Science is a cumulative enterprise. As more studies accumulate, it is important to
integrate them, and meta-analysis is one approach to doing so. But what is the best
way to conduct a meta-analysis? The commentary by Laoutidis and Luckhaus suggests
limitations of two recent meta-analyses, one reported in this journal by Byrd and
Manuck (
1
) and the second published elsewhere by Karg et al. (
2
). These focus, respectively, on two reports of gene-environment (G × E) interactions,
published in 2002 and 2003 (
3
,
4
), that have spawned over 80 replication attempts. The earlier of the two meta-analyses
targeted the interaction of life stress and polymorphic variation in the serotonin
transporter gene on risk for depression, and the second meta-analysis targeted the
interaction of early maltreatment and analogous variation in monoamine oxidase A (MAOA) on later antisocial behaviors. Laoutidis and Luckhaus critique our use of the Liptak-Stouffer
weighted Z-test (LST) for meta-analysis, as opposed to alternative methods involving
aggregated effect sizes, and suggest any conclusions permitted by the LST are limited.
Here, we show why use of the LST is appropriate, and authors from our two groups have
joined in this reply.To read this article in full you will need to make a payment
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References
- MAOA, childhood maltreatment, and antisocial behavior: Meta-analysis of a gene-environment interaction.Biol Psychiatry. 2014; 75: 9-17
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Article Info
Publication History
Published online: February 24, 2014
Footnotes
The authors report no biomedical financial interests or potential conflicts of interest.
Please also see associated correspondence, doi:10.1016/j.biopsych.2013.11.033.
Identification
Copyright
© 2015 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.
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- The Liptak-Stouffer Test for Meta-AnalysesBiological PsychiatryVol. 77Issue 1
- PreviewWe are writing to address a potential statistical limitation in the meta-analyses reported by Byrd and Manuck (1) and by Karg et al. (2). Both meta-analyses followed the same statistical method and investigated the role of gene-environment (G × E) interactions in the development of psychopathology. Byrd and Manuck (1) showed that there is a G × E interaction between the variable number tandem repeat polymorphism of the monoamine oxidase A promoter and childhood maltreatment in the development of antisocial behavior, while Karg et al.
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