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

Borderline Personality Disorder FT4 Mendelian Randomisation Schizophrenia TSH Thyroid function

Journal

Borderline personality disorder and emotion dysregulation
ISSN: 2051-6673
Titre abrégé: Borderline Personal Disord Emot Dysregul
Pays: England
ID NLM: 101650634

Informations de publication

Date de publication:
15 Feb 2024
Historique:
received: 08 08 2023
accepted: 20 01 2024
medline: 15 2 2024
pubmed: 15 2 2024
entrez: 14 2 2024
Statut: epublish

Résumé

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. 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. 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. 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.

Sections du résumé

BACKGROUND 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 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 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 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.

Identifiants

DOI: 10.1186/s40479-024-00246-3 PMID: 38355654
pubmed: 38355654
doi: 10.1186/s40479-024-00246-3
pii: 10.1186/s40479-024-00246-3
doi:

Types de publication

Journal Article

Langues

eng

Pagination

2

Informations de copyright

© 2024. The Author(s).

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Auteurs

Oladapo Babajide (O)

Queen Mary University of London, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, London, UK.

Alisa D Kjaergaard (AD)

Aarhus University Hospital, Steno Diabetes Center, Hedeager Aarhus, Denmark.

Weichen Deng (W)

Queen Mary University of London, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, London, UK.

Aleksander Kuś (A)

Department of Internal Medicine and Endocrinology, Medical University of Warsaw, Warsaw, Poland.

Rosalie B T M Sterenborg (RBTM)

Erasmus Medical Center, Academic Center for Thyroid Diseases, Department of Internal Medicine, Rotterdam, Netherlands.
Erasmus Medical Center, Department of Epidemiology, Rotterdam, Netherlands.
Department of Internal Medicine, Radboud University Medical Center, Nijmegen, Netherlands.

Bjørn Olav Åsvold (BO)

Department of Public Health and Nursing, Department of Endocrinology, Clinic of Medicine, NTNU, Norwegian University of Science and Technology &, St. Olavs Hospital, Trondheim University Hospital, Trondheim, Norway.

Stephen Burgess (S)

University of Cambridge, MRC Biostatistics Unit, Cambridge Institute of Public Health, Cambridge, UK.
Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK.

Alexander Teumer (A)

Institute of Community Medicine, University Medicine Greifswald, Greifswald, Germany.
DZHK German Center for Cardiovascular Research, Berlin, Germany.

Marco Medici (M)

Erasmus Medical Center, Academic Center for Thyroid Diseases, Department of Internal Medicine, Rotterdam, Netherlands.

Christina Ellervik (C)

Department of Laboratory Medicine, Boston Children's Hospital, Boston, MA, USA.
Department of Pathology, Harvard Medical School, Boston, MA, USA.
Faculty of Health and Medical Sciences, Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark.

Bass Nick (B)

Division of Psychiatry, University College London, Mental Health Neuroscience, London, UK.

Panos Deloukas (P)

Queen Mary University of London, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, London, UK.

Eirini Marouli (E)

Queen Mary University of London, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, London, UK. e.marouli@qmul.ac.uk.

Classifications MeSH