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Green spaces are associated with increased well-being and reduced risk of developing psychiatric disorders. In this study, we aimed to investigate how residential proximity to green spaces was associated with stress response buffering during the COVID-19 pandemic in a prospective cohort of young mothers. We collected information on stress in 766 mothers (mean age: 36.6 years) from the ENVIR ON AGE birth cohort at baseline of the study (from 2010 onwards), and during the COVID-19 pandemic (from December 2020 until May 2021). Self-reported stress responses due to the COVID-19 pandemic were the outcome measure. Green space was quantified in several radiuses around the residence based on high-resolution (1 m 2 ) data. Using ordinal logistic regression, we estimated the odds of better resistance to reported stress, while controlling for age, socio-economic status, stress related to care for children, urbanicity, and household change in income during the pandemic. In sensitivity analyses we corrected for pre-pandemic stress levels, BMI, physical activity, and changes in health-related habits during the pandemic. We found that for an inter-quartile range contrast in residential green space 300 m and 500 m around the residence, participants were respectively 24% (OR = 1.24, 95%CI: 1.03 to 1.51) and 29% (OR = 1.29, 95%CI: 1.04 to 1.60) more likely to be in a more resistant category, independent of the aforementioned factors. These results remained robust after additionally controlling for pre-pandemic stress levels, BMI, physical activity, smoking status, urbanicity, psychological disorders, and changes in health-related habits during the pandemic. This prospective study in young mothers highlights the importance of proximity to green spaces, especially during challenging times.

Telomere length (TL) and telomere shortening are biological indicators of aging, and epigenetic associates have been found for TL in adults. However, the role of epigenetic signatures in setting newborn TL and early life telomere dynamics is unknown. In the present study, based on 247 participating newborns from the ENVIRONAGE birth cohort, whole-genome DNA methylation, profiled on the Illumina MethylationEPIC BeadChip microarray, and TL were measured in cord blood. In a follow-up visit at a mean age of 4.58 years, leukocyte TL was evaluated. We combined an epigenome-wide association study and a statistical learning method with re-sampling to select CpGs and their two-way interactions to model baseline (cord blood) TL and early-life telomere attrition rate, where distinct epigenetic signatures were identified for the two outcomes. In addition, a stronger epigenetic regulation was suggested in setting newborn TL than that of telomere dynamics in early life: 47 CpGs and 7 between-CpG interactions explained 76% of the variance in baseline TLs, while 72% of the total variance in telomere attrition rate was explained by 31 CpGs and 5 interactions. Functional enrichment analysis based on the selected CpGs in the two models revealed GLUT4 translocation and immune cell signaling pathways, respectively. These CpGs and interactions, as well as the cellular pathways, are potential novel targets of further investigation of telomere biology and aging.

Aging starts at the beginning of life as evidenced by high variability in telomere length (TL) and mitochondrial DNA content (mtDNAc) at birth. Whether p53 and PGC-1α are connected to these age-related markers in early life is unclear. In this study, we hypothesized that these hallmarks of aging are associated at birth. In 613 newborns from the ENVIRONAGE birth cohort, p53 and PGC-1α protein levels were measured in cord plasma, while TL and mtDNAc were measured in both cord blood and placental tissue. Cord blood methylation data of genes corresponding to the measured protein levels were available from the Human MethylationEPIC 850K BeadChip array. Pearson correlations and linear regression models were applied while accounting for selected covariates. In cord, a 10% increase in TL was associated with 5.22% (95% CI: 3.26 to 7.22; p < 0.0001) higher mtDNAc and −2.66% (95% CI: -5.04 to −0.23%; p = 0.032) lower p53 plasma level. In placenta, a 10% increase in TL was associated with 5.46% (95% CI: 3.82 to 7.13%; p < 0.0001) higher mtDNAc and −2.42% (95% CI: −4.29 to −0.52; p = 0.0098) lower p53 plasma level. Methylation level of TP53 was correlated with TL and mtDNAc in cord blood and with cord plasma p53 level. Our study suggests that p53 may be an important factor both at the protein and methylation level for the telomere-mitochondrial axis of aging at birth.

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