Treating the father’s symptoms of an inherited disease can epigenetically treat the son

This 2014 La Jolla rodent study showed that treating the symptoms of an inherited disease can, through epigenetic DNA methylation, positively treat the symptoms in the subjects’ offspring.

The disease studied was Huntington’s, which is the most common inherited neurodegenerative disease:

  • The treatment induced epigenetic changes in the expression of genes on the male Y chromosome.
  • The treated male subjects were bred, and their sperm carried both the Huntington’s disease and the epigenetic changes that reduced the symptoms.
  • The male offspring showed both delayed onsets of Huntington’s disease and reductions of specific symptoms when compared with both the treated subjects’ female offspring and the control group non-treated subjects’ male offspring.

Per the definitions in A review of epigenetic transgenerational inheritance of reproductive disease and Transgenerational effects of early environmental insults on aging and disease, for the term in the study’s title “transgenerational effects” to apply, the researchers needed to provide evidence in at least the next 2 male and/or 3 female generations of:

“Altered epigenetic information between generations in the absence of continued environmental exposure.”

The study instead provided evidence for intergenerational effects.

http://www.pnas.org/content/112/1/E56.full “HDAC inhibition imparts beneficial transgenerational effects in Huntington’s disease mice via altered DNA and histone methylation”

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”