Traumatic stress and accelerated DNA methylation age: A meta-analysis

Wolf, Erika J.; Maniates, Hannah; Nugent, Nicole R.; Maihofer, Adam X.; Armstrong, Don; Ratanatharathorn, Andrew; Ashley–Koch, Allison; Garrett, Melanie E.; Kimbrel, Nathan A.; Lori, Adriana; Workgroup, VA Mid-Atlantic Mirecc; Aiello, Allison E.; Baker, Dewleen G.; Beckham, Jean C.; Boks, Marco P.; Galea, Sandro; Geuze, Elbert; Hauser, Michael A.; Kessler, Ronald C.; Koenen, Karestan C.; Miller, Mark W.; Ressler, Kerry J.; Risbrough, Victoria B.; Rutten, Bart P. F.; Stein, Murray B.; Ursano, Robert J.; Vermetten, Eric; Vinkers, Christiaan H.; Uddin, Monica; Smith, Alicia K.; Nievergelt, Caroline M.; Logue, Mark W.

doi:10.1016/j.psyneuen.2017.12.007

Cited by 201 publications

(179 citation statements)

References 77 publications

(105 reference statements)

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“…Since cumulative life stress has been shown to be strongly predictive of accelerated epigenetic aging 132 , the persistent symptoms and residual effects of PTSD may themselves be chronic stressors that promote accelerated epigenetic aging. This is in contrast to current PTSD diagnosis or severity, which has not been found to associate with accelerated epigenetic aging 130 . As a matter of fact, a longitudinal study of military personnel reported an apparent reversal of epigenetic aging during development of PTSD symptoms 133 , which suggests an initial attempt at compensation before loss of control and accelerated epigenetic aging.…”

Section: Epigenetic Effects Of Stress/trauma Response In the Brain Ancontrasting

confidence: 61%

“…In fact, lifetime PTSD severity has been found to be associated with accelerated aging 129,130 based on one DNA methylation-based calculation of cellular age 131 , as well as reduced neural integrity (in the genu of the corpus callosum), as indexed by DTI 129 . Since cumulative life stress has been shown to be strongly predictive of accelerated epigenetic aging 132 , the persistent symptoms and residual effects of PTSD may themselves be chronic stressors that promote accelerated epigenetic aging.…”

Section: Epigenetic Effects Of Stress/trauma Response In the Brain Anmentioning

confidence: 99%

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Neuroepigenetics of Post-Traumatic Stress Disorder

Kim

Smith

Nievergelt

et al. 2018

Progress in Molecular Biology and Translational Science

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While diagnosis of PTSD is based on behavioral symptom clusters that are most directly associated with brain function, epigenetic studies of PTSD in humans to date have been limited to peripheral tissues. Animal models of PTSD have been key for understanding the epigenetic alterations in the brain most directly relevant to endophenotypes of PTSD, in particular those pertaining to fear memory and stress response. This chapter provides an overview of neuroepigenetic studies based on animal models of PTSD, with an emphasis on the effect of stress on fear memory. Where relevant, we also describe human-based studies with relevance to neuroepigenetic insights gleaned from animal work and suggest promising directions for future studies of PTSD neuroepigenetics in living humans that combine peripheral epigenetic measures with measures of central nervous system activity, structure and function.

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Section: Epigenetic Effects Of Stress/trauma Response In the Brain Ancontrasting

confidence: 61%

Section: Epigenetic Effects Of Stress/trauma Response In the Brain Anmentioning

confidence: 99%

Neuroepigenetics of Post-Traumatic Stress Disorder

Kim

Smith

Nievergelt

et al. 2018

Progress in Molecular Biology and Translational Science

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“…Given these mixed patterns of results across studies and the variability in findings across the two algorithms, Wolf et al [62] conducted a meta-analysis of over 2000 subjects and nine cohorts contributing to the Psychiatric Genomics Consortium PTSD Epigenetics Workgroup [63] and found that lifetime PTSD symptom severity and childhood trauma (when assessed with a particularly sensitive self-report instrument) were associated with accelerated Hannum DNAm age. No trauma or PTSD-related effects emerged for the Horvath index.…”

Section: Traumatic Stress and Accelerated Cellular Aging In The Epi/gmentioning

confidence: 99%

“…Specifically, robust associations between estimated white blood cell counts and accelerated DNAm age have emerged across studies, such as a negative relationship between CD4 T-cell counts and accelerated Hannum DNAm [55, 60••, 61–62]. There is also preliminary evidence for an association between Horvath epigenetic age acceleration (adjusted for white blood cell counts) and increased C-reactive protein as well as between Hannum epigenetic age acceleration (in an index combined with white blood cell counts, see below) and increased C-reactive protein [78].…”

Section: Potential Mechanisms Linking Traumatic Stress To Acceleratedmentioning

confidence: 99%

Traumatic Stress and Accelerated Cellular Aging: From Epigenetics to Cardiometabolic Disease

Wolf

Morrison

2017

Curr Psychiatry Rep

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Purpose of review The aim of this paper is to review the recent literature on traumatic stress-related accelerated aging, including a focus on cellular mechanisms and biomarkers of cellular aging and on the clinical manifestations of accelerated biological aging. Recent findings Multiple lines of research converge to suggest that PTSD is associated with accelerated aging in the epigenome, and the immune and inflammation systems, and this may be reflected in premature onset of cardiometabolic and cardiovascular disease. Summary The current state of research paves the way for future work focused on identifying the peripheral and central biological mechanisms linking traumatic stress to accelerated biological aging and medical morbidity, with an emphasis on processes involved in inflammation, immune functioning, oxidative stress, autonomic arousal, and stress responding. Ultimately, such work could help reduce the pace of biological aging and improve health and wellness.

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“…In addition to relationships between EAA and growth under energetic constraint, it is also potentially important to understand how concurrent exposure to psychosocial and energetic stressors relates to children's EAA. Multiple studies have shown that individuals experiencing psychosocial adversity prior to adulthood exhibit greater EAA, and children's family environments may play a role in shaping these effects (Brody, Miller, Yu, Beach, & Chen, ; Javed, Chen, Lin, & Liang, ; Jovanovic et al, ; Lawn et al, ; Sumner, Colich, Uddin, Armstrong, & McLaughlin, ; Wolf et al, ). For example, research among African‐American children found that supportive family contexts were protective for children against the effects of racial discrimination on EAA (Brody, Yu, Chen, Beach, & Miller, ).…”

Section: Introductionmentioning

confidence: 99%

Epigenetic aging in children from a small‐scale farming society in The Congo Basin: Associations with child growth and family conflict

Gettler

Lin

Miegakanda

et al. 2019

Developmental Psychobiology

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Developmental environments influence individuals' long‐term health trajectories, and there is increasing emphasis on understanding the biological pathways through which this occurs. Epigenetic aging evaluates DNA methylation at a suite of distinct CpG sites in the genome, and epigenetic age acceleration (EAA) is linked to heightened chronic morbidity and mortality risks in adults. Consequently, EAA provides insights on trajectories of biological aging, which early life experiences may help shape. However, few studies have measured correlates of children's epigenetic aging, especially outside of the U.S. and Europe. In particular, little is known about how children's growth and development relate to EAA in ecologies in which energetic and pathogenic stressors are commonplace. We studied EAA from dried blood spots among Bondongo children (n = 54) residing in a small‐scale, fisher‐farmer society in a remote region of the Republic of the Congo. Here, infectious disease burdens and their resultant energy demands are high. Children who were heavier for height or taller for age, respectively, exhibited greater EAA, including intrinsic EAA, which is considered to measure EAA internal to cells. Furthermore, we found that children in families with more conflict between parents had greater intrinsic EAA. These results suggest that in contexts in which limited energy must be allocated to competing demands, more investment in growth may coincide with greater EAA, which parallels findings in European children who do not face similar energetic constraints. Our findings also indicate that associations between adverse family environments and greater intrinsic EAA were nonetheless observable but only after adjustment for covariates relevant to the energetically and immunologically demanding nature of the local ecology.

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Traumatic stress and accelerated DNA methylation age: A meta-analysis

Cited by 201 publications

References 77 publications

Neuroepigenetics of Post-Traumatic Stress Disorder

Neuroepigenetics of Post-Traumatic Stress Disorder

Traumatic Stress and Accelerated Cellular Aging: From Epigenetics to Cardiometabolic Disease

Epigenetic aging in children from a small‐scale farming society in The Congo Basin: Associations with child growth and family conflict

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