The link between scientific value and content is broken at PNAS.org

Should we expect content posted on the Proceedings of the National Academy of Sciences of the United States of America to have scientific value?

This 2016 Singapore study was a “PNAS Direct Submission” that claimed:

“This paper makes a singular contribution to understanding the association between biological aging indexed by leukocyte telomeres length (LTL) and delay discounting measured in an incentivized behavioral economic task.

LTL is an emerging marker of aging at the cellular level, but little is known regarding its link with poor decision making that often entails being overly impatient.”


Whether measured at the level of a human or of a blood cell, in 2016 there wasn’t incontrovertible evidence to support:

  • “Biological aging indexed by leukocyte telomeres length
  • LTL is an emerging marker of aging at the cellular level”

Using an epigenetic clock to distinguish cellular aging from senescence found:

Cellular ageing is distinct from cellular senescence and independent of DNA damage response and telomere length.”

If that study was too recent, the researchers and reviewer knew or should have known of studies such as this 2009 study that found the correlation between a person’s chronological age and blood cell telomere length was r = −0.51 in women and r = −0.55 in men.

A study of biological aging in young adults with limited findings was cited for evidence that “the seeds of biological aging are widely thought to be planted early in life.” That study didn’t elucidate the point, however, as it didn’t fully link its measurements when the subjects were 38 years old with measurements taken during the subjects’ early lives.

Problematic research with telomere length was cited for evidence that “other factors, such as the early family environment, lifestyle, and stress, also have considerable impact on cellular aging.” The researchers had to be willing to overlook that study’s multiple questionable practices in order to cite it as evidence for anything.

Nevertheless, the study used a one-to-one correspondence of telomere length and cellular aging.


The researchers speciously modeled a relationship between telomere length and the behavioral trait “poor decision making that often entails being overly impatient.” That overreach was further stretched to the breaking point:

“We then asked if genes possibly modulate the effect of impatient behavior on LTL.

The oxytocin receptor gene (OXTR) polymorphism rs53576, which has figured prominently in investigations of social cognition and psychological resources, and the estrogen receptor β gene (ESR2) polymorphism rs2978381, one of two gonadal sex hormone genes, significantly mitigate the negative effect of impatience on cellular aging in females.”


The “significantly mitigate” finding was “fun with numbers” that produced false effects rather than solid evidence. Consider that:

  1. The study’s model disregarded the probability that “Cellular ageing is independent of telomere length.”
  2. The researchers provided no mechanisms that plausibly linked performance “in an incentivized behavioral economic task” with telomere length.
  3. The researchers didn’t characterize any causal mechanisms whereby two gene variants affected the task performance’s purported effect on telomere length.

What’s the real reason the reviewer forwarded this paper to PNAS.org?

http://www.pnas.org/content/113/10/2780.full “Delay discounting, genetic sensitivity, and leukocyte telomere length”

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