Are children with attention-deficit/
hyperactivity disorder (ADHD) more
likely to develop celiac disease?
A prospective study

Mohammadi, Mohammad Hasan; Hesaraki, Mehran

doi:10.5114/ppn.2023.127573

Cited by 1 publication

(2 citation statements)

References 29 publications

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“…For instance, in the case of CeD, diagnostic information encompassed not only clinical s y m p t o m a t o l o g y a n d s e r o l o g i c a l m a r k e r s b u t a l s o histopathological identification (24,26). On the other hand, some past studies might have just used quick diagnostic tests for CeD in the absence of such thorough diagnostic protocols (57,58).…”

Section: Discussionmentioning

confidence: 99%

“…(iv) The disparities in our study findings compared to previous research linking CeD and ADHD may stem from differences in population inclusion and diagnostic criteria for the disease. Our study encompassed a broad spectrum of European countries, incorporating various European ethnic groups, whereas previous studies often focused on large cohorts within a single country or non-European populations ( 17 , 18 , 57 ). Furthermore, the GWAS database we used for our research followed strict guidelines for selecting case samples.…”

Section: Discussionmentioning

confidence: 99%

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Celiac disease and attention-deficit/hyperactivity disorder: a bidirectional Mendelian randomization analysis

Chen,

Zhu,

et al. 2024

Front. Psychiatry

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BackgroundRecent observational research suggests a potential link between celiac disease (CeD) and an increased incidence of attention-deficit/hyperactivity disorder (ADHD). However, the genetic relationship between CeD and ADHD remains unclear. In order to assess the potential genetic causality between these two conditions, we conducted a Mendelian randomization (MR) analysis.MethodsWe performed a bidirectional MR analysis to investigate the relationship between CeD and ADHD. We carefully selected single nucleotide polymorphisms (SNPs) from publicly available large-scale genome-wide association studies (GWAS) databases, employing rigorous quality screening criteria. MR estimates were obtained using four different methods: fixed-effect inverse variance weighted (fe-IVW), random-effect inverse variance weighting (re-IVW), weighted median (WM), and MR-Egger. The robustness and reliability of our findings were confirmed through sensitivity analyses, assessment of instrumental variable (IV) strength (F-statistic), and statistical power calculations.ResultsOur MR analyses did not reveal any significant genetic associations between CeD and ADHD (fe-IVW: OR = 1.003, 95% CI = 0.932–1.079, P = 0.934). Similarly, in the reverse direction analysis, we found no evidence supporting a genetic relationship between ADHD and CeD (fe-IVW: OR = 0.850, 95% CI = 0.591–1.221, P = 0.378). Various MR approaches consistently yielded similar results. Sensitivity analysis indicated the absence of significant horizontal pleiotropy or heterogeneity. However, it’s important to note that the limited statistical power of our study may have constrained the causal analysis of the exposure’s influence on the outcome.ConclusionsOur findings do not provide compelling evidence for a genetic association between CeD and ADHD within the European population. While the statistical power of our study was limited, future MR research could benefit from larger-scale datasets or datasets involving similar traits. To validate our results in real-world scenarios, further mechanistic studies, large-sample investigations, multicenter collaborations, and longitudinal studies are warranted.

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