Physical contact causes long-lasting epigenetic marks in infants
Physical care for babies appears to have lasting biological implications, according to a recent study, which reports that infants exposed to high and low levels of physical early postnatal contact have different overall epigenetic signatures.
Moreover, those exposed to low contact appear to manifest greater distress at younger epigenetic ages, suggesting that “epigenetic age deceleration, rather than acceleration, marks development risk in paediatric samples,” said researchers.
For the study, 94 mother-infant dyads accomplished the baby’s day diary, an e-diary designed to record infant behaviours and interactions at home. Contact was defined as the total of all caregiver diary-reported time spent holding the baby over the 4-day period.
Buccal swabs were then performed to collect buccal epithelial cell (BEC) samples from the infants, which were then subjected to DNA extraction and subsequent analysis of DNA methylation (DNAm).
The mean contact time per day was calculated to be 9 hours and 7 minutes, with a standard deviation (SD) of 2 hours and 52 minutes. Infants who received at least one SD above or below the mean daily contact time were assigned to the high (n=55) or low (n=39) contact groups, respectively. [Dev Psychopathol 2017;29:1517-1538]
In an initial analysis, the researchers found no significant difference between contact groups in the DNAm patterns in four candidate genes involved in pathways of neurobiological processing of physical contact, prompting an epigenome-wide investigation.
Between the high and low contact groups, and across four different chromosomes, the researchers found five differentially methylated regions (DMRs) corresponding to 44 unique CpG sites. Each region had at least two CpG sites that had at least a 5-percent between-group difference in DNAm patterns.
Of the five DMRs, two were intergenic and three fell inside gene bodies: the lactate dehydrogenase A-like 6A gene, the major histocompatibility complex class II gene and the zinc finger AN1-type containing 2A gene.
While it is important to remember that DNAm does not result in direct straightforward outcomes so much so that it is difficult to infer its functional effects, the researchers speculated “that these differential regions may reflect a component of the plasticity mechanisms involved in the biological embedding of early postnatal contact via cellular reprogramming.”
However, further studies that track long-term neurobiological outcomes or investigate causality at a genetic and molecular level are needed to confirm these speculations, they added.
In a subsequent analysis, the researchers showed that infant distress mediated the association between postnatal contact and epigenetic age deviation, with a negative correlation between the two factors observable in the low contact group.
That is, those who received low postnatal contact experienced higher distress at significantly lower epigenetic ages. The opposite is also true, where lower infant distress was associated with higher epigenetic age.
When infant distress levels were removed from the analysis, the relationship between postnatal contact and deviations of epigenetic age was attenuated.
“[T]he relationship between contact and epigenetic age deviation was contingent upon infant distress levels,” said the researchers, noting that such relationship was weak and nonsignificant in the high contact group.
“Higher infant distress in the context of low care thus corresponded with lower epigenetic age relative to chronological age,” they added.