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. 2022 Jun 9;54(6):897–905. doi: 10.1038/s41588-022-01085-0

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — The estimate is given along with the 95% confidence interval. Direct effects are causal effects due to inheritance of alleles; population effects are estimated by standard GWASs and include direct effects, indirect effects from relatives and confounding due to population stratification and AM. We estimated the correlation between direct and population effect estimates using summary statistics derived from a sample of 39,619 individuals from the ‘White British’ subsample of the UKB where parental genotypes were imputed, using the developed methods, or observed (Methods). Phenotypes were adjusted for 40 genetic PCs before analysis. We do not show the results for age at first birth in women and ever-smoked here due to their large standard errors (see Supplementary Table 5).