Evidence map›Paper›PMID 19079817›Full record

ReviewThe British journal of nutrition2009

Nutrition in early life, and risk of cancer and metabolic disease: alternative endings in an epigenetic tale?

Graham C Burdge, Karen A Lillycrop, Alan A Jackson

Open access · bronzeAbstract readReview
In one paragraph

Review in The British journal of nutrition, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
13.1field-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

26 citing papers in PubMed, 85 citations in OpenAlex.

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  18. Exposures in early life: associations with DNA promoter methylation in breast tumors.Journal of developmental origins of health and disease · 2013
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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

3 authors at 2 institutions in 1 country.

Graham C BurdgeInstitute of Human Nutrition, Southampton General Hospital, Tremona Road, Southampton, UK. g.c.burdge@southampton.ac.uk
Karen A Lillycrop
Alan A Jackson
Southampton General Hospital · GBUniversity of Southampton · GB

Funding

British Heart Foundation FS/05/064/19525
6 · The paper itself

Abstract

There is substantial evidence which shows that constraints in the early life environment are an important determinant of risk of metabolic disease and CVD. There is emerging evidence that higher birth weight, which reflects a more abundant prenatal environment, is associated with increased risk of cancer, in particular breast cancer and childhood leukaemia. Using specific examples from epidemiology and experimental studies, this review discusses the hypothesis that increased susceptibility to CVD, metabolic disease and cancer have a common origin in developmental changes induced in the developing fetus by aspects of the intra-uterine environment including nutrition which involve stable changes to the epigenetic regulation of specific genes. However, the induction of specific disease risk is dependent upon the nature of the environmental challenge and interactions between the susceptibility set by the altered epigenome and the environment throughout the life course.

Indexed as

AnimalsBirth WeightDisease Models, AnimalEpigenesis, GeneticFemaleFetal DevelopmentHumansInfant, NewbornMetabolic DiseasesNeoplasmsPregnancyPrenatal Exposure Delayed EffectsPrenatal Nutritional Physiological PhenomenaRisk Factors

Identifiers

PMID19079817
PMCPMC2649281
OpenAlexW2119909792

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.