Epigenetic Research Research Articles

Prenatal chemical exposures and the methylome: current evidence and opportunities for environmental epigenetics.

Exposure to pollutants and chemicals during critical developmental periods in early life can impact health and disease risk across the life course. Research in environmental epigenetics has provided increasing evidence that prenatal exposures affect epigenetic markers, particularly DNA methylation. In this article, we discuss the role of DNA methylation in early life programming and review evidence linking the intrauterine environment to epigenetic modifications, with a focus on exposure to tobacco smoke, metals, and endocrine-disrupting chemicals. We also discuss challenges and novel approaches in environmental epigenetic research and explore the potential of epigenetic biomarkers in studies of pediatric populations as indicators of exposure and disease risk. Overall, we aim to highlight how advancements in environmental epigenetics may transform our understanding of early-life exposures and inform new approaches for supporting long-term health.

Normative implications of postgenomic deterministic narratives: the case study of epigenetic harm.

What do we mean when we talk about epigenetic harm? This paper presents a multidimensional view of epigenetic harm. It is a plea to take a step back from discussions of epigenetic responsibility distributions prevalent in ELSA literature on epigenetics. Instead, it urges researchers to take a closer look at the normative role played by the concept of epigenetic harm. It starts out by showing that the ways in which the object of epigenetic responsibility has already been conceptualized are all related to 'epigenetic harm': something negative that happens in which epigenetic mechanisms play a role, or rather something that needs to be avoided. Epigenetic harm is then characterized as a bridging concept between relatively neutral findings on epigenetics on the one side, and potential ethical and societal implications of those findings, primarily in terms of responsibility ascriptions and distributions, on the other. The paper proposes that a sufficiently nuanced account of epigenetic harm should include at least three dimensions. The dimension of causation alone leads to an overly narrow understanding of harm, and a wrong understanding of this dimension might prompt researchers to support an excessively simplistic epigenetic determinism. It is argued that a multidimensional analysis of epigenetic harm is less vulnerable to this threat and more reflective of the various kinds of harm that may be experienced by the subjects of epigenetic alterations. The paper applies insights from disability studies and feminist philosophy to draw attention to two other dimensions of epigenetic harm, namely lived experiences and relationality. The paper concludes by exploring what a shift towards a multidimensional approach to epigenetic harm might mean for epigenetic research and responsibility ascriptions by formulating some concrete implications.

Epigenetic dynamics of partially methylated domains in human placenta and trophoblast stem cells

BackgroundThe placenta is essential for nutrient exchange and hormone production between the mother and the developing fetus and serves as an invaluable model for epigenetic research. Most epigenetic studies of the human placenta have used whole placentas from term pregnancies and have identified the presence of partially methylated domains (PMDs). However, the origin of these domains, which are typically absent in most somatic cells, remains unclear in the placental context.ResultsUsing whole-genome bisulfite sequencing and analysis of histone H3 modifications, we generated epigenetic profiles of human cytotrophoblasts during the first trimester and at term, as well as human trophoblast stem cells. Our study focused specifically on PMDs. We found that genomic regions likely to form PMDs are resistant to global DNA demethylation during trophectoderm reprogramming, and that PMDs arise through a slow methylation process within condensed chromatin near the nuclear lamina. In addition, we found significant differences in histone H3 modifications between PMDs in cytotrophoblasts and trophoblast stem cells.ConclusionsOur findings suggest that spatiotemporal genomic features shape megabase-scale DNA methylation patterns, including PMDs, in the human placenta and highlight distinct differences in PMDs between human cytotrophoblasts and trophoblast stem cells. These findings advance our understanding of placental biology and provide a basis for further research into human development and related diseases.

Epigenetic Explorations of Neurological Disorders, the Identification Methods, and Therapeutic Avenues.

Neurodegenerative disorders are major health concerns globally, especially in aging societies. The exploration of brain epigenomes, which consist of multiple forms of DNA methylation and covalent histone modifications, offers new and unanticipated perspective into the mechanisms of aging and neurodegenerative diseases. Initially, chromatin defects in the brain were thought to be static abnormalities from early development associated with rare genetic syndromes. However, it is now evident that mutations and the dysregulation of the epigenetic machinery extend across a broader spectrum, encompassing adult-onset neurodegenerative diseases. Hence, it is crucial to develop methodologies that can enhance epigenetic research. Several approaches have been created to investigate alterations in epigenetics on a spectrum of scales-ranging from low to high-with a particular focus on detecting DNA methylation and histone modifications. This article explores the burgeoning realm of neuroepigenetics, emphasizing its role in enhancing our mechanistic comprehension of neurodegenerative disorders and elucidating the predominant techniques employed for detecting modifications in the epigenome. Additionally, we ponder the potential influence of these advancements on shaping future therapeutic approaches.

Epigenetic modulation of fungal pathogens: a focus on Magnaporthe oryzae.

Epigenetics has emerged as a potent field of study for understanding the factors influencing the effectiveness of human disease treatments and for identifying alternations induced by pathogens in host plants. However, there has been a paucity of research on the epigenetic control of the proliferation and pathogenicity of fungal plant pathogens. Fungal plant pathogens such as Magnaporthe oryzae, a significant threat to global rice production, provide an important model for exploring how epigenetic mechanisms govern fungal proliferation and virulence. In M. oryzae, epigenetic alterations, such as DNA methylation, histone modification, and non-coding RNAs, regulate gene expression patterns that influence the pathogen's ability to infect its host. These modifications can enhance fungal adaptability, allowing the pathogen to survive in diverse environments and evade host immune responses. Our primary objective is to provide a comprehensive review of the existing epigenetic research on M. oryzae and shed light on how these changes influence the pathogen's lifecycle, its ability to invade host tissues, and the overall severity of the disease. We begin by examining the epigenetic alterations occurring in M. oryzae and their contributions to the virulence and proliferation of the fungus. To advance our understanding of epigenetic mechanisms in M. oryzae and similar plant diseases, we emphasize the need to address unanswered questions and explore future research directions. This information is crucial for developing new antifungal treatments that target epigenetic pathways, which could lead to improved disease management.

Toxicity as process: tracing a new epigenetic regime of im/perceptibility in environmental toxicology

ABSTRACT Science and Technology Studies (STS) research has paid considerable attention to how toxicology produces knowledge on toxicity and how this knowledge has changed. For example, modern toxicological approaches of dose–response and threshold levels and genetic/genomic approaches for tracing exposure-induced DNA damage have been found to yield specific notions of toxicity. However, some of the toxicants’ latent exposure effects have remained invisible with these two established epistemic perspectives. To tackle this issue, environmental toxicologists have recently turned to environmental epigenetics, offering a promising biomolecular perspective to better understand the role of latent exposure effects on health. Analysing environmental toxicology literature on epigenetics and interviews with key researchers demonstrates how an epigenetic perspective yields a novel notion of toxicity as process. This temporal emphasis foregrounds the idea that bodies are not just exposed to toxicants but dynamically respond to the exposures they experience. In particular, environmental toxicologists draw on a specific combination of an epigenetic theory of toxicity and new but compatible methods and technologies, which establish a new epistemic understanding of toxicity. Characterising these developments as a Regime of Im/Perceptibility shows how novel regimes can emerge in both difference and continuity with prior regimes such as modern and genetic/genomic toxicology. The case study on epigenetic research in environmental toxicology adds to STS scholarship on epistemic developments in scientific fields by illuminating how a new epistemic perspective is successfully adopted while co-existing with established regimes of knowledge production in a given field.

DNA methylation stability in cardiac tissues kept at different temperatures and time intervals

Investigating DNA methylation (DNAm) in cardiac tissues is vital for epigenetic research in cardiovascular diseases (CVDs). During cardiac surgery, biopsies may not be immediately stored due to a lack of human or technical resources at the collection site. Assessing DNAm stability in cardiac samples left in suboptimal conditions is crucial for applying DNAm analysis. We investigated the stability of DNAm in human cardiac tissues kept at 4 °C and 22 °C for periods of 1, 7, 14, and 28 days (exposed samples) using the Illumina Infinium MethylationEPIC v1.0 BeadChip Array. We observed high correlations between samples analysed immediately after tissue collection and exposed ones (R2 > 0.992). Methylation levels were measured as β-values and median absolute β-value differences (|∆β|) ranged from 0.0093 to 0.0119 in all exposed samples. Pairwise differentially methylated position (DMP) analysis revealed no DMPs under 4 °C (fridge temperature) exposure for up to 28 days and 22 °C (room temperature) exposure for one day, while 3,437, 6,918, and 3,824 DMPs were observed for 22 °C samples at 7, 14, and 28 days, respectively. This study provides insights into the stability of genome-wide DNAm, showing that cardiac tissue can be used for reliable DNAm analysis even when stored suboptimally after surgery.

Epigenetic changes in patients with post-acute COVID-19 symptoms (PACS) and long-COVID: A systematic review.

Up to 30% of people infected with SARS-CoV-2 report disabling symptoms 2 years after the infection. Over 100 persistent symptoms have been associated with Post-Acute COVID-19 Symptoms (PACS) and/or long-COVID, showing a significant clinical heterogeneity. To develop effective, patient-targeted treatment, a better understanding of underlying mechanisms is needed. Epigenetics has helped elucidating the pathophysiology of several health conditions and it might help unravelling inter-individual differences in patients with PACS and long-COVID. As accumulating research is exploring epigenetic mechanisms in PACS and long-COVID, we systematically summarized the available literature on the topic. We interrogated five databases (Medline, Embase, Web of Science, Scopus and medXriv/bioXriv) and followed PRISMA and SWiM guidelines to report our results. Eight studies were included in our review. Six studies explored DNA methylation in PACS and/or long-COVID, while two studies explored miRNA expression in long-COVID associated with lung complications. Sample sizes were mostly small and study quality was low or fair. The main limitation of the included studies was a poor characterization of the patient population that made a homogeneous synthesis of the literature challenging. However, studies on DNA methylation showed that mechanisms related to the immune and the autonomic nervous system, and cell metabolism might be implicated in the pathophysiology of PACS and long-COVID. Epigenetic changes might help elucidating PACS and long-COVID underlying mechanisms, aid subgrouping, and point towards tailored treatments. Preliminary evidence is promising but scarce. Biological and epigenetic research on long-COVID will benefit millions of people suffering from long-COVID and has the potential to be transferable and benefit other conditions as well, such as Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). We urge future research to employ longitudinal designs and provide a better characterization of included patients.

“In the Footsteps of Our Ancestors” Polish Traditions of Westward Migration Meets Modern Epigenetics of Trauma

For several years, there have been ongoing considerations regarding the interdisciplinary connections between the natural sciences and the humanities. The same holds true for the question as to whether trauma can be inherited biologically as well as culturally. Today, this topic is increasingly steering the scientific debate in the direction of epigenetic research, which currently combines molecular biology and social psychology with their respective hallmarks. Can culture-related traumas be inherited and, if this was possible, can transgenerational consequences of trauma be passed on to subsequent generations? The focus remains on educational and socialization-related conduct as well on biologically inherited processes of how individual deals with their own trauma. Can migration be inherited by subsequent generations via transgenerational transmission of trauma? In order to answer this question, both consequences and causes of the long-running migration from Poland to Western European countries need to be considered. This article thus seeks to establish a connection between now and then, while also focusing on tragic passages in Poland’s history that were characterized by suffering, statelessness, and occupation (until 1989). Consequently, multi-layered and repeated habitus breakages as well as specific Polish “worldviews” may have emerged, which tend to favour migration. The causal links between the transgenerational transmission of such traumas and their causal connections to ongoing migration from Poland to countries such as Germany are addressed by using modern epigenetics.

Investigating the Association of TaqI (rs731236), ApaI (rs7975232), and BsmI (rs1544410) With Diabetic Nephropathy: A Case for Broader Genetic and Epigenetic Research

Investigating the Association of TaqI (rs731236), ApaI (rs7975232), and BsmI (rs1544410) With Diabetic Nephropathy: A Case for Broader Genetic and Epigenetic Research

Rapid and direct detection of m6A methylation by DNAzyme-based and smartphone-assisted electrochemical biosensor

m6A methylation detection is crucial for understanding RNA functions, revealing disease mechanisms, guiding drug development and advancing epigenetics research. Nevertheless, high-throughput sequencing and liquid chromatography-based traditional methods still face challenges to rapid and direct detection of m6A methylation. Here we report a DNAzyme-based and smartphone-assisted electrochemical biosensor for rapid detection of m6A. We initially identified m6A methylation-sensitive DNAzyme mutants through site mutation screening. These mutants were then combined with tetrahedral DNA to modify the electrodes, creating a 3D sensing interface. The detection of m6A was accomplished by using DNAzyme to capture and cleave the m6A sequence. The electrochemical biosensor detected the m6A sequence at nanomolar concentrations with a low detection limit of 0.69 nM and a wide detection range from 10 to 104 nM within 60 min. As a proof of concept, the 3′-UTR sequence of rice was selected as the m6A analyte. Combined with a smartphone, our biosensor shows good specificity, sensitivity, and easy-to-perform features, which indicates great prospects in the field of RNA modification detection and epigenetic analysis.

What's in the Blood? Temporalities at Play in Diet-Related Risk Management Testing Practices

In this paper, I look at two different sets of practices that are part of the risk management apparatus in place in Québec & Canada to apprehend and control risks associated with food consumption. More specifically, I contrast diabetes and chemical contaminants risk management testing practices, so as to compare how both frame and approach risks, in a context where recent research in social sciences, epigenetics and environmental sciences increasingly points to “environmental” pathways of disease causation while many chronic conditions remain highly individualized in public and health discourses. The analysis pays close attention to the different temporalities discursively created, considered, and neglected in these practices in order to understand how risk is approached and worked on. This highlights the power relations that inform how we care (or not) for (certain) bodies, inflecting in particular ways their—uneven—becomings. I argue that the Canadian biotechnological apparatus of testing practices meant to apprehend and control diet-related risks contributes to foreclosing the temporalities of health and illness considered and acted upon. As such, the apparatus contributes to (re)producing inequalities, here mostly health related ones, as well as creating differentiated biological materialities.

Benchmarking sample pooling for epigenomics of natural populations.

DNA methylation (DNAm) is a mechanism for rapid acclimation to environmental conditions. In natural systems, small effect sizes relative to noise necessitates large sampling efforts to detect differences. Large numbers of individually sequenced libraries are costly. Pooling DNA prior to library preparation may be an efficient way to reduce costs and increase sample size, yet there are to date no recommendations in ecological epigenetics research. We test whether pooled and individual libraries yield comparable DNAm signals in a natural system exposed to different pollution levels by generating whole-epigenome data from two invasive molluscs (Corbicula fluminea, Dreissena polymorpha) collected from polluted and unpolluted localities (Italy). DNA of the same individuals were used for pooled and individual epigenomic libraries and sequenced with equivalent resources per individual. We found that pooling effectively captures similar genome-wide and global methylation signals as individual libraries, highlighting that pooled libraries are representative of the global population signal. However, pooled libraries yielded orders of magnitude more data than individual libraries, which was a consequence of higher coverage. We would therefore recommend aiming for a high initial coverage of individual libraries (15×) in future studies. Consequently, we detected many more differentially methylated regions (DMRs) with the pooled libraries and a significantly lower statistical power for regions from individual libraries. Computationally pooled data from the individual libraries produced fewer DMRs and the overlap with wet-lab pooled DMRs was relatively low. We discuss possible causes for discrepancies, list benefits and drawbacks of pooling, and provide recommendations for future epigenomic studies.

Ligation-driven hyperbranched DNA assembly for label-free and sequence-specific measurement of RNA N6-methyladenosine in human breast tissues

N6-methyladenosine (m6A) is a critical post-transcriptional regulator, and it is linked to various biological functions (e.g., degradation, export, and translation) and multiple human diseases (e.g., cancers, immune disorders, and neurodegenerative diseases). The current methods for sequence-specific detection of m6A usually suffer from radioactive risk, large sample consumption, washing/separation steps, and false-positive signal. Herein, we develop a ligation-driven hyperbranched DNA assembly-based fluorescent biosensor for label-free and sequence-specific detection of m6A. In this assay, the unmethylated RNA can be identified and cleaved by m6A-sensitive endoribonuclease MazF. The retained intact m6A-RNA is complementary to the padlock probe to form a circular DNA, subsequently initiating ligation-driven hyperbranched rolling circle amplification (HRCA). The obtained HRCA products can be simply quantified with SYBR Gold as a fluorescent indicator. This method can be homogeneously carried out in an isothermal, label-free and antibody-free manner. The limit of detection can reach 0.079 pM. Moreover, this method can differentiate even 0.01 % m6A level in excess coexisting interferences, monitor cellular m6A RNA level with single-cell sensitivity, and differentiate m6A level in breast tumor tissues and normal adjacent tissues, with promising applications in m6A-releated epigenetic research and clinical diagnosis.

Decoding the genetic landscape of autism: A comprehensive review.

Autism spectrum disorder (ASD) is a complex neurodevelopmental condition characterized by heterogeneous symptoms and genetic underpinnings. Recent advancements in genetic and epigenetic research have provided insights into the intricate mechanisms contributing to ASD, influencing both diagnosis and therapeutic strategies. To explore the genetic architecture of ASD, elucidate mechanistic insights into genetic mutations, and examine gene-environment interactions. A comprehensive systematic review was conducted, integrating findings from studies on genetic variations, epigenetic mechanisms (such as DNA methylation and histone modifications), and emerging technologies [including Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)-Cas9 and single-cell RNA sequencing]. Relevant articles were identified through systematic searches of databases such as PubMed and Google Scholar. Genetic studies have identified numerous risk genes and mutations associated with ASD, yet many cases remain unexplained by known factors, suggesting undiscovered genetic components. Mechanistic insights into how these genetic mutations impact neural development and brain connectivity are still evolving. Epigenetic modifications, particularly DNA methylation and non-coding RNAs, also play significant roles in ASD pathogenesis. Emerging technologies like CRISPR-Cas9 and advanced bioinformatics are advancing our understanding by enabling precise genetic editing and analysis of complex genomic data. Continued research into the genetic and epigenetic underpinnings of ASD is crucial for developing personalized and effective treatments. Collaborative efforts integrating multidisciplinary expertise and international collaborations are essential to address the complexity of ASD and translate genetic discoveries into clinical practice. Addressing unresolved questions and ethical considerations surrounding genetic research will pave the way for improved diagnostic tools and targeted therapies, ultimately enhancing outcomes for individuals affected by ASD.

Imprinting as Basis for Complex Evolutionary Novelties in Eutherians.

The epigenetic phenomenon of genomic imprinting is puzzling. While epigenetic modifications in general are widely known in most species, genomic imprinting in the animal kingdom is restricted to autosomes of therian mammals, mainly eutherians, and to a lesser extent in marsupials. Imprinting causes monoallelic gene expression. It represents functional haploidy of certain alleles while bearing the evolutionary cost of diploidization, which is the need of a complex cellular architecture and the danger of producing aneuploid cells by mitotic and meiotic errors. The parent-of-origin gene expression has stressed many theories. Most prominent theories, such as the kinship (parental conflict) hypothesis for maternally versus paternally derived alleles, explain only partial aspects of imprinting. The implementation of single-cell transcriptome analyses and epigenetic research allowed detailed study of monoallelic expression in a spatial and temporal manner and demonstrated a broader but much more complex and differentiated picture of imprinting. In this review, we summarize all these aspects but argue that imprinting is a functional haploidy that not only allows a better gene dosage control of critical genes but also increased cellular diversity and plasticity. Furthermore, we propose that only the occurrence of allele-specific gene regulation mechanisms allows the appearance of evolutionary novelties such as the placenta and the evolutionary expansion of the eutherian brain.

Research trend of lung cancer epigenetics research: Bibliometric and visual analysis of top-100 cited documents

BackgroundLung cancer is a highly prevalent cancer on a global scale and its oncogenic process is driven by the accumulation of multiple pathological events. Epigenetics has gained significant recognition in recent years as a crucial contributor to the development of lung cancer. Epigenetics include processes such as DNA methylation, histone modification, chromatin remodeling, and RNA modification. These pathways lead to enduring alterations in genetic phenotypes, which are crucial in the advancement and growth of lung cancer. However, the specific mechanisms and roles of epigenetics in lung cancer still need to be further elucidated. MethodsWe obtained publications from the Web of Science databases and applied a rigorous search method to filter them. Ultimately, we gathered high-quality publications that had received the highest 100 number of citations. The data were processed and visualized by various bibliometric tools. ResultsThe 100 papers had varying numbers of citations, with the lowest being 491 and the most being 6316. On average, each work received 1119 citations. A total of 1056 co-authors were involved in publishing these papers in 59 journals from 185 institutions in 27 countries. The majority of high-caliber research in the subject of lung cancer epigenetics is conducted in advanced countries, with the United States taking the lead in terms of both the quantity of articles produced and their academic influence. The study of DNA methylation has been a longstanding research priority in the discipline. With the development of next-generation sequencing technology in recent years, research related to non-coding RNA has become a research hotspot. Future research directions may focus more on exploring the mechanisms of action of messenger RNA and circular RNA and developing targeted treatment strategies based on non-coding RNA drugs. ConclusionWe analyzed 100 top lung cancer and epigenetics documents through various bibliometric analysis tools. This study provides a concise overview of the findings from prior research, anticipates future research directions, and offers potential avenues for additional investigation.

Update on the pathophysiology, diagnosis and management of Ménière's disease.

The aim of this work is to summarize the main advances on the pathophysiology, diagnosis, and treatment of Meniere's disease (MD). Different immune responses to biotic stimuli may trigger MD, with subgroups identified based on cytokine and genetic profile, suggesting potential benefits from immune therapy, including antiallergic medication. Genetic and epigenetic research, along with imaging studies, reveal the complexity of MD, involving inflammation, immunity, and metabolic processes. Advanced imaging techniques define specific temporal bone features and endolymphatic hydrops, while machine learning models enhance diagnostic accuracy through clinical and laboratory data analysis. Differentiating MD from vestibular migraine remains challenging due to overlapping symptoms, but combining vestibular tests, audiological assessments, and biomarkers like cytokines and chemokines shows promise. Pharmacological treatments such as betahistine or corticosteroids show varying effectiveness and require further research according to immune subgroups. Surgical options like endolymphatic sac decompression, semicircular canal occlusion and labyrinthectomy are restricted to intractable cases. Research into MD aims to improve diagnosis and treatment through genetic, immunological, and advanced imaging studies. Current treatments include pharmacological, intratympanic, and surgical interventions, but current research supports a personalized approach based on clinical and molecular re-definition of patient subgroups.

CRISPR/dCas9-Mediated DNA Methylation Editing on emx2 in Chinese Tongue Sole (Cynoglossus semilaevis) Testis Cells.

DNA methylation is a key epigenetic mechanism orchestrating gene expression networks in many biological processes. Nonetheless, studying the role of specific gene methylation events in fish faces challenges. In this study, we validate the regulation of DNA methylation on empty spiracles homeobox 2 (emx2) expression with decitabine treatment in Chinese tongue sole testis cells. We used the emx2 gene as the target gene and developed a new DNA methylation editing system by fusing dnmt3a with catalytic dead Cas9 (dCas9) and demonstrated its ability for sequence-specific DNA methylation editing. Results revealed that utilizing dCas9-dnmt3a to target emx2 promoter region led to increased DNA methylation levels and decreased emx2 expression in Chinese tongue sole testis cells. More importantly, the DNA methylation editing significantly suppressed the expression of MYC proto-oncogene, bHLH transcription factor (myc), one target gene of emx2. Furthermore, we assessed the off-target effects of dCas9-dnmt3a and confirmed no significant impact on the predicted off-target gene expression. Taken together, we developed the first DNA methylation editing system in marine species and demonstrated its effective editing ability in Chinese tongue sole cells. This provides a new strategy for both epigenetic research and molecular breeding of marine species.

Constructing maternal responsibility: narratives of “motherly love” and maternal blame in epigenetics research

Research in epigenetics is demonstrating the importance of maternal care towards offspring early in life for long-term health and behavioral outcomes. Although most of this research has been conducted in rodents, these findings are increasingly framing broader debates about mothers’ moral responsibilities for the health of their offspring. In this paper, I investigate the implications of scientific narratives and research agendas of maternal care for current discourses surrounding maternal epigenetic responsibility. I show how despite clear differences between rodent and human contexts of care, researchers tend to construct rodent maternal care as a form of love or emotional commitment. This construction, which ignores fathers’ care for their offspring, reflects widespread social assumptions about mothers’ particular or “natural” capacities to love their children. This has important implications for how we assign moral blame. Because love is important to our widespread understandings of parental virtues, mothers who act “unlovingly” are prone to being judged in an especially harsh manner. By embedding simplistic and gendered assumptions about mothers’ love for their children, then, epigenetics research perpetuates the tendency to consider mothers especially blameworthy where they are perceived as failing to sufficiently care for or love their children.