Evidence mapPaperPMID 37953248Full record

ArticleBMC medicine2023

Advancing the communication of genetic risk for cardiometabolic diseases: a critical interpretive synthesis.

Jing Hui Law, Najia Sultan, Sarah Finer, Nina Fudge

Abstract read
In one paragraph

Article in BMC medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
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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

4 authors.

Jing Hui LawCentre for Primary Care, Wolfson Institute of Population Health, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK. jing.law@qmul.ac.uk.ORCID 0000-0002-3080-9623
Najia SultanCentre for Primary Care, Wolfson Institute of Population Health, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Sarah FinerCentre for Primary Care, Wolfson Institute of Population Health, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Nina FudgeCentre for Primary Care, Wolfson Institute of Population Health, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.

Funding

Wellcome TrustWellcome Trust 218584/Z/19/Z
6 · The paper itself

Abstract

backgroundGenetics play an important role in risk for cardiometabolic diseases-including type 2 diabetes, cardiovascular disease and obesity. Existing research has explored the clinical utility of genetic risk tools such as polygenic risk scores-and whether interventions communicating genetic risk information using these tools can impact on individuals' cognitive appraisals of disease risk and/or preventative health behaviours. Previous systematic reviews suggest mixed results. To expand current understanding and address knowledge gaps, we undertook an interpretive, reflexive method of evidence synthesis-questioning the theoretical basis behind current interventions that communicate genetic risk information and exploring how the effects of genetic risk tools can be fully harnessed for cardiometabolic diseases.

methodsWe obtained 189 records from a combination of database, website and grey literature searches-supplemented with reference chaining and expert subject knowledge within the review team. Using pre-defined critical interpretive synthesis methods, quantitative and qualitative evidence was synthesised and critiqued alongside theoretical understanding from surrounding fields of behavioural and social sciences.

findingsExisting interventions communicating genetic risk information focus predominantly on the "self", targeting individual-level cognitive appraisals, such as perceived risk and perceived behavioural control. This approach risks neglecting the role of contextual factors and upstream determinants that can reinforce individuals' interpretations of risk. It also assumes target populations to embody an "ascetic subject of compliance"-the idea of a patient who strives to comply diligently with professional medical advice, logically and rationally adopting any recommended lifestyle changes. We developed a synthesising argument-"beyond the ascetic subject of compliance"-grounded in three major limitations of this perspective: (1) difficulty applying existing theories/models to diverse populations, (2) the role of familial variables and (3) the need for a life course perspective.

conclusionsInterventions communicating genetic risk information should account for wider influences that can affect individuals' responses to risk at different levels-including through interactions with their family systems, socio-cultural environments and wider health provision. PROTOCOL REGISTRATION: PROSPERO CRD42021289269.

Indexed as

Diabetes Mellitus, Type 2CommunicationHumansLife StylePatient ComplianceRisk FactorsCardiometabolic diseasesCardiovascular diseaseCognitive appraisalsFamily historyGenetic riskHealth behavioursObesityPolygenic risk scoresRisk perceptionsType 2 diabetes

Identifiers

PMID37953248
PMCPMC10641935

What Socratic holds

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Registered trials

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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 Socratic graph.