Lifespan adversity and later adulthood telomere length in the nationally representative US Health and Retirement Study

Abstract

Stress over the lifespan is thought to promote accelerated aging and early disease. Telomere length is a marker of cell aging that appears to be one mediator of this relationship. Telomere length is associated with early adversity and with chronic stressors in adulthood in many studies. Although cumulative lifespan adversity should have bigger impacts than single events, it is also possible that adversity in childhood has larger effects on later life health than adult stressors, as suggested by models of biological embedding in early life. No studies have examined the individual vs. cumulative effects of childhood and adulthood adversities on adult telomere length. Here, we examined the relationship between cumulative childhood and adulthood adversity, adding up a range of severe financial, traumatic, and social exposures, as well as comparing them to each other, in relation to salivary telomere length. We examined 4,598 men and women from the US Health and Retirement Study. Single adversities tended to have nonsignificant relations with telomere length. In adjusted models, lifetime cumulative adversity predicted 6% greater odds of shorter telomere length. This result was mainly due to childhood adversity. In adjusted models for cumulative childhood adversity, the occurrence of each additional childhood event predicted 11% increased odds of having short telomeres. This result appeared mainly because of social/traumatic exposures rather than financial exposures. This study suggests that the shadow of childhood adversity may reach far into later adulthood in part through cellular aging. cellular aging | telomeres | lifespan adversity | childhood adversity A ging cells play a crucial role in the pathogenesis of noncommunicable diseases, and telomere shortening in cells plays a part of this aging process (1, 2). Telomeres are DNAprotein caps at the ends of chromosomes that protect genetic material from degradation, and their lengths indicate cellular aging (2, 3). Experiments in rodents implicate shortened telomeres and lower activity of telomerase, the enzyme that lengthens telomeres, as causes of mitochondrial and tissue damage associated with disease pathogenesis (4-6).Telomere length is linked cross-sectionally and prospectively with human disease states in many studies. A recent meta-analysis suggests that individuals with observed short leukocyte telomeres are at an ∼80% increased risk of concurrent reports of cardiovascular disease and an ∼40% increased risk of developing cardiovascular disease in the future (7). Other recent meta-analyses support the concurrent associations between short telomeres and diabetes (8) and several cancers (9, 10). Several studies indicate that short telomeres from varied sources, including leukocytes and saliva, are related to early mortality (11-17), including a study with >60,000 adults (18), although null studies also exist (19)(20)(21)(22).Although these studies suggest that telomere length plays a role in disease, they are observational, and studies directly linking genetics...

Young adult survivors of childhood acute lymphoblastic leukemia show evidence of chronic inflammation and cellular aging

“…36,37 It has been demonstrated that adverse life events at a young age increase the odds of short telomeres; in contrast, comparable experiences in adults have not demonstrated a similar biologic impact. 38 The current study has several limitations. First, temporal changes in the survivors' clinical or biochemical parameters could not be assessed, because only crosssectional data were available.…”

“…In addition, social, traumatic, and psychological experiences associated with having cancer in childhood may become embedded epigenetically and lead to long‐term, or even permanent, alterations in gene expression . It has been demonstrated that adverse life events at a young age increase the odds of short telomeres; in contrast, comparable experiences in adults have not demonstrated a similar biologic impact …”

Measuring biological aging in humans: A quest

“…Interestingly, significant amounts of telomere shortening were explained by decreased telomerase activity in the cells that express this enzyme, suggesting that measuring telomerase activity in human cells may be informative (Lin et al, ). Several reports indicate that short telomeres may be associated with central obesity (García‐Calzón et al, ; Mundstock et al, ), lifetime accumulation of stress (Epel et al, ; Osler, Bendix, Rask, & Rod, ; Puterman et al, ), increased risk of cardiovascular events (Baragetti et al, ; Hammadah et al, ), reduced immune response to influenza vaccination (Najarro et al, ), mortality (Batsis et al, ; Goglin et al, ; Heidinger et al, ), and several adverse health outcomes (Lin et al, ; Lorenzi et al, ; Lustig et al, ; Sanders & Newman, ). Genetic mutations associated with short telomeres have been shown to cause dyskeratosis congenita, pulmonary fibrosis, and several other severe medical conditions that are grouped under the definition of “telomere syndrome” (El‐Chemaly et al, ; Ungar et al, ).…”

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

“…The evidence on the relation between childhood SSS and telomere length is inconsistent. While several recent studies are supportive of the association (Cohen et al, ; Puterman et al, ), an early meta‐analysis found no relation (see, Robertson et al, ). Developing a better understanding of the conditions under which childhood SSS is associated with telomere length is important given that telomere length is an indicator of cellular aging.…”

“…The evidence on the relation between childhood SSS and telomere length is inconsistent. While several recent studies are supportive of the association (Cohen et al, 2013;Puterman et al, 2016), an early meta-analysis found no relation (see, Robertson et al, 2013).…”