Hostname: page-component-77f85d65b8-45ctf Total loading time: 0 Render date: 2026-04-18T08:08:17.885Z Has data issue: false hasContentIssue false
  • English
  • Français

A disanalogy with RCTs and its implications for second-generation causal knowledge

Published online by Cambridge University Press:  11 September 2023

Kate E. Lynch Open the ORCID record for Kate E. Lynch [Opens in a new window] ,
Rachael L. Brown Open the ORCID record for Rachael L. Brown [Opens in a new window] ,
Jeremy Strasser  and
Shang Long Yeo Open the ORCID record for Shang Long Yeo [Opens in a new window]
Kate E. Lynch
Affiliation:
Department of Philosophy, University of Sydney, Sydney, Australia kate.lynch@sydney.edu.au www.katelynch.net Charles Perkins Centre, University of Sydney, Sydney, Australia
Rachael L. Brown
Affiliation:
Centre for Philosophy of the Sciences, School of Philosophy, Australian National University, Canberra, Australia rachael.brown@anu.edu.au http://rachaelbrown.net
Jeremy Strasser
Affiliation:
School of Philosophy, Australian National University, Canberra, Australia jeremy.strasser@anu.edu.au
Shang Long Yeo
Affiliation:
Department of Philosophy, National University of Singapore, Singapore, Singapore phiysl@nus.edu.sg http://shang.isaphilosopher.com
Get access Rights & Permissions [Opens in a new window]

Abstract

We are less optimistic than Madole & Harden that family-based genome-wide association studies (GWASs) will lead to significant second-generation causal knowledge. Despite bearing some similarities, family-based GWASs and randomised controlled trials (RCTs) are not identical. Most RCTs assess a relatively homogenous causal stimulus as a treatment, whereas GWASs assess highly heterogeneous causal stimuli. Thus, GWAS results will not translate so easily into second-generation causal knowledge.

Information

Type
Open Peer Commentary
Information
Behavioral and Brain Sciences , Volume 46 , 2023 , e194
Check for updates
Copyright
Copyright © The Author(s), 2023. Published by Cambridge University Press

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

Article purchase

Temporarily unavailable

References

Belsky, D. W., & Harden, K. P. (2019). Phenotypic annotation: Using polygenic scores to translate discoveries from genome-wide association studies from the top down. Current Directions in Psychological Science, 28, 82–90. doi: 10.1177/0963721418807729CrossRefGoogle Scholar
Belsky, D. W., Moffitt, T. E., Corcoran, D. L., Domingue, B., Harrington, H., Hogan, S., … Caspi, A. (2016). The genetics of success: How single-nucleotide polymorphisms associated with educational attainment relate to life-course development. Psychological Science, 27, 957–972. doi: 10.1177/0956797616643070CrossRefGoogle ScholarPubMed
Davey Smith, G., & Ebrahim, S. (2003). “Mendelian randomization”: Can genetic epidemiology contribute to understanding environmental determinants of disease? International Journal of Epidemiology, 32(1), 1–22.CrossRefGoogle Scholar
Lynch, K. E. (2017). Heritability and causal reasoning. Biology & Philosophy, 32(1), 25–49.CrossRefGoogle Scholar
Lynch, K. E. (2021). The meaning of cause in genetics. In Smith, G. D., Richmond, R., & Pingault, J.-B. (Eds.), Cold Spring Harbour Perspectives in Medicine, 11(9), A0405019. doi: 10.1101/cshperspect.a040519Google Scholar
Lynch, K. E., Parke, E, & O'Malley, M. (2019). How causal are microbiomes? A comparison with the Helicobacter pylori explanation of ulcers. Biology and Philosophy, 34, 62.CrossRefGoogle Scholar
Matthews, L. J., & Turkheimer, E. (2022). Three legs of the missing heritability problem. Studies in History and Philosophy of Science, 93, 183–191.CrossRefGoogle ScholarPubMed
Pearl, J. (2014). Interpretation and identification of causal mediation. Psychological Methods, 19(4), 459.CrossRefGoogle ScholarPubMed