0-1 star Wasted resources

Research that wasted resources

Are a child’s genes the causes for their anxiety?

gettingwell4 0-1 star Wasted resources, Amygdala, Brain development, Brainstem, Cerebrum, Epigenetics, Limbic system, Lower brain, Stress , , ,

This 2015 Wisconsin macaque study was another attempt to justify the school’s continuing captivity of thousands of monkeys. The researchers performed a study that – if its experimental design was truly informative for helping humans – could have been done with humans.

A problem I saw in the news coverage was that the finding of:

“35 percent of variation in anxiety-like tendencies is explained by family history”

was attributed to genetics, with headlines such as “Anxious Brains Are Inherited, Study Finds.” The lead researcher encouraged this misinterpretation with statements such as:

“Over-activity of these three brain regions are inherited brain alterations that are directly linked to the later life risk to develop anxiety and depression.”

However, the researchers produced this finding by running numbers on family trees, not by studying genetic samples to assess the contributions of genetic and epigenetic factors!

The study’s “family history” correlation was different than finding an inherited genetic causation that wasn’t influenced by the subjects’ caged environments!

The study found:

“Metabolism within a tripartite prefrontal-limbic-midbrain circuit mediates some of the inborn risk for developing anxiety and depression.

The brain circuit that was genetically correlated with individual differences in early-life anxiety involved three survival-related brain regions. These regions were located in the brain stem, the most primitive part of the brain; the amygdala, the limbic brain fear center; and the prefrontal cortex, which is responsible for higher-level reasoning and is fully developed only in humans and their primate cousins.”

The 592 subjects were the human-equivalent ages of 3 to 12 years old. Primate brainstems and limbic systems are fully-developed BEFORE these ages.

The researchers skipped over potential evidence for the important contributions of epigenetic factors to “the later life risk to develop anxiety and depression” that change the studied brain areas during womb-life, infancy, and early childhood. Studies such as:

show:

  1. A developing fetus adapts to being constantly stressed by an anxious mother.
  2. When these adaptations persist after birth, they may present as physiological and behavioral maladaptations of the infant and young child to a non-stressful environment.
  3. Later in life, these enduring changes may be among the causes of symptoms such as the anxious overreactions the current study found.

http://www.pnas.org/content/112/29/9118.full “Intergenerational neural mediators of early-life anxious temperament”

Perpetuating the meme that rodent PTSD experiments necessarily apply to humans

gettingwell4 0-1 star Wasted resources, Cerebrum, Limbic system, Lower brain, Memory, Neurochemicals, Stress

This 2015 Texas A&M rodent study found:

“Propranolol administration dampened the stress-induced impairment in extinction observed when extinction training is delivered shortly after fear conditioning.”

The researchers were way off base in extrapolating this study to humans:

“Propranolol may be a helpful adjunct to behavioral therapy for PTSD, particularly in patients who have recently experienced trauma.”

Would National Institutes of Health Grant R01MH065961 money have been available without perpetuating the meme that rodent PTSD experiments necessarily apply to humans? Or are a priori findings necessary in order to get research funded?

In rodent studies such as this one, the origins of both the disease and the “cure” are all exerted externally. But humans aren’t lab rats. We can perform effective therapy that doesn’t involve some outside action being done to us.

Studies such as Fear extinction is the learned inhibition of retrieval of previously acquired responses make clear that extinction is equivalent to suppression. “Behavioral therapy for PTSD” that suppresses symptoms can’t be a “cure” for humans since the original causes for the symptoms aren’t treated.

Even if this study’s recommendation to administer a drug applied to humans, neither drugs nor “behavioral therapy for PTSD” address the underlying causes.

http://www.pnas.org/content/112/28/E3729.full “Noradrenergic blockade stabilizes prefrontal activity and enables fear extinction under stress”

A study of biological aging in young adults with limited findings

gettingwell4 0-1 star Wasted resources, Epigenetics, Telomeres ,

This 2015 New Zealand human study used the same subjects of the More from the researchers that found people have the same personalities at age 26 that they had at age 3 study. These researchers used 10 biologic age markers of subjects at age 38 to find that their biological ages ranged from 28 to 61.

F2.large

Researchers assessed subjects’ pace of aging at ages 26, 32, and 38 with 11 more biomarkers, including leukocyte telomere length. Three of the initial 10 biomarkers weren’t used because measurements were taken only at age 38.

These researchers also assessed physical functioning, physical limitations, cognitive testing, retinal imaging, self-rated health, and facial aging. There was a fascinating graph in the supplementary material of the effect on each of these assessments of successively leaving out each of 18 pace-of-aging biomarkers.

There were three areas I expected to see covered that weren’t addressed in this study:

  1. Where were links back to all relevant measurements and predictions made when these subjects were ages 3, 5, 7..? Other studies of these same subjects made such links, but only cognitive testing was linked back in this study. Were these researchers trying to pretend that these dramatic later-life physical measurements weren’t effects of earlier-life causes?
  2. Where were psychological measurements? Are we to believe that subjects’ states of mind had no relationships to their biomarkers?
  3. I didn’t see any effort to use newer measures such as The degree of epigenetic DNA methylation may be used as a proxy to measure biological age study. I’d expect that these subjects’ historical tissue samples were available. The peer reviewer certainly was familiar with newer biomarkers.

http://www.pnas.org/content/112/30/E4104.full “Quantification of biological aging in young adults”

A study on alpha brain waves and visual processing that had limited findings

gettingwell4 0-1 star Wasted resources, Amygdala, Beliefs, Cerebrum, Hippocampus, Limbic system, Memory

This 2015 Wisconsin human study found:

“Forming predictions about when a stimulus will appear can bias the phase of ongoing alpha-band oscillations toward an optimal phase for visual processing, and may thus serve as a mechanism for the top-down control of visual processing guided by temporal predictions.”

The researchers measured delta (1-4 Hz), theta (4-7 Hz), alpha (9-13 Hz), and low beta (15-20 Hz) brain waves. Their findings applied only to the alpha band in their experimental tasks, which excluded emotional content.

Brain waves studies such as Are hippocampal place cells controlled by theta brain waves from grid cells? and Research that identifies the source of generating gamma brain waves established different experimental conditions that elicited brain waves in non-alpha frequency bands. Such studies may have been relevant to further explain this study’s negative findings.

Visual perception studies such as We are attuned to perceive what our brains predict will be rewarding and Our long-term memory usually selects what we pay closer visual attention to provided insight into possible causes for the observed effects. It may have provided additional findings if the researchers of this study were also interested in causal factors that affected visual processing.

Other studies on visual perception such as The amygdala is where we integrate our perception of human facial emotion provided reasons to not exclude emotional content in brain studies. The current study’s researchers claimed that they provided insights relevant to neurological disorders by stating:

“Because forming the appropriate sensory predictions can have a large impact on our visual experiences and visually guided behaviors, a mechanism thought to be disrupted in certain neurological conditions like autism and schizophrenia, an understanding of the neural basis of these predictions is critical.”

However, I didn’t see that the researchers provided such an understanding since their experimental designs excluded emotional content. I wonder what the reviewer saw that justified this Significance section statement.

http://www.pnas.org/content/112/27/8439.full “Top-down control of the phase of alpha-band oscillations as a mechanism for temporal prediction”

An observational instead of experimental study on direction and place recognition

gettingwell4 0-1 star Wasted resources, Hippocampus, Limbic system, Memory

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”

Do popular science memes justify researchers’ cruelties to monkeys?

gettingwell4 0-1 star Wasted resources, Anterior cingulate cortex, Cerebrum, Limbic system

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”

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

gettingwell4 0-1 star Wasted resources, Epigenetics, Neurochemicals, Oxytocin ,

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?

http://www.pnas.org/content/111/33/12258.full “Plasma oxytocin concentrations and OXTR polymorphisms predict social impairments in children with and without autism spectrum disorder”

Separating genetic from environmental factors when assessing educational achievement

gettingwell4 0-1 star Wasted resources, Brain development, Epigenetics , ,

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:

F2

“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!

http://www.pnas.org/content/111/42/15273.full “The high heritability of educational achievement reflects many genetically influenced traits, not just intelligence”

What causes disconnection between the limbic system and the cerebrum?

gettingwell4 0-1 star Wasted resources, Cerebrum, Dopamine, Glutamate, Hippocampus, Limbic system, Memory, Neurochemicals

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.

http://www.pnas.org/content/111/49/17654.full “Elevated hippocampal resting-state connectivity underlies deficient neurocognitive function in aging”

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.

Kids who have a larger and better-connected hippocampus learn math better when tutored

gettingwell4 0-1 star Wasted resources, Brain development, Cerebrum, Hippocampus, Limbic system, Memory, Thalamus ,

This 2013 Stanford study of 24 eight- and nine-year-old children found that measurements of limbic system areas predicted how well the 11 boys and 13 girls would respond to 8 weeks of one-on-one math tutoring!

“Pretutoring hippocampal volume predicted performance improvements. Furthermore, pretutoring intrinsic functional connectivity of the hippocampus with dorsolateral and ventrolateral prefrontal cortices and the basal ganglia also predicted performance improvements.

Brain regions associated with learning and memory, and not regions typically involved in arithmetic processing, are strong predictors of responsiveness to math tutoring in children. More generally, our study suggests that quantitative measures of brain structure and intrinsic brain organization can provide a more sensitive marker of skill acquisition than behavioral measures.”

None of the assessments, such as IQ and working memory tests, predicted how much benefit a child would receive from one-on-one math tutoring. The 16 children in the control group who didn’t receive one-on-one math tutoring didn’t improve their math performance over the 8-week period. Adults use different brain areas when solving math problems.

Much of the news coverage was from vested interests who dismissed the findings. A typical headline was “Your child’s brain on math: Don’t bother?”

The No Child Left Behind people were concerned that science could predict that some children were better suited to math tutoring than others. Psychiatrists and psychologists responded with general dismissals like small sample size, and the journalist let that stand without asking them how they disagreed with any of the specific P-, T- and other values found in the study’s supplementary material.

The researchers were careful to invoke a politically-correct meme of “individual differences“ 19 times, including the study’s title!

“Individual differences” isn’t a causal explanation, however. The journalist whiffed and also gave a pass to the researchers on this uninformative-but-PC meme.

It certainly would have been within the scope of this study for the researchers to inquire further into causes for the findings. It possibly could have informed us of causal factors had the children’s test battery included emotional content, as did the subjects in the Early emotional experiences change our brains: Childhood maltreatment is associated with reduced volume in the hippocampus study.

http://www.pnas.org/content/110/20/8230.full “Neural predictors of individual differences in response to math tutoring in primary-grade school children”

Wasting public science funds on voodoo dolls

gettingwell4 0-1 star Wasted resources

This 2014 Ohio State human study found:

“Low glucose levels might be one factor that contributes to intimate partner violence.”

The study used pins stuck in voodoo dolls and noise blasts to measure aggression towards the subjects’ spouses. These measures had neither been correlated with “intimate partner violence” nor standardized, though.

The experimental data led to some fun-with-number associations:

“Lower evening glucose levels related to blasting one’s spouse with more intense and prolonged noise.

Lower levels of evening glucose were more aggressive in part because they also had greater aggressive impulses.”

Both the study’s design and implementation were such that they couldn’t provide evidence for causes of the effects. The expert opinion here expressed:

“Concerns to which extent this particular study is helpful in explaining the role of self-control (or lack thereof) in the etiology of intimate partner violence.”

and pointed out several methodological and statistical lacks.

National Science Foundation Grant BCS1104118 was a waste of public money while deserving areas of research go begging.

http://www.pnas.org/content/111/17/6254.full “Low glucose relates to greater aggression in married couples”

Translating PTSD research findings from animals to humans

gettingwell4 0-1 star Wasted resources, Amygdala, Cortisol, Hippocampus, Limbic system, Neurochemicals, Stress

This 2014 rodent study stressed the animals, measured their stress responses, then killed them and sampled genes in their amygdala, hippocampus, and blood. The researchers found that glucocorticoid receptor signaling genes were the primary pathway associated with “exposure-related individual differences“ in stress responses for the amygdala and blood. This pathway also placed first for the hippocampus in female rats (glucocorticoid receptor was second in male rats and prostate cancer signaling was first).

I’ll quote one press article’s coverage to show where the researchers wanted to go with the study’s findings:

“We found that most of the genes and pathways that are different in PTSD [post-traumatic stress disorder]-like animals compared to resilient animals are related to the glucocorticoid receptor, which suggests we might have identified a therapeutic target for treatment of PTSD.”

How about this lead sentence:

“There may some day be a blood test to determine whether someone suffers from Post-Traumatic Stress Disorder or is at risk for the psychiatric condition.”

Here’s another article’s paraphrase of a different researcher:

“Those are genes that become activated in the presence of stress. Like a key fitting into a lock, the hormone corticosterone, produced naturally by the body, connects to the receptor and has a calming effect.

In some rodents, and apparently in some people, the pathway appears to be defective, and this puts them at higher risk for PTSD.”

Also, from the study’s abstract:

“Corticosterone treatment 1 h[our] after PSS [predator-scent-stress]-exposure prevented anxiety and hyperarousal 7 d[ays] later in both sexes, confirming the GR [glucocorticoid receptor] involvement in the PSS behavioral response.”

Like other researchers continue to do, they stopped this study short of finding causes for the effects:

  1. What were the causes for genes in the glucocorticoid receptor signaling pathway being differentially expressed? “Exposure-related individual differences” isn’t a causal finding.
  2. If this pathway is “defective,” what exactly happened to make it that way?
  3. Did dampening the effects of stress with a shot of cortisol one hour after the stress treat the cause such that the rats were cured? Since the readers of the study and associated articles were led to infer that this treatment was a cure, why destroy the treated animals afterwards before the proofs of long-term efficacy were thoroughly documented and tested?

When studies like this are carried forward with humans, researchers should try to find the causes for these effects. It isn’t sufficient to pretend that there aren’t early-life causes for these effects. Such a pretense leads to the follow-on pretense that later-life consequences are mysteries such as “exposure-related individual differences” and not effects.

Researchers should act like the subjects are feeling human beings who can participate in treatments of both the causes and effects. They should remember that humans are not lab rats who need to be fixed.

http://www.pnas.org/content/111/37/13529.full “Expression profiling associates blood and brain glucocorticoid receptor signaling with trauma-related individual differences in both sexes”

A missed opportunity to study odor-evoked emotional memories

gettingwell4 0-1 star Wasted resources, Anterior cingulate cortex, Cerebrum, Hippocampus, Limbic system, Memory

The researchers of Can a study exclude the limbic system and adequately find how we process value? published another study. In this 2015 human study, subjects were monitored with fMRI scans while making choices on the identity and pleasantness of rewarding food odors.

I feel that the researchers missed quite a few good opportunities to advance science. Instead of making peripheral assessments of limbic system areas and citing numerous other studies, they could have included emotional content in their study and drawn their own conclusions.

Consider these opportunities:

  • Wouldn’t the odors used in the study such as chocolate cake and pizza and strawberry and potato chips – and other “comfort” foods – potentially be associated with emotional responses?
  • Don’t most humans have memories that include pleasant food odors?
  • Wouldn’t it have been informative to ask the subjects during fMRI scans to identify what emotions were evoked by the pleasant food odors?
  • Wouldn’t these resultant fMRI scans be expected to potentially show more strongly activated limbic system areas, given the hippocampus’ position as the seat of emotional memories?
  • Wouldn’t the additional emotional responses and memories and subsequent limbic system area activations potentially influence the subjects’ value judgments?

Instead, the researchers peripherally included limbic system areas in the study. The supplementary material included passages such as:

“Identity-specific value signals were found in not only the OFC, [orbitofrontal cortex] but also the ACC [anterior cingulate cortex] and hippocampus.”

Like the previous study, the current study’s focus was to provide evidence that areas of the cerebrum were in control when people made value judgments. The term “value” in the current study meant:

“the pleasantness of the odor.”

Like the previous study, areas of the limbic system weren’t addressed until the tail end of the supplementary material. The researchers cited other studies in an attempt to dismiss the role of the ACC in making value judgments, then said:

“Although we are unable to distinguish between these alternative explanations, our findings suggest that value-related signals in ACC—whether signed or unsigned—are specific to the identity of the expected outcome.”

Since the current study found that “identity” was encoded by cerebral areas, the above sentence was written to nudge the reader into inferring that the cerebrum dominated value judgments of “the pleasantness of the odor.”

The researchers similarly cited other studies in the last paragraph instead of specifically discussing how they studied the participation of the hippocampus part of the limbic system. They then speculated that the hippocampus’ contributions to value judgments in the current study were explained by the referenced studies:

“We speculate that the hippocampus is involved in retaining sensory-based information about specific rewards, which may be linked to value-based representations in OFC for later consolidation.”

Like the previous study, the researchers were begrudgingly diverted away from their focus on cerebral areas when they were forced to acknowledge the limbic system’s contributions to value judgments of “the pleasantness of the odor.”

http://www.pnas.org/content/112/16/5195.full “Identity-specific coding of future rewards in the human orbitofrontal cortex”

The amygdala part of the limbic system doesn’t process beliefs

gettingwell4 0-1 star Wasted resources, Amygdala, Beliefs, Cerebrum, Limbic system

Does your desk light switch on or off when other people in the office switch their desk lights on or off? Something in the wiring would probably be wrong if it did.

And wouldn’t you expect that other desk lights would still operate normally if your desk light’s bulb burned out, although everyone may be plugged into the same electrical circuit?

It surprised the researchers of this 2015 CalTech/MIT study when:

“Two patients with bilateral amygdala lesions performed a belief reasoning test.

Both patients showed typical test performance and cortical activity when compared with nearly 500 healthy controls.”

The study’s overall frame of reference was expressed as:

“Humans use a so-called “theory-of-mind” to reason about the beliefs of others. Neuroimaging studies of belief reasoning suggest it activates a specific cortical network. The amygdala is interconnected with this network and plays a fundamental role in social behavior.”

The experimental test:

“Was designed to optimize functional contrast in those brain regions thought to be involved in attempts, be they successful or unsuccessful, to evaluate the veracity of another person’s belief about the world.”

A “belief reasoning test..to reason about the beliefs of others” is a cerebral exercise. The amygdala, in contrast, is an emotional center of a person’s limbic system.

The logic by which the study may be viewed is:

  1. The “belief reasoning test” had no emotional content to activate the subjects’ amygdalae.
  2. fMRI scans confirmed that limbic system areas in the 2 lesioned subjects weren’t activated during the test.
  3. Apply the logic of Occam’s razor, and we arrive at the findings of “typical test performance and cortical activity.”

Task performance and beliefs about task responses are solely cerebral exercises had a similar methodology and result in that those subjects’ limbic systems were monitored during fMRI scans and subsequent reporting, but the subjects’ limbic system areas weren’t activated during any of the experiments.

The researchers stated the results:

“Suggest a reevaluation of the role of the amygdala and its cortical interactions in human social cognition.”

But per the beginning analogy – if your desk light’s bulb burned out, would you be surprised that it didn’t affect the normal operations of desk lights in other offices, although they all may be plugged into the same circuit?

This study informed us that the amygdala isn’t slaved to the cerebrum. It’s hard to change the current research mindset/social meme of cerebral dominance, though, so maybe this information will be overlooked.

http://www.pnas.org/content/112/15/4827.full “Amygdala lesions do not compromise the cortical network for false-belief reasoning”

Can you give emotionally informed yet reasoned responses to moral questions within 3 seconds?

gettingwell4 0-1 star Wasted resources, Beliefs, Cerebrum, Limbic system, Memory

Could you give a 3-second informed decision that reflected your true feelings about this statement?

“Inflicting emotional harm is just as bad as inflicting physical harm.”

Could you then express your confidence about your answer on a 1-7 scale within 1 second? How about your 3-second response to this statement:

“Developing a child’s character is central to raising it good.”

The researchers of this 2015 Swedish study asserted that it:

“Demonstrates that moral choices are no different from their preferential and perceptual counterparts; they are highly constrained and coupled to the immediate environment through sensory interaction.”

The subjects’ moral choices about statements such as:

“One should never intentionally harm another person.”

weren’t weighted any differently than their “top of the head” answers to questions such as:

“Is Denmark larger than Sweden?”

There was a time limit of 3 seconds for the subjects to answer 63 “moral” and 35 “factual” questions. The subjects were asked to express their confidence in the answer during an additional 1-second time frame. Answers after these time limits were discarded.

In the supplementary material, the researchers:

“Justified our design. When no time-out condition was included, 33% of participants realized that their eye movements were influencing the timing of the trial.”

So the 3-second time frame was imposed to keep the subjects from gaming the experiment. The experiment’s time limit of 3 seconds didn’t have anything to do with properly modeling moral decision-making.

The time period wasn’t the only questionable area. The researchers focused on eye gaze as the important homogenous factor influencing the subjects as they made their “moral” choices.

However, one person’s eye gaze is not necessarily the same as the next person’s, as demonstrated by studies such as:

An individual’s attention and perception that are incorporated into their eye gaze are behaviors that may have many differing historical components. For example, one subject may have kept their gaze on the:

“Value animals equally.”

answer to the:

“Animal welfare should not be valued equally with human welfare.”

question because their initial reaction involved their cuddly pet. Another subject may have kept their gaze on the same answer because their initial reaction involved a stray dog that attacked them.

Did the study shed light on its initial statement?

“Moral cognition arises from the interplay between emotion and reason.”

I didn’t see that the study’s design allowed its subjects to produce emotionally informed yet reasoned responses to the 98-question battery.

http://www.pnas.org/content/112/13/4170.full “Biasing moral decisions by exploiting the dynamics of eye gaze”