Uncontrolled eating: rE = .54, 95% CI [.43, .64]; BMI–Cognitive restraint: rE = .15, 95% CI [.01, .28]). In contrast to BMI, individual differences in eating behaviors are mostly explained by nonshared environmental factors, which also accounted for the phenotypic correlation between eating behaviors and BMI. Due to the sample size, analyses were underpowered to detect contributions of additive genetic or shared environmental factors to variation and covariation of the phenotypes. Although more research is granted, these results support that eating behaviors could be viable intervention targets to help individuals maintain a healthy weight.


2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Bojing Liu ◽  
Arvid Sjölander ◽  
Nancy L. Pedersen ◽  
Jonas F. Ludvigsson ◽  
Honglei Chen ◽  
...  

AbstractTo examine whether irritable bowel syndrome (IBS) was related to the future risk of Parkinson’s disease (PD), we conducted a nested case-control study in the Swedish total population including 56,564 PD cases identified from the Swedish Patient Register and 30 controls per case individually matched by sex and year of birth. Odds ratios (ORs) with 95% confidence intervals (CIs) for having a prior diagnosis of IBS were estimated using conditional logistic regression. We furthermore conducted a cohort study using the Swedish Twin Registry following 3046 IBS patients identified by self-reported abdominal symptoms and 41,179 non-IBS individuals. Through Cox proportional hazard models, we estimated hazard ratios (HRs) and 95% CIs for PD risk. In the nested case-control study, 253 (0.4%) PD cases and 5204 (0.3%) controls had a previous IBS diagnosis. IBS diagnosis was associated with a 44% higher risk of PD (OR = 1.44, 95% CI 1.27–1.63). Temporal relationship analyses showed 53% and 38% increased risk of PD more than 5 and 10 years after IBS diagnosis, respectively. In the cohort analysis based on the Swedish Twin Registry, there was no statistically significantly increased risk of PD related to IBS (HR = 1.25, 95% CI = 0.87–1.81). Our results suggest a higher risk of PD diagnosis after IBS. These results provide additional evidence supporting the importance of the gut–brain axis in PD.


1997 ◽  
Vol 81 (2) ◽  
pp. 635-639
Author(s):  
Motoko Hayashi ◽  
Isao Fukunishi

This study examined what kinds of social support are related to mood states in a sample of 50 HIV-positive patients without AIDS (46 men and 4 women; M age 36.5 yr., SD = 9.8). In the early stage of HIV infection, HIV patients without AIDS may be prone to depressive symptoms although none of these HIV-positive patients' symptoms fulfilled the DSM-III-R Mood Disorders including Major Depression. The depressive symptoms were not significantly related to lack of ordinary social support such as friends and family but were significantly associated with dissatisfaction with HIV/AIDS-related medical support


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