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. 2024 Apr 22;116(8):1303–1312. doi: 10.1093/jnci/djae089

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© The Author(s) 2024. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 4. — Metabolic mediators of the relationships between modifiable risk factors and CRC. A) Phylum Actinobacteria effect on CRC mediated by plasma galactonate and urinary lactose. B) Class Actinobacteria effect on CRC mediated by plasma galactonate and urinary lactose. C) Smoking initiation effect on CRC mediated by plasma 1-lignoceroyl-GPC (24:0), 1-linoleoyl-2-linolenoyl-GPC (18:2/18:3)*. D) BMI effect on CRC mediated by plasma 1-lignoceroyl-GPC, mannonate*, mannose, deoxycholic acid glucuronide, 1,2-dilinoleoyl-GPC(18:2/18:2), and 1-linoleoyl-2-linolenoyl-GPC(18:2/18:3)*. E) Waist to hip ratio effect on CRC mediated by plasma 1,2-dilinoleoyl-GPC (18:2/18:2), hydroxypalmitoyl sphingomyelin (d18:1/16:0(OH))**, and mannose. F) Fasting insulin effect on CRC mediated by plasma mannose. BMI = body mass index; CRC = colorectal cancer.