scholarly journals Stress exposure in intrauterine life is associated with shorter telomere length in young adulthood

2011 ◽  
Vol 108 (33) ◽  
pp. E513-E518 ◽  
Author(s):  
S. Entringer ◽  
E. S. Epel ◽  
R. Kumsta ◽  
J. Lin ◽  
D. H. Hellhammer ◽  
...  
2019 ◽  
Vol 8 (11) ◽  
pp. 1824 ◽  
Author(s):  
Catharina A. Hartman ◽  
Nanda Rommelse ◽  
Cees L. van der Klugt ◽  
Rob B.K. Wanders ◽  
Marieke E. Timmerman

Background: Compared to typically developing individuals, individuals with attention-deficit-hyperactivity disorder (ADHD) are on average more often exposed to stressful conditions (e.g., school failure, family conflicts, financial problems). We hypothesized that high exposure to stress relates to a more persistent and complex (i.e., multi-problem) form of ADHD, while low-stress exposure relates to remitting ADHD over the course of adolescence. Method: Longitudinal data (ages 11, 13, 16, and 19) came from the Tracking Adolescents’ Individual Life Survey (TRAILS). We selected children diagnosed with ADHD (n = 244; 167 males; 77 females) from the TRAILS clinical cohort and children who screened positive (n = 365; 250 males; 115 females) and negative (gender-matched: n = 1222; 831 males; 391 females) for ADHD from the TRAILS general population sample cohort (total n = 1587). Multivariate latent class growth analysis was applied to parent- and self-ratings of stress exposure, core ADHD problems (attention problems, hyperactivity/impulsivity), effortful control, emotion dysregulation (irritability, extreme reactivity, frustration), and internalizing problems (depression, anxiety, somatic complaints). Results: Seven distinct developmental courses in stress exposure and psychopathology were discerned, of which four related to ADHD. Two persistent ADHD courses of severely affected adolescents were associated with very high curvilinear stress exposure peaking in mid-adolescence: (1) Severe combined type with ongoing, severe emotional dysregulation, and (2) combined type with a high and increasing internalization of problems and elevated irritability; two partly remitting ADHD courses had low and declining stress exposure: (3) inattentive type, and (4) moderate combined type, both mostly without comorbid problems. Conclusions: High-stress exposure between childhood and young adulthood is strongly intertwined with a persistent course of ADHD and with comorbid problems taking the form of either severe and persistent emotion dysregulation (irritability, extreme reactivity, frustration) or elevated and increasing irritability, anxiety, and depression. Conversely, low and declining stress exposure is associated with remitting ADHD and decreasing internalizing and externalizing problems. Stress exposure is likely to be a facilitating and sustaining factor in these two persistent trajectories of ADHD with comorbid problems into young adulthood. Our findings suggest that a bidirectional, continuing, cycle of stressors leads to enhanced symptoms, in turn leading to more stressors, and so forth. Consideration of stressful conditions should, therefore, be an inherent part of the diagnosis and treatment of ADHD, to potentiate prevention and interruption of adverse trajectories.


2014 ◽  
Vol 28 (6) ◽  
pp. 967-972 ◽  
Author(s):  
Steven R. H. Beach ◽  
Man Kit Lei ◽  
Gene H. Brody ◽  
Tianyi Yu ◽  
Robert A. Philibert

2019 ◽  
Vol 104 ◽  
pp. 210-218 ◽  
Author(s):  
Stefanie E. Mayer ◽  
Aric A. Prather ◽  
Eli Puterman ◽  
Jue Lin ◽  
Justine Arenander ◽  
...  

Author(s):  
Richard S Lee ◽  
Peter P Zandi ◽  
Alicia Santos ◽  
Anna Aulinas ◽  
Jenny L Carey ◽  
...  

Abstract Context Chronic exposure to glucocorticoids (GCs) or stress increases the risk of medical disorders, including cardiovascular and neuropsychiatric disorders. GCs contribute to an accelerated aging, while the link between chronic GCs exposure and disease onset is well established, the underpinning mechanisms are not clear. Objective we explored the potential nexus between GCs or stress exposure and telomere length. Design, Setting, and Participants rats exposed to three weeks of chronic stress; an iatrogenic mouse model of Cushing’s syndrome (CS); a mouse neuronal cell line; 33 patients with CS and 75 healthy human people were studied. Results 1.Telomere length is associated with exposure to stress in rats: 54.5% (P=0.036) reduction in telomere length in the stressed animals. Genomic DNA extracted from the dentate gyrus of stressed and unstressed rats showed 43.2% reduction in telomere length (P=0.006). 2. Mice were exposed to corticosterone (CORT), this treatment produced a 61.4% reduction in telomere length in the blood gDNA (P=5.75x 10-5). 3. We observed a 40.8% reduction in the telomere length in patients with active CS compared to healthy controls (P=0.006). There was a 17.8% reduction in telomere length in cured CS patients, no different from controls (P=0.08). For both cured and active CS, telomere length correlated significantly with the duration of hypercortisolism (R2=0.22, P=0.007). 4. There was a 27.6% reduction in telomere length between low vs. high tertiles in bedtime cortisol levels (P=0.019). Conclusions Our findings demonstrate that exposure to stress and/or glucocorticoids is associated with shortened telomeres, and that shortening may be partially reversible.


2014 ◽  
Vol 281 (1782) ◽  
pp. 20133151 ◽  
Author(s):  
Katherine A. Herborn ◽  
Britt J. Heidinger ◽  
Winnie Boner ◽  
Jose C. Noguera ◽  
Aileen Adam ◽  
...  

Exposure to stressors early in life is associated with faster ageing and reduced longevity. One important mechanism that could underlie these late life effects is increased telomere loss. Telomere length in early post-natal life is an important predictor of subsequent lifespan, but the factors underpinning its variability are poorly understood. Recent human studies have linked stress exposure to increased telomere loss. These studies have of necessity been non-experimental and are consequently subjected to several confounding factors; also, being based on leucocyte populations, where cell composition is variable and some telomere restoration can occur, the extent to which these effects extend beyond the immune system has been questioned. In this study, we experimentally manipulated stress exposure early in post-natal life in nestling European shags ( Phalacrocorax aristotelis ) in the wild and examined the effect on telomere length in erythrocytes. Our results show that greater stress exposure during early post-natal life increases telomere loss at this life-history stage, and that such an effect is not confined to immune cells. The delayed effects of increased telomere attrition in early life could therefore give rise to a ‘time bomb’ that reduces longevity in the absence of any obvious phenotypic consequences early in life.


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