This 2015 Swiss human study’s Abstract began:
“It is known that increased circulating glucocorticoids in the wake of excessive, chronic, repetitive stress increases anxiety and impairs Brain-Derived Neurotrophic Factor (BDNF) signaling.”
The study had several statements that were unconvincingly supported by the study’s findings. One such statement in the Conclusions section was:
“This study supports the view that early-life adversity may induce long-lasting epigenetic changes in stress-related genes, thus offering clues as to how intergenerational transmission of anxiety and trauma could occur.”
However, the study’s evidence for “intergenerational transmission of anxiety and trauma” as summarized in the Limitations section was:
“This study did not directly associate child behavior or biology to maternal behavior and biology.”
In another example, the Discussion section began with:
“The severity of maternal anxiety was significantly correlated with mean overall methylation of 4 CpG sites located in exon IV of the BDNF promoter region as measured from DNA extracted from mothers’ saliva.
In addition, methylation at CpG3 was also significantly associated with maternal exposure to domestic violence during childhood, suggesting that BDNF gene methylation levels are modulated by early adverse experiences.”
The researchers assessed five DNA methylation values (four individual sites and the overall average). The CpG3 site was “significantly associated with maternal exposure to domestic violence during childhood” and the three other CpG sites’ methylation values were not.
IAW, the researchers found only one of four sites’ methylation values significantly associated to only one of many studied early adverse experiences. This finding didn’t provide sufficient evidence to support the overarching statement:
“BDNF gene methylation levels are modulated by early adverse experiences.”
To make such a generally applicable statement – more than one BDNF gene’s methylation levels could be directly altered by more than one early adverse experience – the researchers would, AT A MINIMUM, need to provide evidence that:
- The one category of significantly associated early adverse experience directly altered the one significantly associated CpG site’s DNA methylation level
- Other categories of early adverse experiences were fairly represented by the one significantly associated experience category
- Other categories of early adverse experiences could directly alter other BDNF genes’ DNA methylation levels
- The significantly associated DNA methylation level of only one out of four CpG sites was fairly represented by the overall average of the four sites
- Other BDNF gene’s methylation levels were fairly represented by the overall average of the four sites
If researchers and sponsors must have agendas, a worthwhile, evidence-supported one would be to investigate prenatal and perinatal epigenetic causes for later-life adverse effects.
As Grokking an Adverse Childhood Experiences (ACE) score pointed out, environmental factors that disrupt neurodevelopment may be the largest originators of epigenetic changes that are sustained throughout an individual’s entire lifespan.
What’s the downside of conducting studies that may “directly associate child behavior or biology to maternal behavior and biology” during time periods when a child’s environment has the greatest impact on their development?
When prenatal and perinatal periods aren’t addressed, researchers and sponsors neglect the times during which many harmful epigenetic consequences may be prevented. It is known.
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0143427 “BDNF Methylation and Maternal Brain Activity in a Violence-Related Sample”