TPC Journal-Vol 11-Issue-1

The Professional Counselor | Volume 11, Issue 1 109 cues. Weaver et al. looked at HPA response of rodent pups who received low licking and grooming from their mother (a negative environmental effect) who exhibited higher HPA response to environmental cues in adulthood. Epigenetically, they found lower DNA methylation in a specific promotor region in these adult rodents. They hypothesized that they could reverse this hypomethylation by giving an infusion of methionine, an essential amino acid that is a methyl group donor. They discovered the ability to reverse low methylation, which improved the minimally licked and groomed adult rodents’ response to stress. This connects with counseling in that epigenetic information is not set for life but reversible through interventions such as diet. Others have investigated mindfulness and its epigenetic effects on stress. Chaix et al. (2020) looked at DNA methylation at the genome level for differences between skilled meditators who meditated for an 8-hour interval compared to members of a control group who engaged in leisure activities for 8 hours. The control group did not have any changes in genome DNA methylation, but the skilled meditators showed 61 differentially methylated sites post-intervention. This evidence can potentially support the use of mindfulness with our clients as an intervention for treatment of stress. Childhood Maltreatment Childhood maltreatment includes sexual abuse, physical abuse and/or neglect, and emotional abuse and/or neglect. Through this lens, Suderman et al. (2014) examined differences in 45-year-old males’ blood samples between those who experienced abuse in childhood and those who did not, with the aim of determining whether gene promoter DNA methylation is linked with child abuse. After 30 years, the researchers found different DNA methylation patterns between abused versus non-abused individuals and that a specific hypermethylation of a gene was linked with the adults who experienced child abuse. Suderman et al. (2014) believed that adversity, such as child abuse, reorganizes biological pathways that last into adulthood. These DNA methylation differences have been associated with biological pathways leading to cancer, obesity, diabetes, and other inflammatory paths. Other researchers have also found epigenetic interactions at CpG sites predicting depression and anxiety in participants who experienced abuse. Though these interactions were not statistically significant (Smearman et al., 2016), increased methylation at specific promoter regions was discovered (Perroud et al., 2011; Romens et al., 2015). Furthermore, in a hallmark study, McGowan et al. (2009) discovered that people with child abuse histories who completed suicide possessed hypermethylation of a particular promotor region when compared to controls. Perroud et al. (2011) noted that frequency, age of onset, and severity of maltreatment correlated positively with increased methylation in adult participants suffering from borderline personality disorder, depression, and PTSD. Yehuda et al. (2016) reported that in a smaller subset of an overall sample of Holocaust survivors, the impact of trauma was intergenerationally associated with increased DNA methylation. Continued study of these particular regions may provide evidence of DNA methylation as a predictor of risk in developing anxiety or depressive disorders. Major Depressive Disorder Most studies of mental illness, genetics, and depression have used stress animal models. Through these models, histone modification, chromatin remodeling, miRNA, and DNA methylation mechanisms have been found in rats and mice (Albert et al., 2019; Nestler et al., 2016). When an animal or human experiences early life stress, epigenetic biomarkers may serve to detect the development or progression of major depressive disorder (Saavedra et al., 2016). Additionally, histone modification markers may also indicate an increase in depression (Tsankova et al., 2007; Turecki, 2014). Beyond animal models, Januar et al. (2015) found that buccal tissue in older patients with major depressive disorder provided evidence that the BDNF gene modulates depression through hypermethylation of specific CpGs in promoter regions.