On Primal Therapy with Drs. Art and France Janov

Experiential feeling therapy addressing the pain of the lack of love.

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A limited study of parental transmission of anxiety/stress-reactive traits

BehavioralTraitsThis 2016 New York rodent study found:

“Parental behavioural traits can be transmitted by non-genetic mechanisms to the offspring.

We show that four anxiety/stress-reactive traits are transmitted via independent iterative-somatic and gametic epigenetic mechanisms across multiple generations.

As the individual traits/pathways each have their own generation-dependent penetrance and gender specificity, the resulting cumulative phenotype is pleiotropic. In the context of genetic diseases, it is typically assumed that this phenomenon arises from individual differences in vulnerability to the various effects of the causative gene. However, the work presented here reveals that pleiotropy can be produced by the variable distribution and segregated transmission of behavioural traits.”


A primary focus was how anxiety was transmitted from parents to offspring:

“The iterative propagation of the male-specific anxiety-like behaviour is most compatible with a model in which proinflammatory state is propagated from H [serotonin1A receptor heterozygote] F0 to F1 [children] females and in which the proinflammatory state is acquired by F1 males from their H mothers, and then by F2 [grandchildren] males from their F1 mothers.

We propose that increased levels of gestational MIP-1β [macrophage inflammatory protein 1β] in H and F1 mothers, together with additional proinflammatory cytokines and bioactive proteins, are required to produce immune system activation in their newborn offspring, which in turn promotes the development of the anxiety-like phenotype in males.

In particular, increase in the number of monocytes and their transmigration to the brain parenchyma in F1 and F2 males could be central to the development of anxiety.”


The researchers studied transmission of behavioral traits and epigenetic changes. Due to my quick take on the study title – “Behavioural traits propagate across generations..” – I had expectations of this study that weren’t born out. What could the researchers have done versus what they did?

The study design removed prenatal and postnatal parental behavioral transmission of behavioral traits and epigenetic changes as each generation’s embryos were implanted into foster wild-type (WT) mothers.

The study design substituted the foster mothers’ prenatal and postnatal parental environments for the biological parents’ environments. So we didn’t find out, for example:

  • To what extents the overly stress-reactive F1 female children’s prenatal environments and postnatal behaviors induced behaviors and/or epigenetic changes in their children; and
  • Whether the F2 grandchildren’s parental behaviors subsequently induced behaviors and/or epigenetic changes in the F3 great-grandchildren.

How did the study meet the overall goal of rodent studies: to help humans?

    1. Only a minority of humans experienced an early-life environment that included primary caregivers other than our biological parents.
    2. Very, very few of us experienced a prenatal environment other than our biological mothers.
    3. The study’s thorough removal of parental behavior was an outstanding methodology to confirm by falsifiability whether parental behavior was both an intergenerational and transgenerational epigenetic inheritance mechanism.
    4. Maybe the researchers filled in some gaps in previous rodent studies, such as determining what is or isn’t a “true transgenerational mechanism.”

As an example of a rodent study that more closely approximated human conditions, the behavior of a mother whose DNA was epigenetically changed by stress induced the same epigenetic changes to her child’s DNA when her child was 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.”


How did parental behavioral transmission of behavioral traits and epigenetic changes become a subject not worth investigating? These traits and effects can be seen everyday in real-life human interactions, and in every human’s physiology.

But when investigating human correlates with behavioral epigenetic changes of rodents in the laboratory, parental behavioral transmission of behavioral traits is often treated the way this study treated it: as a confounder.

I doubt that people who have reached some degree of honesty about their early lives and concomitant empathy for others would agree with this prioritization. The papers of Transgenerational epigenetic inheritance week show the spectrum of opportunities to advance science that were intentionally missed.

http://www.nature.com/ncomms/2016/160513/ncomms11492/full/ncomms11492.html “Behavioural traits propagate across generations via segregated iterative-somatic and gametic epigenetic mechanisms”

Observing pain in others had long-lasting brain effects

This 2016 Israeli human study used whole-head magnetoencephalography (MEG) to study pain perception in military veterans:

Our findings demonstrate alterations in pain perception following extreme pain exposure, chart the sequence from automatic to evaluative pain processing, and emphasize the importance of considering past experiences in studying the neural response to others’ states.

Differences in brain activation to ‘pain’ and ‘no pain’ in the PCC [posterior cingulate cortex] emerged only among controls. This suggests that prior exposure to extreme pain alters the typical brain response to pain by blurring the distinction between painful and otherwise identical but nonpainful stimuli, and that this blurring of the ‘pain effect’ stems from increased responses to ‘no pain’ rather than from attenuated response to pain.”


Limitations included:

  • “The pain-exposed participants showed posttraumatic symptoms, which may also be related to the observed alterations in the brain response to pain.
  • We did not include pain threshold measurements. However, the participants’ sensitivity to experienced pain may have had an effect on the processing of observed pain.
  • The regions of interest for the examination of pain processing in the pain-exposed group were defined on the basis of the results identified in the control group.
  • We did not detect pain-related activations in additional regions typically associated with pain perception, such as the anterior insula and ACC. This may be related to differences between the MEG and fMRI neuroimaging approaches.”

The subjects self-administered oxytocin or placebo per the study’s design. However:

“We chose to focus on the placebo condition and to test group differences at baseline only, in light of the recent criticism on underpowered oxytocin administration studies, and thus all following analyses are reported for the placebo condition.”


A few questions:

  1. If observing others’ pain caused “increased responses to ‘no pain’,” wouldn’t the same effect or more be expected from experiencing one’s own pain?
  2. If there’s evidence for item 1, then why aren’t “increased responses to ‘no pain'” of affected people overtly evident in everyday life?
  3. If item 2 is often observed, then what are the neurobiological consequences for affected people’s suppression of “increased responses to ‘no pain’?”
  4. Along with the effects of item 3, what may be behavioral, emotional, and other evidence of this suppressed pain effect?
  5. What would it take for affected people to regain a normal processing of others’ “‘pain’ and ‘no pain’?”

https://www.researchgate.net/publication/299546838_Prior_exposure_to_extreme_pain_alters_neural_response_to_pain_in_others “Prior exposure to extreme pain alters neural response to pain in others” Thanks to one of the authors, Ruth Feldman, for providing the full study

Empathy, value, pain, control: Psychological functions of the human striatum

This 2016 US human study found:

“A link between existing data on the anatomical and physiological characteristics of striatal regions and psychological functions.

Because we did not limit our metaanalysis to studies that specifically targeted striatal function, our results extend previous knowledge of the involvement of the striatum in reward-related decision-making tasks, and provide a detailed functional map of regional specialization for diverse psychological functions, some of which are sometimes thought of as being the exclusive domain of the PFC [prefrontal cortex].”

The analysis led to dividing the striatum into five segments:

Ventral striatum (VS):

  • Stimulus Value
  • Terms such as “reward,” “losses,” and “craving”
  • The most representative study reported that monetary and social rewards activate overlapping regions within the VS.
  • Together with the above finding of a reliable coactivation with OFC [orbitofrontal cortex] and ventromedial PFC, this finding suggests a broad involvement of this area in representing stimulus value and related stimulus-driven motivational states.

Anterior caudate (Ca) Nucleus:

  • Incentive Behavior
  • Terms such as “grasping,” “reaching,” and “reinforcement”
  • The most representative study reported a stronger blood-oxygen level-dependent (BOLD) response in this region during trials in which participants had a chance of winning or losing money in a card guessing game, in comparison to trials where participants merely received feedback about the accuracy of their guess.
  • This result suggests a role in evaluating the value of different actions, contrasting with the above role of the VS in evaluating the value of stimuli.

Posterior putamen (Pp):

  • Sensorimotor Processes
  • Terms such as “foot,” “noxious,” and “taste”
  • The most representative study reported activation of this region in response to painful stimulation at the back of the left hand and foot of participants. Anatomically, the most reliable and specific coactivation is with sensorimotor cortices, and the posterior and midinsula and operculum (secondary somatosensory cortex SII) in particular, some parts of which are specifically associated with pain.
  • Together, these findings suggest a broad involvement of this area in sensorimotor functions, including aspects of their affective qualities.

Anterior putamen (Pa):

  • Social- and Language-Related Functions
  • Terms such as “read,” “vocal,” and “empathic”
  • The most representative study partially supports a role of this area in social- and language-related functions; it reported a stronger activation of the Pa in experienced singers, but not when novices were singing.
  • It is coactivated with frontal areas anterior to the ones coactivated with the Pp, demonstrating topography in frontostriatal associations. These anterior regions have been implicated in language processes.

Posterior caudate (Cp) Nucleus:

  • Executive Functions
  • Terms such as “causality,” “rehearsal,” and “arithmetic”
  • The representative study reported this region to be part of a network that included dorsolateral PFC and ACC, which supported inhibitory control and task set-shifting.
  • These results suggest a broad, and previously underappreciated, role for the Cp in cognitive control.

The authors presented comparisons of the above striatal segments with other analyses of striatal zones.


One of the coauthors was the lead researcher of the 2015 Advance science by including emotion in research. The current study similarly used a coactivation view rather than a connectivity paradigm of:

“Inferring striatal function indirectly via psychological functions of connected cortical regions.”

Another of the coauthors was a developer of the system used by the current study and by The function of the dorsal ACC is to monitor pain in survival contexts, and he provided feedback to those authors regarding proper use of the system.


The researchers’ “unbiased, data-driven approach” had to work around the cortical biases evident in many of the 5,809 human imaging studies analyzed. The authors referred to the biases in statements such as:

“The majority of studies investigating these psychological functions report activity preferentially in cortical areas, except for studies investigating reward-related and motor functions.”

The methods and results of research with cortical biases influenced the study’s use of:

“Word frequencies of psychological terms in the full text of studies, rather than a detailed analysis of psychological tasks and statistical contrasts.”

http://www.pnas.org/content/113/7/1907.full “Regional specialization within the human striatum for diverse psychological functions”

What was not, is not, and will never be

Neuroskeptic’s blog post Genetic Testing for Autism as an Existential Question related the story of “A Sister, a Father and a Son: Autism, Genetic Testing, and Impossible Decisions.”

“I decided to put the question to my sister, Maria. Although she is autistic, she is of high intelligence.

Maria was excited to be an aunt soon, and was willing to do what she could to help my baby – even if what she was helping with was to avoid her own condition.

She is high enough functioning to know some of what she’s missing in life, and has longed her entire life to be “normal.” If she could save her niece or nephew some of the pain and awkwardness her condition had caused her, she was willing to help.”

In the concluding paragraph:

“What struck me about this story is the way in which the prospect of the genetic test confronted Maria with a very personal decision: will you do something that might help prevent someone else becoming like you?

Isn’t this very close to the ultimate existential question: all things considered, would you wish to live your life over again?”


Aren’t the majority of humans also “high enough functioning to know some of what she’s missing in life?”

Aren’t our feelings of what we’re missing one of the impetuses for us to have also “longed her entire life to be normal?”

This feeling was aired in Dr. Arthur Janov’s blog post What a Waste:

“What it was, was the feeling of great loss, something missing that could never again be duplicated.

It was no love where it could have been the opposite if the parent’s gates could have been open. But it could not be because that would have meant terrible pain and suffering for them; and their whole neurologic system militated against any conscious-awareness.”


We long for what was and is impossible:

  • For many of us, the impossibilities of having normal lives started with prenatal epigenetic changes.
  • Our experiences of our postnatal environment prompted us into adapting to its people, places, and contents. These neurological, biological, and behavioral adaptations were sometimes long-lasting deviations from developmental norms.
  • Other genetic factors combined with the above to largely make us who we were and are.

Our longing for an impossible-to-reconstruct life doesn’t go away.

We often may not be aware of our longing for what “could not be” and of its extensive impacts. Such feelings impel us into many hundreds of ideas, hundreds of beliefs, and hundreds of behaviors, a sample of which were referred to above:

  • Behaviors to “do something that might help prevent someone else becoming like you;”
  • Ideas such as existential philosophy; and
  • Beliefs that manifest the “wish to live your life over again.”

Spending our time on these ideas, beliefs, and behaviors won’t ameliorate their motivating causes. Our efforts distance us from our truths, with real consequences: a wasted life.

What keeps us from understanding our reality? I invite readers to investigate Dr. Arthur Janov’s Primal Therapy for effective therapeutic approaches.

Where do our beliefs about our children come from? An autism example

A 2015 case study by Ohio physicians highlighted:

“Although only a small minority of patients with autism have a mitochondrial disease, many patients with mitochondrial myopathies have autism spectrum disorder symptoms.

These symptoms may be the presenting symptoms, which presents a diagnostic challenge for clinicians.

The case of a 15-year-old boy with a history of autism spectrum disorder and neurocardiogenic syncope, admitted to the inpatient unit for self-injury, whose young mother, age 35, was discovered to suffer from mitochondrial myopathy, dysautonomia, neurocardiogenic syncope, Ehler-Danlos syndrome, and other uncommon multisystem pathologies likely related to mitochondrial dysfunction.”

I was somewhat taken aback by the Abstract and Introduction statements:

“All autism spectrum disorders are known to be heritable, via genetic and/or epigenetic mechanisms, but specific modes of inheritance are not well characterized.

This form of ASD is known to be heritable, as are all forms of ASD, despite the previous belief to the contrary, though the mechanisms of inheritance, both genetic and epigenetic, are not well characterized.”

The definition of heritable as used was “able to be passed from parent to child before birth.” The reference provided for the statements was a 2014 French review Gene × Environment Interactions in Autism Spectrum Disorders: Role of Epigenetic Mechanisms.

I didn’t see the “known to be heritable” phrase mentioned in the referenced review. However, I also didn’t see anything stated in the review or cited from its 217 references that disproved the phrase.


I shouldn’t have been surprised by “despite the previous belief to the contrary” in the above quotation. I’d guess that the physicians frequently encountered parents who needed such beliefs when faced with their child’s condition.

A relevant hypothesis of Dr. Arthur Janov’s Primal Therapy is: a major function that our cerebrums have evolutionarily adapted is to use ideas and beliefs to repress pain and make us more comfortable.

I value this inference as an empathetic method of interpreting people’s behaviors and expressions of thoughts and feelings.

When a “known to be heritable” phrase can unleash pain, it likely won’t be understood in its appropriate context. Among the physicians’ challenges was a barrier that kept the parent’s pain from being felt – the belief.

http://innovationscns.com/autism-in-the-son-of-a-woman-with-mitochondrial-myopathy-and-dysautonomia-a-case-report/ “Autism in the Son of a Woman with Mitochondrial Myopathy and Dysautonomia: A Case Report”

Is the purpose of research to define opportunities for interventions?

In this 2014 review, a social scientist first presented an interpretive history of what he found to be important in the emergence of epigenetics. He proceeded into his ideas of “a possible agenda of the social studies of the life-sciences” in the “postgenomic age” with headings such as “Postgenomic biopolitics: “upgrade yourself” or born damaged for ever?”

This perspective included:

“The upgradable epigenome may become the basis for a new motivation to intervene, control and improve it through pharmacological agents or social interventions.

An important trend is the use of epigenetic and developmental findings in the so-called early-intervention programmes.

It is possible that epigenetic findings will become increasingly relevant in social policy strategies.”


In this blog I often highlight research that may help us understand details of how each of us is a unique individual. It’s my view that insofar as research helps each of us understand our unique, real self, we may be able to empathetically understand others’ unique qualities.

Click individual differences for a sample of how researchers explain away uniqueness in order to converge on a study’s desired objectives. There’s seldom an attempt to further understand what caused each subject to develop their unique qualities.

Why would this reviewer advocate that

  • Researchers,
  • People working in the social sciences,
  • People employed or involved in social services, and
  • Their sponsors and employers

intentionally disregard another individual’s unique qualities?

I’ll answer this question from a perspective that explains how this common, reflexive action derives from a person being unable to face the facts of their own life. Pertinent fundamentals of Dr Arthur Janov’s Primal Therapy are:

  1. Pain motivates a person’s unconscious act-outs of their underlying problems.
  2. The behavior that caused a problem is sometimes also the act-out behavior.
  3. Act-outs enable a person to re-experience the feelings of their historical struggles, in a vain attempt to resolve them.
  4. Due to pain barriers, people seldom become consciously aware of and – more importantly – address the causes for their own problematic behavior.
  5. “The patient has the power to heal himself.”

A consequent hypothesis is that a person will often glorify their unconscious act-outs and surround themself with justifications for these actions. For example, a person who can’t sit still may refer to their incessant activity with socially acceptable phrases such as “I’m always busy” or “I love to travel.” They’ll structure their life to enable their unconscious behavior, never questioning how they were attracted to an always-on-the-go occupation such as flight attendant, only vaguely feeling that they were made for it.

The behavior relevant to the current review may be exhibited by a person with a history of having no control over their own life. Following the above first two fundamentals, the pain of historically not having control over their life may motivate them to control other people’s lives.

Unfortunately for everyone who’s affected, such unconscious act-outs don’t resolve anything:

  1. The initiator may achieve some symbolic satisfaction by controlling others’ lives.
  2. This temporary satisfaction doesn’t make the initiator’s underlying problems less painful.
  3. The motivation impelling these unconscious act-outs isn’t thereby reduced.
  4. So the initiator soon repeats their controlling behavior, stuck in a loop of unresolved feelings.
  5. Since the self-chosen interests of someone who’s being controlled are lesser concerns to the initiator than exercising control, the controlled person may or may not be helped by the controller’s act-outs.

Research provides abundant evidence that we are unique individuals.

This is a strong indicator of who is best qualified to direct each of our unique lives.

A person who is driven to control others’ lives won’t accept epigenetic research as instructive for understanding, honoring, and respecting others as unique individuals. They’ll use research as a way to enable their own unconscious act-outs, and view it as offering opportunities for interventions into the lives of others.

This is the way that “pharmacological agents or social interventions” are often the intended “use of epigenetic and developmental findings.” Interventions receive justifications with “a possible agenda of the social studies of the life-sciences.”

Becoming aware of one’s own act-outs – and then individually addressing one’s own underlying problems – often take backseats to employment and other concerns to keep enabling one’s own behavior. That makes it likely that interventions justified by “epigenetic findings..in social policy” will continue, whether or not the subjects agree that they’re being helped.

For examples, take a look at a few of the YouTube presentations by people employed in the social sciences and social services on a topic of epigenetics. Compare them with the current state of epigenetic research in Grokking an Adverse Childhood Experiences (ACE) score.

What did you notice? How many presentations emphasized disrupted prenatal development – a period when problems can be prevented? Did you instead see that many more of the presentations emphasized controlling behavior?

http://journal.frontiersin.org/article/10.3389/fnhum.2014.00309/full “The social brain meets the reactive genome: neuroscience, epigenetics and the new social biology