Evidence map›Paper›PMID 27465381›Full record

ArticleThe American journal of clinical nutrition2016

Sugar-sweetened beverage consumption and genetic predisposition to obesity in 2 Swedish cohorts.

Louise Brunkwall, Yan Chen, George Hindy, Gull Rukh, Ulrika Ericson, Inês Barroso, Ingegerd Johansson, Paul W Franks, Marju Orho-Melander, Frida Renström

Abstract read
In one paragraph

Article in The American journal of clinical nutrition, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 4 pooled it
–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

41 citing papers in PubMed, 4 syntheses or guidelines pooled it.

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  3. Associations ofNutrients · 2019
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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

10 authors.

Louise BrunkwallDiabetes and Cardiovascular Disease-Genetic Epidemiology and.
Yan ChenGenetic and Molecular Epidemiology Unit, Department of Clinical Sciences, Lund University, Malmö, Sweden;
George HindyDiabetes and Cardiovascular Disease-Genetic Epidemiology and.
Gull RukhDiabetes and Cardiovascular Disease-Genetic Epidemiology and.
Ulrika EricsonDiabetes and Cardiovascular Disease-Genetic Epidemiology and.
Inês BarrosoNational Institute for Health Research Cambridge Biomedical Research Centre and University of Cambridge, Metabolic Research Laboratories, Institute of Metabolic Science, Addenbrooke's Hospital, Cambridge, United Kingdom; Wellcome Trust Sanger Institute, Cambridge, United Kingdom;
Ingegerd JohanssonDepartments of Odontology.
Paul W FranksGenetic and Molecular Epidemiology Unit, Department of Clinical Sciences, Lund University, Malmö, Sweden; Public Health and Clinical Medicine, Section for Medicine, and Department of Nutrition, Harvard School of Public Health, Boston, MA.
Marju Orho-MelanderDiabetes and Cardiovascular Disease-Genetic Epidemiology and.
Frida RenströmGenetic and Molecular Epidemiology Unit, Department of Clinical Sciences, Lund University, Malmö, Sweden; Biobank Research, Umeå University, Umeå, Sweden; and frida.renstrom@med.lu.se.

Funding

Wellcome Trust
6 · The paper itself

Abstract

backgroundThe consumption of sugar-sweetened beverages (SSBs), which has increased substantially during the last decades, has been associated with obesity and weight gain.

objectiveCommon genetic susceptibility to obesity has been shown to modify the association between SSB intake and obesity risk in 3 prospective cohorts from the United States. We aimed to replicate these findings in 2 large Swedish cohorts.

designData were available for 21,824 healthy participants from the Malmö Diet and Cancer study and 4902 healthy participants from the Gene-Lifestyle Interactions and Complex Traits Involved in Elevated Disease Risk Study. Self-reported SSB intake was categorized into 4 levels (seldom, low, medium, and high). Unweighted and weighted genetic risk scores (GRSs) were constructed based on 30 body mass index [(BMI) in kg/m(2)]-associated loci, and effect modification was assessed in linear regression equations by modeling the product and marginal effects of the GRS and SSB intake adjusted for age-, sex-, and cohort-specific covariates, with BMI as the outcome. In a secondary analysis, models were additionally adjusted for putative confounders (total energy intake, alcohol consumption, smoking status, and physical activity).

resultsIn an inverse variance-weighted fixed-effects meta-analysis, each SSB intake category increment was associated with a 0.18 higher BMI (SE = 0.02; P = 1.7 × 10(-20); n = 26,726). In the fully adjusted model, a nominal significant interaction between SSB intake category and the unweighted GRS was observed (P-interaction = 0.03). Comparing the participants within the top and bottom quartiles of the GRS to each increment in SSB intake was associated with 0.24 (SE = 0.04; P = 2.9 × 10(-8); n = 6766) and 0.15 (SE = 0.04; P = 1.3 × 10(-4); n = 6835) higher BMIs, respectively.

conclusionsThe interaction observed in the Swedish cohorts is similar in magnitude to the previous analysis in US cohorts and indicates that the relation of SSB intake and BMI is stronger in people genetically predisposed to obesity.

Indexed as

Genetic LociGenetic Predisposition to DiseasePolymorphism, Single NucleotideBeveragesBody Mass IndexCarbonated BeveragesCohort StudiesConfounding Factors, EpidemiologicCross-Sectional StudiesDietary CarbohydratesDiet RecordsFemaleFruit and Vegetable JuicesGenetic Association StudiesHumansMaleDietary CarbohydratesBMIgene-lifestyle interactiongenetic risk scoresugar-sweetened beverageSweden

Identifiers

PMID27465381
PMCPMC4997292

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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.