Evidence map›Paper›PMID 26354530›Full record

Trial reportThe American journal of clinical nutrition2015

Dietary inflammatory index and telomere length in subjects with a high cardiovascular disease risk from the PREDIMED-NAVARRA study: cross-sectional and longitudinal analyses over 5 y.

Sonia García-Calzón, Guillermo Zalba, Miguel Ruiz-Canela, Nitin Shivappa, James R Hébert, J Alfredo Martínez, Montserrat Fitó, Enrique Gómez-Gracia, Miguel A Martínez-González, Amelia Marti

Open access · bronzeAbstract readRandomized Controlled Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in The American journal of clinical nutrition, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 8 pooled it
14.2field-weighted citation impact, top 1% 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

65 citing papers in PubMed, 8 syntheses or guidelines pooled it, 135 citations in OpenAlex.

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5 more citing papers are in PubMed but not listed here.

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 at 5 institutions in 2 countries.

Sonia García-CalzónDepartments of Nutrition, Food Science and Physiology, Navarra Institute for Health Research, Pamplona, Spain;
Guillermo ZalbaBiochemistry and Genetics, and Navarra Institute for Health Research, Pamplona, Spain;
Miguel Ruiz-CanelaPreventive Medicine and Public Health and Navarra Institute for Health Research, Pamplona, Spain; Center of Biomedical Research in Physiopathology of Obesity and Nutrition (CIBEROBN), Institute of Health Carlos III, Madrid, Spain;
Nitin ShivappaCancer Prevention and Control Program and Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC;
James R HébertCancer Prevention and Control Program and Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC;
J Alfredo MartínezDepartments of Nutrition, Food Science and Physiology, Centre for Nutrition Research, University of Navarra, Pamplona, Spain; Navarra Institute for Health Research, Pamplona, Spain; Center of Biomedical Research in Physiopathology of Obesity and Nutrition (CIBEROBN), Institute of Health Carlos III, Madrid, Spain;
Montserrat FitóCenter of Biomedical Research in Physiopathology of Obesity and Nutrition (CIBEROBN), Institute of Health Carlos III, Madrid, Spain; Cardiovascular Risk and Nutrition Research Group (Regicor Study Group), Barcelona, Spain; and.
Enrique Gómez-GraciaDepartment of Preventive Medicine, University of Malaga, Malaga, Spain.
Miguel A Martínez-GonzálezPreventive Medicine and Public Health and Navarra Institute for Health Research, Pamplona, Spain; Center of Biomedical Research in Physiopathology of Obesity and Nutrition (CIBEROBN), Institute of Health Carlos III, Madrid, Spain;
Amelia MartiDepartments of Nutrition, Food Science and Physiology, Navarra Institute for Health Research, Pamplona, Spain; Center of Biomedical Research in Physiopathology of Obesity and Nutrition (CIBEROBN), Institute of Health Carlos III, Madrid, Spain; amarti@unav.es.
Instituto de Salud Carlos III · ESUniversity of South Carolina · USNavarre Institute of Health Research · ESUniversidad de Málaga · ESUniversidad de Navarra · ES

Funding

Developing the Dietary Inflammatory Index for Clinical ApplicationR44DK103377 · NIDDK · CONNECTING HEALTH INNOVATIONS, LLC · PI SHIVAPPA, NITIN, WIRTH, MICHAEL DAVID · 2014 to 2016
$1.8M
NIDDK NIH HHS R44DK103377
6 · The paper itself

Abstract

backgroundDietary factors can affect telomere length (TL), a biomarker of aging, through oxidation and inflammation-related mechanisms. A Dietary Inflammatory Index (DII) could help to understand the effect of the inflammatory potential of the diet on telomere shortening.

objectiveThis study aimed to determine the association of the DII with TL and to examine whether diet-associated inflammation could modify the telomere attrition rate after a 5-y follow-up of a Mediterranean dietary intervention.

designThis was a prospective study of 520 participants at high cardiovascular disease risk (mean ± SD age: 67.0 ± 6.0 y, 45% males) from the PREDIMED-NAVARRA (PREvención con DIeta MEDiterránea-NAVARRA) trial. Leukocyte TL was measured by quantitative real-time polymerase chain reaction at baseline and after 5 y of follow-up. The DII was calculated from self-reported data by using a validated 137-item food-frequency questionnaire.

resultsLonger telomeres at baseline were found in participants who had a more anti-inflammatory diet (lowest DII score) (P-trend = 0.012). Longitudinal analyses further showed that a greater anti-inflammatory potential of the diet (i.e., a decrease in the DII) could significantly slow down the rate of telomere shortening. Moreover, the multivariable-adjusted OR for short telomeres (z score ≤20th percentile) was 1.80 (95% CI: 1.03, 3.17) in a comparison between the highest (proinflammatory) and the lowest (anti-inflammatory) DII tertiles. Similarly, a greater DII (greatest proinflammatory values) after a 5-y follow-up was associated with almost a 2-fold higher risk of accelerated telomere attrition compared with the highest decrease in DII (greatest anti-inflammatory values) during this period (P-trend = 0.025).

conclusionsThis study showed both cross-sectional and longitudinal associations between the inflammatory potential of the diet and telomere shortening in subjects with a high cardiovascular disease risk. Our findings are consistent with, but do not show, a beneficial effect of adherence to an anti-inflammatory diet on aging and health by slowing down telomere shortening. These results suggest that diet might play a key role as a determinant of TL through proinflammatory or anti-inflammatory mechanisms. This trial was registered at controlled-trials.com as ISRCTN35739639.

Indexed as

Feeding BehaviorAgedAged, 80 and overAgingBody Mass IndexCardiovascular DiseasesCholesterol, HDLCholesterol, LDLCross-Sectional StudiesDietary CarbohydratesDietary FatsDietary ProteinsDiet, Fat-RestrictedDiet, MediterraneanEnergy IntakeFemaleCholesterol, HDLCholesterol, LDLDietary CarbohydratesDietary FatsDietary ProteinsGenetic MarkersMicronutrientsOlive OilTriglyceridesagingcardiovascular diseasedietinflammationtelomeres

Identifiers

PMID26354530
PMCPMC4588745
OpenAlexW2138684035

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.