Key result
Delayed puberty links to a ~0.11 SD dodecanedioylcarnitine increase per year, driven by adulthood adiposity.
Why the study?
The long-term impact of puberty timing on human plasma metabolites has been uncertain due to confounding factors in conventional observational studies.
Does genetically predicted puberty timing affect plasma metabolic profiles in adulthood?
Observational (n=329,345)
Does genetically predicted puberty timing affect plasma metabolic profiles in adulthood?
Genetically predicted later puberty timing has a causal effect on specific plasma metabolites in adulthood, largely mediated by adulthood adiposity.
Answers are grounded in this paper and cite their sources.
Later puberty timing may alter specific adult metabolites via adiposity; extends MR evidence but leaves clinical translation open.
There has been uncertainty regarding the long-term impact of puberty timing on human plasma metabolites. This lack of clarity can be attributed to the influence of confounding factors present in conventional observational studies. To determine the causal effect of puberty timing on plasma metabolites, we employed a two-sample Mendelian randomization (MR) analysis, complemented by MR mediation analysis assessing the direct effect. We utilized data from a large-scale meta-analysis of genome-wide association studies (GWAS) on puberty timing, consisting of 329,345 women of European ancestry, and a meta-analysis of GWAS on plasma metabolites, involving up to 86,507 individuals. Our findings provide moderate evidence supporting a causal effect of puberty timing on 23 out of 174 plasma metabolites. After excluding 7 single nucleotide polymorphisms (SNPs) related to birth weight and childhood adiposity, causal effects remained for 16 metabolites. Through two-step MR analysis, we observed strong evidence that adulthood adiposity mediated the causal relationships of puberty timing on 35 plasma metabolites. We also observed moderate evidence for an independent causal effect of puberty timing on 10 metabolites through multivariable MR analysis. We further used metabolomic data measured in the UK Biobank (UKB) to perform a replication analysis to validate the causal effect estimated. Nine amino acids were identified in the UKB, and the replication analysis supported our main findings.
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Li et al. (2023) conducted an observational in Puberty timing and plasma metabolic profiles (n=329,345). Puberty timing (per year delayed) vs. Earlier puberty timing was evaluated on Plasma level of dodecanedioylcarnitine (beta 0.11, 95% CI 0.04-0.17, p=9.09 × 10-4). Each year of delayed puberty onset was causally associated with a 0.11 standard deviation increase in plasma dodecanedioylcarnitine levels, with effects largely mediated by adulthood adiposity.
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