Evidence map›Paper›PMID 10967953›Full record

ReviewTheoretical medicine and bioethics2000

Schizophrenia epigenesis?

J S Robert

Abstract readReview
PubMed Publisher
In one paragraph

Review in Theoretical medicine and bioethics, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.8field-weighted citation impact, top 23% 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

2 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. 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

1 author at 1 institution in 1 country.

J S RobertDepartment of Philosophy, McMaster University, Hamilton, Ontario, Canada. robertjs@mcmaster.ca
McMaster University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

I begin by examining how genetics drives schizophrenia research, and raise both familiar and relatively novel criticisms of the evidence putatively supporting the genetic basis of schizophrenia. In particular, I call attention to a set of concerns about the effects of placentation on concordance rates of schizophrenia in monozygotic twins, which further weakens the case for schizophrenia's so-called strong genetic component. I then underscore two critical points. First, I emphasize the importance of taking seriously considerations about the complexity of both ontogenesis and the development of hereditary diseases. The recognition of developmental constraints and supports is crucial, for attention to development exposes the naivete of too many models of gene action in the aetiology of disease. Secondly, I attend to those schizophreniologists who ignore methodological criticisms and thus presume a genetic basis for schizophrenia, and then seek the 'schizophrenic genotype' lacking an adequate phenotype. In response I attempt to demonstrate the necessity of a sustained effort at characterizing the phenotype of schizophrenia as an enabling condition for the whole enterprise of psychiatric genetics--and for psychiatry itself. Without the organism-level phenotype, research at the level of genes will remain unproductive--assuming of course that research at the genetic level is appropriate at all.

Indexed as

Genetic Predisposition to DiseaseEnvironmentFemaleHumansPhenotypePlacentationPregnancySchizophreniaTwin Studies as Topic

Identifiers

PMID10967953
OpenAlexW4237563494

What OpenQuestion holds

Textmetadata
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.