Low childhood subjective social status and telomere length in adulthood: The role of attachment orientations

Abstract

Low subjective social status (SSS) in childhood places one at greater risk of a number of health problems in adulthood. Theoretical and empirical evidence indicates that exposure to supportive parenting may buffer the negative effects of low childhood SSS on adult health. Given the importance of supportive caregivers and close others for the development of attachment orientations throughout the lifespan, attachment theory may be important for understanding why some individuals are resilient to the negative effects of low childhood SSS on adult health while others are not. We examined if attachment anxiety and attachment avoidance altered the association between childhood subjective social status (SSS) and length of telomeres in white blood cells in adulthood. Shorter telomere length is associated with increased risk of age-related diseases including cancer, type 2 diabetes, and cardiovascular disease. Participants (N = 128) completed self-report measures of childhood SSS and attachment orientations, as well as a blood draw. We found that among those with low childhood SSS, low attachment anxiety was associated with longer telomere length in white blood cells in comparison to high attachment anxiety controlling for participant age, sex, race, body mass index, and adult SSS. Among those with high childhood SSS, low attachment anxiety was associated with a slight decrease in telomere length. Attachment avoidance was unrelated to length of telomeres. Such findings provide further evidence for the role that close relationships may have on buffering SSS related health disparities.

Connecting cognition, cardiology, and chromosomes: Cognitive reappraisal impacts the relationship between heart rate variability and telomere length in CD8+CD28– cells

“…Previous literature, however, shows that telomere length is impacted by several different factors (e.g., physical activity and gender) (Arsenis et al, 2017;Starkweather et al, 2014). Although these associations were not present in the current sample, other telomere length-related studies control for these factors; accordingly, we controlled for these factors to maintain consistency across studies (e.g., Murdock et al, 2018).…”

“…All samples were run in duplicate (Cohen et al, 2016). Replicate values were averaged to determine a final T:S ratio (Murdock et al, 2018). Higher T:S ratios signify longer telomere length (Kroenke et al, 2011).…”

“…We included the following in the model as a priori covariates or fixed factors based on previous research related to T:S ratio and psychoneuroimmunology: age, sex, body mass index, race, education, employment, smoking status, alcohol consumption, and exercise (Fagundes et al, 2012;Murdock et al, 2018).…”

The Psychobiology of Bereavement and Health: A Conceptual Review From the Perspective of Social Signal Transduction Theory of Depression

“…Consistent with this theory, research has shown that genetic factors, epigenetic processes, personality traits (e.g., neuroticism), and social environmental conditions during childhood and adolescence (e.g., social/financial stress, uncertainty, abuse, or neglect) play a role in shaping individuals' sensitivity to lateroccurring adverse life events (25,36). At the molecular level, epigenetic regulation of gene transcription can play an important role in helping individuals adapt to challenges posed by the external social environmental (37).…”

“…Specifically, stress exposure during childhood can alter behavioral and physiological responses to acute and chronic stress in adulthood that in turn influence later-life risk for mental and physical health problems, including anxiety disorder, depression, CVD, and autoimmune and neurodegenerative disorders ( 20 , 39 , 47 , 140 , 179 ). Epigenetic changes and immune system dysregulation may be potential pathways that underlie this link ( 36 , 39 , 180 ). Indeed, the presence of multiple childhood adversities has been found to heighten emotional and physical reactivity to subsequent stress, which in turn activates genetic and epigenetic processes that may promote a proinflammatory phenotype ( 20 ).…”