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Background: Previous studies have shown the interaction between age and socioeconomic status (SES) on the risk of infertility in the UK, but the association is still unclear in the United States. Therefore, the present study investigated the effect of age on the relationship between SES and the risk of infertility in American women. Methods: The study included adults who participated in the National Health and Nutrition Examination Survey (NHANES) from 2013 to 2018. The poverty income ratio (PIR) was used to represent the SES of the population. With participants stratified according to age category (< 35 years; ≥ 35 years), we further assessed differences in the relationship between PIR and infertility risk among participants of different age groups using multivariate logistic regression and interaction tests. Results: Approximately 3,273 participants were enrolled in the study. There were 399 cases of infertility and 2,874 cases without infertility. In women ≥ 35 years of age, PIR levels were significantly higher in infertile participants than in non-infertile participants, but no such difference was found in those < 35 years of age. The association of PIR with the risk of infertility appeared to differ between age < 35 years and age ≥ 35 years (OR: 0.99, 95%Cl: 0.86–1.13 vs. OR: 1.24, 95%Cl: 1.12–1.39) in a fully adjusted model. Furthermore, an interaction between age and PIR increased the risk of infertility (p-value for interaction < 0.001). Conclusion: Our study found that age may influence the association between PIR and infertility. It is imperative to perform further studies to provide more evidence. [ABSTRACT FROM AUTHOR]

Mitochondrial DNA (mtDNA) variants influence the risk of late-onset human diseases, but the reasons for this are poorly understood. Undertaking a hypothesis-free analysis of 5,689 blood-derived biomarkers with mtDNA variants in 16,220 healthy donors, here we show that variants defining mtDNA haplogroups Uk and H4 modulate the level of circulating N-formylmethionine (fMet), which initiates mitochondrial protein translation. In human cytoplasmic hybrid (cybrid) lines, fMet modulated both mitochondrial and cytosolic proteins on multiple levels, through transcription, post-translational modification and proteolysis by an N-degron pathway, abolishing known differences between mtDNA haplogroups. In a further 11,966 individuals, fMet levels contributed to all-cause mortality and the disease risk of several common cardiovascular disorders. Together, these findings indicate that fMet plays a key role in common age-related disease through pleiotropic effects on cell proteostasis., (© 2021. The Author(s), under exclusive licence to Springer Nature America, Inc.)