Substantial and accumulating evidence exists to link adverse early life environments with long term health outcomes, including increased risk for hypertension, obesity and diabetes, the main causes of chronic disease in adulthood (Barker et al., 2002; Gluckman and Hanson, 2004; Hales and Barker, 1992; Hoffman et al., 2021; Lillycrop and Burdge, 2011). However, the precise biological mechanisms that explain how such early life events influence adult chronic disease risk are not well resolved (Mposhi and Turner, 2023). It is possible that adverse early life events may result in accelerated biological aging and increase disease risk later in life.

One measure that is considered a biomarker of biological aging is telomere length (Entringer et al., 2018; Lin and Epel, 2022; Shalev et al., 2013a). Telomeres are specialized DNA structures located at the ends of chromosomes that function to maintain genomic stability. Telomere length across the lifespan is a product of both telomere shortening (e.g., through mitotic division) and telomere lengthening via the telomeric DNA elongating enzyme telomerase. Telomeres gradually diminish in length with age, with the greatest attrition from birth to three years of age (Cowell et al., 2021). Data indicate that there is a correlation between telomere length at birth and at 4 and 23 years of age (Martens et al., 2021). Notably, accelerated telomere shortening has been observed in individuals experiencing stressful or adverse environments (Shalev et al., 2013a, Shalev et al., 2013b). Shorter telomere length, in turn, is associated with increased risk of non-communicable diseases, including obesity (Mundstock et al., 2015; Qureshi et al., 2023; Xi et al., 2013), and diabetes (Cheng et al., 2022; Dudinskaya et al., 2015; Hunt et al., 2015).

Previous research has explored the relationship between early environments and telomere length measured in adulthood, including a recent meta-analysis that using 41 datasets found that an individual's early-life adversity is associated with shorter telomere length (Cohen's d effect size = −0.35) (Ridout et al., 2017). The specific type and timing of the adverse event exposure predicted variation in telomere length. Specifically, studies evaluating adversity during early development (prenatal to four years) found a more pronounced effect than exposure to adversity in childhood (4–12 years) or during adolescence (13–18 years)(Ridout et al., 2017). Significant effect sizes were found for studies evaluating leukocytes or lymphocytes, saliva samples, or buccal swabs but not cord blood, indicating that source tissue is a moderator of the effect size. Taken together these results indicate that early exposure could be important for cellular aging, and that this association can be measured in multiple tissues. However, publication bias could contribute to these positive associations.

Despite the hypothesized impacts of the early environment on telomere length, few studies have measured telomere length in early childhood. Studies utilizing samples derived from cord blood or dried blood spots taken at-birth have reported that prenatal stress is associated with shorter telomere length at-birth (Marchetto et al., 2016; Naudé et al., 2023; Send et al., 2017; Wojcicki et al., 2015) A meta-analysis that included 11 studies that utilized DNA either from buccal swabs, saliva or peripheral blood, found that stress was associated with telomere attrition in children aged 3–11(Coimbra et al., 2017). Finally, postnatal maternal depression but not antenatal depression was associated with telomere shortening among a cohort of 151 four and five year old Hispanic children (Wojcicki et al., 2015). Although these results suggest that early life adversity may impact telomere length measured in childhood, more research in larger, more socioeconomically and ethnically diverse cohorts is needed to more fully appreciate the factors that determine telomere length variation at this important life stage.

The Growing Up in New Zealand longitudinal study, which is a nationally representative birth cohort that includes all of the major ethnic groups in New Zealand, provides a unique opportunity to measure the impact of environmental influences such as maternal psychosocial health on telomere length, and to provide important new knowledge of the interaction between the early-life environment and genome. Consistent with reports from others, we have also identified and reported marked differences in telomere length between sex and between ethnic groups in young children (Ly et al., 2019). The aim of this study was to evaluate if maternal prenatal and early post-natal depression and anxiety is associated with telomere length of their children in early life.