Evidence map›Paper›PMID 19396697›Full record

ArticleUpsala journal of medical sciences2009

Smoking as a product of gene-environment interaction.

Kent W Nilsson, Lars Oreland, Robert Kronstrand, Jerzy Leppert

Open access · diamondAbstract read
In one paragraph

Article in Upsala journal of medical sciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

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  11. Contribution of hypothalamic-pituitary-adrenal activity and environmental stress to vulnerability for smoking in adolescents.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2009
    Article
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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

4 authors at 3 institutions in 1 country.

Kent W NilssonCentre for Clinical Research, Uppsala University, Central Hospital, Västerås, Sweden. kent.nilsson@ltv.se
Lars Oreland
Robert Kronstrand
Jerzy Leppert
Uppsala University Hospital · SESwedish National Board of Forensic Medicine · SEUppsala University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A strong hereditary influence on smoking has been demonstrated. As one of the candidate genes in relation to smoking, the serotonin transporter gene (5-HTTLPR) has been suggested, however with conflicting results. In recent studies, it has been shown that genotypic and environmental (G*E) factors interact in the shaping of a variety of phenotypic expressions. The objective of the present study was to investigate the interaction between a variation in the 5-HTTLPR and family environment in relation to smoking habits, nicotine dependence, and nicotine and cotinine levels in hair samples. A random Swedish adolescent population sample (n = 785), from which 200 individuals were stratified regarding behaviour, was genotyped for 5-HTTLPR and assessed with semi-structured interviews, a questionnaire, and hair analyses of nicotine and cotinine. The 5-HTTLPR gene interacted with a poor family environment to predict smoking habits, as well as nicotine and cotinine levels. The risk of being a smoker was increased 13 times for an individual with a combination of the 5-HTTLPR LS genotype and a poor family environment in comparison with the Homozygous Long-Long (LL) genotype and a good family environment.

Indexed as

EnvironmentGenetic Predisposition to DiseaseAdolescentAdultCotinineFamilyHairHumansNicotinePolymerase Chain ReactionSerotonin Plasma Membrane Transport ProteinsSmokingSurveys and QuestionnairesCotinineNicotineSerotonin Plasma Membrane Transport Proteins

Identifiers

PMID19396697
PMCPMC2852756
OpenAlexW2053779519

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.