Are stress-induced epigenetic changes to DNA inherited across generations?

This 2014 Geneva/Cambridge plant study ended by stating:

“The unequivocal demonstration of transgenerational transmission of environmentally-induced epigenetic traits remains a significant challenge.

One of the critical activities erasing stress memories is conserved between plants and mammals.”

However, the researchers didn’t demonstrate that their findings were broadly applicable for mammals or organisms other than the specific plant variety they studied. Possible reasons for these limited findings were given in a 2015 Australian study referenced by Mechanisms of stress memories in plants:

“The majority of DNA methylation analyses performed in plants to date have focused on Arabidopsis, despite being relatively depleted of TEs [transposable elements] (15–20% of the genome) and being poorly methylated compared to other plant genomes.

These studies have lacked the resolution to provide the specific context and genomic location of the changes in DNA methylation.”

There are also significant differences in how epigenetic inheritance across generations may operate among different species per Epigenetic reprogramming in plant and animal development.


Neither the current study nor the above review addressed the behavioral aspect of stress-induced epigenetic inheritance across generations. For example, the behavior of a mother whose DNA was epigenetically changed by stress can induce the same epigenetic changes to her child’s DNA when her child is stressed per One way that mothers cause fear and emotional trauma in their infants:

“Our results provide clues to understanding transmission of specific fears across generations and its dependence upon maternal induction of pups’ stress response paired with the cue to induce amygdala-dependent learning plasticity.”

http://www.pnas.org/content/111/23/8547.full “Identification of genes preventing transgenerational transmission of stress-induced epigenetic states”

Problematic research that excluded the most influential human epigenetic environments

This 2014 ivy league human study found that what appeared to be genetic links may have been epigenetic responses to our environment.

Curiously, none of the news articles covering this study highlighted the lack of the most influential environments on epigenetic DNA changes:

  • The mother’s prenatal environment provided for the fetus, and
  • The family environment during infancy and early childhood.

This omission may have been because the study intentionally didn’t support such an interpretation. Here’s a partial explanation from the study’s supplementary material of the “family fixed-effects model” the researchers developed:

“The family fixed-effects model blocks both genetic factors and parental characteristics/behaviors that are common to family members (e.g., siblings), including unmeasured factors; therefore, from the perspective of confounding, the fixed-effect specification is preferred.”

When the preferred model blocked the most important environments in which epigenetic DNA changes occur, what environments remained?

“These results suggest genetic influences on complex traits like obesity can vary over time, presumably because of global environmental changes that modify allelic penetrance.”

Although a finding attributing “global environmental changes” made more funding available to the researchers, it was rightly an outlier from the majority of epigenetic studies.

This finding made me start a negative rating for studies that DETRACT from science!

Why was the reviewer okay with the study’s model omitting the most important factors in human development? The study’s model defined away both the:

  • Out-of-favor genetic factors, and the
  • Predominant but nonpolitically-correct epigenetic factors

in order to manufacture a politically-correct epigenetics meme!

How else to interpret this statement, if not intended to generate a meme?

“Our results underscore the importance of interpreting any genetic studies with a grain of salt and leave open the possibility that new genetic risk factors may be seen in the future due to different genetically driven responses to our ever-changing environment.”

http://www.pnas.org/content/112/2/354.full “Cohort of birth modifies the association between FTO genotype and BMI”

Early human brain development can be greatly modified by environmental factors

This 2014 Brazilian human study found that the brains of people born without the corpus callosum, the major connection between brain hemispheres, adapted to this loss:

“The authors believe that the development of alternative pathways results from the brain’s ability for long-distance plasticity and occurs in the utero during embryo development, which indicates that connections formed in the human brain early in development can be greatly modified, and most likely by environmental or genetic factors.”

BRAVO! MORE STUDIES LIKE THIS ONE!

People have limited capability to adapt later in life to corpus callosum injuries or to brain hemisphere disconnection.

http://www.pnas.org/content/111/21/7843.full “Structural and functional brain rewiring clarifies preserved interhemispheric transfer in humans born without the corpus callosum”

Problematic research with telomere length

This 2014 study purportedly linked the effect of shorter telomere length in children to twin causes of a disadvantaged social environment and genetics. Two questionable areas were even more egregious than the study’s lack of a control group.

The first questionable area was that the researchers purposely measured telomere length using methods that couldn’t be directly compared with the telomere length measurements found in almost all other telomere studies. There was no attempt to make findings equivalent, no map with cited studies! They offered up rationale after rationale, but the direct incomparability with other studies remained.

The largest questionable area was the way the researchers produced the study’s concluding sentence:

“We suggest that an individual’s genetic architecture moderates the magnitude and direction of the physiological response to exogenous stressors.”

The researchers’ process deliberately skewed the sample of forty 9-year old boys. Next, they split this forty-member sample in half according to maternal depression! Maternal depression is an experimentally proven contributor to epigenetic changes that are detrimental to developing fetuses, infants, and young children.

The researchers asserted that the results of compounding their questionable choices represented something about stress and genetics in a larger population of children.

Of course, “an individual’s genetic architecture moderates the magnitude and direction of the physiological response to exogenous stressors.” These researchers didn’t do the work to determine whether it was the genetic architecture that the 9-year-olds were either epigenetically changed into or conceived.

I presume that this additional work on genetic architecture wasn’t pursued by the researchers because it may not produce the race-baiting headlines of the press coverage this study achieved. If the additional work pointed to epigenetic causes of adverse effects, the headline may have been non-politically correct like “Maternal depression and poor caregiving damages fetuses, infants, and young children.”

Was this study published to further an agenda? If so, did this study also represent a failure of the peer review process?

Was it predetermined that this study would be published in PNAS regardless of its methods? Were the researchers and reviewers even interested in advancing science?

http://www.pnas.org/content/111/16/5944.full “Social disadvantage, genetic sensitivity, and children’s telomere length”