Evidence map›Paper›PMID 16841242›Full record

ArticleMedicine, health care, and philosophy2006

Some causal limitations of pharmacogenetic concepts.

David Badcott

Abstract read
PubMed Publisher
In one paragraph

Article in Medicine, health care, and philosophy, 2006. 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
–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

2 citing papers in PubMed.

  1. Article
  2. Complex causation and the virtue of pluralism.Medicine, health care, and philosophy · 2006
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author.

David BadcottCentre for Applied Ethics, Cardiff University, PO Box 94, Cardiff, CF10 3XB, UK. badcottd@cardiff.ac.uk

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pharmacogenetics and pharmacogenomics are related facets of cutting edge therapeutic research in a field that relates pharmacological properties to the genetic characteristics of human beings. An optimistic interpretation suggests that "One-Size-Fits-All" therapeutics, whose effects can only be predicted in probabilistic terms, will give way eventually to individual tailor-made therapies with entirely predictable properties in each patient. Yet the concept of anticipating individual pharmacotherapeutic response appears to disregard some of the fundamental limitations of causal understanding in the biological world of structure-action relationships. It is not simply a problem of confronting complexity - which might be overcome in time with advances in biotechnology and computing power - but the inescapable paradox of the genetic characteristics of individuals within the human species. The aleatory process of evolution ensures that with the exception of monozygotic twins, every human being is genetically unique. At the same time there appears to be more in common than divides. Pharmacogenomics provides a climate in which to explore and better understand the variable causal relationships between genetic element, protein and therapeutic or toxic actions, but can only do so in abstraction. Thus predictive power may be enhanced but is ultimately constrained by insuperable probabilistic considerations.

Indexed as

CausalityPhilosophy, MedicalDrug ResistanceGenetic MarkersGenetic Predisposition to DiseaseGenetic VariationHumansModels, GeneticPharmacogeneticsPolymorphism, Single NucleotideReproducibility of ResultsGenetic Markers

Identifiers

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.