Maria Meier

Childhood maltreatment (CM) has long-lasting effects on physical and mental health with CM type specific effects being reported. Epigenetic processes, like deoxyribonucleic acid methylation (DNAm), might mediate this link, and CM types might be linked to differential alterations in DNAm. While a study by Cecil et al. [1] suggests that different forms of CM share common but also exhibit distinct epigenetic signatures, it is unclear whether these results are generalizable to other high-risk samples. The aim of this preregistered study was to replicate the study of Cecil and colleagues [1] in a sample of N = 116 previously out-of-home placed young adults (32% women, age mean = 26.38, SD = 3.49). Participants completed the Childhood Trauma Questionnaire - Short Form (CTQ-SF), DNA was extracted from whole blood and DNAm was assayed using the Illumina Infinium MethylationEPIC BeadChip Microarray. Using state-of the-art processing pipelines, we failed to replicate the original finding of common and shared epigenetic signatures by CM type. When using a pipeline that was closely matched to the original study, we found that DNAm of cg07032930 was significantly linked to emotional neglect, but in the reverse direction as in the original report. Overall, replication rates per CM subtype were only modest. These findings highlight challenges in independently replicating reported epigenetic associations in high-risk samples and underscore the importance of replication attempts in the field of behavioral epigenetics. Further research is needed to clarify the robustness and specificity of DNAm signatures linked to distinct CM types.

Childhood maltreatment (CM) is a key risk factor for psychopathology, physical morbidity and premature mortality, potentially mediated by epigenetic processes like DNA methylation. While differential links between type and timing of CM and psychopathology are increasingly acknowledged, it remains unclear how type- and timing-specific characteristics of CM are associated with epigenetic measures of biological aging, including age acceleration, mortality risk, and the pace of aging. We thus aimed to explore these links in an at-risk sample of formerly out-of-home placed adults who often report significant exposure to CM and high rates of adverse health outcomes. One-hundred-sixteen young adults previously placed in youth residential care (33% women, age M = 26.3 years, SD = 3.6) completed the Maltreatment and Abuse Chronology of Exposure (MACE-X) and provided blood samples to estimate DNA methylation using the Illumina Infinium MethylationEPIC BeadChip Microarray. In preregistered analyses, conditional random forest regressions were used to estimate the importance of CM types (abuse, neglect, peer victimization, sexual abuse), timing (ages 3-18), and global measures (severity, multiplicity, duration) for the prediction of markers of epigenetic aging (Hannum’s and Pheno’s age acceleration and DunedinPACE). Abuse from age 9 until late adolescence predicted Hannum’s age acceleration more strongly than global CM measures and was consistently and negatively associated with it. BMI was positively linked to Hannum’s age acceleration. We found no association between CM and newer epigenetic clocks (i.e., Pheno’s age acceleration and DunedinPACE). In an at-risk sample of formerly out-of-home-placed young adults with high rates of CM, we provide first evidence that parental abuse from mid childhood until late adolescence – a potential sensitive period – was linked to decelerated epigenetic aging. CM should therefore be assessed dimensionally, rather than as a single, undifferentiated cumulative exposure.

In psychoneuroendocrinology (PNE), data is valuable due to its high clinical and health-related relevance and resource-intensive data collection yet sharing it openly alongside publications remains uncommon. If shared, data remain highly fragmented and non-standardized, which hinders data reuse and integration across studies. To address this, we formed a consortium and, as a first step, conducted this study using a modified Delphi approach across two survey rounds to inform about important considerations regarding data structure, metadata, subject-level variables, and implementation requirements before a data standard for PNE may be developed. The panel in the final round consisted of 50 responders from the field of PNE. In two online survey rounds, respondents rated their agreement with 84 statements anonymously on a 5-point Likert scale. Consensus (> 70% [dis]agreement) was achieved for 80 items. The results highlight a broad agreement within the PNE community on the need for, and key components of, a standardized data structure, including a balance between flexibility and standardization to allow for adaptability across many use cases as well as comparability. Developing and establishing a standard for PNE data will be a central next step to foster transparency, sustainable use of resources, and the translational potential of our work.

Stress has been linked to the consumption of palatable food and may contribute to the development of obesity. Interindividual differences in cortisol stress reactivity are discussed as mediating mechanisms, yet findings linking food craving to cortisol reactivity are heterogeneous. Methodological differences in whether participants receive a sugary preload or are invited fasted may contribute to these divergences. Hence, this study set out to systematically investigate the effect of glucose and psychosocial stress on food craving in healthy adults. Overall, 62 healthy, fasted adults (mean age = 23.13; SD = 3.02; 54.84 % female, 45.16 % male) reported current food craving on the Food Craving Questionnaire, received either glucose or water and were later exposed to psychosocial stress or a friendly control condition. After stressor exposure, food craving was assessed a second time. We repeatedly assessed salivary cortisol and blood glucose and used linear mixed models to test whether the experimental manipulations predicted changes in craving and explored associations with sex and stress-eating tendency.Blood glucose increased in those consuming glucose and the stress test increased cortisol significantly. Higher cortisol reactivity, and even stronger, a greater increase in blood glucose led to significant reductions in food craving over time. We found no supportive evidence that glucose and cortisol reactivity interactively affected craving. These findings suggest that short-term metabolic signals may be more influential in shaping immediate food craving than acute stress, and that acute cortisol elevations may not universally promote food craving.

Replicability is a cornerstone of scientific progress. Yet, replications are often undervalued, and are sometimes seen as redundant, unimportant, or lacking novelty. This impedes their broader adoption in research and beyond. In response, the credibility revolution calls for slower, more deliberate science and greater responsiveness to fallibility. In this perspective piece, we argue that (a) replications are essential for validating scientific claims, (b) replications need to be made more visible, recognized, and integrated into research and educational practices, and (c) we can change the way we view and judge replication results. We propose a framework where replication studies can be systematically tracked and normalized through the Replication Hub as part of the Framework for Open and Reproducible Research Training (FORRT) initiative, with the goal of enhancing the visibility, integration, and cumulative impact of replication research across disciplines.

Childhood maltreatment (CM) has long-lasting effects on physical and mental health with CM type specific effects being reported. Epigenetic processes, like deoxyribonucleic acid methylation (DNAm), might mediate this link, and CM types might be linked to differential alterations in DNAm. While a study by Cecil et al. (2016) suggests that different forms of CM share common but also exhibit distinct epigenetic signatures, it is unclear whether these results are generalizable to other high-risk samples. The aim of this preregistered study was to replicate the study of Cecil and colleagues (2016) in a sample of N = 116 previously out-of-home placed young adults (32% women, age mean = 26.38, SD = 3.49). Participants completed the Childhood Trauma Questionnaire - Short Form (CTQ-SF), DNA was extracted from whole blood and DNAm was assayed using the Illumina Infinium MethylationEPIC BeadChip Microarray. Using state-of the-art processing pipelines, we failed to replicate the original finding of common and shared epigenetic signatures by CM type. When using a pipeline that was closely matched to the original study, we could replicate that DNAm of cg07032930 was linked to emotional neglect, but in the reverse direction as in the original report. Overall, replication rates per CM subtype were only modest. These findings highlight challenges in independently replicating reported epigenetic associations in high-risk samples and underscore the importance of replication attempts in the field of behavioral epigenetics. Further research is needed to clarify the robustness and specificity of DNAm signatures linked to distinct CM types.