If research provides evidence for the causes of stress-related disorders, why only focus on treating the symptoms?

This 2014 rodent research reliably induced many disorders common to humans. Here are some post-birth problems the researchers caused, primarily by applying different types of stress, as detailed in the study’s supplementary material:

Yet the researchers’ goal was to identify a brain receptor for:

“Novel therapeutic targets for stress-related disorders.”

In other words, develop new drugs to treat the symptoms.


Where are the studies that have goals to prevent these common problems being caused in humans by humans?

Where is the research on treatments to reverse the enduring physiological impacts to stress by treating the causes?


What do you think of this excerpt?

“Accumulating evidence suggests that traumatic events particularly during early life (e.g., parental loss or neglect) coupled with genetic factors are important risk factors for the development of depression and anxiety disorders.

Moreover, the brain is particularly vulnerable to the effects of stress during this period.

Maternal separation in rodents is a useful model of early-life stress that results in enduring physiological and behavioral changes that persist into adulthood, including increased hypothalamic–pituitary–adrenal (HPA)–axis sensitivity, increased anxiety, and visceral hypersensitivity.”

http://www.pnas.org/content/111/42/15232.fullGABAB(1) receptor subunit isoforms differentially regulate stress resilience”

How to make a child less capable even before they are born: stress the pregnant mother-to-be

This 2014 rodent study showed how to make a less-capable pup by stressing the mother early in gestation. The study centered on a placental enzyme (OGT) that translates a mother’s stress into neuroprogramming of her developing fetus.

One finding was that this enzyme was less plentiful when the fetus was male compared with female.

Another finding was that the enzyme was less plentiful when the mother was stressed early in gestation, compared with unstressed mothers.

Informed by the first two findings, the researchers studied the placentae of male pups where the mother was stressed early in gestation. They found that these placentae had lower levels of an enzyme (Hsd17b3) that converts the precursor androstenedione into testosterone.

The resultant finding was that the male pups of stressed mothers had lower levels of testosterone than the control group of male pups.

A fourth finding was that offspring of both sexes born with a placenta where the OGT enzyme was less plentiful had 10-20% less body weight, a condition that developed after weaning. The researchers attributed this finding to reduced mitochondrial function in the hypothalamus compared with normal mice.

http://www.pnas.org/content/111/26/9639.full “Targeted placental deletion of OGT recapitulates the prenatal stress phenotype including hypothalamic mitochondrial dysfunction”

Are stress-induced epigenetic changes to DNA inherited across generations?

This 2014 Geneva/Cambridge plant study ended by stating:

“The unequivocal demonstration of transgenerational transmission of environmentally-induced epigenetic traits remains a significant challenge.

One of the critical activities erasing stress memories is conserved between plants and mammals.”

However, the researchers didn’t demonstrate that their findings were broadly applicable for mammals or organisms other than the specific plant variety they studied. Possible reasons for these limited findings were given in a 2015 Australian study referenced by Mechanisms of stress memories in plants:

“The majority of DNA methylation analyses performed in plants to date have focused on Arabidopsis, despite being relatively depleted of TEs [transposable elements] (15–20% of the genome) and being poorly methylated compared to other plant genomes.

These studies have lacked the resolution to provide the specific context and genomic location of the changes in DNA methylation.”

There are also significant differences in how epigenetic inheritance across generations may operate among different species per Epigenetic reprogramming in plant and animal development.


Neither the current study nor the above review addressed the behavioral aspect of stress-induced epigenetic inheritance across generations. For example, the behavior of a mother whose DNA was epigenetically changed by stress can induce the same epigenetic changes to her child’s DNA when her child is stressed per One way that mothers cause fear and emotional trauma in their infants:

“Our results provide clues to understanding transmission of specific fears across generations and its dependence upon maternal induction of pups’ stress response paired with the cue to induce amygdala-dependent learning plasticity.”

http://www.pnas.org/content/111/23/8547.full “Identification of genes preventing transgenerational transmission of stress-induced epigenetic states”

DNA methylation is the most frequent way that duplicate genes are epigenetically silenced

This 2014 human study showed that DNA methylation was the most frequent way that duplicate genes were epigenetically silenced. Current thinking is that at least half of the genes in the human genome are inactive duplicates.

The study stated:

“Duplicate genes are essential and ongoing sources of genetic material.”

What the researchers didn’t show, however, was that duplicate genes evolve per the study’s title “evolution of duplicate genes.” It was misleading to imply in the study’s headline that duplicate genes evolve.

Evolution occurs as organisms adapt to their environments. Duplicate genes aren’t active in the adaptation process when they are silenced.

http://www.pnas.org/content/111/16/5932.full “DNA methylation and evolution of duplicate genes”

Hypothalamic oxytocin and vasopressin have sex-specific effects on pair bonding, gregariousness, and aggression

This 2014 bird study showed the complementary effects of neurochemicals vasopressin and oxytocin in the hypothalamus.

Oxytocin neurons in the hypothalamus promote pair bonding and gregariousness in females.

Vasopressin neurons in the hypothalamus promote maternal care, social recognition, and gregariousness in both males and females, and aggression in males toward females.

Vasopressin and oxytocin released generally and in other parts of the brain have different effects. For example:

“Central administration of oxytocin also attenuates stress-induced effects on the brain and reverses stress-induced social avoidance.”

http://www.pnas.org/content/111/16/6069.full “Hypothalamic oxytocin and vasopressin neurons exert sex-specific effects on pair bonding, gregariousness, and aggression in finches”

Flooding the hypothalamus with neurochemicals affects reward-seeking, motivated, and depressive behavior

This 2014 rodent study showed the opposing effects of neurochemicals orexin (excitator) and dynorphin (inhibitor) in the hypothalamus.

The hypothalamus plays a role in behaviors such as addiction and impulsiveness. Food and cocaine self-administration were the main techniques used.

Flooding the hypothalamus with orexin produced reward-seeking and motivated behavior. That was greatly reduced when dynorphin levels were increased, and depressive behavior set in.

http://www.pnas.org/content/111/16/E1648.full “Hypocretin (orexin) facilitates reward by attenuating the antireward effects of its cotransmitter dynorphin in ventral tegmental area”

Do researchers have to be cruel to our fellow primates to adequately research oxytocin?

This 2014 primate study found:

“Oxytocin increased infants’ affiliative communicative gestures and decreased salivary cortisol, and higher oxytocin levels were associated with greater social interest.”

One would have to take an anti-evolutionist stance and believe that primates do not feel what humans feel to consider this process to NOT be cruel:

“To test these macaques, we took advantage of ongoing experiments requiring infants to be separated from their mother on the day of birth. Infants were nursery-reared, housed individually, with a cloth surrogate mother. They could see and hear other infants, but could not touch them.”

We know that primate infants, like humans, need nourishment, transportation, warmth, protection, and socialization from their mothers. What level of findings about oxytocin can a research study make that would justify this deprivation?

It surely wasn’t the findings this study made. We knew without doing the study that getting oxytocin from a nebulizer would be nowhere near an acceptable substitute for a mother’s touch and care.

http://www.pnas.org/content/111/19/6922.full “Inhaled oxytocin increases positive social behaviors in newborn macaques”

Problematic research on oxytocin: If the study design excludes women, its findings cannot include women

This 2014 study’s findings that “the hormone oxytocin promotes group-serving dishonesty” can’t apply generally to humans because its subjects were ALL men.

Regarding oxytocin, the researchers certainly knew or should have known previous studies’ findings about sex differences, as did Is oxytocin why more women than men like horror movies? which cited:

“Oxytocin modulates brain activity differently in male and female subjects.”

Regarding differing reciprocal behaviors, the researchers also knew or should have been better informed about associated brain areas through studies such as Reciprocity behaviors differ as to whether we seek cerebral vs. limbic system rewards and its references.

And how could the study produce reliable, replicable evidence of:

Dishonesty to be plastic and rooted in evolved neurobiological circuitries”

when the researchers performed NO measurements of “neurobiological circuitries” that supported that finding?

What was the agenda in play here? What did the female Princeton reviewer see in this study that advanced science?

http://www.pnas.org/content/111/15/5503.full “Oxytocin promotes group-serving dishonesty”


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Is oxytocin why more women than men like horror movies?

This 2014 human study showed how oxytocin regulates serotonin with the involvement of the right part of the amygdala.

The following passage caught my eye as a possible explanation of why more women than men prefer horror movies: oxytocin?

“We have chosen to enroll male subjects only to avoid the confounding effects linked to sex and a possible interaction with gonadal steroids. Indeed, as shown by previous studies, oxytocin modulates brain activity differently in male and female subjects.

For instance, oxytocin suppresses amygdala response to emotionally threatening stimuli in males but enhances the same response in females.

http://www.pnas.org/content/111/23/8637.full “Switching brain serotonin with oxytocin”

Who benefits when research with no practical application becomes a politically correct meme?

Do you take a risk, as this 2013 University of Texas/Yale study concluded, because you don’t foresee how you can avoid the risk?

By making this finding, the study essentially assigned the bases of a person’s risky decisions to their cerebrum.

I wasn’t persuaded. The conclusion was reached because the study’s design only engaged the subjects’ cerebrums with a video game task involving popping balloons. See Task performance and beliefs about task responses are solely cerebral exercises for a similar point.

If the researchers had instead designed a study that also engaged the subjects’ limbic system and lower brains, the findings may have been different.


Only one of the news articles covered this story with some accuracy, io9.com:

Helfinstein (the lead researcher) doesn’t see any direct, practical applications of the research. After all, people don’t spend their lives in fMRI scanners, so it’s not as if we can tell when people are going to make a risky decision in their day-to-day activities.”

Compare that with the majority of the news coverage that hijacked the study’s findings to try to develop a politically correct meme:

“Many health-relevant risky decisions share this same structure, such as when deciding how many alcoholic beverages to drink before driving home or how much one can experiment with drugs or cigarettes before developing an addiction.”

The study found that “risk taking may be due, in part, to a failure of the control systems necessary to initiate a safe choice.” The brain areas were “primarily located in regions more active when preparing to avoid a risk than when preparing to engage in one.” These areas included the “bilateral parietal and motor regions, anterior cingulate cortex, bilateral insula, and bilateral lateral orbitofrontal cortex.”

Notice that just one of the studied brain areas (the anterior cingulate cortex) is part of the limbic system or lower brains, although the bilateral insula connects to the limbic system. Yet the limbic system and lower parts of the brain are most often the brain areas that drive real-world risky behaviors such as smoking, drug use, sexual risk taking, and unsafe driving.

A video game task of popping balloons that engaged the cerebrum was NOT informative to the cause-and-effect of the emotions and instincts and impulses from limbic system and lower brains that predominantly drive risky behavior.

Who may benefit from the misinterpretations and misdirections of the study’s findings? We can take clues from the five applicable NIH grants (UL1-DE019580, RL1MH083268, RL1MH083269, RL1DA024853, PL1MH083271) and the researchers’ statement:

“We were able to predict choice category successfully in 71.8% of cases.”

Anybody ever read Philip K. Dick?

http://www.pnas.org/content/111/7/2470.full “Predicting risky choices from brain activity patterns”

We pay attention to the present through the windows of perception that we’ve developed from our past

My paraphrase of the 2013 study’s findings:

  • We pay attention to the present through the windows of perception that we’ve developed from our past;
  • The rest of the world is blocked by our consciousness’ perceptual thresholds.

It was good to read an attention study that didn’t zap the subjects’ brains.

http://www.pnas.org/content/111/4/E417.full “Prestimulus oscillatory power and connectivity patterns predispose conscious somatosensory perception”

Our long-term memory usually selects what we pay closer visual attention to

This 2014 human study at Vanderbilt found that our long-term memory usually selects what we pay closer visual attention to:

“Improvements in attentional tuning were accompanied by changes in an electrophysiological signal hypothesized to index long-term memory.”

The focus was on electrical fields, leading to predictable statements:

“Follow-up studies using neuroimaging techniques are needed to identify definitively the brain areas and associated networks responsible for the rapid changes in perceptual attention we observed.”

The researchers also found that 20 minutes of electrical brain stimulation helps tune perceptual attention. Is it in vogue that attention studies like this one and Can psychologists exclude the limbic system and adequately study awareness and social cognition? seemed to need gadgets that zapped the subjects’ brains?

http://www.pnas.org/content/112/2/625.full “Enhancing long-term memory with stimulation tunes visual attention in one trial”

Task performance and beliefs about task responses are solely cerebral exercises

This 2013 human study provided details of which areas of the cerebrum participated in objective performance of a task vs. the subjects’ subjective confidence in their task responses:

“These results suggest the existence of functional brain networks indexing objective performance and accuracy of subjective beliefs distinctively expressed in a set of stable mental states.”

The subjects’ limbic systems were monitored during the fMRI and subsequent reporting, but the subjects’ limbic system areas weren’t activated during any of the experiments.

The researchers demonstrated that both task participation and subjective beliefs about the tasks were only cerebral exercises.

These findings should inform studies such as:

to neither characterize subjects’ task responses as “positive feelings” nor to ascribe emotions such as happiness to the subjects’ cerebral exercises.

http://www.pnas.org/content/110/28/11577.full “Distinct patterns of functional brain connectivity correlate with objective performance and subjective beliefs”

Can psychologists exclude the limbic system and adequately study awareness and social cognition?

This 2014 Princeton human study was proof that cognitive researchers are stuck in the cerebrum. That and gadgets.

The researchers didn’t measure limbic system or lower brain areas, yet from their use of cartoon faces and magnetically zapping their subjects’ brains they proclaimed:

“The findings suggest a fundamental connection between private awareness and social cognition.”

For just one example of the gross omissions of the study’s design, look at the limbic system’s part in “social cognition” for The amygdala is where we integrate our perception of human facial emotion.

And it’s a very limited scope of “private awareness” that excludes conscious awareness of what’s in our own feeling, instinctual, and impulsive levels of consciousness.

http://www.pnas.org/content/111/13/5012.full “Attributing awareness to oneself and to others”


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