Evidence map›Paper›PMID 19037211›Full record

ArticleObesity (Silver Spring, Md.)2008

Genotype-phenotype associations: modulation by diet and obesity.

Jose M Ordovas

Open access · greenAbstract read
In one paragraph

Article in Obesity (Silver Spring, Md.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 11% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Circadian rhythmicity as a predictor of weight-loss effectiveness.International journal of obesity (2005) · 2014
    Article
  15. Article
  16. Review
  17. Appetite control: methodological aspects of the evaluation of foods.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2010
    Review
  18. A strategy for analyzing gene-nutrient interactions in type 2 diabetes.Journal of diabetes science and technology · 2009
    Article
  19. Article
  20. Article
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

1 author at 1 institution in 1 country.

Jose M OrdovasNutrition and Genetics, JM-USDA-HNRCA at Tufts University, Boston, Massachusetts, USA. jose.ordovas@tufts.edu
Jean Mayer Human Nutrition Research Center on Aging · US

Funding

Genetic and Environmental Determinants of TriglyceridesU01HL072524 · NHLBI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI ARNETT, DONNA K · 2002 to 2008
$11.9M
GENE/DIET EFFECTS ON PLASMA LIPOPROTEIN LEVELSR01HL054776 · NHLBI · TUFTS UNIVERSITY BOSTON · PI ORDOVAS, JOSE M. · 1996 to 2010
$2.6M
PAT PROTEINS: GENE-DIET INTERACTIONS OBESITY RISK AND HEALTHR01DK075030 · NIDDK · TUFTS UNIVERSITY BOSTON · PI ORDOVAS, JOSE M. · 2007 to 2009
$989k
NHLBI NIH HHS HL54776NHLBI NIH HHS HL72524NHLBI NIH HHS R01 HL054776NHLBI NIH HHS U01 HL072524NIDDK NIH HHS DK075030NIDDK NIH HHS R01 DK075030
6 · The paper itself

Abstract

Changes in diet are likely to reduce chronic disorders, but after decades of active research and heated discussion, the question still remains: what is the optimal diet to achieve this elusive goal? Is it a low-fat diet, as traditionally recommended by multiple medical societies? Or a high monounsaturated fat (MUFA) diet as predicated by the Mediterranean diet? Perhaps a high polyunsaturated fat (PUFA) diet based on the cholesterol-lowering effects? The right answer may be all of the above but not for everybody. A well-known phenomenon in nutrition research and practice is the dramatic variability in interindividual response to any type of dietary intervention. There are many other factors influencing response, and they include, among many others, age, sex, physical activity, alcohol, and smoking as well as genetic factors that will help to identify vulnerable populations/individuals that will benefit from a variety of more personalized and mechanistic-based dietary recommendations. This potential could and needs to be developed within the context of nutritional genomics that in conjunction with systems biology may provide the tools to achieve the holy grail of dietary prevention and therapy of chronic diseases and cancer. This approach will break with the traditional public health approach of "one size fits all." The current evidence based on nutrigenetics has begun to identify subgroups of individuals who benefit more from a low-fat diet, whereas others appear to benefit more from high MUFA or PUFA diets. The continuous progress in nutrigenomics will allow some time in the future to provide targeted gene-based dietary advice.

Indexed as

DietNutrigenomicsBody Mass IndexDietary FatsEnvironmentEpigenesis, GeneticGenetic VariationGenotypeHumansMetabolic SyndromeObesityPhenotypeDietary Fats

Identifiers

PMID19037211
PMCPMC2771769
OpenAlexW1984765859

What OpenQuestion holds

Textmetadata
LicenceTDM
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.