Evidence map›Paper›PMID 31160693›Full record

ArticleMolecular psychiatry2021

Familial risk and heritability of diagnosed borderline personality disorder: a register study of the Swedish population.

Charlotte Skoglund, Annika Tiger, Christian Rück, Predrag Petrovic, Philip Asherson, Clara Hellner, David Mataix-Cols, Ralf Kuja-Halkola

Open access · hybridAbstract read
In one paragraph

Article in Molecular psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 3 pooled it
7.8field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

36 citing papers in PubMed, 3 syntheses or guidelines pooled it, 80 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Charlotte Skoglund *Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet, & Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden.
Annika Tiger *Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Christian RückCentre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet, & Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden.ORCID http://orcid.org/0000-0002-8742-0168
Predrag PetrovicDepartment of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Philip AshersonSocial, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology, and Neuroscience, King's College, London, UK.
Clara HellnerCentre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet, & Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden.
David Mataix-ColsCentre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet, & Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden.
Ralf Kuja-HalkolaDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. Ralf.Kuja-Halkola@ki.se.ORCID http://orcid.org/0000-0002-3765-2067
Stockholm County Council · SEKarolinska Institutet · SEKing's College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Family and twin studies of Borderline Personality Disorder (BPD) have found familial aggregation and genetic propensity for BPD, but estimates vary widely. Large-scale family studies of clinically diagnosed BPD are lacking. Therefore, we performed a total-population study estimating the familial aggregation and heritability of clinically diagnosed BPD. We followed 1,851,755 individuals born 1973-1993 in linked Swedish national registries. BPD-diagnosis was ascertained between 1997 and 2013, 11,665 received a BPD-diagnosis. We identified relatives and estimated sex and birth year adjusted hazard ratios, i.e., the rate of BPD-diagnoses in relatives to individuals with BPD-diagnosis compared to individuals with unaffected relatives, and used structural equation modeling to estimate heritability. The familial association decreased along with genetic relatedness. The hazard ratio was 11.5 (95% confidence interval (CI) = 1.6-83.8) for monozygotic twins; 7.4 (95% CI = 1.0-55.3) for dizygotic twins; 4.7 (95% CI = 3.9-5.6) for full siblings; 2.1 (95% CI = 1.5-3.0) for maternal half-siblings; 1.3 (95% CI = 0.9-2.1) for paternal half-siblings; 1.7 (95% CI = 1.4-2.0) for cousins whose parents were full siblings; 1.1 (95% CI = 0.7-1.8) for cousins whose parents were maternal half-siblings; and 1.9 (95% CI = 1.2-2.9) for cousins whose parents were paternal half-siblings. Heritability was estimated at 46% (95% CI = 39-53), and the remaining variance was explained by individually unique environmental factors. Our findings pave the way for further research into specific genetic variants, unique environmental factors implicated, and their interplay in risk for BPD.

Indexed as

Borderline Personality DisorderGenetic Predisposition to DiseaseHumansRegistriesRisk FactorsSwedenTwins, DizygoticTwins, Monozygotic

Identifiers

PMID31160693
PMCPMC7910208
OpenAlexW2948054808

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.