Epidemiological Study of Parental Obstructive Sleep Apnea and Subsequent Risk of ADHD in Their Children: A Nationwide Population-Based Study
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Published on: December 6, 2016
Iwen Chen1, Jing-Yang Huang2, Renin Chang1
1Kaohsiung Veterans General Hospital.
Insights
Parental obstructive sleep apnea (OSA) may increase the risk of attention-deficit/hyperactivity disorder (ADHD) in children. This study found a significant association between parental OSA and offspring ADHD, suggesting a potential link requiring further investigation.
Area of Science:
- Pediatric Neurology
- Sleep Medicine
- Genetics and Genomics
Background:
- Obstructive sleep apnea (OSA) is linked to systemic inflammation and oxidative stress.
- These physiological changes may impact neurodevelopmental outcomes in children.
Purpose of the Study:
- To investigate the association between parental obstructive sleep apnea (OSA) and the risk of attention-deficit/hyperactivity disorder (ADHD) in offspring.
- To explore potential links between parental sleep disorders and neurodevelopmental conditions in children.
Main Methods:
- A nested case-control study utilizing Taiwan's National Birth Registry and National Health Insurance Research Database (2006-2015).
- Included 1,723,873 singleton live births, comparing children with ADHD to matched controls.
- Conditional logistic regression analysis was used to determine adjusted odds ratios (aOR).
Main Results:
- Offspring ADHD risk was elevated with paternal OSA (aOR: 1.758) and maternal OSA (aOR: 2.159).
- Subgroup analyses indicated varying effects of parental diseases based on the child's gender.
Conclusions:
- Parental OSA is associated with an increased risk of ADHD in children.
- Further research is warranted to elucidate the underlying mechanisms connecting parental OSA and childhood ADHD.
Objective:
Obstructive sleep apnea (OSA), with daytime drowsiness, nocturnal hypoxia, could result in systemic inflammation and oxidative damage. We hypothesize that parental OSA, with chronic systemic inflammation and oxidative stress, might contribute to children's neurodevelopmental disorders, such as ADHD.
Method:
By linking National Birth Registry with the National Health Insurance Research Database, Taiwan, we identified 2006-2015 birth cohort, which comprised 1,723,873 singleton live births, and conducted a nested case-control study. We included children with ADHD and compared them with non-ADHD controls matched with ADHD case on index date. Conditional logistic regression was utilized to calculate adjusted odds ratio (aOR) when investigating the association between parental diseases with risk of ADHD in their offspring.
Results:
The aOR (95% CI) of offspring's ADHD was 1.758 (1.458-2.119) with paternal OSA and 2.159 (1.442-3.233) with maternal OSA. The subgroup analysis revealed different effects of parental diseases among children's gender.
Conclusion:
Our study demonstrates an association in parental OSA and offspring ADHD, which could inspire further research to clarify the mechanisms.
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