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Special Issue "Epigenetic and Molecular Consequences of Early-Life Trauma"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (15 February 2021).

Special Issue Editor

Dr. Jonathan Turner
E-Mail Website
Guest Editor
Principal Investigator, Immune Endocrine and Epigenetics Research Group, Luxembourg Institute of Health, Esch-sur-Alzette, Luxembourg
Interests: behavioural epigenetics; molecular consequences of early life adversity; DNA methylation; HPA axis; glucocorticoid receptor; genetics and epigenetics of the stress response

Special Issue Information

Dear Colleagues,

The environment in the early life period has a significant long-term impact on health and disease. This early-life exposome includes socioeconomic conditions, trauma exposure, parental separation, maltreatment, and many other factors. In many cases, suboptimal early-life conditions are a major contributor, not only to the lifelong disease burden but also to the cost of acute and chronic care. There is growing evidence that the early life social environment affects both the parents and the offspring. The direct action of the environment on the early-life epigenome as well as the inheritance of parental epigenetic marks is a rapidly expanding area of research. New and emerging research in the areas of epigenetics, biomedicine, and neuro-endocrinology hold great promise in relation to the development of our understanding of the complexity of the early life (social) environment and the multiplicity of factors that result in the long-term phenotype.

In this Special Issue of the International Journal of Molecular Sciences, the developmental origins of health and disease will be explored in the context of the early-life (social) environment. Potential topics include but are not limited to the early life (social) environment; methods of conceptualizing the early life environment, including SES, trauma, parental illness, or PTSD; long-term health consequences of the early life environment; long-term pathophysiological and phenotypic differences; biological markers of early-life exposure; and epigenetic or immunological mechanisms encoding exposure. Manuscripts exploring the relative strengths and weaknesses of competing hypotheses such as but limited to the hygiene hypothesis/microbiome establishment vs. EPIIC (Epigenetic Impact of Childbirth) that may explain long term differences in immune response are particularly welcome.

Although the impetus for this Special Issue comes from the COST Action CA18211 (Perinatal Mental Health and Birth-Related Trauma: Maximising Best Practice and Optimal Outcomes” (DEVoTION)), submissions are encouraged from the wider scientific community as well as action members.

Dr. Jonathan Turner
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Early-life exposome
  • Trauma
  • Epigenetic mechanisms
  • Behavioural epigenetics
  • Social epigenetics

Published Papers (6 papers)

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Research

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Article
Fetal Middle Cerebral Artery Pulsatility Index in No-Risk Pregnancies: Effects of Auditory Stimulation and Pregnancy Order
Int. J. Mol. Sci. 2020, 21(11), 3855; https://doi.org/10.3390/ijms21113855 - 29 May 2020
Viewed by 618
Abstract
Pulsatility index (PI) values in a fetal middle cerebral artery (MCA) were compared in no-risk pregnancies to examine the differences related to auditory stimulation test and pregnancy order. The study included 196 women with no-risk pregnancies selected from the database of more than [...] Read more.
Pulsatility index (PI) values in a fetal middle cerebral artery (MCA) were compared in no-risk pregnancies to examine the differences related to auditory stimulation test and pregnancy order. The study included 196 women with no-risk pregnancies selected from the database of more than 1000 pregnant women divided into two groups. Group 1 consisted of 98 nulliparous women (C1 = 98) and Group 2 consisted of 98 parous women (C2 = 98). All pregnant women were of comparable age and fetal gestational age (GA) when MCA-PI values were recorded. Measurements of PI values in fetal MCA were obtained before and immediately after the application of fetal auditory stimulation test. The MCA-PI measuring was conducted in the period between the 36th and the 41st week of GA. The results showed that PI baseline values and PI values after defined auditory stimulation were significantly different when measured in nulliparous women compared to parous women (p = 0.001; p = 0.003, respectively), while no group differences were observed in relative PI value changes due to auditory stimulation. These findings suggest that hemodynamic changes in fetal MCA caused by defined auditory stimulation measured by PI value changes may be valuable in the assessment of fetal auditory perception functionality and its development. Full article
(This article belongs to the Special Issue Epigenetic and Molecular Consequences of Early-Life Trauma)
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Review

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Review
The ‘Jekyll and Hyde’ of Gluconeogenesis: Early Life Adversity, Later Life Stress, and Metabolic Disturbances
Int. J. Mol. Sci. 2021, 22(7), 3344; https://doi.org/10.3390/ijms22073344 - 25 Mar 2021
Viewed by 766
Abstract
The physiological response to a psychological stressor broadly impacts energy metabolism. Inversely, changes in energy availability affect the physiological response to the stressor in terms of hypothalamus, pituitary adrenal axis (HPA), and sympathetic nervous system activation. Glucocorticoids, the endpoint of the HPA axis, [...] Read more.
The physiological response to a psychological stressor broadly impacts energy metabolism. Inversely, changes in energy availability affect the physiological response to the stressor in terms of hypothalamus, pituitary adrenal axis (HPA), and sympathetic nervous system activation. Glucocorticoids, the endpoint of the HPA axis, are critical checkpoints in endocrine control of energy homeostasis and have been linked to metabolic diseases including obesity, insulin resistance, and type 2 diabetes. Glucocorticoids, through the glucocorticoid receptor, activate transcription of genes associated with glucose and lipid regulatory pathways and thereby control both physiological and pathophysiological systemic energy homeostasis. Here, we summarize the current knowledge of glucocorticoid functions in energy metabolism and systemic metabolic dysfunction, particularly focusing on glucose and lipid metabolism. There are elements in the external environment that induce lifelong changes in the HPA axis stress response and glucocorticoid levels, and the most prominent are early life adversity, or exposure to traumatic stress. We hypothesise that when the HPA axis is so disturbed after early life adversity, it will fundamentally alter hepatic gluconeogenesis, inducing hyperglycaemia, and hence crystalise the significant lifelong risk of developing either the metabolic syndrome, or type 2 diabetes. This gives a “Jekyll and Hyde” role to gluconeogenesis, providing the necessary energy in situations of acute stress, but driving towards pathophysiological consequences when the HPA axis has been altered. Full article
(This article belongs to the Special Issue Epigenetic and Molecular Consequences of Early-Life Trauma)
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Review
Are There Epigenetic Oxytocin-Mediated Effects on the Mother and Infant during Physiological Childbirth?
Int. J. Mol. Sci. 2020, 21(24), 9503; https://doi.org/10.3390/ijms21249503 - 14 Dec 2020
Viewed by 610
Abstract
Introduction: Studies have shown that long-term positive behavioural and physiological changes are induced in connection with vaginal, physiological birth, and skin-to-skin contact after birth in mothers and babies. Some of these effects are consistent with the effect profile of oxytocin. This scoping review [...] Read more.
Introduction: Studies have shown that long-term positive behavioural and physiological changes are induced in connection with vaginal, physiological birth, and skin-to-skin contact after birth in mothers and babies. Some of these effects are consistent with the effect profile of oxytocin. This scoping review explores whether epigenetic changes of the oxytocin gene and of the oxytocin receptor gene (OTR) are involved in these effects. Methods: We searched Pubmed, Medline, BioMed Central, Cochrane Library, OVID, and Web of Science for evidence of epigenetic changes in connection with childbirth in humans, with a particular focus on the oxytocin system. Results: There were no published studies identified that were related to epigenetic changes of oxytocin and its receptor in connection with labour, birth, and skin-to-skin contact after birth in mothers and babies. However, some studies were identified that showed polymorphisms of the oxytocin receptor influenced the progress of labour. We also identified studies in which the level of global methylation was measured in vaginal birth and caesarean section, with conflicting results. Some studies identified differences in the level of methylation of single genes linked to various effects, for example, immune response, metabolism, and inflammation. In some of these cases, the level of methylation was associated with the duration of labour or mode of birth. We also identified some studies that demonstrated long-term effects of mode of birth and of skin-to-skin contact linked to changes in oxytocin function. Conclusion: There were no studies identified that showed epigenetic changes of the oxytocin system in connection with physiological birth. The lack of evidence, so far, regarding epigenetic changes did not exclude future demonstrations of such effects, as there was a definite role of oxytocin in creating long-term effects during the perinatal period. Such studies may not have been performed. Alternatively, the oxytocin linked effects might be indirectly mediated via other receptors and signalling systems. We conclude that there is a significant lack of research examining long-term changes of oxytocin function and long-term oxytocin mediated adaptive effects induced during physiological birth and skin-to-skin contact after birth in mothers and their infants. Full article
(This article belongs to the Special Issue Epigenetic and Molecular Consequences of Early-Life Trauma)
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Review
The COVID-19 Pandemic: Does Our Early Life Environment, Life Trajectory and Socioeconomic Status Determine Disease Susceptibility and Severity?
Int. J. Mol. Sci. 2020, 21(14), 5094; https://doi.org/10.3390/ijms21145094 - 19 Jul 2020
Cited by 6 | Viewed by 2508
Abstract
A poor socioeconomic environment and social adversity are fundamental determinants of human life span, well-being and health. Previous influenza pandemics showed that socioeconomic factors may determine both disease detection rates and overall outcomes, and preliminary data from the ongoing coronavirus disease (COVID-19) pandemic [...] Read more.
A poor socioeconomic environment and social adversity are fundamental determinants of human life span, well-being and health. Previous influenza pandemics showed that socioeconomic factors may determine both disease detection rates and overall outcomes, and preliminary data from the ongoing coronavirus disease (COVID-19) pandemic suggests that this is still true. Over the past years it has become clear that early-life adversity (ELA) plays a critical role biasing the immune system towards a pro-inflammatory and senescent phenotype many years later. Cytotoxic T-lymphocytes (CTL) appear to be particularly sensitive to the early life social environment. As we understand more about the immune response to SARS-CoV-2 it appears that a functional CTL (CD8+) response is required to clear the infection and COVID-19 severity is increased as the CD8+ response becomes somehow diminished or exhausted. This raises the hypothesis that the ELA-induced pro-inflammatory and senescent phenotype may play a role in determining the clinical course of COVID-19, and the convergence of ELA-induced senescence and COVID-19 induced exhaustion represents the worst-case scenario with the least effective T-cell response. If the correct data is collected, it may be possible to separate the early life elements that have made people particularly vulnerable to COVID-19 many years later. This will, naturally, then help us identify those that are most at risk from developing the severest forms of COVID-19. In order to do this, we need to recognize socioeconomic and early-life factors as genuine medically and clinically relevant data that urgently need to be collected. Finally, many biological samples have been collected in the ongoing studies. The mechanisms linking the early life environment with a defined later-life phenotype are starting to be elucidated, and perhaps hold the key to understanding inequalities and differences in the severity of COVID-19. Full article
(This article belongs to the Special Issue Epigenetic and Molecular Consequences of Early-Life Trauma)
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Review
Nutri-Epigenetics and Gut Microbiota: How Birth Care, Bonding and Breastfeeding Can Influence and Be Influenced?
Int. J. Mol. Sci. 2020, 21(14), 5032; https://doi.org/10.3390/ijms21145032 - 16 Jul 2020
Cited by 5 | Viewed by 1646
Abstract
Maternal lifestyle is an important factor in the programming of an infant’s epigenome, in particular when considered alongside the mode of birth and choice of feeding method (i.e., breastfeeding or formula feeding). Beginning in utero, and during the first two years of an [...] Read more.
Maternal lifestyle is an important factor in the programming of an infant’s epigenome, in particular when considered alongside the mode of birth and choice of feeding method (i.e., breastfeeding or formula feeding). Beginning in utero, and during the first two years of an infant’s life, cells acquire an epigenetic memory of the neonatal exposome which can be influential across the entire lifespan. Parental lifestyle (e.g., malnutrition, alcohol intake, smoke, stress, exposure to xenobiotics and/or drugs) can modify both the maternal and paternal epigenome, leading to epigenetic inheritance in their offspring. This review aims to outline the origin of early life modulation of the epigenome, and to share this fundamental concept with all the health care professionals involved in the development and provision of care during childbirth in order to inform future parents and clinicians of the importance of the this process and the key role it plays in the programming of a child’s health. Full article
(This article belongs to the Special Issue Epigenetic and Molecular Consequences of Early-Life Trauma)

Other

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Concept Paper
Twin Research in the Post-Genomic Era: Dissecting the Pathophysiological Effects of Adversity and the Social Environment
Int. J. Mol. Sci. 2020, 21(9), 3142; https://doi.org/10.3390/ijms21093142 - 29 Apr 2020
Cited by 4 | Viewed by 1072
Abstract
The role of twins in research is evolving as we move further into the post-genomic era. With the re-definition of what a gene is, it is becoming clear that biological family members who share a specific genetic variant may well not have a [...] Read more.
The role of twins in research is evolving as we move further into the post-genomic era. With the re-definition of what a gene is, it is becoming clear that biological family members who share a specific genetic variant may well not have a similar risk for future disease. This has somewhat invalidated the prior rationale for twin studies. Case co-twin study designs, however, are slowly emerging as the ideal tool to identify both environmentally induced epigenetic marks and epigenetic disease-associated processes. Here, we propose that twin lives are not as identical as commonly assumed and that the case co-twin study design can be used to investigate the effects of the adult social environment. We present the elements in the (social) environment that are likely to affect the epigenome and measures in which twins may diverge. Using data from the German TwinLife registry, we confirm divergence in both the events that occur and the salience for the individual start as early as age 11. Case co-twin studies allow for the exploitation of these divergences, permitting the investigation of the role of not only the adult social environment, but also the salience of an event or environment for the individual, in determining lifelong health trajectories. In cases like social adversity where it is clearly not possible to perform a randomised-controlled trial, we propose that the case co-twin study design is the most rigorous manner with which to investigate epigenetic mechanisms encoding environmental exposure. The role of the case co-twin design will continue to evolve, as we argue that it will permit causal inference from observational data. Full article
(This article belongs to the Special Issue Epigenetic and Molecular Consequences of Early-Life Trauma)
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