Metabolic costs and evolutionary implications of human brain development

This 2014 human study framed many of the other studies that relate to children’s brain development:

“The researchers found instead that the brain maxes out its glucose use at age 5. At age 4 the brain consumes glucose at a rate comparable to 66 percent of the body’s resting metabolic rate (43 percent of the body’s total energy expenditure).

To compensate for these heavy energy demands of our big brains, children grow more slowly and are less physically active during this age range.”

http://www.pnas.org/content/111/36/13010.full “Metabolic costs and evolutionary implications of human brain development”

Conscious mental states should not be the first-choice explanation of behavior

Here are some 2014 ruminations by Joseph LeDoux, the grandfather of studies of the amygdala. He attempted to disambiguate feeling brain structures’ activations and responses from ideas of what feelings are, specifically regarding fear:

“Damage to the hippocampus in humans disrupts explicit conscious memory of having been conditioned but has no effect on fear conditioning itself, whereas damage to the amygdala disrupts fear conditioning but not the conscious memory of having been conditioned.

Conscious mental states should not, in the absence of direct evidence, be the first-choice explanation of behavior.

Neither amygdala activity nor amygdala-controlled responses are telltale signatures of fearful feelings.

Conscious fear can cause us to act in certain ways, but it is not the cause of the expression of defensive behaviors and physiological responses elicited by conditioned or unconditioned threats.”

http://www.pnas.org/content/111/8/2871.full “Coming to terms with fear”

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”

Shorter telomere length in older men but not older women

This 2014 UK human study was the first on telomere length I’ve curated, so here’s some background information:

“Telomeres are..structures..that cap the ends of..chromosomes, protecting them from end-to-end fusion and degradation during cell division.

Human telomeric DNA naturally shortens with age during..cell divisions and as a result of oxidative attack.

At critical shortness, telomeres exhibit impaired function, leading to genomic instability, apoptosis, and cell senescence, often with altered transcriptional programming and mitochondrial dysfunction.

In humans, mutations that directly compromise telomere maintenance cause premature mortality and onset of a spectrum of diseases overlapping with the age-related diseases common in the population.

Shorter telomere length in white blood cells is linked and, in some cases, anticipates aging-related morbidity and mortality from conditions with immune system involvement, such as infectious diseases, cancer, and cardiovascular diseases, as well as risk factors, including hypertension, diabetes, obesity, and smoking.

A critical determinant of telomere length is the enzyme telomerase, which has the capacity to add..onto the..ends of telomeric DNA, extending telomere length and promoting genomic stability.

Acute mental stress appears to increase telomerase enzymatic activity at least transiently, and it has been suggested that high telomerase activity in conjunction with shorter telomere length may be indicative of a stressed system.”

The study put UK civil service men and women ages 54 through 76 through a series of stress tests. They found that men with longer telomeres had quicker recovery times than did men with shorter telomeres.

Men with shorter telomeres and low telomerase activity also had quicker recovery times than did men with shorter telomeres and high telomerase activity:

“In addition, we found that the (shorter telomeres and high telomerase activity men) had blunted reactivity to acute stress in diastolic blood pressure, heart rate, and cortisol.”

No telomere-based differences occurred with women:

“The explanation for the sex difference in response profiles in our study is not clear. Hormonal processes are unlikely to be directly responsible, because women in this study were postmenopausal.”

http://www.pnas.org/content/111/12/4519.full “Shorter telomeres with high telomerase activity are associated with raised allostatic load and impoverished psychosocial resources”