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”

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.

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


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

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”

A missed opportunity to research the oxytocin receptor gene and autism

This 2013 study:

“Examined whether genetic variants of the OXTR [oxytocin receptor] affect face recognition memory in families with an autistic child.

We investigated whether common polymorphisms in the genes encoding the oxytocin and vasopressin 1a receptors influence social memory for faces.”

I feel that the researchers missed an opportunity to improve their assessment of the autism-related genetic contribution to the study’s findings by separating the degree of environmental influence on the oxytocin receptor gene expression, as did the How epigenetic DNA methylation of the oxytocin receptor gene affects the perception of anger and fear study.

An assessment of epigenetic DNA methylation of the oxytocin receptor gene may have been even more compelling because the researchers genetically sampled one non-autistic sibling in each of the autistic children’s families. I hope the study’s samples are still available, because they may offer the possibility of evaluating the contribution of the autistic children’s historical environment with potential confirmation from their siblings.

Both studies gave their subjects similar facial emotion recognition tests, with the current one deriving from findings about autism, and the second from findings about the amygdala. The studies also had common references, such as a 2010 study, A common allele in the oxytocin receptor gene (OXTR) impacts prosocial temperament and human hypothalamic-limbic structure and function.

http://www.pnas.org/content/111/5/1987.full “Common polymorphism in the oxytocin receptor gene (OXTR) is associated with human social recognition skills”

Agenda-driven research on emotional memories

I curated this 2013 study because one of the authors has made a career out of denying that people accurately remember and re-experience emotional memories. I’ll show how this viewpoint created problems with the study.

For background, one relevant hypothesis of Dr. Arthur Janov’s Primal Therapy is that there are differences in the levels of consciousness of: (1) an emotional memory; (2) the recall of an emotional memory; and (3) a verbal description of the recall of an emotional memory.

  1. The retrieval and re-experiencing of an emotional memory can engage our lower-level brain areas without our higher-level brain areas’ participation.
  2. The recall of 1 above is a product of our cerebrum in response to input from limbic system and lower brain areas.
  3. The verbal description of 2 above is a product of our brain’s language areas in response to input from the cerebral areas that recalled the emotional memory.

Clinical principles of Primal Therapy that follow are:

  • A patient won’t re-experience an emotional memory when they only just recall it.
  • It’s another level of consciousness even further removed from an emotional memory when someone describes their recall of the memory.

The researchers asserted that they studied emotional memories in one part of this study. Their method was to ask the subjects to recall and verbally describe the emotions they felt the week after 9/11/2001.

The researchers introduced factors to try to confuse the subjects about their recall of their emotions, and their verbal descriptions of their recall. The researchers were very sure that confusing the subjects’ cerebral recalls and descriptions produced evidence that the subjects’ emotional memories were changed and falsified.

Can you see how far removed the researchers were from studying emotional memories? They didn’t demonstrate that they understood how emotional memories were stored because they didn’t attempt to engage the subjects’ limbic system and lower brain areas.


Let’s illustrate the study’s inappropriate characterizations with an example. I burned my left index fingertip last week while toasting bread on an infrared oven grill. The pain is still stored with my emotional memory, and is probably why my memory is very clear.

I can recall the visual details of the grill, how my fingertip looked, the pain I initially felt, and the relief I felt when I held my finger under running cold water. I can retrieve and re-experience my emotional memory in a calm environment such as lying in bed with no aural or visual distractions.

Let’s imagine that the researchers analogously studied my burned fingertip accident. They would deny that I can accurately retrieve and re-experience my emotional memory of the accident if they could create problems with my verbal descriptions of my recall. For example, if I initially said that I pushed the kitchen faucet handle all the way in the cold direction, then after repeated questioning, I said that I wasn’t sure that the handle was pushed all the way over to Cold.


The researchers intentionally conflated the falsifiability of emotional memories with a strawman definition of false emotional memories.

They purposely misidentified both:

  • The subjects’ recalls of post-9/11 emotions; and
  • The subjects’ descriptions of their recalls

as emotional memories.

The study was designed to be lawyering, not science. The researchers DETRACTED from science.

Maybe their purposeful error could be overlooked if it was confined to this study. But it isn’t.

Imagine the damage this viewpoint creates when mental health professionals deny the reality of their patients’ feelings, experiences, and emotional memories!

http://www.pnas.org/content/110/52/20947.full “False memories in highly superior autobiographical memory individuals”

Who benefits when research promotes a meme of self-sacrifice?

The main purpose of this 2014 Illinois human study was to make findings directed toward high school students that:

“Well-being may depend on attending to higher values related to family, culture, and morality, rather than to immediate, selfish pleasure.”

The study’s messages to young people and to those who control young people were:

  • You have to give up trying to live your own life if you want to be happy.
  • For your own “well-being” just follow the “higher values” where other people tell you what to do and think.
  • Other people know how you should live your life better than you do. Science says so.

The researchers embedded many assertions into the study, most of which weren’t supported by the study’s data. The researchers’ main assertion was:

“Optimal well-being may be achieved through eudaimonic activities.”

The researchers repeated this assertion multiple times in multiple ways, such as citing philosophy and other research. The short version of the term “eudaimonic” was defined as: “Meaning and purpose, a life well-lived.”

The study’s ONLY measurement of “eudaimonic” activities was the subjects’

“Neural activation when making a donation to the family that involves self-sacrifice.”

The study’s main finding involving this SOLE measurement was:

“Eudaimonic decisions predicted longitudinal declines in depressive symptoms.”

Depressive symptoms were determined by “a self-report measure” where the subjects, 47 adolescents aged 15-17:

  • “Completed the internalizing symptoms subscale of the Youth Self-Report form of the Child Behavior Checklist
  • Underwent a brain scan during which they completed a family donation task and a risk-taking task.”

39 of the subjects returned one year later to reanswer the checklist.


I wonder what bases the reviewer used to approve the researchers’ methods.

1. In the study’s verbiage the researchers extrapolated the significance of the sole measurement of eudaimonic activities – the initial fMRI scan – many times past what it actually measured. One-time measurements of the blood flow in the ventral striatum of a few Los Angeles teenagers can’t validly be assigned as the bases for all of what the researchers went on and on about to glorify “prosocial eudaimonic decisions.”

2. No method checked the subjects’ personal impact of the experiments’ monetary rewards and donations. The subjects didn’t scale their personal relative importance of the monetary rewards and donations.

Consider the relative importance of a dime for a kid whose parents gave them a BMW to drive to high school. Compare that with a kid who searched the sidewalk for dropped coins as they walked to high school.

Absent subjective scaling, the monetary rewards and donations data couldn’t be used as the basis to produce informative results.

3. The balloon test used in this study to measure “risky hedonic decisions” was the same as in the Who benefits when research with no practical application becomes a politically correct meme? study. The same objection applies here: a video game task of popping balloons that engages the cerebrum was NOT informative to the cause-and-effect of the emotions and instincts and impulses from limbic system and lower brain areas that predominantly drive risky behavior.


Scientific justification for memes like the self-sacrifice promoted by this study helps rush people past what really happened in their lives. A popular cultural meme is to “live in the present” and purposefully overlook how we arrived at our present lives.

I wonder how we would evaluate the “higher values related to family, culture, and morality” if we felt and honestly understood our real history.

Do you feel that young people benefit when they sacrifice their lives in the name of “family, culture, and morality?” Who benefits when people don’t pause to reflect on how their history impacts what’s going on now with their lives?

http://www.pnas.org/content/111/18/6600.full “Neural sensitivity to eudaimonic and hedonic rewards differentially predict adolescent depressive symptoms over time”

Problematic research on suppressing unwanted memories

This 2014 French/UK human study found:

“Motivated forgetting mechanisms, known to disrupt conscious retention, also reduce unconscious expressions of memory, pointing to a neurobiological model of this process.”

There were multiple problems with this study.

1. The researchers excluded emotional content, although the study involved areas of the brain involved in processing emotions:

roi

How could the study’s findings apply to:

“The distressing intrusions that accompany posttraumatic stress disorder“

when emotional memories were excluded? It was an unsupported assertion for one of the researchers to state:

“The better understanding of the neural mechanisms underlying this process arising from this study may help to better explain differences in how well people adapt to intrusive memories after a trauma.”

2. The term “unconscious” was used 27 times, including in the title, without defining it. The cited studies defined “unconscious” several meaningfully different ways. How could the findings achieve validity when they contained an undefined term?

3. The experiments involved short-term memories and visual perception, and the subjects took longer to visually perceive objects that they had been directed to suppress than those that they had been directed to think about. However, the researchers didn’t show that these experimental results could be extrapolated into findings about long-term unconscious memories.

4. Data manipulation:

  • The researchers noted:

    “We did not observe less hippocampal activation during no-think than think trials.”

  • This data didn’t fit what they wanted to find, so they:

    “Restricted the search volume to anatomically defined regions of interest.”

  • They still couldn’t make their predetermined finding, so they discarded:

    “An outlier which compromised the significance of this effect.”

The above process didn’t support the statement that immediately followed:

“Thus, suppression robustly engaged the brain regions associated with memory control, and this was accompanied by reduced activation in the hippocampus.”

Didn’t the reviewer have something to say about these four problem areas?

It was a letdown to read the details of the study when its title held out such promise for informing us about the unconscious influence of memories. Per the Scientific evidence page, it would really help a person as a first step to become somewhat aware of their unconscious memories and feelings, especially when these are expressed through behavior.

http://www.pnas.org/content/111/13/E1310.full “Suppressing unwanted memories reduces their unconscious influence via targeted cortical inhibition”

Translating PTSD research findings from animals to humans

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”

Can a Romanian orphan give informed consent to be an experimental subject?

This 2015 study used Romanian orphans as lab rats for findings of which I failed to see the value. The world didn’t really need any further research to demonstrate that foster care would be better for a child than staying in an orphanage.

The researchers placed the orphans in five separate stressful situations, and measured their cortisol and DHEA-S levels, along with their electrocardiograph and impedance cardiograph activity. The findings were:

“Children who were removed from the Romanian institutions and placed with foster parents before the age of 24 months had stress system responses similar to those of children being raised by families in the community.

The children raised in institutions showed blunted responses in the sympathetic nervous system, associated with the flight or fight response, and in the HPA axis, which regulates cortisol.”

One unsupported assertion from the researchers was:

“We provide evidence for a causal link between the early caregiving environment and stress response system reactivity in humans with effects that differ markedly from those observed in rodent models.”

The researchers stated that rodent studies have converged to find:

“Early-life adversity results in hyperreactivity of the sympathetic nervous system (SNS) and hypothalamic–pituitary–adrenal (HPA) axis.”

It’s baloney that the same results from early life adversity in rodents haven’t also been present in humans. Even the lead researcher herself said in a news article:

“More significantly, McLaughlin said, their [the orphans] stress response systems might have been initially hyperactive at earlier points in development, then adapted to high levels of stress hormones.”

The difference was that the rodents were monitored 24/7 until researchers killed and dissected them. The children’s periods of adversity likely started while in the womb, and their lives had been monitored for research purposes sporadically after their births.

Everybody knows that just because adverse events and effects in these children’s lives weren’t recorded by researchers didn’t mean these effects weren’t present at some point.

Particularly irksome was another unsupported assertion from the lead reviewer:

“The children involved in the study are now about 16 years old, and researchers next plan to investigate whether puberty has an impact on their stress responses. It could have a positive effect, McLaughlin said, since puberty might represent another sensitive period when stress response systems are particularly tuned to environmental inputs. “It’s possible that the environment during that period could reverse the impacts of early adversity on the system,” she said.”

No, this is NOT possible. We may as well expect an apple to fall upward.

The impacts of early adversity persist with enduring physiological changes as shown in experimental studies. Studies have NOT provided evidence that the subjects’ environment can cause the effects of complete reversal of all these changes, no matter the stage of life of the subjects.

This point was addressed in The effects of early-life stress are permanent alterations in the child’s brain circuitry and function rodent study:

“The current study manipulates the type and timing of a stressor and the specific task and age of testing to parallel early-life stress in humans reared in orphanages.

The results provide evidence of both early and persistent alterations in amygdala circuitry and function following early-life stress.

These effects are not reversed when the stressor is removed nor diminished with the development of prefrontal regulation regions.”

That study had the same reviewer as the current study. The current study’s lead researcher knew or should have known of this and other relevant research. She knew or should have known of the irreversibility of critical periods, during which developments either occurred or were forever missed.

Did the lead researcher make assertions not supported by the study or relevant research – assertions made counter to her scientific knowledge – show her unease about treating the orphans as lab rats? Was there was some other agenda in play?

The larger problem was the study’s informed consent with this group of Romanian orphans. If you were in contact with a damaged person, and implicitly gave them hope that you would improve their life, then who are you as a feeling human being when you don’t personally carry through? Does the legal documentation matter?


Also, I’ve noticed problems with several studies that had this particular reviewer:

Add the current study to the list.

http://www.pnas.org/content/112/18/5637.full “Causal effects of the early caregiving environment on development of stress response systems in children”


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Emotion inclusion in basic research drives discovery

What happens when a meme influences science? It would seem that researchers’ perceptions start to wheel around its axis.

A meme was the driver of this short 2015 commentary that stated:

“Most preclinical biomedical research, however, has been conducted with inadequate consideration of sex.”

If researchers discovered that gender hadn’t been adequately considered in research, maybe other “evolutionarily fundamental” factors had “inadequate consideration” as well.

Maybe one day soon, researchers will stop the current widespread exclusion of emotional content in studies, especially when the studies already included areas of the brain that are the biological bases of emotions.


To imagine a potentially beneficial future meme, I substituted the word “emotion” for “sex” in the title and part of two paragraphs of this commentary. How well does this fit?

“[Emotion] inclusion in basic research drives discovery”

“Why is [emotion] so important?

Although many factors can influence an outcome, [emotion] is evolutionarily fundamental and affects the whole of the population

Across diverse disciplines, researchers risk drawing erroneous conclusions when they extrapolate outcome data from [emotional to non-emotional and vice versa].”

See A missed opportunity to study odor-evoked emotional memories for one deliberate exclusion of emotional content, although including emotions may have been appropriate, informative, and contributed to advancing science.

Click the hippocampus category to see a sample of human studies that may have included the biological seat of emotional memories, but only a scarce few of which included emotional content.

http://www.pnas.org/content/112/17/5257.full “Opinion: Sex inclusion in basic research drives discovery”

Genetic programming of hypothalamic neurons regulates food intake and body weight

These 2015 Michigan/Argentinian fish and rodent studies were of the genetic programming of specific neurons in the hypothalamus. The study linked below found:

“Food intake and body weight regulation depend on proper expression of the gene” in these neurons.

In a second study released at the same time from the same researchers:

“The researchers found that the two enhancers act in ways that complement one another, both encouraging the expression of the Pomc gene at key times. One of the two is found in the same form among all mammals, the other among all placental mammals – suggesting that they’ve been kept intact throughout the evolutionary process.”

Genetic programming of these neurons begins during early brain development. One of the researchers said:

“This work represents the first example of a neuron-specific gene in vertebrates where we have found both the enhancers and a shared transcription factor that control gene expression in the developing brain and then throughout the life span of the adult.”

The first study showed that if the genetic expression of these hypothalamic neurons was disrupted, the individual lost control of their eating (hyperphagia) and the usual result was severe obesity:

“We don’t know, but we think it likely, that it [regulation of these specific hypothalamic neurons in humans] may be similar to the mouse model, where its role is like a dial, with a linear relationship between the amount of Pomc [the gene] expression and the degree of obesity.”

I hope that when extending this research to humans, the researchers don’t exclude emotional content like most studies involving areas of the limbic system have done. Everyone has feelings intermixed with eating and foods. It’s a great disservice to have publicly funded studies not include aspects of emotion that could potentially help people.

http://www.pnas.org/content/112/15/E1861.full “Islet 1 specifies the identity of hypothalamic melanocortin neurons and is critical for normal food intake and adiposity in adulthood”

Epigenetic production of new brain neurons in the hippocampus

This 2015 La Jolla rodent study provided further details on the production of new neurons in the adult hippocampus:

“We propose that SOX2 sets a permissive epigenetic state in neural progenitor cells, thus enabling proper activation of the neuronal differentiation program under neurogenic cue.”

The researchers stated that the functions of these new brain neurons were:

“Newborn granule neurons generated from neural progenitor cells in the adult hippocampus play a key role in spatial learning and pattern separation.”

http://www.pnas.org/content/112/15/E1936.full “SOX2 primes the epigenetic landscape in neural precursors enabling proper gene activation during hippocampal neurogenesis“

A missed opportunity to study odor-evoked emotional memories

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”