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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
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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.

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

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