Evidence mapPaperPMID 29796113Full record

ArticleGenes & nutrition2018

Dietary and genetic risk scores and incidence of type 2 diabetes.

Ulrika Ericson, George Hindy, Isabel Drake, Christina-Alexandra Schulz, Louise Brunkwall, Sophie Hellstrand, Peter Almgren, Marju Orho-Melander

Open access · goldAbstract read
In one paragraph

Article in Genes & nutrition, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Gene-lifestyle interaction on risk of type 2 diabetes: A systematic review.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2019
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  11. Tolerable upper intake level for dietary sugars.EFSA journal. European Food Safety Authority · 2022
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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 1 institution in 1 country.

Ulrika Ericson1Diabetes and Cardiovascular Disease, Genetic Epidemiology, Department of Clinical Sciences, Malmö, Lund University, Malmö, Sweden.ORCID 0000-0003-4629-4318
George Hindy1Diabetes and Cardiovascular Disease, Genetic Epidemiology, Department of Clinical Sciences, Malmö, Lund University, Malmö, Sweden.
Isabel Drake1Diabetes and Cardiovascular Disease, Genetic Epidemiology, Department of Clinical Sciences, Malmö, Lund University, Malmö, Sweden.
Christina-Alexandra Schulz1Diabetes and Cardiovascular Disease, Genetic Epidemiology, Department of Clinical Sciences, Malmö, Lund University, Malmö, Sweden.
Louise Brunkwall1Diabetes and Cardiovascular Disease, Genetic Epidemiology, Department of Clinical Sciences, Malmö, Lund University, Malmö, Sweden.
Sophie Hellstrand1Diabetes and Cardiovascular Disease, Genetic Epidemiology, Department of Clinical Sciences, Malmö, Lund University, Malmö, Sweden.
Peter Almgren1Diabetes and Cardiovascular Disease, Genetic Epidemiology, Department of Clinical Sciences, Malmö, Lund University, Malmö, Sweden.
Marju Orho-Melander1Diabetes and Cardiovascular Disease, Genetic Epidemiology, Department of Clinical Sciences, Malmö, Lund University, Malmö, Sweden.
Malmö University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBoth lifestyle and genetic predisposition determine the development of type 2 diabetes (T2D), and studies have indicated interactions between specific dietary components and individual genetic variants. However, it is unclear whether the importance of overall dietary habits, including T2D-related food intakes, differs depending on genetic predisposition to T2D. We examined interaction between a genetic risk score for T2D, constructed from 48 single nucleotide polymorphisms identified in genome-wide association studies, and a diet risk score of four foods consistently associated with T2D in epidemiological studies (processed meat, sugar-sweetened beverages, whole grain and coffee). In total, 25,069 individuals aged 45-74 years with genotype information and without prevalent diabetes from the Malmö Diet and Cancer cohort (1991-1996) were included. Diet data were collected with a modified diet history method.

resultsDuring 17-year follow-up, 3588 incident T2D cases were identified. Both the diet risk score (HR in the highest risk category 1.40; 95% CI 1.26, 1.58;

conclusionsThe findings thus show that both genetic heredity and dietary habits previously associated with T2D add to the risk of T2D, but they seem to act in an independent fashion, with the consequence that all individuals, whether at high or low genetic risk, would benefit from favourable food choices.

Indexed as

Cohort studyDietFood intakeGene-environment interactionsType 2 diabetes

Identifiers

PMID29796113
PMCPMC5956794
OpenAlexW2806213947

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.