What is Primal Therapy by Dr. Arthur Janov

“We have needs that we are all born with.

When those basic needs are not met, we hurt.

And when that hurt is big enough, it is imprinted into the system.

It changes the system, our whole physiologic system.

What our therapy does, it goes back to those early brains, those hurt brains, and relive the pain, and get it out of the system.

Because meanwhile, that pain is being held in storage, and just waiting for its exit, so to speak.

So Primal Therapy is a way of accessing our feeling brain, and down below even the feeling brain, to the brainstem, to get to all of the hurts that started very early in our lives.

And bring them up to consciousness for connection and integration.

It is a very systematic therapy, by the patient.

The patient decides when he comes and when he leaves and how long he stays.

There’s no 50-minute hour anymore.

It’s the feelings of the patient that determine when he stops.”

If rodent training had beneficial epigenetic effects, how can the next step be human gene therapy?

This 2014 rodent study detailed significant and lasting epigenetic DNA methylation in the hippocampus part of the limbic system as a result of fear-extinction training.

The researchers missed the boat when explaining in interviews how their research could apply to humans. What I understood from the interviews was that the researchers were focused on targeting human genes with some outside action.

Recommending human gene therapy smelled like an agenda. If these epigenetic modifications were induced by training in rodents, wouldn’t the next step be research into reversal training or therapeutic activity for humans?


The researchers also found:

“Importantly, these effects were specific to extinction training and did not occur in mice that had been fear conditioned, followed by a single reactivation trial, therefore arguing against the possibility that such epigenetic modifications are nonspecifically induced by the retrieval or reconsolidation of the original fear memory.”

This was fine for rodent studies where the origins of both the disease and the cure were all exerted externally. I didn’t see that it necessarily applied to humans.

After all, we’re not lab rats. We can perform effective therapy that doesn’t involve some outside action being done to us.

http://www.pnas.org/content/111/19/7120.full “Neocortical Tet3-mediated accumulation of 5-hydroxymethylcytosine promotes rapid behavioral adaptation”

What happens next after a detox program predictably fails?

This 2014 study was a misguided example of looking solely at the presenting parts of a person’s condition rather than the whole historical person.

What did this study’s researchers decide after finding:

“Alcohol-dependent subjects..remained with high scores of depression, anxiety, and alcohol craving after a short-term detoxification program.”

Was it that the detox program didn’t work because it dealt with suppressing symptoms rather than addressing causes?

NO!

The researchers decided:

“Gut microbiota seems to be a previously unidentified target in the management of alcohol dependence.”

The researchers proceeded on some trendy, in-vogue aspect of their patients with which to tinker.

The researchers ignored that the correlation of the new treatment course didn’t show causation. They also ignored underlying causes for the ineffectiveness of the preceding treatments of symptoms.

Hard to see how the reviewer believed that this study would advance science.

Meanwhile, the researchers continued to ignore the elephants in the room: the relationships of the patients’ histories and their pain.

http://www.pnas.org/content/111/42/E4485.full “Intestinal permeability, gut-bacterial dysbiosis, and behavioral markers of alcohol-dependence severity”

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”

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”

Problematic research: If you don’t feel empathy for a patient, is the solution to fake it?

If you don’t experience empathy for another person, this 2014 Harvard study showed how to use your cerebrum to manipulate your limbic system into displaying a proxy of empathy.

Is this what we want from our human interactions? To have a way to produce an emotion the same way that an actor would as they read their lines?

How to finesse the effect of “no empathy” was the focus. Because these researchers didn’t define a lack of genuine empathy as a symptom of a fundamental problem, they absolved themselves from investigating any underlying causes.

Nice trick in the academic world.


In the real world, in which we are feeling human beings, what may be a cause of no empathy?

Let’s say that someone is in a position that helps people. They have daily encounters where they may be expected to be empathetic, but they seldom have these feelings for others.

One hypothesis of Dr. Arthur Janov’s Primal Therapy is this condition’s origin may be that in the past, a person needed help as a matter of survival, and they weren’t helped. Their unconscious memories of being helpless impel them to act out being helpful in their current life.

This person’s frequent reaction to any hint in the present of the agony of not receiving help back when they desperately needed it is to act out what they needed to have done back then. Helping others also gives them momentary distraction from such painful memories, but any relief is transitory. So they repeat the process.

Let’s say that unconscious needs pressed them into making a career choice of actively helping people. They’re usually too caught up in their own thoughts and feelings and behavior, though, to sense feelings of the people they’re helping.

Something isn’t right, but what’s the problem? They see indicators such as: their actions that should feel fulfilling aren’t fulfilling, they seldom feel empathy, and so on.


Primal Therapy allows patients to therapeutically address origins of such conditions. A symptom such as lack of empathy for others will resolve as historical pains are ameliorated.

Or we can do as this study suggested: produce an inauthentic display – and thereby ignore the lack of empathy as a symptom – and never address causes of no empathy.

http://www.pnas.org/content/111/12/4415.full “Episodic simulation and episodic memory can increase intentions to help others”

One way that mothers cause fear and emotional trauma in their infants

This 2014 rodent study showed that infants learned to fear specific items in the environment that their mothers feared. The imprinting memory happened at a stage in the infants’ lives when they hadn’t yet developed the physiology to respond to the environment with fear on their own.

The learning cue was the mothers’ fear response – in this case, her distress odor, even when the mother was not present – coupled with the infants’ stress. The fear memory was stored in the infants’ amygdalae:

“These memories are acquired at younger ages compared with amygdala-dependent odor-shock conditioning and are more enduring following minimal conditioning.

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.”

There’s no scientific reason why this and related studies shouldn’t inform researchers who ignore the earliest stages of human life when studying limbic system disorders in humans.

For an example of researchers choosing to NOT be informed, look at Is this science, or a PC agenda? Problematic research on childhood maltreatment and its effects.

http://www.pnas.org/content/111/33/12222.full “Intergenerational transmission of emotional trauma through amygdala-dependent mother-to-infant transfer of specific fear”

How painful long-lasting memories are stored and why they are so strong

This 2014 rodent study provided evidence for a portion of the neurophysiology that underlies how painful long-lasting memories are stored and why they are so strong. The amygdala was the brain area studied.

The researchers were misguided in news coverage by focusing on solutions such as external mechanisms to forget these memories. The researchers should think in terms of how their research can help people who can help themselves instead of having something externally done to them.

After all, we’re humans who can participate in therapy, not lab rats who need to be fixed.

http://www.pnas.org/content/111/51/E5584.full “Hebbian and neuromodulatory mechanisms interact to trigger associative memory formation”

Are 50 Shades of Grey behaviors learned in infancy?

Ever wonder how someone could become attached to their early childhood abuser?

Ever wonder what underlying neurobiological conditions may account for the popularity of Fifty Shades of Grey?

This 2014 rodent study “Enduring good memories of infant trauma” linked below showed how trauma changed infants’ limbic system and lower brains. As adults, they derived a neurochemical benefit from re-experiencing the traumatic conditions:

“Trauma and pain experienced in infancy clearly led to higher rates of adult rat depression-like behavior..(but) the infant brain has limited ability to link trauma to fear areas in the brain, such as the amygdala.

These results are surprising because cues associated with trauma experienced as adults provoke fear and do not rescue depressive behavior.

It is possible that giving SSRI medications to children could be detrimental to mental health in adulthood,” Dr. Sullivan says. “We believe that our research offers the first evidence for the impact of serotonin pathways.

The infant trauma increases serotonin to produce brain programming of later life depression, and the infant trauma cue increases serotonin to alleviate the adult depressive like symptoms.”


As the study may apply to humans, let’s say that as an infant, someone was traumatized by a caregiver who, for example, bound them too tightly and left them alone for too long. What adult behaviors and other symptoms may develop as results? The person may:

  • Show depression-like symptoms that would strangely be alleviated by being bound tightly and left alone for an extended period.
  • Develop attachments to people who treated them poorly in a way that triggered them to re-experience their early childhood traumas.
  • Feel their mood lift when their infancy traumas were cued.
  • Be unable to explain and integrate with their cerebrum what was going on with their limbic system and lower brains.
  • Be caught in a circle of acting out their feelings and impulses, with unfulfilling results.

Isn’t it curious that this acting-out behavior – driven by unconscious memories of traumatic conditions – is a subject for popular entertainment? It may have resonated with personal experiences of the people who read the books and watched the movie.


What about people who want to be relieved of their symptomatic behavior? Is it a justifiable practice:

  • To pass affected people over to talk therapies that aren’t interested in directly treating the cause – a neurobiological condition that exists in the limbic system and lower brains – only the symptoms?
  • To drug affected people with the neurochemicals that their condition makes scarce – the symptoms – instead of addressing the source?

A principle of Dr. Arthur Janov’s Primal Therapy is that people are capable of treating their own originating neurobiological conditions. One of the therapeutic results is that the patient is relieved of being caught in endless circles of acting-out behavior.

That way we can have our own lives, and not be driven by what happened during early stages of our lives.

http://www.pnas.org/content/112/3/881.full “Enduring good memories of infant trauma: Rescue of adult neurobehavioral deficits via amygdala serotonin and corticosterone interaction”

Conscious mental states should not be the first-choice explanation of behavior

Here are some 2014 ruminations by Joseph LeDoux, the grandfather of studies of the amygdala. He attempted to disambiguate feeling brain structures’ activations and responses from ideas of what feelings are, specifically regarding fear:

“Damage to the hippocampus in humans disrupts explicit conscious memory of having been conditioned but has no effect on fear conditioning itself, whereas damage to the amygdala disrupts fear conditioning but not the conscious memory of having been conditioned.

Conscious mental states should not, in the absence of direct evidence, be the first-choice explanation of behavior.

Neither amygdala activity nor amygdala-controlled responses are telltale signatures of fearful feelings.

Conscious fear can cause us to act in certain ways, but it is not the cause of the expression of defensive behaviors and physiological responses elicited by conditioned or unconditioned threats.”

http://www.pnas.org/content/111/8/2871.full “Coming to terms with fear”