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Newborn thyroxine levels and childhood ADHD
Offie Porat Soldin1, Arvind K N Nandedkar, Knoxley M Japal
1Consultants in Epidemiology and Occupational Health, Inc., 2428 Wisconsin Avenue, N.W., Washington, DC 20007, USA. offie@ceoh.com
Insights
Neonatal thyroxine levels do not indicate prenatal thyroid issues in children who later develop Attention Deficit Hyperactivity Disorder (ADHD). This study found no link between newborn thyroid status and ADHD diagnosis, suggesting it
Area of Science:
- Neurodevelopmental disorders
- Endocrinology
- Pediatric health
Background:
- Normal brain development relies on sufficient iodine and thyroid hormone.
- Prenatal thyroid endocrine disruption is hypothesized to contribute to Attention Deficit Hyperactivity Disorder (ADHD).
Purpose of the Study:
- To investigate the association between neonatal thyroxine levels and the subsequent development of ADHD.
- To determine if neonatal thyroxine levels serve as a biomarker for prenatal thyroid status in relation to ADHD.
Main Methods:
- A matched case-control study design was employed.
- Cases were children diagnosed with ADHD; controls were children born in the same hospital on the same day.
- Conditional logistic regression analysis was used.
Main Results:
- Neonatal thyroxine levels were within normal ranges for all children.
- There was no significant difference in the distribution of neonatal thyroxine levels between children who developed ADHD and their matched controls.
Conclusions:
- Children diagnosed with ADHD do not exhibit evidence of prenatal thyroid dysfunction based on newborn thyroxine levels.
- Neonatal thyroxine levels are not a reliable biomarker for predicting the subsequent development of ADHD.
Objectives:
Normal brain development is highly dependent on adequate levels of iodine and thyroid hormone. It has been suggested that Attention Deficit Hyperactivity Disorder (ADHD) is the consequence of prenatal thyroidal endocrine disruption. The hypothesis was examined using neonatal thyroxine levels as a bio-marker of prenatal thyroid status and comparing it to subsequent development of ADHD.
Design And Methods:
In a matched case-control study, cases were defined as children diagnosed with ADHD, while children born in the same hospital and tested on the same day served as matched controls. Conditional logistic regression analysis with unequal numbers of controls was performed.
Results:
The neonatal thyroxine levels were within normal limits for each of the children who were subsequently diagnosed as having ADHD, and their distribution was no different from that of their controls.
Conclusions:
Children diagnosed with ADHD do not demonstrate prenatal thyroidal dysfunction as reflected in the newborn thyroxine levels, therefore neonatal thyroxine levels are not a bio-marker for the subsequent development of ADHD.