Do scientists have to perpetuate memes in order to keep their jobs?

I was disgusted by this 2015 Korean human study. Is the current state of science such that researchers won’t be funded unless their studies will produce politically correct findings?

It seemed to me that the primary reason for the study’s main finding of:

“Neural markers reflecting individual differences in human prosociality”

was to perpetuate a non-causal “individual differences” meme.

Per my view in If research treats “Preexisting individual differences” as a black box, how can it find causes for stress and depression? it isn’t sufficient in 2015 to pretend that there are no early-life causes for the observed behavior and fMRI scan results of the subjects. Such a pretense leads to the follow-on pretense that later-life consequences are not effects, but are instead, a “mystery” due to “individual differences.”

The researchers asserted:

“Our present findings shed some light on the mystery of human altruism.”

Yet the findings of the People who donated a kidney to a stranger have a larger amygdala 2014 study of extraordinary altruists weren’t big enough clues for these researchers to feature the amygdala part of the limbic system in the fMRI scans.

The main experiment had the female, college student, right-handed subjects try to “reduce the duration of exposure to stressful noise.” Why weren’t brain areas that are especially susceptible to stress like the hippocampus featured in the fMRI scans?

The secondary reason for the study seemed to be to perpetuate the harmful “self-sacrifice = good, individuality = bad” meme.

The main reason this meme is harmful is that it condones a subset of people’s unconscious act outs. People are encouraged to avoid conscious awareness both of who they really are and of what drives their feelings, thoughts, and actions.

Despite not asking the subjects directly about either their motivations or their histories, these researchers asserted that the study demonstrated:

“The automatic and intuitive nature of prosocial motivation.”

In my view, what was largely observed were the subjects’ unconscious act outs, not some higher-order functions as the researchers mischaracterized them.

Similar to my view in Who benefits when research promotes a meme of self-sacrifice? I suspect that a major motivation behind scientific justification for memes like the self-sacrifice promoted by this study is to rush people past what really happened in their lives.

I wonder what value we would place on the “social norms internalized within an individual” if we felt and honestly understood our real history.

This study and the Do you know a stranger’s emotional motivations for smiling? study had the same reviewer, and shared several of the burden-of-proof problems. Both studies similarly demonstrated a lack of researcher interest in finding causes for the observed effects.

What was the agenda with these researchers and the reviewer? Why would the researchers glorify the factors that cause an individual difficulties when one tries to live a life of one’s own choosing? “Spatial gradient in value representation along the medial prefrontal cortex reflects individual differences in prosociality”

Dopamine may account for differences in cognitive performance

This 2015 German human study found:

“Dopamine may account for adult age differences in brain signal variability.”

The researchers administered amphetamine to the subjects to boost their dopamine levels, and measured their cognitive performance on several working memory tests under fMRI:

“Older adults expressed lower brain signal variability at placebo, but met or exceeded young adult..”

brain signal variability levels when on speed.

The order of the tests also influenced the results. Older adults who received amphetamine during the initial series of tests performed better on placebo during the second series of tests.

As is often done, the researchers focused on effects and not causes. I didn’t see questionnaires or investigation into possible historical or biological factors for reduced dopamine levels, leaving the researchers with age as the only correlated-but-not-causative explanation. “Amphetamine modulates brain signal variability and working memory in younger and older adults”

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.

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.” “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 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.” “Classical conditioning of analgesic and hyperalgesic pain responses without conscious awareness”

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”? “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. “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.” “GIRK3 gates activation of the mesolimbic dopaminergic pathway by ethanol”