2021 ◽  
Vol 84 ◽  
pp. 106961
Author(s):  
Lauren Micalizzi ◽  
Kristine Marceau ◽  
Allison S. Evans ◽  
Leslie A. Brick ◽  
Rohan H.C. Palmer ◽  
...  

2011 ◽  
Vol 168 (12) ◽  
pp. 1286-1294 ◽  
Author(s):  
Manuela Heins ◽  
Claudia Simons ◽  
Tineke Lataster ◽  
Stefanie Pfeifer ◽  
Dagmar Versmissen ◽  
...  

2014 ◽  
Vol 20 (14) ◽  
pp. 1881-1891 ◽  
Author(s):  
Viktoria Johansson ◽  
Cecilia Lundholm ◽  
Jan Hillert ◽  
Thomas Masterman ◽  
Paul Lichtenstein ◽  
...  

Background: Psychiatric disorders are known to be prevalent in multiple sclerosis (MS). Objective: The objective of this paper is to study comorbidity between MS and bipolar disorder, schizophrenia and depression in a nationwide cohort and to determine whether shared genetic liability underlies the putative association. Methods: We identified ICD-diagnosed patients with MS ( n = 16,467), bipolar disorder ( n = 30,761), schizophrenia ( n = 22,781) and depression ( n = 172,479) in the Swedish National Patient Register and identified their siblings in the Multi-Generation Register. The risk of MS was compared in psychiatric patients and in matched unexposed individuals. Shared familial risk between MS and psychiatric disorders was estimated by sibling comparison. Results: The risk of MS was increased in patients with bipolar disorder (hazard ratio (HR) 1.8, 95% confidence interval (CI) 1.6–2.2, p < 0.0001) and depression (HR 1.9, 95% CI 1.7–2.0, p < 0.0001). MS risk in schizophrenia was decreased (HR 0.6, 95% CI 0.4–0.9, p = 0.005). The association between having a sibling with a psychiatric disorder and developing MS was not significant. Conclusion: We found a strong positive association between MS and bipolar disorder and depression that could not be explained by genetic liability. The unexpected negative association between MS and schizophrenia might be spurious or indicate possible protective mechanisms that warrant further exploration.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
David Carslake ◽  
Per Tynelius ◽  
Gerard J. van den Berg ◽  
George Davey Smith

AbstractPeople are having children later in life. The consequences for offspring adult survival have been little studied due to the need for long follow-up linked to parental data and most research has considered offspring survival only in early life. We used Swedish registry data to examine all-cause and cause-specific adult mortality (293,470 deaths among 5,204,433 people, followed up to a maximum of 80 years old) in relation to parental age. For most common causes of death adult survival was improved in the offspring of older parents (HR for all-cause survival was 0.96 (95% CI: 0.96, 0.97) and 0.98 (0.97, 0.98) per five years of maternal and paternal age, respectively). The childhood environment provided by older parents may more than compensate for any physiological disadvantages. Within-family analyses suggested stronger benefits of advanced parental age. This emphasises the importance of secular trends; a parent’s later children were born into a wealthier, healthier world. Sibling-comparison analyses can best assess individual family planning choices, but our results suggested a vulnerability to selection bias when there is extensive censoring. We consider the numerous causal and non-causal mechanisms which can link parental age and offspring survival, and the difficulty of separating them with currently available data.


2013 ◽  
Vol 177 (7) ◽  
pp. 638-644 ◽  
Author(s):  
Johan Håkon Bjørngaard ◽  
Ottar Bjerkeset ◽  
Lars Vatten ◽  
Imre Janszky ◽  
David Gunnell ◽  
...  

2018 ◽  
Vol 188 (1) ◽  
pp. 22-23
Author(s):  
Annette K Regan ◽  
Stephen J Ball ◽  
Joshua L Warren ◽  
Eva Malacova ◽  
Cicely Marston ◽  
...  

2014 ◽  
Vol 205 (5) ◽  
pp. 355-361 ◽  
Author(s):  
Quetzal A. Class ◽  
Martin E. Rickert ◽  
Henrik Larsson ◽  
Paul Lichtenstein ◽  
Brian M. D'Onofrio

BackgroundIt is unclear whether associations between fetal growth and psychiatric and socioeconomic problems are consistent with causal mechanisms.AimsTo estimate the extent to which associations are a result of unmeasured confounding factors using a sibling-comparison approach.MethodWe predicted outcomes from continuously measured birth weight in a Swedish population cohort (n = 3 291 773), while controlling for measured and unmeasured confounding.ResultsIn the population, lower birth weight (⩽2500 g) increased the risk of all outcomes. Sibling-comparison models indicated that lower birth weight independently predicted increased risk for autism spectrum disorder (hazard ratio for low birth weight = 2.44, 95% CI 1.99–2.97) and attention-deficit hyperactivity disorder. Although attenuated, associations remained for psychotic or bipolar disorder and educational problems. Associations with suicide attempt, substance use problems and social welfare receipt, however, were fully attenuated in sibling comparisons.ConclusionsResults suggest that fetal growth, and factors that influence it, contribute to psychiatric and socioeconomic problems.


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