Running a marathon, cortisol, depression, causes, effects, and agendas

Let’s imagine that you decide you want to run a marathon. You haven’t run in six months, and you know you’ll have to train.

On the first day of training, as you run your first mile a friend pops out of nowhere and says, “You’re sweating! That means you’re going up to Mile 14 today! Good job, you’re on your way!”

You may appreciate the encouragement, but would a friend’s assessment have anything to do with your physical reality? Before you’ve run one mile, can an observer of your sweat say with certainty that you’ll run 14 miles on your first day of training?

Yeah. That’s how I felt when reading this 2014 UK study that found:

“Adolescent boys who have high levels of stress hormone ‘cortisol’ along with some symptoms of depression are at a 14 times higher risk of the condition than their peers.”

The researchers latched onto teenagers (12-16 years old, mean 13.7) to assess a psychiatric condition. They stated that a physical effect as common as visible sweat was a biomarker that predicted where some of the teenagers were going with their lives.

The study’s only physical measurements were cortisol from saliva samples at 8:00 a.m. on four consecutive days, then repeated a year later. For comparison, a standard lab test is to measure cortisol from saliva taken four times in one day at 9:00 a.m., 1:00 p.m., 5:00 p.m., and 9:00 p.m.

Cortisol is an effect of multiple potential causes, including stress, which itself is often an effect of multiple potential causes. One common cause of stress and its cortisol byproduct is diet, for example, when a person consumes caffeine.

“Mean time between waking and morning-cortisol collection was 50 min.”

I found it hard to believe that teenagers who:

  • woke up at 7:10 a.m.,
  • gulped down who knows what for breakfast,
  • got ready for, and then
  • went to school for an 8:00 a.m. cortisol test

wouldn’t have relatively “elevated morning cortisol” from the resultant stress.

Subjects self-reported depressive symptoms via a 33-item questionnaire initially and again every four months. They were interviewed for psychiatric diagnoses.

The largest separator used for stratification within subjects was an autobiographic memory test. Without this test, the study wouldn’t have made its main finding, so let’s look at the test’s details:

Anxious and depressed adolescent patients report significantly elevated levels of over-general categoric memories compared with well controls. Six positive and six negative words are presented on flashcards in pseudorandom order, and participants are instructed to recall a particular memory of an event in their life after each word. Sixty seconds were allowed for each response.

Responses were categorized as specific if they referred to an event with a specific time and place, lasting no longer than 1 d[ay]. Responses were considered overgeneral if they formed a general class of repeated events.”

We can see that the autobiographical memory test only considered the subjects’ verbal expressions – within a short time period – of their recalls of emotionally triggered memories. As informed by the principles described in Agenda-driven research on emotional memories, the recall of an emotional memory is a product of the cerebrum responding to input from limbic system and lower brain areas. When someone describes their recall of an emotionally triggered memory, it’s yet another level further removed from the brain areas that store emotional memories.

We can also see that test scores of the subjects’ verbal expressions aren’t capable of providing any etiologic evidence for an effect of high cortisol. A correlation is the best that could ever be shown by an autobiographic memory test. Again, the study’s main finding hinged on this third-order observational method of trying to figure out what’s going on inside subjects’ brains.

The researchers developed a control group, and made only a token attempt to trace the control group teenagers’ histories:

“The primary caregiver was interviewed about the quality of the family environment in three epochs (0–5, 6–11, and 12–14 y of age).

Four classes were found: optimal class, aberrant parenting, discordant, and hazardous.”

Were we supposed to believe that any primary caregiver would tell the truth about anything in a teenager’s history that indicated they had damaged their child? Good luck with that.

Anyway, the researchers didn’t act as though teenagers’ histories had any significant relationships with any present or future conditions. Their ahistoric biases showed by subsequently processing the entire history of each of the control group teenagers into a 1 or a 0 for the model.

The researchers then modeled this binary assessment to be relevant to the study’s main subjects!

The researchers’ agenda led to predetermined findings. Was the reviewer onboard with this agenda?

  • By disregarding the main subjects’ histories, it couldn’t provide etiologic evidence for any present or future effects.
  • By measuring only early morning cortisol, are we surprised that model numbers could be processed into some correlation?
  • Comparing this sole measurement to 325 measurements taken of subjects in Assessing a mountain climber’s condition without noticing their empty backpack made me wonder about the study designers’ real intentions.

News coverage of the study jumped on its flimsy finding to demand that something must be done. What did researchers offer teenagers who needed help?

  • After citing research that:

    “Showed null effects for two active treatments [cognitive behavioral therapy (CBT) and attentional training, respectively]”

    they recommended some unspecific:

    “New models of public mental health education and intervention in the youth population.”

  • After citing research that found:

    “Current diagnostic classifications [e.g., the Diagnostic and Statistical Manual for Mental Disorders (DSM) and the International Classification of Diseases (ICD)] have proved to have low diagnostic validity for investigations on the etiology, prevention, or treatment of MD [major depression]

    the study relied on these diagnoses anyway, and then disclaimed:

    “It may also be the case that current classifications, as used in this study, such as DSM and ICD are simply not optimally specified.”

They didn’t make their case that “elevated morning cortisol” effect was an adequate biomarker for teenagers who needed help. They did a disservice to their subjects by neither investigating nor providing any etiologic evidence for observed effects.

Who really benefited from this underlying agenda? I didn’t see that it was teenagers who may have actually needed assistance.

Did the study’s funders know that these efforts had enormous lacks? And what did:

“New models of public mental health education and intervention in the youth population”

really mean? “Elevated morning cortisol is a stratified population-level biomarker for major depression in boys only with high depressive symptoms”

One way beliefs produce pleasure and reward in the cerebrum

This 2014 Singapore human study found:

“Differences in belief learning – the degree to which players were able to anticipate and respond to the actions of others, or to imagine what their competitor is thinking and respond strategically – was associated with variation in three genes which primarily affect dopamine functioning in the medial prefrontal cortex.

In contrast, differences in trial-and-error reinforcement learning – how quickly they forget past experiences and how quickly they change strategy – was associated with variation in two genes that primarily affect striatal dopamine.”

One of the researchers said:

“The findings correlate well with previous brain studies showing that the prefrontal cortex is involved in belief learning, while the striatum is involved in reinforcement learning.”

The study didn’t demonstrate cause and effect, however, and the researchers cautioned:

“It would be mistaken to interpret our results as suggesting that dopamine genes function as “belief learning genes.”

The study added to the science of how beliefs act on the pleasure and reward parts of the cerebrum. “Dissociable contribution of prefrontal and striatal dopaminergic genes to learning in economic games” (the pdf file is linked because the html had errors)

Changing an individual’s future behavior even before they’re born

This 2015 Harvard fruit fly research was a companion of the Is what’s true for a population what’s true for an individual? study.

The researchers began with the question:

“If we could rear genetically identical individuals from a variety of genetic backgrounds and rear them in the same environment, how much phenotypic variation between individuals of the same genotype would we see?”

They answered with:

“We show that different genotypes vary dramatically in their propensity for variability, that phenotypic variability itself, as a trait, can be heritable, and that loci affecting variability can be mapped.”

The specific problem that probably prompted this study was that the methodology of genome-wide association studies (GWAS) usually:

“Focuses on the average effect of alternative alleles averaged in a population.”

What this methodology often missed was:

“When phenotypic variation results from alleles that modify phenotypic variance rather than the mean, this link between genotype and phenotype will not be detected.”

The researchers altered the environment during a critical period of fruit flies’ development in order to induce epigenetic changes in the fruit fly pupae brains:

“Disruption of Ten-a [the synaptic target recognition gene Tenascin accessory] expression in midpupa affects behavioral variance [the standard statistical dispersion parameter].

In all cases, disrupting Ten-a increased the variability [the median of the absolute deviation from each observation’s median] in turning bias with no effect on the mean.”

I fully expect researchers to demonstrate that this finding has general applicability for humans, especially during womb-life. Research such as:

are steps in this direction just for one factor in the human fetal environment – stress. The effects of stressing a human fetus should be at least as significant as the effects produced on the study’s subjects with increased temperature during pupation. “Behavioral idiosyncrasy reveals genetic control of phenotypic variability”

Is what’s true for a population what’s true for an individual?

This 2015 Harvard fruit fly study found:

“Genetically identical individuals display variability in their behaviors even when reared in essentially identical environments.

Individual flies exhibit significant bias in their left vs. right locomotor choices during exploratory locomotion.”

Here’s an example of why population statistics such as in GWAS didn’t necessarily apply to an individual:

“The probability of turning right averaged across all individuals within each line was statistically indistinguishable from 50%. However, an individual fly’s probability of turning right often diverged markedly from the population average.

For example, nearly one quarter (23.5%) of CS [Canton-S] flies turned right greater than 70% of the time or less than 30% of the time. This distribution would be unlikely indeed if all flies were choosing to turn right with identical probabilities.”

The researchers noted other species with similar findings:

“Individuals can develop idiosyncratic behaviors, morphology, and gene expression profiles. For example, stochastic DNA methylation may contribute to phenotypic variation that is uncorrelated to genetic variation.”

This study should inform other studies such as the Separating genetic from environmental factors when assessing educational achievement, to the degree its findings apply to humans.

As the findings applied to neurological areas:

“The magnitude of locomotor handedness is under the control of neurons within a brain region implicated in motor planning and execution.”

I was surprised that the study’s news coverage included this opinion:

“They are suggesting that variation [read: individuality] itself might be a genetic trait.”

The researchers stated their case in the companion study Changing an individual’s future behavior even before they’re born. “Neuronal control of locomotor handedness in Drosophila”

Limits of dMRI brain studies

This 2015 macaque study found:

“∼50% of the cortical surface was effectively inaccessible for long-range diffusion tracking.

Current and future high-resolution dMRI [diffusion magnetic resonance imaging] studies of the human brain will need to develop methods to overcome the challenges posed by superficial white matter systems to determine long-range anatomical connections accurately.”

The researchers stated:

“Although in many respects the macaque brain is a good approximation of the human brain, both species have undergone profound evolutionary changes since the time of their most recent common ancestor living more than 20 million years ago, particularly in regard to the massive expansion of the cerebral cortex in the human brain. Thus, it is of great value to assess human anatomical connections directly and comprehensively.”

Sound familiar? That’s also the point I made in Do popular science memes justify researchers’ cruelties to monkeys? “Superficial white matter fiber systems impede detection of long-range cortical connections in diffusion MR tractography”

An observational instead of experimental study on direction and place recognition

Occasionally a study appears in the Psychological and Cognitive Sciences section of PNAS that isn’t much more than graduate students wasting resources. This 2015 Pennsylvania rodent study was such an item.

The study’s design was observational, and it couldn’t be used as a reliable source to make statements of fact. Yet the researchers hyped that their:

“Finding has important implications for understanding the cognitive architecture underlying spatial navigation.

A similar cognitive architecture may underlie human navigational behavior.”

No reason was provided for not experimentally exploring the “cognitive architecture underlying spatial navigation.” So the study’s results didn’t advance science concerning grid cells, hippocampal place cells, head direction cells, boundary cells, and cells that encode object locations, as did the research referenced in the Are hippocampal place cells controlled by theta brain waves from grid cells? study.

It seemed to me that one of the researchers recognized this lack when they referred to new research instead of this study in one of the covering news articles. We’ll see what the graduate students do next. “Place recognition and heading retrieval are mediated by dissociable cognitive systems in mice”

The thalamus part of the limbic system has a critical period for connections

This highly-jargoned 2015 UK study found that connections made by the thalamus of the developing human fetus had a critical period of the last trimester of womb-life. Babies born before the 33rd week of gestation experienced thalamic disconnections compared with normal-term babies and adults. The disconnections increased with a shorter womb-life.

The thalamus of premature babies also developed stronger connections with areas of the face, lips, tongue, jaw, and throat. They presumably needed these connections for survival actions such as breathing and feeding that aren’t a part of the last trimester of womb-life.

The study confirmed that the structures of thalamic connections of normal-term babies were very similar to those of adults. The study added to the research that shows that human limbic systems and lower brains closely approximate their lifelong functionalities at the normal time of birth.

It was difficult to measure the thalamus at this stage of life with current technology, and the researchers had to discard over two-thirds of their results. The researchers recommended monitoring these premature babies for difficulties in later childhood that may be caused by their early-life experiences.

Why would this monitoring recommendation apply to just the study’s subjects? We know from other studies that a main purpose of thalamic connections is to actively control and gate information to and from the cerebrum.

Would it make sense for a medical professional to disregard any patient’s birth history if they had problems in their brain’s gating functions or connectivity?

One researcher said:

“The ability of modern science to image the connections in the brain would have been inconceivable just a few years ago, but we are now able to observe brain development in babies as they grow, and this is likely to produce remarkable benefits for medicine.”

This study’s results provided evidence for a principle of Dr. Arthur Janov’s Primal Therapy: the bases for disconnection from aspects of oneself are often set down during gestation. The “remarkable benefits for medicine” are more likely to be along the lines of what I describe in my Scientific evidence page. “Specialization and integration of functional thalamocortical connectivity in the human infant”

Do strong emotions cause our brain hemispheres to interact more closely?

This 2015 human/macaque study found:

“The functional coordination between the two hemispheres of the brain is maintained by strong and stable interactions.

These findings suggest a notable role for the corpus callosum in maintaining stable functional communication between hemispheres.”

The human subjects were asked to:

“Generate four negative autobiographical memories and create word cues that reminded them of each event. Participants then underwent a 6-min IR fMRI scan during which they were cued with the words they had created to recall the two most negative autobiographic memories generated outside the scanner.”

However, the study’s supplementary material didn’t address why the researchers used this particular technique.

Does recalling strong emotional memories that engage our limbic systems cause our brain hemispheres to interact more closely than do cerebral exercises?

This study demonstrated that including emotional content in brain studies was essential. It may have provided additional information had the researchers also used the two least-negative emotional memories.

As noted in Agenda-driven research on emotional memories, one hypothesis of Dr. Arthur Janov’s Primal Therapy is that recalling an emotional memory engages one’s brain differently than does re-experiencing an emotional memory. Asking the subjects to attempt to re-experience the two least-negative emotional memories may have provided data relevant to the study.

I didn’t understand why macaques were used as subjects. The researchers didn’t provide any tasks for the monkeys during the scans. The information this study gained only duplicated other studies.

Also, the monkeys were anesthetized throughout the experiments. An assumption that wasn’t addressed: fMRI scan data on anesthetized macaques provided comparable evidence to fMRI scan data on normal non-anesthetized humans who were recalling emotional memories?

Did the researchers use macaques simply because they were available? “Stable long-range interhemispheric coordination is supported by direct anatomical projections”

Chaos – not balance – and competition for resources are the natural order

This 2015 Amsterdam/New Zealand/Cornell shore-life study found:

“Species abundances in natural ecosystems may never settle at a stable equilibrium.

Species in one of the world’s oldest marine reserves showed chaotic fluctuations for more than 20 years. The species replaced each other in cyclic order, yet the exact timing and abundances of the species were unpredictable.

Our findings provide a field demonstration of nonequilibrium coexistence of competing species through a cyclic succession at the edge of chaos.

Our findings show that natural ecosystems can sustain continued changes in species abundances.”

chaos “Species fluctuations sustained by a cyclic succession at the edge of chaos”

The University of Amsterdam also participated in a 2013 study Evolution of microbial markets where evolutionary biologists studied microbes. Their related findings included:

“Cooperative interactions between individuals of different species.

Strategies important for microbes to optimize their success in potential biological markets:

  • (i) avoid bad trading partners;
  • (ii) build local business ties;
  • (iii) diversify or specialize;
  • (iv) become indispensable;
  • (v) save for a rainy day; and
  • (vi) eliminate the competition.”

A 2015 study How a well-adapted immune system is organized (the *.pdf file is linked because the html has errors) had a related finding that applied to our body’s immune system. The researchers found that the primary reason why each of our immune systems is unique is due to the effect of:

“Competition between receptor clones..NOT a biologically implausible centralized mechanism distributing resources system-wide.

The repertoire of lymphocyte receptors in the adaptive immune system protects organisms from diverse pathogens. A well-adapted repertoire should be tuned to the pathogenic environment to reduce the cost of infections.

Competitive dynamics can allow the immune repertoire to self-organize into a state that confers high protection against infections.”

Chaos and competition for resources are facts of life observed within ourselves and in nature from ocean life down to the microbe level.

Why are we often presented – as a fact of life – that what’s natural is for all aspects of our lives to be in balance? Emotional, economic, social, intellectual – you name it, we’re told that the natural model is one of “stable equilibrium.”

Two hypotheses of Dr. Arthur Janov’s Primal Therapy are relevant:

Trying for closure, though, becomes an act-out – a temporary fulfillment of a substitute need. But the underlying need remains unsatisfied, and soon drives further act-outs. Balance is never achieved.

With this viewpoint, can you see how behavior like the following shows the internal state of the actor as they attempt to thwart the natural reality of the situation?

  • A person in authority who demands that people cease their competition for a resource and instead, accept what the authority figure determines is fair and balanced. An example is limiting supplies with price controls after a disaster.
  • A person who disrupts cooperative behavior that provides a solution for the cooperators’ needs/wants and instead, interposes themselves in a directed solution. An example is requiring licenses for cooperative childcare.
  • A person who insists that peoples’ responses to chaos to form an optimal adaptation cease, and instead, conform to some other responses. An example is prohibiting free movement after a disaster.

It reveals even more about the internal states of people that the above examples become codified. Children are taught that the natural and solely acceptable way to behave is in accordance with these unnatural solutions.

There are some signs that unnatural solutions in society can be reversed. For example, here is a 2013 article about a UK village that benefited from removing all of its traffic signals and reverting to the natural order of human cooperation and competition.

At the individual level, though, it’s up to each one of us to recognize and reverse our unnatural states. We and the people around us will be pleased when we and they are no longer adversely affected by our unconscious act-outs that are driven by our internal states. There’s enough natural chaos without adding more with act-outs.

Our internal systems will suffer damage, for example, when our unconscious act-out is to be busy, always doing something, and we can’t relax. Stress adversely affects our internal systems until we understand and reverse the driving unnatural states.

Do popular science memes justify researchers’ cruelties to monkeys?

This 2015 Oxford study of 38 humans and 25 macaques drew correlations of brain activities between the two species. The study title included buzzwords such as “reward” and “decision making” and the study focused on the ever-popular “frontal cortex.”

Humans and macaques are separated by 25 million years of evolutionary adaptations and developments. Studies done with macaque subjects don’t automatically have human applicability.

Was a major reason for the study’s comparisons to provide justifications for keeping macaques as study subjects? Accepting these justifications and going along with the popular memes would ease the way for whatever cruelties researchers want to inflict on our primate relatives. “Connectivity reveals relationship of brain areas for reward-guided learning and decision making in human and monkey frontal cortex”

A mixed bag of findings about oxytocin, its receptor, and autism

This 2014 Stanford human study found:

“No empirical support for the OXT [oxytocin] deficit hypothesis of ASD [autism spectrum disorder], nor did plasma OXT concentrations differ by sex, OXTR [oxytocin receptor] SNPs [single nucleotide polymorphisms], or their interactions.”

Apparently, there was a:

“Prevalent but not well-interrogated OXT deficit hypothesis of ASD.”

The researchers followed up this worthwhile finding with three weak findings. The first, as stated by one of the study’s lead researchers, was:

“It didn’t matter if you were a typically developing child, a sibling or an individual with autism: Your social ability was related to a certain extent to your oxytocin levels.”

The second weak finding was that, regarding OXTR SNPs:

“The minor allele of rs2254298 predicted global social impairments on the SRS [Social Responsiveness Scale] and diagnostic severity on the ADI-R [Autism Diagnostic Interview-Revised]. In contrast, the major allele of rs53576 predicted impaired affect recognition performance on the NEPSY [A Developmental NEuroPSYchological Assessment].”

This was at odds with other relevant research, leading the researchers to state:

The functional significance of these two intronic variants remains unknown.”

The third weak finding irked me:

“Plasma OXT concentrations were highly heritable.”

because the researchers didn’t attempt to differentiate the contribution of the environment for the observed blood oxytocin levels, as did the similar How epigenetic DNA methylation of the oxytocin receptor gene affects the perception of anger and fear study.

I wonder what the reviewer’s feedback was about these weak findings. Did he make the researchers insert specific language into the lengthy paragraph about the study’s limitations, or did he give them a pass? “Plasma oxytocin concentrations and OXTR polymorphisms predict social impairments in children with and without autism spectrum disorder”

Do our unique visual perceptions arise from brain structural differences?

This 2014 UK/German human study involved fMRI scans of the subjects inferior temporal cortex while viewing images:

“Brain representational idiosyncrasies accessible to fMRI are expressed in an individual’s perceptual judgments.

We found evidence for an individually unique representation predictive of perceptual idiosyncrasies in hIT [human inferior temporal cortex] (but not in early visual areas) and for personally meaningful (but not for unfamiliar) objects.”

Citing other studies, the researchers said:

“The size of primary visual cortex varies across individuals by a factor of about 2.5.

Although other areas might vary by smaller factors, many parts of the brain, including cortical and subcortical structures, show gross anatomical variation across individuals that is predictive of cognitive and behavioral differences.”

The researchers asserted:

“Functional differences as reported here ultimately must arise from differences in the physical structure of each individual brain.”

However, no evidence was provided for this assertion.

The researchers acknowledged this lack of evidence, but in a way that required further evidence:

“Our study demonstrates individual differences in high-level semantic representations but cannot address their structural basis. Our current interpretation is that the representational idiosyncrasies might arise from the microstructural plasticity of cortex, which is driven by individual experience.”

The researchers’ assertion beyond the study’s supporting data was at best a statement of their goal. Further, their bias to focus on the inferior temporal cortex area of the cerebrum led them to not investigate other areas of the brain that may have been involved with the “personally meaningful (but not for unfamiliar) objects” finding, such as the subjects’ limbic systems.

I hope that researchers won’t think that their research is complete when they reach their goal of finding “differences in the physical structure of each individual brain.” It would be far more informative to understand the causes for these effects. “Unique semantic space in the brain of each beholder predicts perceived similarity”

Separating genetic from environmental factors when assessing educational achievement

This 2014 UK study of identical and fraternal twins found that an average of 62% of the differences among their scores on a significant test given at age 16 were due to genetic factors:

“Genetic influence is greater for achievement than for intelligence, and other behavioral traits are related to educational achievement largely for genetic reasons.”

However, the “genetic reasons” term didn’t mean that the researchers actually took genetic samples. From one news article:

“Identical twins share 100 percent of their genes while non-identical twins share just 50 percent of their genes. Because these sets of twins share the same environment, the scientists were able to compare identical and non-identical twins to estimate the relative contributions of genetic and environmental factors.”

This estimation method produced an artificial divide between genetic and environmental factors. Identical twins start out sharing 100% of their genes, but then their genes become expressed differently – often because of environmental factors – to produce unique individuals even before birth.

The sets of identical twins were definitely not the 100% same genetic makeup between themselves at age 16 as they were at conception, and that assumption was the foundation of the researchers’ model:


“Bivariate estimates for additive genetic (A), shared environmental (C), and nonshared environmental (E) contributions to the correlations between GCSE and nine predictors. The total length of the bar indicates the phenotypic correlations.”

The researchers didn’t provide evidence that “genetic reasons” were causal factors to the stated extent. Although the model’s numbers may have indicated that the method’s results were valid, that didn’t necessarily mean that the reality of genetic and epigenetic influences on the subjects were represented to the stated precision by the results.

The weather analogy of Scientific evidence applies to this study’s methods:

“We can think about what we mean by evidence. For example, that when you see dark storm clouds overhead, that’s strong evidence that it’s about to rain. If you smell a certain scent, that’s maybe weak evidence that it’s about to rain. And if we see the dark storm clouds and then we smell the scent, the evidence doesn’t get weaker: if anything, it gets stronger.

But P-values in a circumstance like that, where you have a very small P-value in one dataset and a not-so-small P-value in a second dataset, you put the data together and the P-value will tend to sort of average.

So the P-value is not behaving like evidence.”

Better methods of estimating “the relative contributions of genetic and environmental factors” are available with actual genetic sampling. One way is to measure the degree of DNA methylation of genes as did:

The study and its news coverage were full of politically-correct buzzwords – for example, the researchers’ statement:

“The results also support the trend in education toward personalized learning.”

This “personalized learning” is a teacher not telling a student:

“You’re doing poorly at math. You need to pay attention in class and do the homework.”

but instead saying:

“You have a different learning style. We’ll tailor the math lessons to your style.”

The funniest thing I saw in the study’s news coverage was this one where someone argued that the researchers were wrong and that they needed educational psychologists on their staff to interpret the data. Guess the profession of the arguer! “The high heritability of educational achievement reflects many genetically influenced traits, not just intelligence”

People who donated a kidney to a stranger have a larger amygdala

This 2014 Georgetown study was of people who had donated a kidney to a stranger. The study found that the subjects had a larger right amygdala part of their limbic systems:

“Our results support the possibility of a neural basis for extraordinary altruism.

In sum, our findings suggest that individuals who have performed an act of extraordinary altruism can be distinguished from healthy controls by increased right amygdala volume, as well as heightened responsiveness in right amygdala to fearful facial expressions, which may support enhanced recognition of these expressions.”

The researchers stopped short of causal explanations. They stated in the study’s abstract that:

“Individual variation in altruistic tendencies may be genetically mediated”

but didn’t develop any evidence to support this statement.

It would have been within the scope of the study had the researchers continued on to examine:

  • What may have happened in the subjects’ lives to possibly cause their neurobiological and psychological attributes?
  • What were the causes for the subjects’ extreme altruistic behavior?
  • Were these the same causes for their larger, more sensitive amygdala?

An accompanying PNAS commentary from a Harvard researcher made other points. However, the author showed his biases that the cerebrum rules human behavior with an out-of-left-field question at the end of a paragraph in which he developed specious reasoning.

The commentator was completely off base when he stated:

“Could it be that extraordinary altruists such as Maupin [a study participant] and the 19 individuals studied by Marsh et al. [the researchers] are special, not only because of how they feel when they see people in distress, but because of how they think?”

I don’t imagine that the brilliant commentator’s attempt to upstage the study’s subjects and put the spotlight on himself for some brilliant idea was much appreciated by anyone involved.

The amygdala is the central hub of a person’s limbic system. The study’s findings had very little to say about the subjects’ cerebral activity – thinking.

To postulate that the researchers missed that there was something different about the subjects’ thinking was out of touch with the realities of both the researchers’ scientific bases and the subjects. It’s another example of the current research mindset/social meme of cerebral dominance. “Neural and cognitive characteristics of extraordinary altruists”

What causes disconnection between the limbic system and the cerebrum?

This 2014 Swedish human study with 339 subjects aged 25-80 years old found that as the subjects’ age increased, their hippocampus became less connected to their cerebrums:

“Age-related cortico–hippocampal functional connectivity disruption leads to a more functionally isolated hippocampus at rest, which translates into aberrant hippocampal decoupling and deficits in active mnemonic processing.”

The lead researcher said:

“What we can now show is that memory problems that come with increased age are most likely due to a process where the interaction among different regions of the hippocampus increases in response to less inhibitory cortical input. This in turn means that the hippocampus risks being more isolated from other important networks in the brain which impacts our ability to actively engage the hippocampus, for example to remember different events.”

Like other researchers commonly do, they excluded emotional content from the study. See another Swedish study Emotional memories and out-of-body–induced hippocampal amnesia as an example of why emotional memories are necessary in order to properly study the hippocampus.

1) As a result of excluding emotional content and other aspects of the study’ design such as using 25 as the beginning age of the subjects, all the researchers could muster as a explanatory factor was age. However, they had to couch their findings as “age-related” because age in and of itself wasn’t a causal explanation for the observed effects.

2) The findings weren’t even truly “age-related”  because, for example, the study didn’t necessarily apply to people below the age of 25. Had the study included 10-18 year old subjects, the researchers may have found that “less inhibitory cortical input” may also be present before puberty, as The prefrontal cortex develops more repressive function at puberty study indicated.

3) Had the study design included neurochemicals, the researchers may have found that “cortico–hippocampal functional connectivity disruption” was due to factors that influenced dopamine and glutamate levels, as A mechanistic study of neurotransmitters in the hippocampus indicated.

4) A finding that “cortico–hippocampal functional connectivity disruption” was influenced by other factors may also have been made had the study design included the subjects’ histories. Per my Welcome page, the findings of much of the recent research I’ve curated on this blog, and the references in those studies show that when basic needs aren’t met, especially early in people’s lives, and the painful conditions persist, enduring physiological changes may occur.

5) What the researchers noted in the study’s limitation paragraph were references to fMRI scans rather than limitations such as those mentioned above regarding the study design. The study provided unconvincing evidence for causes of “cortico–hippocampal functional connectivity disruption” and it wasn’t because of fMRI limitations. “Elevated hippocampal resting-state connectivity underlies deficient neurocognitive function in aging”

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