Autonomic and Adrenocortical Reactivity and Buccal Cell Telomere Length in Kindergarten Children

Abstract

Objective To examine associations between autonomic nervous system and adrenocortical reactivity to laboratory stressors and buccal cell telomere length (BTL) in children. Methods The study sample comprised 78 five- and six-year-old children from a longitudinal cohort study of kindergarten social hierarchies, biological responses to adversity, and child health. Buccal cell samples and reactivity measures were collected in the spring of the kindergarten year. BTL was measured by realtime PCR, as the telomere-to-single copy gene (T/S) ratio. Parents provided demographic information; parents and teachers reported children’s internalizing and externalizing behavior problems. Components of children’s autonomic (heart rate (HR), respiratory sinus arrhythmia (RSA), pre-ejection period (PEP)) and adrenocortical (salivary cortisol) responses were monitored during standardized laboratory challenges. We examined relations between reactivity, internalizing and externalizing behavior, and BTL, adjusted for age, race, and gender. Results Heart rate and cortisol reactivity were inversely related to BTL, PEP was positively related to BTL, and RSA was unrelated. Internalizing behaviors were also inversely related to BTL (standardized β=−0.33, p=0.004). Split at the median of reactivity parameters, children with high sympathetic activation (decreasing PEP) and high parasympathetic withdrawal (decreasing RSA) did not differ with regard to BTL. However, children with both this profile and high cortisol reactivity (N=12) had significantly shorter BTL (0.80 vs. 1.00, χ2=7.6, p=0.006), compared with other children. Conclusions Autonomic and adrenocortical reactivity in combination were associated with shorter buccal cell telomere length in children. These data suggest that psychophysiological processes may influence, and that BTL may be a useful marker of, early biological aging.

Telomere length analysis in Cushing's syndrome

“…Accelerated telomere shortening was observed in a group of 647 women (who had a sister with breast cancer) with higher perceived stress and higher levels of urinary free cortisol and cathecolamines (6). Similarly, shorter buccal cell TL was observed in children exposed to laboratory stressors with higher levels of salivary cortisol and higher autonomic reactivity (26). Greater cortisol responses and dysregulated patterns of daily cortisol secretion were associated with shorter leukocyte TL in 14 postmenopausal women caregivers of a partner with dementia compared with matched noncaregiver controls (27).…”

Early-life stress and reproductive cost: A two-hit developmental model of accelerated aging?

“…With regard to glucocorticoids, several studies of humans document significant associations between stress-related hypothala mus-pituitary-adrenal (HPA) axis indices and shorter TL [74][75][76], including research in children [77,78]. When it comes to inflammation, increased proliferation of immune cells in response to stress result in more telomere erosion [79], and a history of childhood adversity, by itself a strong predictor of elevated inflammation [80], is associated with shorter TL in white blood cells [81].…”

Childhood abuse, parental warmth, and adult multisystem biological risk in the Coronary Artery Risk Development in Young Adults study

“…Childhood toxic stress has also been associated with a less healthy cardiovascular system profile (e.g., elevated blood pressure), increases in inflammation suggestive of proinflammatory immune system programming, and accelerated cellular aging (17)(18)(19)(20)(21)(22)(23)(24)(25). In addition to alterations in adult levels of these biomarkers of risk, several of these markers have been observed in children with stress (18,23,(26)(27)(28)(29)(30), with one study reporting more pronounced effects of cumulative childhood stress on stress hormones, blood pressure, and fat deposition among those with mothers who were cold and unresponsive to their needs (27). This work indicates that the impact of childhood stress on these regulatory systems may begin in childhood, but might be buffered by a nurturing relationship with an adult.…”