Evidence map›Paper›PMID 36807592›Full record

ArticleScientific reports2023

The necessity of incorporating non-genetic risk factors into polygenic risk score models.

Sipko van Dam, Pytrik Folkertsma, Jose Castela Forte, Dylan H de Vries, Camila Herrera Cunillera, Rahul Gannamani, Bruce H R Wolffenbuttel

Abstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
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  5. The Early-Onset Alzheimer's Disease Whole-Genome Sequencing Project: Study design and methodology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023
    Article
  6. Review
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

7 authors.

Sipko van Dam *Department of Endocrinology, University of Groningen, University Medical Center Groningen, P.O. Box 30001, 9700 RB, Groningen, The Netherlands. Sipkovandam@gmail.com.
Pytrik Folkertsma *Department of Endocrinology, University of Groningen, University Medical Center Groningen, P.O. Box 30001, 9700 RB, Groningen, The Netherlands.
Jose Castela ForteAncora Health B.V., Herestraat 106, 9711 LM, Groningen, The Netherlands.
Dylan H de VriesDepartment of Endocrinology, University of Groningen, University Medical Center Groningen, P.O. Box 30001, 9700 RB, Groningen, The Netherlands.
Camila Herrera CunilleraDepartment of Endocrinology, University of Groningen, University Medical Center Groningen, P.O. Box 30001, 9700 RB, Groningen, The Netherlands.
Rahul GannamaniAncora Health B.V., Herestraat 106, 9711 LM, Groningen, The Netherlands.
Bruce H R WolffenbuttelDepartment of Endocrinology, University of Groningen, University Medical Center Groningen, P.O. Box 30001, 9700 RB, Groningen, The Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The growing public interest in genetic risk scores for various health conditions can be harnessed to inspire preventive health action. However, current commercially available genetic risk scores can be deceiving as they do not consider other, easily attainable risk factors, such as sex, BMI, age, smoking habits, parental disease status and physical activity. Recent scientific literature shows that adding these factors can improve PGS based predictions significantly. However, implementation of existing PGS based models that also consider these factors requires reference data based on a specific genotyping chip, which is not always available. In this paper, we offer a method naïve to the genotyping chip used. We train these models using the UK Biobank data and test these externally in the Lifelines cohort. We show improved performance at identifying the 10% most at-risk individuals for type 2 diabetes (T2D) and coronary artery disease (CAD) by including common risk factors. Incidence in the highest risk group increases from 3.0- and 4.0-fold to 5.8 for T2D, when comparing the genetics-based model, common risk factor-based model and combined model, respectively. Similarly, we observe an increase from 2.4- and 3.0-fold to 4.7-fold risk for CAD. As such, we conclude that it is paramount that these additional variables are considered when reporting risk, unlike current practice with current available genetic tests.

Indexed as

Coronary Artery DiseaseDiabetes Mellitus, Type 2Genetic Predisposition to DiseaseGenetic TestingHumansRisk Factors

Identifiers

PMID36807592
PMCPMC9941118

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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.