Contending with epigenetic consequences of violence to women

This 2016 UK review subject was the interplay of genomic imprinting and intergenerational epigenetic information transfer:

“A range of evolutionary adaptations associated with placentation transfers disproportionate control of this process to the matriline, a period unique in mammalian development in that there are three matrilineal genomes interacting in the same organism at the same time (maternal, foetal, and postmeiotic oocytes).

Genomic imprinting is absent in egg laying mammals and only around 6 imprinted genes have been detected in a range of marsupial species; this is in contrast to eutherian mammals where around 150 imprinted genes have been described.

The interactions between the maternal and developing foetal hypothalamus and placenta can provide a template by which a mother can transmit potentially adaptive information concerning potential future environmental conditions to the developing brain.

In circumstances either where the early environment provides inaccurate cues to the environmental conditions prevailing when adult due to rapid environmental change or when disruptions to normal neural development occur, the mismatch between the environmental predictions made during early development and subsequent reality may mean that an organism may have a poorly adapted phenotype to its adult environment. An appreciation of these underlying evolutionary salient processes may provide a novel perspective on the casual [causal] mechanisms of a range of health problems.

The concept of a brain that is not pathological in the classical sense but it is simply mismatched to its environment has been most extensively studied in the context of ancestral and early developmental nutrition. However, this concept can be extended to provide insights into the development of a range of alternative neural phenotypes.”

The review’s final sentence was:

“Examination of the adaptive potential of a range of neural and cognitive deficits in the context of evolutionary derived foetocentric brain and placental development, epigenetics and environmental adaptation may provide novel insights into the development and potential treatment of a range of health, neurological, and cognitive disorders.”

One of the reviewers was cited in Epigenetic DNA methylation and demethylation with the developing fetus, which the review cited along with Epigenetic changes in the developing brain change behavior.


Researchers who avoid hypotheses that can’t be proven wrong could certainly test the subject matter of this review if they investigated their subjects’ histories.

For example, let’s say a patient/subject had symptoms where the “150 imprinted genes” were implicated. What are the chances a clinician or researcher would be informed by this review’s material and investigate the mother’s and grandmother’s histories?

For clinicians or researchers who view histories as irrelevant busywork: how many tens of millions of people alive today have mothers who were fetuses when their grandmothers were adversely affected by violence? Wouldn’t it be appropriate to assess possible historical contributions of:

“The mismatch between the environmental predictions made during early development and subsequent reality”

to the patient’s/subject’s current symptoms?

http://www.hindawi.com/journals/np/2016/6827135/ “Placental, Matrilineal, and Epigenetic Mechanisms Promoting Environmentally Adaptive Development of the Mammalian Brain”

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2 thoughts on “Contending with epigenetic consequences of violence to women

  1. https://www.researchgate.net/publication/298724574_Placental_Matrilineal_and_Epigenetic_Mechanisms_Promoting_Environmentally_Adaptive_Development_of_the_Mammalian_Brain

    Are researchers and clinicians clued in enough to symptoms of the affected 150 genes to investigate the mother’s and grandmother’s histories?
    For example, one effect of genomic imprinting on male sexual behavior is if the processes didn’t proceed normally at an early stage of the male fetus’ development, the result could be suboptimal adult sexual behavior that didn’t change with experience.

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    • https://www.researchgate.net/publication/298724574_Placental_Matrilineal_and_Epigenetic_Mechanisms_Promoting_Environmentally_Adaptive_Development_of_the_Mammalian_Brain

      There is this paper, normally virgin male mice cannot tell the difference between oestrus and dioestrus urine. But the first time a male mouse gets laid they develop a stimulus reward association between just getting laid and oestrus female urine, they then develop a behavioural preference for oestrus urine. Peg3 knockout mice whilst being able to perform sexually are not able to develop this discriminatory ability and then approach female mice out of oestrus (they are only receptive during oestrus which is 5-8 hours every 5 days) who often react very aggressively. Sex then becomes an aversive stimulus. Peg3 is also called Prada Willi 1 and there is a clump of imprinted genes on the same chromosome which can be mutated in Prad Willi Disease, which does have a sexual phenotype
      Try these papers
      Proc Natl Acad Sci U S A. 2015 Jun 2;112(22):6789-95.
      Epigenetic changes in the developing brain: Effects on behavior.
      Keverne EB, Pfaff DW, Tabansky I.
      The paternally expressed gene Peg3 regulates sexual experience-dependent preferences for estrous odors.
      Swaney WT, Curley JP, Champagne FA, Keverne EB.
      Behav Neurosci. 2008 Oct;122(5):963-73. doi: 10.1037/a0012706
      Genomic imprinting mediates sexual experience-dependent olfactory learning in male mice.
      Swaney WT, Curley JP, Champagne FA, Keverne EB.
      Proc Natl Acad Sci U S A. 2007 Apr 3;104(14):6084-9. Epub 2007 Mar 26.
      Loss of the imprinted snoRNA mbii-52 leads to increased 5htr2c pre-RNA editing and altered 5HT2CR-mediated behaviour.
      Doe CM, Relkovic D, Garfield AS, Dalley JW, Theobald DE, Humby T, Wilkinson LS, Isles AR.
      Hum Mol Genet. 2009 Jun 15;18(12):2140-8. doi: 10.1093/hmg/ddp137. Epub 2009 Mar 20.

      Kevin

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