Childhood Trauma, DNA Methylation of Stress-Related Genes, and Depression: Findings From Two Monozygotic Twin Studies

Peng, Hao; Zhu, Yun; Strachan, Eric; Fowler, Emily; Bacus, Tamara J.; Roy‐Byrne, Peter; Goldberg, Jack; Vaccarino, Viola; Zhao, Jinying

doi:10.1097/psy.0000000000000604

Cited by 81 publications

(75 citation statements)

References 52 publications

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“…In addition to the primary Bdnf exon IV, other isoforms of Bdnf mRNA were also influenced by stress-related DNA methylation. Notably, altered DNA methylation at the BDNF promoters were found in blood samples of stressed humans with depressive symptoms [130,131].…”

Section: Dna Methylation and Bdnfmentioning

confidence: 99%

The Relationships Between Stress, Mental Disorders, and Epigenetic Regulation of BDNF

Zhang

Wang

Sun

2020

IJMS

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Brain-derived neurotrophic factor (BDNF), a critical member of the neurotrophic family, plays an important role in multiple stress-related mental disorders. Although alterations in BDNF in multiple brain regions of individuals experiencing stress have been demonstrated in previous studies, it appears that a set of elements are involved in the complex regulation. In this review, we summarize the specific brain regions with altered BDNF expression during stress exposure. How various environmental factors, including both physical and psychological stress, affect the expression of BDNF in specific brain regions are further summarized. Moreover, epigenetic regulation of BDNF, including DNA methylation, histone modification, and noncoding RNA, in response to diverse types of stress, as well as sex differences in the sensitivity of BDNF to the stress response, is also summarized. Clarification of the underlying role of BDNF in the stress process will promote our understanding of the pathology of stress-linked mental disorders and provide a potent target for the future treatment of stress-related illness.

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Section: Dna Methylation and Bdnfmentioning

confidence: 99%

The Relationships Between Stress, Mental Disorders, and Epigenetic Regulation of BDNF

Zhang

Wang

Sun

2020

IJMS

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“…The reduced IL-6 promoter was accompanied by an increased acute stress-induced IL-6 response, and a blunted cortisol response. On the other hand, ELS seemed to contribute to the increased DNAm of BNDF in individuals with ELS, and this epigenetic alteration was long-lasting and possibly impacted the offspring of the females (Braithwaite et al, 2015;Peng et al, 2018). Furthermore, the functional single nucleotide polymorphisms (SNPs) of BDNF were moderated by the DNAm values at BDNF specific promoter sites and the interaction between SNPs and DNAm enhanced the susceptibility to depression (Ferrer et al, 2019).…”

Section: Epigenetic Studies Focused On Human Beingsmentioning

confidence: 99%

Effect of Early Life Stress on the Epigenetic Profiles in Depression

Xie

et al. 2020

Front. Cell Dev. Biol.

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Depression is one of the most common mental disorders and has caused an overwhelming burden on world health. Abundant studies have suggested that early life stress may grant depressive-like phenotypes in adults. Childhood adversities that occurred in the developmental period amplified stress events in adulthood. Epigenetic-environment interaction helps to explain the role of early life stress on adulthood depression. Early life stress shaped the epigenetic profiles of the HPA axis, monoamine, and neuropeptides. In the context of early adversities increasing the risk of depression, early life stress decreased the activity of the glucocorticoid receptors, halted the circulation and production of serotonin, and reduced the molecules involved in modulating the neurogenesis and neuroplasticity. Generally, DNA methylation, histone modifications, and the regulation of non-coding RNAs programmed the epigenetic profiles to react to early life stress. However, genetic precondition, subtypes of early life stress, the timing of epigenetic status evaluated, demographic characteristics in humans, and strain traits in animals favored epigenetic outcomes. More research is needed to investigate the direct evidence for how early life stress-induced epigenetic changes contribute to the vulnerability of depression.

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“…Childhood trauma also increases the risk of respiratory, heart, and metabolic diseases [ 13 ]. Childhood trauma deteriorates health through various mechanisms such as systemic inflammation [ 14 ], reducing telomere length [ 15 , 16 , 17 , 18 ], and DNA methylation [ 19 , 20 , 21 ]. Exposure to childhood trauma also impacts the developing brain [ 22 ].…”

Section: Introductionmentioning

confidence: 99%

Family Socioeconomic Status and Exposure to Childhood Trauma: Racial Differences

Assari

2020

Children

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Background: Minorities’ diminished returns (MDRs) refer to weaker effects of socioeconomic status (SES) indicators such as parental educational attainment and family income in generating tangible childhood outcomes for racial and ethnic minorities compared to the majority group, a pattern prevalent in the US. Our existing knowledge is minimal, however, about diminished returns of family SES on reducing exposure to childhood trauma. Aim: To determine if there was a difference between non-Hispanic whites (NHW) and non-Hispanic blacks (NHB) in the effect of SES on exposure to childhood trauma among children ages 8–11 years old. Materials and methods: In this cross-sectional study, we analyzed data from 4696 NHW or NHB American 8–11-year-old children who were participants in the Adolescent Brain Cognitive Development (ABCD) Study. The independent variables were parental educational attainment and family income. The primary outcome was exposure to 1 or 2+ childhood traumas, measured by the Kiddie Schedule for Affective Disorders and Schizophrenia (K-SADS) semi-structured interview. Polynomial regression was used for data analysis. Results: Parental education and family income had statistically significant protective (negative) effects on childhood trauma, indicating children from high income and highly educated families were exposed to a lower level of childhood trauma. However, race/ethnicity showed statistically significant interactions with parental education and family income on exposure to childhood trauma, indicating weaker protective effects of parental education and family income on reducing exposure to trauma for NHB compared to NHW children. Race-specific models showed protective effects of parental education and family income on exposure to childhood trauma for NHW but not NHB children. Conclusion: The protective effects of parental education and family income against exposure to childhood trauma are systematically diminished for NHBs compared to NHWs. To minimize the racial/ethnic health gaps, diminished returns of parental education and family income should be addressed. There is a need for programs and interventions that equalize not only SES but also the marginal returns of SES for ethnic groups. Such efforts require addressing structural and societal barriers that hinder NHB families from translating their SES resources into tangible outcomes. There is a need for studies that can minimize MDRs for NHB families, such that SES can similarly secure tangible outcomes in the presence of SES resources.

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Childhood Trauma, DNA Methylation of Stress-Related Genes, and Depression: Findings From Two Monozygotic Twin Studies

Cited by 81 publications

References 52 publications

The Relationships Between Stress, Mental Disorders, and Epigenetic Regulation of BDNF

The Relationships Between Stress, Mental Disorders, and Epigenetic Regulation of BDNF

Effect of Early Life Stress on the Epigenetic Profiles in Depression

Family Socioeconomic Status and Exposure to Childhood Trauma: Racial Differences

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