Familial co-aggregation of attention-deficit/hyperactivity disorder and autoimmune diseases

Introduction:The etiology of attention-deficit/hyperactivity disorder (ADHD) remains largely unknown. In later years, ADHD has been associated with several autoimmune diseases (AD) and traits, potentially reflecting common... [ view full abstract ]

Introduction:
The etiology of attention-deficit/hyperactivity disorder (ADHD) remains largely unknown. In later years, ADHD has been associated with several autoimmune diseases (AD) and traits, potentially reflecting common underlying mechanisms. Still, most studies have investigated intraindividual relationships that reveal little regarding etiology. In addition, some of the findings in previous studies have not been replicated in independent samples.

To further elucidate the relationship between autoimmunity and ADHD, we conducted a familial co-aggregation study using Swedish population-wide national registers.

Materials and methods:
We linked several Swedish population-wide national registries to define a birth cohort with their biological relatives and to identify the individuals who had been diagnosed with ADHD and ADs of interest. The base cohort included more than 5 million individuals born between 1960 and 2010. Logistic regression was used to investigate the associations between different ADs and ADHD, both within individuals, and across biological family members of differing relatedness. 

Results:
In the preliminary analyses, ADHD was in intraindividual models associated with several relatively common ADs with odds ratios (OR) in the range of 1.1 - 1.7, including, but not limited to celiac disease (OR = 1.19, 95% confidence interval = 1.12-1.28), psoriasis (OR = 1.48, 95%CI = 1.41-1.55), Sjögren’s disease (OR = 1.64; 95%CI = 1.27-2.12), and type 1 diabetes mellitus (OR = 1.32, 95%CI = 1.24-1.41). Moreover, results supporting familial co-aggregation, with attenuation of the association estimates with decreasing relatedness, were noted for several offspring ADHD – relative AD-relationships. For example ADHD was more strongly associated with psoriasis in full siblings (OR = 1.26, 95%CI = 1.20-1.32) than full cousins (OR = 1.07, 95%CI = 1.04-1.09). Though this was not the case for all ADHD-AD associations.

Discussion and conclusion:
Our study supports some of the previous findings on the intraindividual associations between ADHD and ADs, and also indicate that there could be common underlying genetic architecture between ADHD and some of the ADs. However, the absence of clear familial co-aggregation for many ADHD-AD associations dissuades us from stating general conclusions regarding common genetic risk factors between ADHD and ADs. (We aim to present replication of some our findings with the use of similar Norwegian register data).