Evidence map›Paper›PMID 22190153›Full record

ReviewHuman genetics2012

Genetics of schizophrenia and smoking: an approach to studying their comorbidity based on epidemiological findings.

Jose de Leon, Francisco J Diaz

Abstract readReview
In one paragraph

Review in Human genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–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

15 citing papers in PubMed.

  1. Chronic obstructive pulmonary disease in severe mental illness: A timely diagnosis to advance the process of quitting smoking.European psychiatry : the journal of the Association of European Psychiatrists · 2021
    Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
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  10. Article
  11. Article
  12. Article
  13. The genetics of addiction.Human genetics · 2012
    Article
  14. Role of Statistical Random-Effects Linear Models in Personalized Medicine.Current pharmacogenomics and personalized medicine · 2012
    Article
  15. 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

2 authors.

Jose de LeonUniversity of Kentucky Mental Health Research Center at Eastern State Hospital, 627 West Fourth St., Lexington, KY 40508, USA. jdeleon@uky.edu
Francisco J Diaz

Funding

HEARTLAND INSTITUTE FOR CLINICAL AND TRANSLATIONAL RESEARCHUL1RR033179 · NCRR · UNIVERSITY OF KANSAS MEDICAL CENTER · PI BAROHN, RICHARD J. · 2011 to 2011
$3.2M
Heartland Institute for Clinical and Translational ResearchTL1RR033178 · NCRR · UNIVERSITY OF KANSAS MEDICAL CENTER · PI BAROHN, RICHARD J. · 2011 to 2011
$132k
NCRR NIH HHS RR033178NCRR NIH HHS TL1 RR033178NCRR NIH HHS UL1 RR033179
6 · The paper itself

Abstract

The association between schizophrenia and tobacco smoking has been described in more than 1,000 articles, many with inadequate methodology. The studies on this association can focus on: (1) current smoking, ever smoking or smoking cessation; (2) non-psychiatric controls or controls with severe mental illness (e.g., bipolar disorder); and (3) higher smoking frequency or greater usage in smokers. The association with the most potential for genetic studies is that between ever daily smoking and schizophrenia; it may reflect a shared genetic vulnerability. To reduce the number of false-positive genes, we propose a three-stage approach derived from epidemiological knowledge. In the first stage, only genetic variations associated with ever daily smoking that are simultaneously significant within the non-psychiatric controls, the bipolar disorder controls and the schizophrenia cases will be selected. Only those genetic variations that are simultaneously significant in the three hypothesis tests will be tested in the second stage, where the prevalence of the genes must be significantly higher in schizophrenia than in bipolar disorder, and significantly higher in bipolar disorder than in controls. The genes simultaneously significant in the second stage will be included in a third stage where the gene variations must be significantly more frequent in schizophrenia patients who did not start smoking daily until their 20s (late start) versus those who had an early start. Any genetic approach to psychiatric disorders may fail if attention is not given to comorbidity and epidemiological studies that suggest which comorbidities are likely to be explained by genetics and which are not. Our approach, which examines the results of epidemiological studies on comorbidities and then looks for genes that simultaneously satisfy epidemiologically suggested sets of hypotheses, may also apply to the study of other major illnesses.

Indexed as

Genetic VariationResearch DesignComorbidityFemaleGenome-Wide Association StudyHumansMaleOdds RatioPrevalenceSchizophreniaSmoking

Identifiers

PMID22190153
PMCPMC3536540

What OpenQuestion holds

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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.