The principal way science advances is through the principle Einstein expressed as:
“No amount of experimentation can ever prove me right; a single experiment can prove me wrong.”
Members of the scientific community and of the public should be satisfied that the scientific process is working well when hypotheses are discarded due to nonconfirming evidence. Researchers should strive to develop evidence that rejects paradigms, and be lauded for their efforts.
The opposite took place with this 2018 commentary on two studies where the evidence didn’t confirm current biases. I curated one of these studies in DNA methylation and childhood adversity.
The commentators’ dismissive tone was set in the opening paragraph:
“Is early exposure to adversity associated with a genetic or an epigenetic signature? At first glance, two articles in this issue -..and the other from Marzi et al., who measured genome-wide DNA methylation in a prospective twin cohort assessed at age 18 – appear to say that it is not.”
The two commentators, one of whom was a coauthor of Manufacturing PTSD evidence with machine learning, went on to protect their territory. Never mind the two studies’ advancement of science that didn’t coincide with the commentators’ vested interests.
My main concern with the curated study was that although the children had been studied at ages 5, 7, 10, 12, and 18, the parents had never been similarly evaluated! The researchers passed up an opportunity to develop the parents as a F0 generation for understanding possible human transgenerational inherited epigenetic causes and effects.
The curated study focused on the children’s intergenerational epigenetic effects. However, animal studies have often demonstrated transgenerational effects that skip over the F1 generation children! For example:
- Transgenerational pathological traits induced by prenatal immune activation found a F2 grandchild and F3 great-grandchild phenotype of impaired sociability, abnormal fear expression and behavioral despair – effects that weren’t present in the F1 children;
- A self-referencing study of transgenerational epigenetic inheritance found histone modifications in the F3 generation that weren’t found in the F1 and F2 generations; and
- A study not cited in – but completely appropriate for – The lack of oxygen’s epigenetic effects on a fetus found heart disease effects in the F1 generation that were different from the heart disease effects found in the F2 and F3 generations.
https://ajp.psychiatryonline.org/doi/pdf/10.1176/appi.ajp.2018.18020156 “Considering the Genetic and Epigenetic Signature of Early Adversity Within a Biopsychosocial Framework” (not freely available)