Parental lying thwarted both their children and researchers

This 2017 German human study explored the relationship between birth stress and handedness. The authors summarized previous research which, among other points, estimated epigenetic contributions to handedness as great as 75%.

The study hit a snag in its reliance on the sixty participants (average age 24) completing, with the assistance of their parents and medical records, a 24-item questionnaire of maternal health problems during pregnancy, substance use during pregnancy, and birth complications. The subjects didn’t provide accurate information. For example:

  • Only one of the subjects reported maternal alcohol use during pregnancy. An expected number would have been 26.
  • None of the subjects reported maternal mental illness during pregnancy. An expected number would have been at least 7.

The subjects’ parents willingly misled their children about facts of their child’s important earliest development periods. The absence of evidence greatly increased the difficulty for researchers and individuals in determining causes of epigenetic effects still present in the subjects’ lives.

http://www.tandfonline.com/doi/full/10.1080/1357650X.2017.1377726 “DNA methylation in candidate genes for handedness predicts handedness direction” (not freely available)

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How one person’s paradigms regarding stress and epigenetics impedes relevant research

This 2017 review laid out the tired, old, restrictive guidelines by which current US research on the epigenetic effects of stress is funded. The reviewer rehashed paradigms circumscribed by his authoritative position in guiding funding, and called for more government funding to support and extend his reach.

The reviewer won’t change his beliefs regarding individual differences and allostatic load since he helped to start those memes. US researchers with study ideas to develop evidence beyond such memes may have difficulties finding funding.

Here’s one example of the reviewer’s restrictive views taken from the Conclusion section:

Adverse experiences and environments cause problems over the life course in which there is no such thing as “reversibility” (i.e., “rolling the clock back”) but rather a change in trajectory [10] in keeping with the original definition of epigenetics [132] as the emergence of characteristics not previously evident or even predictable from an earlier developmental stage. By the same token, we mean “redirection” instead of “reversibility”—in that changes in the social and physical environment on both a societal and a personal level can alter a negative trajectory in a more positive direction.”

What would happen if US researchers proposed tests of his “there is no such thing as reversibility” axiom? To secure funding, his sphere of influence would probably steer the prospective studies’ experiments toward altering “a negative trajectory in a more positive direction” instead.

However, I found nothing in citation [10] (of which the reviewer is a coauthor) where the rodent study researchers even attempted to directly reverse the epigenetic changes! The researchers under his guidance simply asserted:

“..a history of stress exposure can permanently alter gene expression patterns in the hippocampus and the behavioral response to a novel stressor”

without making any therapeutic efforts to test the permanence assumption! Never mind that researchers outside the reviewer’s sphere of influence have done exactly that. In any event, citation [10] didn’t support an “there is no such thing as reversibility” axiom.

The reviewer also implied that humans respond just like lab rats and can be treated as such. Notice that the above graphic conflated rodent and human behaviors. Further examples of this inappropriate merger of behaviors are in the Conclusion section.


What may be a more promising research approach to human treatments of the epigenetic effects of stress now that it’s 2017? I pointed out in The current paradigm of child abuse limits pre-childhood causal research:

“If the current paradigm encouraged research into treatment of causes, there would probably already be plenty of evidence to demonstrate that directly reducing the source of the damage would also reverse the damaging effects. There would have been enough studies done so that the generalized question of reversibility wouldn’t be asked.

Aren’t people interested in human treatments of originating causes so that their various symptoms don’t keep bubbling up? Why wouldn’t research paradigms be aligned accordingly?”

http://journals.sagepub.com/doi/full/10.1177/2470547017692328 “Neurobiological and Systemic Effects of Chronic Stress”

Epigenetic stress effects in preterm infants

This 2017 Italian review selected 9 human studies on the epigenetic effects of:

“..one of the major adverse events in human development. Preterm infants are hospitalized in the Neonatal Intensive Care Unit where they are exposed to life-saving yet pain-inducing procedures and to protective care.”

Highlights of the referenced studies included:

  • “..early exposure to adverse events during the third trimester of pregnancy is capable to alter the epigenetic status of imprinted and placenta-related genes which have relevant implications for fetal development and preterm infants’ HPA [hypothalamic–pituitary–adrenal] stress reactivity during infancy.”
  • “..there was an association between DNAm [DNA methylation] and white matter tract tissue integrity and shape inferred from dMRI [diffusion MRI], suggesting that epigenetic variation may contribute to the cerebral phenotype of preterm birth.”

Limitations of the referenced studies included:

  • “A multiple sampling design that includes parental samples, placental tissue, cord blood and extends across the life-course would be required to investigate the relative contributions of in utero and postnatal exposures to changes in DNAm, and the extent to which preterm birth leaves a legacy on the methylome.”
  • Saliva, blood, and other tissues’ DNA methylation may not produce valid links to brain tissue DNA methylation of the same gene, which may hamper conclusive inferences about behavior, etc.

http://www.sciencedirect.com/science/article/pii/S0149763417302117 “Preterm Behavioral Epigenetics: A systematic review” (not freely available)

http://www.nature.com/tp/journal/v6/n1/full/tp2015210a.html “Epigenomic profiling of preterm infants reveals DNA methylation differences at sites associated with neural function” (one of the studies selected, quoted above)

Epigenetic effects on genetic diseases

This 2017 review provided evidence for epigenetic effects on a disease widely considered to be of genetic origins:

“..for a T1D [type 1 diabetes] identical twin the concordance rate (both twins affected)..is consistently less than 100%, which implies a non-genetically determined effect. However, the concordance rate declines with age at diagnosis of the index twin, indicating that in adult-onset T1D the genetic impact is limited, and certainly lower than that in childhood-onset disease.

Genes associated with T1D are well-established and have four broad functions..However, T1D is unlikely to be a single disease since there is disease heterogeneity..the incidence of T1D has even increased several-fold in the last 30 years-a timeframe which rules out genetic evolution. In addition, studies of the incidence of T1D in migrant populations have shown a convergence towards the risk of the host population.

Alongside histone modifications and transcription factors, several cis-regulatory elements, including enhancers, promoters, silencers and insulators, are crucial to the function of the genome..There are more than a million enhancers; therefore, many more than there are genes, so that a number of genes are regulated by the same enhancer, which may co-localise with CpGs. Gene enhancers can be found upstream or downstream of genes and do not necessarily act on the closest promoter..Enhancers may be accompanied by insulators, which are located between the enhancers and promoters of adjacent genes and can limit phenotypic gene expression despite genetic activation.”


The review was weak in a few areas. The authors repeated a laughable claim for gross national product as a non-genetic effect for Type 1 diabetes. They also made other hyperbolic statements such as “..this observation illustrates the power of epigenetic analysis to identify those cells which are actively using the genes associated with a given tissue, given that all cells contain every gene..” that were out of place with the review’s evidential bases.

https://link.springer.com/article/10.1007/s11892-017-0916-x “The Role of Epigenetics in Type 1 Diabetes”

What are we to believe?

This 2017 blog post from Antiwar.com’s Justin Raimondo outlines the latest instance of exploiting beliefs:

“..neither the sources of this story nor those who are reporting it can be trusted..journalism is not a means of discovering knowledge, but a weapon to be deployed in a political-ideological conflict.”

Similar to the development of other beliefs, this current one discourages inquiries into “..information about the real world..giving us a highly distorted version of events.” It follows the blueprint of Using citations to develop beliefs instead of evidence in that once the faulty information becomes widely cited, refuting evidence is ignored, and the false belief is used for other purposes.

http://original.antiwar.com/justin/2017/08/10/what-are-we-to-believe/ “What Are We To Believe? Fake news plus phony “intelligence” equals disaster”

Using citations to develop beliefs instead of evidence

This 2009 Harvard study analyzed how citations were used as tools to establish a belief.

The researched data was gathered from 1992 to 2007 on a specific subject of Alzheimer’s research. The belief was that “β amyloid is produced by inclusion body myositis myofibres or is uniquely present in inclusion body myositis muscle.”

The author used social network analysis to determine:

“..four primary data papers, five model papers, and one review paper constituted the 10 most authoritative papers..that the claim was true.

The supportive papers received 94% of the 214 citations to these primary data, whereas the six papers containing data that weakened or refuted the claim received only 6% of these citations.

95% of all citation paths flow through four review papers by the same research group..Amplification of a claim is instead introduced into belief systems through the citing of review papers and other papers that lack data addressing the claim.”

Some of the benefits believers received included:

  1. It became easier to build models if a researcher believed “..animal and cell culture experiments are valid models of inclusion body myositis” although “The uncited data suggest that the animal and cell culture experiments are no more models of inclusion body myositis than any other neuromuscular disease in which muscle regeneration occurs.”
  2. Believers used exaggerations in their confirming research that diverted the original claim’s meaning. As an example, “..three supportive citations developed into 7848 supportive citation paths—chains of false claim in the network.”
  3. Citation biases and diversions could be used to support proposals for new funding.

Just imagine how compressed this phenomenon’s timeframe is now with our social networks! The tools available for creating memes and widespread nonfactual distortions are children’s play.

A few questions:

  • What do we believe in that isn’t thoroughly investigated, where we haven’t found the time or inclination to search for opposing results?
  • What causes us to believe these things?
  • What are the positive and negative consequences of our beliefs?

http://www.bmj.com/content/339/bmj.b2680 “How citation distortions create unfounded authority: analysis of a citation network”

Hat tip to Jon in the comments section of Neuroskeptic’s blog post “The Ethics of Citation” http://blogs.discovermagazine.com/neuroskeptic/2017/03/12/the-ethics-of-citation

Hope sells

I used a browser yesterday that didn’t have ad blocker software installed. The below pictures came from one of the ads that displayed:

helpless

hope

A young girl in a dance position and outfit juxtaposed with an appeal: “No situation is HELPLESS because there is HOPE.” How interesting!

I didn’t click through the ad yesterday to see what was being sold by engaging customers’ beliefs, within which lay hope. When I clicked the ad today, it asked for donations to “Sponsor a Child,” develop “the perfect recipe for sustainable success,” and, at the bottom of the page, “We love because Jesus loves.”

What do we know about this ad’s appeal from reading Dr. Arthur Janov’s May 2016 book Beyond Belief? Can hope change a helpless situation per the ad?

On one level – yes, in a believer’s brain, by blocking helpless feelings. Otherwise – no. Hope ultimately isn’t a remedy for the causes of what created helpless feelings.

I donated to a similar organization for a few years, but not anymore.