The role of thyroid function in borderline personality disorder and schizophrenia: a Mendelian Randomisation study

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2024年2月15日

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Oladapo Babajide,
Alisa D. Kjaergaard,
Weichen Deng,
Aleksander Kuś,
Rosalie B. T. M. Sterenborg,
Bjørn Olav Åsvold,
Stephen Burgess,
Alexander Teumer,
Marco Medici,
Christina Ellervik,
Bass Nick,
Panos Deloukas,
Eirini Marouli

摘要

Background

Genome-wide association studies have reported a genetic overlap between borderline personality disorder (BPD) and schizophrenia (SCZ). Epidemiologically, the direction and causality of the association between thyroid function and risk of BPD and SCZ are unclear. We aim to test whether genetically predicted variations in TSH and FT4 levels or hypothyroidism are associated with the risk of BPD and SCZ.

Methods

We employed Mendelian Randomisation (MR) analyses using genetic instruments associated with TSH and FT4 levels as well as hypothyroidism to examine the effects of genetically predicted thyroid function on BPD and SCZ risk. Bidirectional MR analyses were employed to investigate a potential reverse causal association.

Results

Genetically predicted higher FT4 was not associated with the risk of BPD (OR: 1.18; P = 0.60, IVW) or the risk of SCZ (OR: 0.93; P = 0.19, IVW). Genetically predicted higher TSH was not associated with the risk of BPD (OR: 1.11; P = 0.51, IVW) or SCZ (OR: 0.98, P = 0.55, IVW). Genetically predicted hypothyroidism was not associated with BPD or SCZ. We found no evidence for a reverse causal effect between BPD or SCZ on thyroid function.

Conclusions

We report evidence for a null association between genetically predicted FT4, TSH or hypothyroidism with BPD or SCZ risk. There was no evidence for reverse causality.