This 2016 California human study found:
“A persistency of DNA methylation over time at key genomic loci associated with diabetic complications. Two sets of DNAs collected at least 16–17 years apart from the same participants are used to show the persistency of DNA-me over time.
Twelve annotated differentially methylated loci were common in both WB [whole blood] and Monos [blood monocytes], including thioredoxin-interacting protein (TXNIP), known to be associated with hyperglycemia and related complications.
The top 38 hyperacetylated promoters in cases included 15 genes associated with the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) inflammatory pathway, which is strongly associated with diabetic complications.”
The researchers built on a series of studies that showed how subjects with early intensive interventions didn’t develop further complications, whereas subjects with later intensive interventions:
“Continued to develop complications, such as nephropathy, retinopathy, and macrovascular diseases, at significantly higher rates.
This persistence of benefit from early application of intensive therapy, called ‘metabolic memory,’ is an enigma.”
I’d say that the researchers needed to also consider a point of Enduring memories? Or continuous toxic stimulation? that:
“The lasting epigenomic effect would not be due to memory, but continuous stimulation by persistent pathogens or persistent components.”
Other studies that involved specific genes of this study include:
- Lack of oxygen’s epigenetic effects (NF-κB)
- A followup study of DNA methylation and age (NF-κB)
- Epigenetic memories of stress as therapeutic targets (TXNIP)
http://www.pnas.org/content/113/21/E3002.full “Epigenomic profiling reveals an association between persistence of DNA methylation and metabolic memory in the DCCT/EDIC type 1 diabetes cohort”