Evidence map›Paper›PMID 25008580›Full record

ArticleThe Journal of nutrition2014

Genetic variation in FADS1 has little effect on the association between dietary PUFA intake and cardiovascular disease.

Sophie Hellstrand, Ulrika Ericson, Bo Gullberg, Bo Hedblad, Marju Orho-Melander, Emily Sonestedt

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of nutrition, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 17% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 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

6 authors at 3 institutions in 4 countries.

Sophie HellstrandDiabetes and Cardiovascular Disease-Genetic Epidemiology sophie.hellstrand@med.lu.se.
Ulrika EricsonDiabetes and Cardiovascular Disease-Genetic Epidemiology.
Bo GullbergNutrition Epidemiology, and.
Bo HedbladCardiovascular Epidemiology, Department of Clinical Sciences in Malmö, Lund University, Lund, Sweden.
Marju Orho-MelanderDiabetes and Cardiovascular Disease-Genetic Epidemiology.
Emily SonestedtDiabetes and Cardiovascular Disease-Genetic Epidemiology.
Diabetes Australia · AULund University · SENutrition 21 (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The unclear link between intake of polyunsaturated fatty acids (PUFAs) and risk of cardiovascular disease (CVD) could depend on genetic differences between individuals. Minor alleles of single-nucleotide polymorphisms (SNPs) in the ∆5 fatty acid desaturase (FADS) 1 gene were associated with lower blood concentrations of long-chain ω-3 (n-3) and ω-6 (n-6) PUFAs, indicating an associated loss of function effect. We examined whether the SNP rs174546 in FADS1 modifies the association between PUFA intakes and CVD risk. We included 24,032 participants (62% women, aged 44-74 y) from the Malmö Diet and Cancer cohort without prevalent CVD and diabetes. During a mean follow-up of 14 y, 2648 CVD cases were identified. Diet was assessed by a modified diet history method. A borderline interaction was observed between the α-linolenic acid (ALA) (18:3n-3)-to-linoleic acid (LA) (18:2n-6) intake ratio and FADS1 genotype on CVD incidence (P = 0.06). The ALA-to-LA intake ratio was inversely associated with CVD risk only among participants homozygous for the minor T-allele (HR for quintile 5 vs. quintile 1 = 0.72; 95% CI: 0.50, 1.04; P-trend = 0.049). When excluding participants reporting unstable food habits in the past (35%), the interaction between the ALA-to-LA intake ratio and FADS1 genotype on CVD incidence was strengthened and statistically significant (P = 0.04). Additionally, we observed a significant interaction between ALA and FADS1 genotype on ischemic stroke incidence (P = 0.03). ALA was inversely associated with ischemic stroke only among TT genotype carriers (HR for quintile 5 vs. quintile 1 = 0.50; 95% CI: 0.27, 0.94; P-trend = 0.02). In this large cohort, we found some weak, but not convincing, evidence of effect modification by genetic variation in FADS1 on the associations between PUFA intakes and CVD risk. For the 11% of the population homozygous for the minor T-allele of rs174546 that associates with lower ∆5 FADS activity, high ALA intake and ALA-to-LA intake ratio may be preferable in the prevention of CVD and ischemic stroke.

Indexed as

DietPolymorphism, Single NucleotideAdultAgedAllelesalpha-Linolenic AcidCardiovascular DiseasesDelta-5 Fatty Acid DesaturaseDietary FatsDiet SurveysEnergy IntakeFatty Acid DesaturasesFeeding BehaviorFemaleGenotypeHumansalpha-Linolenic AcidDelta-5 Fatty Acid DesaturaseDietary FatsFADS1 protein, humanFatty Acid DesaturasesLinoleic Acid

Identifiers

PMID25008580
PMCPMC4130826
OpenAlexW2144828895

What OpenQuestion holds

Textmetadata
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.