Evidence map›Paper›PMID 16770336›Full record

ArticleMolecular psychiatry2006

Why do young women smoke? II. Role of traumatic life experience, psychological characteristics and serotonergic genes.

E Lerer, K Kanyas, O Karni, R P Ebstein, B Lerer

Abstract read
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In one paragraph

Article in Molecular psychiatry, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 2 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

19 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Common and unique biological pathways associated with smoking initiation/progression, nicotine dependence, and smoking cessation.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2010
    Article
  11. Review
  12. Review
  13. Smoking as a product of gene-environment interaction.Upsala journal of medical sciences · 2009
    Article
  14. Article
  15. ADHD and smoking: from genes to brain to behavior.Annals of the New York Academy of Sciences · 2008
    Review
  16. Article
  17. Article
  18. Article
  19. Review
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

5 authors.

E LererResearch Laboratory, Sara Herzog Memorial Hospital, Jerusalem, Israel. lerer@cc.huji.ac.il
K Kanyas
O Karni
R P Ebstein
B Lerer

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cigarette smoking is a complex behavioral phenotype to which environmental, psychological and genetic factors contribute. The purpose of this study was to investigate these multifactorial effects with a specific focus on young women and on genes that encode serotonin (5-HT) receptors and the 5-HT transporter. A case-control sample of female Israeli college students provided comprehensive background data and details of cigarette smoking and completed a battery of psychological instruments. They were divided into smoking initiators (SI, n=242) or non-initiators (NI, n=148); SI were further subdivided into high (HND, n=127) and low nicotine-dependent smokers (LND, n=115) on the basis of their scores on the Fagerstrom Tolerance Questionnaire (FTQ). Single-nucleotide polymorphisms (SNPs) in five serotonin receptor genes (HTR1A, HTR1B, HTR2A, HTR2C and HTR6) and the 5-HT transporter-linked polymorphic region (5-HTTLPR) were genotyped. In a logistic regression model for SI (chi2=117.90, P=1.6 x 10(-19), Nagelkerke R2=0.42), novelty seeking (odds ratio (OR)=1.134, P=0.00009) was a significant risk factor. A five SNP CACCC haplotype in HTR6 was a strong protective factor against SI (OR=0.26; P=0.007). The interaction of HTR6-C276T genotype and lifetime traumatic experience contributed strongly to the risk of SI (OR=13.88, P=0.0001). Specifically, subjects homozygous for the HTR6-C276T C allele showed significantly increased risk of SI if they had experienced trauma. Although significant (chi2=42.85, P=1.00 x 10(-7)), the best-fitting model for ND was less predictive than the model for SI (Nagelkerke R2=0.24). HTR1B-G861C GG genotype (OR=2.29, P=0.01) was a significant risk factor for HND. Further studies should consider the interactive contribution of life events and relevant gene variants to cigarette smoking and other complex behavioral traits.

Indexed as

Life Change EventsPersonalityAdultCase-Control StudiesFemaleHaplotypesHumansIsraelLogistic ModelsPolymorphism, Single NucleotideReceptor, Serotonin, 5-HT1AReceptor, Serotonin, 5-HT1BReceptor, Serotonin, 5-HT2AReceptor, Serotonin, 5-HT2CReceptors, SerotoninRisk FactorsHTR1B protein, humanReceptor, Serotonin, 5-HT1AReceptor, Serotonin, 5-HT1BReceptor, Serotonin, 5-HT2AReceptor, Serotonin, 5-HT2CReceptors, Serotoninserotonin 6 receptor

Identifiers

PMID16770336

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.