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In the context of the present findings, it is notable that the most frequent psychiatric disorder, PTSD, is observed in approximately 20% of subjects with TSC. In this cohort, approximately 50% of females and 30% of males with TSC met criteria for lifetime PTSD. Thus, childhood adversities have enduring effects on the development of neuroendocrine and mental health in TSC. The finding of increased methylation at NR3C1 in this study suggests that the NR3C1 promoter methylation observed in chronic PTSD may represent a mechanism of NR3C1 downregulation and altered GR signaling, as recently hypothesized by others [58]. We suggest that the CpG sites most vulnerable to the stress of childhood adversity are those that promote methylation at this site.
Decreased levels of NR3C1 and of cortisol are observed in many conditions, including PTSD [6], [59] and depression [60], [61], [62]. We predict that altered NR3C1 promoter methylation may be a common factor explaining these associations. The effects of DNA methylation at NR3C1 are more likely to be observed in the context of early adversity than in the context of current distress, as they are occurring outside of the 24-hour cortisol cycle. Moreover, the negative association of NR3C1 methylation and salivary cortisol concentrations in this study is consistent with the finding of decreased cortisol reactivity in PTSD. In contrast, increased CpG 1 methylation in adults with PTSD has been observed [63]. This apparent contradiction may be explained by the greater number of adverse childhood experiences as compared to those in our study [27], which may be associated with a greater degree of methylation in adulthood. Further study of NR3C1 methylation is warranted.
The findings of higher methylation of NR3C1 in this sample with a history of childhood adversity is encouraging. It may suggest that people with this history have some type of resilience in terms of the GR gene. It also raises the possibility that epigenetic modifications that occur in response to childhood adversity are reversible, or at least that they can be mitigated by interventions. It will be important to consider the role of NR3C1 in resilience and the potential for modifying epigenetic changes, especially in populations with a higher frequency of adverse childhood experiences (e.g., in samples of low socioeconomic status, minority populations, immigrant groups, and urban populations).
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