How brains mature during critical periods

This 2015 German rodent study found:

“Once silent synapses are consolidated in any neural circuit, initial experience-dependent functional optimization and critical periods end.

Silent synapses are thought to be immature, still-developing excitatory synapses.”

The number of silent synapses related to visual processing was measured at ~50% at eye opening. Visual experience reduced this to 5% or less by adulthood in the study’s control group. Removing a protein in the subjects’ hippocampus silenced the synapses back up to ~50%, even in adults.

Critical periods are:

“Characterized by the absolute requirement for experience in a restricted time window for neural network optimization.

Although some functions can be substantially ameliorated after the CP [critical period], they are rarely optimally restored.”

Two human studies were cited on critical periods in second-language and musical skills development, Sensitive periods in human development: Evidence from musical training (not freely available).

The researchers generalized their findings as:

“Experience-dependent unsilencing of silent synapses constitutes an important general maturational process during CPs of cortical development of different functional domains and suggest an interplay with inhibitory circuits in regulating plasticity.”

http://www.pnas.org/content/112/24/E3131.full “Progressive maturation of silent synapses governs the duration of a critical period”

Unconscious stimuli have a pervasive effect on our brain function and behavior

This 2015 Swedish human study, performed at the institution that awards the Nobel Prize in Physiology or Medicine, found:

“Pain responses can be shaped by learning that takes place outside conscious awareness.”

Images of neutral male faces were used as conditioning stimuli which the subjects were trained to associate with levels of pain.

The concluding sentence of the study:

“Our results demonstrate that conscious awareness of conditioned stimuli is not required during either acquisition or activation of conditioned analgesic and hyperalgesic responses, and that low levels of the brain’s hierarchical organization are susceptible for learning that affects higher-order cognitive processes.”

From the study’s abstract:

“Our results support the notion that nonconscious stimuli have a pervasive effect on human brain function and behavior and may affect learning of complex cognitive processes such as psychologically mediated analgesic and hyperalgesic responses.”


Principles of Dr. Arthur Janov’s Primal Therapy related to this study’s findings are:

  • Experiences associated with pain can be remembered below our conscious awareness.
  • Unconscious memories associated with pain, when activated, have varying forms of expression as they pass up through our levels of consciousness.
  • These memories, when activated, have effects on our feelings, thinking, health, brain functioning, and behavior that are usually below our conscious awareness.

I’ll use one of Dr. Janov’s 2011 blog posts, On Being Alone, to show an example of how the study’s findings of:

  • “Conscious awareness of conditioned stimuli is not required during either acquisition or activation of conditioned..responses” and
  • “Nonconscious stimuli have a pervasive effect on human brain function and behavior”

are seen through the lens of Primal Therapy:

Unconscious memories associated with the pain of being left alone may be stored, especially in the developing brain, in our lower brain areas below conscious awareness: “Pain of being left alone a lot in childhood and infancy, added to the ultimate aloneness right after birth when no one was there for the newborn. That imprints a primal terror where a naïve, innocent and vulnerable baby has no one to lean on, to be held by, to snuggle up to, to be comforted. To be loved.”
As we develop, the cumulative memories associated with the pain of being left alone, when activated, may affect our feelings, thoughts, and behavior: “And that also has multiple meanings: no one wants me; there is no one there for me: no one wants to be with me; I have no love and no one who cares. One races to phone others so as not to feel alone. One runs from the feeling and struggles mightily not to be alone. Or, depending on earlier events one stays alone out of that same feeling. These are by and large the depressives.”
Although memories associated with the pain of being left alone may be formed in our early lives, they remain decades later, and can be activated below our conscious awareness: “When something in the present occurs which is similar to an old feeling “I am all alone and no one wants me,” the old feelings are triggered off..and the whole feeling rises toward conscious/awareness where it must be combated. Either the person wallows in the feeling and is overwhelmed by it even when she doesn’t even know what “it” is. Or the compounded feeling drives the act-out, forcing the person into some kind of social contact.”

A PNAS commentary on the study stated:

“Pain, analgesia, and hyperalgesia represent higher-order cognitive functions.”

and attempted to draw conclusions from this reasoning.

The commentator was incorrect regarding pain. I didn’t see where this study showed or even postulated that pain was always a higher-order cognitive function. In fact, the researchers cited a sea slug study and stated:

“It would not be surprising if vestiges of simpler nonconscious processes would also be operative under some conditions.”

Maybe it would have provided clarifications if the researchers specifically defined “low” and “higher” used throughout the study in statements such as the closing sentence:

“Low levels of the brain’s hierarchical organization are susceptible for learning that affects higher-order cognitive processes.”

http://www.pnas.org/content/112/25/7863.full “Classical conditioning of analgesic and hyperalgesic pain responses without conscious awareness”


This post has somehow become a target for spammers, and I’ve disabled comments. Readers can comment on other posts and indicate that they want their comment to apply here, and I’ll re-enable comments.

The effects of inescapable, uncontrollable, repeated stress on the hippocampus

This 2015 MIT rodent study found:

Behavioral stress impairs cognitive function via activation of a specific direct neural circuit from the basolateral amygdala to the dorsal hippocampus. Moreover, we delineate a molecular mechanism by which behavioral stress is translated to hippocampal dysfunction via a p25/Cdk5 (cyclin-dependent kinase 5)-dependent pathway and epigenetic alterations of neuroplasticity-related gene expression.”

The researchers made several intermediate findings to develop their main finding:

1. “Repeated stress is accompanied by

  • generation of p25,
  • up-regulation and phosphorylation of glucocorticoid receptors,
  • increased HDAC2 [the gene encoding the histone deacetylase 2 enzyme] expression, and
  • reduced expression of memory-related genes [most, but not all that were tested] in the hippocampus.”

2. “BLA [basolateral amygdala] activation is both necessary and sufficient for stress-associated molecular changes and memory impairments.”

3. “This effect [2. above] relies on direct glutamatergic projections from the BLA to the dorsal hippocampus.”

4. “p25 generation is necessary for the stress-induced memory dysfunction.”

From the Results section:

“Control mice showed a significant preference for the novel over the familiar object or location, whereas RFS [repetitive foot shock]-treated mice performed no better than chance.”

The subject adult mice underwent:

“Inescapable, uncontrollable repeated stress.”

Do humans also experience impaired “cognitive function” and “hippocampal dysfunction” and “epigenetic alterations of neuroplasticity-related gene expression” caused by “inescapable, uncontrollable repeated stress”?

And what are the real histories of people who aren’t curious, who don’t show “a significant preference for the novel over the familiar object or location”?

http://www.pnas.org/content/112/23/7291.full “Basolateral amygdala bidirectionally modulates stress-induced hippocampal learning and memory deficits through a p25/Cdk5-dependent pathway”

Measuring the signal-to-noise ratio of a brain neuron

This 2015 study found that a single brain neuron’s

“Spiking history is often a more informative predictor of spiking propensity than the signal or stimulus activating the neuron.

Characterizing the reliability with which neurons represent and transmit information is an important question in computational neuroscience.”

Three of the four brain neuron areas studied were of the limbic system: a rat thalamus, a monkey hippocampus, and a human subthalamus area.

http://www.pnas.org/content/112/23/7141.full.pdf “Measuring the signal-to-noise ratio of a neuron” (pdf file is linked because the html has errors)

An inhibitory gene that affects alcohol binge behavior

This 2015 La Jolla rodent study found that an inhibitory gene affected alcohol binging behavior:

“Our study reveals the behavioral impact of this cellular effect, whereby the level of GIRK3 [the gene] expression in the VTA [ventral tegmental area] tunes ethanol intake under binge-type conditions: the more GIRK3, the less ethanol drinking.”

GIRK3-silenced mice still binged, though, and got alcohol’s rewarding effects through dopamine’s other neural pathways.

High concentrations of the gene were found in the thalamus part of the limbic system of wild-type mice, the control group. Per the study’s title, this gene presumably contributes to the thalamus’ overall function of gating information from limbic system and lower brain areas to reach the cerebrum and vice versa.

And the potential causes for reduced GIRK3 expression are..?? Hopefully – someday – researchers will be focused on finding causes for abnormal gene expression rather than being content to just study effects of abnormal gene expression. Until then, the usual practice of considering only the effects led these researchers to:

“Believe that a compound selectively targeting GIRK3-containing channels may hold promise for reducing alcohol consumption in heavy binge drinkers.”

http://www.pnas.org/content/112/22/7091.full “GIRK3 gates activation of the mesolimbic dopaminergic pathway by ethanol”

Epigenetic changes in the developing brain change behavior

This 2015 review cited 143 studies to tie together findings in epigenetic chemistry and behavioral neuroscience.

In addition to studies I’ve previously curated, other research included:

  • a 2012 study which completely abolished mouse maternal behavior by silencing a gene encoding an estrogen receptor;
  • a 2012 study which found that stress-induced changes in the rat hippocampus were heritable;
  • a 2014 study that distinguished between transgenerational and intergenerational epigenetic effects such as:

    in utero exposure to nutritional status, stress, or toxic environmental factors that act on the developing embryo and its germ line”

  • a 2013 study that showed how genomic imprinting coordinated:

    “Genetic coadaptation where beneficially interacting alleles evolve to become coinherited.”

The current status of research incorporating both epigenetic chemistry and behavioral neuroscience was summed up as:

“A large number of behavioral epigenetic studies attempt to correlate epigenetic marker changes at global levels and in mixed populations of cells with phenotypic changes.

Specific changes at specific gene levels and at single cell levels correlating with behavioral changes remain largely unknown.”

http://www.pnas.org/content/112/22/6789.full “Epigenetic changes in the developing brain: Effects on behavior”

RNA as a proxy signal for context-specific biological activity

This 2015 Harvard/MIT rodent study was of long (more than 200 nucleotides) noncoding (non-protein coding) RNAs (ribonucleic acids). These are of interest because:

“Within the mammalian body, the largest repertoire and diversity of lncRNA genes outside the germ line occurs in the brain, where lncRNAs exhibit regional and cell-specific localization.

The expression patterns of lncRNAs may serve as a proxy signal for important, context-specific biological activity.”

The researchers explained what they could and couldn’t determine with current techniques and technologies:

“The whole-gene ablation method used here is often a first approach to determine the functionality of a locus.

Although each of these loci contains a lncRNA, it is important to consider that any observation resulting from this strategy could reflect the loss of any regulatory element in the deleted region.

The rate of lncRNA gene discovery has significantly outpaced our ability to evaluate both the physiological significance and function of these genes. It is difficult to predict whether the loss of any particular lncRNA locus will present a phenotype, but crucial information on the spatiotemporal dynamics of expression from each locus can provide significant direction and focus to downstream mechanistic studies by highlighting those loci most likely to have a physiological impact.

It is important to stress that no single method exists that can account for all possible mechanisms of action of a noncoding locus. Within these limits, the phenotypes observed after ablation of specific lncRNA loci confirm that expression of this class of noncoding RNAs can serve as a proxy signal to identify functional genomic loci with physiological relevance to disease and development, independent of whether this activity is directly ascribed to a functional lncRNA molecule.”

http://www.pnas.org/content/112/22/6855.full “Spatiotemporal expression and transcriptional perturbations by long noncoding RNAs in the mouse brain”

Stress in early life can alter physiology and behavior across the entire lifespan

I’ll quote a few sections of this 2014 summary of 111 studies concerning stress, including the authors’ research:

“The brain is the central organ of stress and adaptation to stressors because:

  • It not only perceives what is threatening or potentially threatening and initiates behavioral and physiological responses to those challenges,
  • But also is a target of the stressful experiences and the hormones and other mediators of the stress response.

The stress history of parents is a significant factor in the resilience of their offspring.

Environmental stress transduces its effects into lasting changes on physiology and behavior, which can vary even among genetically identical individuals.

Stress in early life can alter physiology and behavior across the entire lifespan.

Structural stress memory is even more apparent with regard to gene expression in stress-sensitive brain regions like the hippocampus.

Individual history is important and that there is a memory of stress history retained by neurons at the cellular level in regions like the hippocampus.

Stress has a number of known effects on epigenetic marks in the brain, producing alterations in DNA methylation and histone modifications in most of the stress-sensitive brain regions examined, including the hippocampus, amygdala, and prefrontal cortex.”


It seemed to be taboo to note that most of – and the largest of – detrimental effects of stress occurred during womb-life in the mother’s environment. The authors instead opted for a politically correct “the stress history of parents” phrase.

Referenced studies had findings relevant to the earliest periods of life, including Figure 1:

interactions

“Those organs that show the highest levels of retrotransposon [a repeat element (mobile DNA sequences often involved in mutations) type formed by copy-and-paste mechanisms] activity, such as the brain and placenta, also seem to be both steroidogenic and steroid-sensitive.”

However, Figure 1 was given a beneficial context, and other studies’ findings weren’t mentioned in their contexts of detrimental effects on fetuses of mothers who were stressed while pregnant.

http://www.pnas.org/content/112/22/6828.full “Stress and the dynamic genome: Steroids, epigenetics, and the transposome”

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?

http://www.pnas.org/content/111/9/3638.full “Elevated morning cortisol is a stratified population-level biomarker for major depression in boys only with high depressive symptoms”

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.

http://www.pnas.org/content/112/20/6503.full “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.

http://www.pnas.org/content/112/20/6485.full “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?

http://www.pnas.org/content/112/20/6473.full “Stable long-range interhemispheric coordination is supported by direct anatomical projections”

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.

http://www.pnas.org/content/112/20/E2695.full “Connectivity reveals relationship of brain areas for reward-guided learning and decision making in human and monkey frontal cortex”

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.

http://www.pnas.org/content/111/40/14565.full “Unique semantic space in the brain of each beholder predicts perceived similarity”

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.

http://www.pnas.org/content/111/42/15036.full “Neural and cognitive characteristics of extraordinary altruists”