“Our therapy is centered on needs.
As we grow up we have different kinds of needs.
The need right after birth is be touched.
The need at birth is to have a good birth with oxygen, etc.
Then it’s to be held, to be listened to, and so on.
For each of the needs that are not fulfilled, there’s pain.
And it’s registered on different levels of the brain.
What we have found a way to do is to go back down into the brain and take those pains out of the system.
So you don’t have to take pills to stuff it back.
What we do is, little by little, take the pain out of the system that is based on not-fulfilled needs.
So that’s basically what Primal Therapy is about.”
Author: gettingwell4
Our cerebrums use ideas and beliefs to repress pain and make us more comfortable
One hypothesis of Primal Therapy is that a major function our cerebrums have evolutionarily adapted is to use ideas and beliefs to repress pain and make us more comfortable.
Is it any wonder why this 2014 study found:
“Beliefs are more prevalent among societies that inhabit poorer environments and are more prone to ecological duress.”
http://www.pnas.org/content/111/47/16784.full “The ecology of religious beliefs”
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 a study didn’t measure feelings, then its findings may not pertain to genuine empathy
This 2014 UK study tried to show that empathetic actions were very context-dependent. It mainly studied causing overt pain to another person.
The lead researcher stated:
“We were interested in quantifying how much people care about others, relative to themselves. A lack of concern for others’ suffering lies at the heart of many psychiatric disorders such as psychopathy, so developing precise laboratory measures of empathy and altruism will be important for probing the brain processes that underlie antisocial behavior.”
The researchers didn’t provide direct evidence of genuine empathy – the subjects’ emotions of sensing and sharing the emotions of another person.
The study was designed to cause sensations of pain and draw conclusions about empathetic feelings. The subjects’ limbic system and lower brains were never measured, however.
Why did the researchers decide to only infer these feelings and sensations from actions and reports? Why wasn’t this inferred evidence confirmed with direct measurements of the brain areas that primarily process feelings and sensations?
- At no time during the experiment did the subjects see or hear or touch the person whom they caused pain. Wouldn’t it be difficult for the subjects to feel authentic empathy for a disembodied presence?
- We’re informed by the Task performance and beliefs about task responses are solely cerebral exercises study that it’s inaccurate to characterize subjects’ task responses as feelings.
- We know from the Problematic research: If you don’t feel empathy for a patient, is the solution to fake it? study that people’s cerebrums are easily capable of generating a proxy for empathy.
This study’s findings concerning empathy involved inauthentic empathy – the non-feeling, cerebral exercise, faking-it kind.
http://www.pnas.org/content/111/48/17320.full “Harm to others outweighs harm to self in moral decision making”
If research treats “Preexisting individual differences” as a black box, how can it find causes for stress and depression?
This 2014 research studied both humans and rodents to provide further evidence on the physiology of defeat. The researchers demonstrated that with mice:
“Bone marrow transplants of stem cells that produce leucocytes lacking IL-6 (the cytokine interleukin 6) or when injected with antibodies that block IL-6 prior to stress exposure, the development of social avoidance was reduced.”
The researchers also showed in humans that standard antidepressants didn’t act to lower IL-6.
So, what were we to make of this finding?
“Preexisting differences in the sensitivity of a key part of each individual’s immune system to stress confer a greater risk of developing stress-related depression or anxiety.”
- Was it sufficient for the researchers and the news articles covering the research to treat “preexisting differences” as a black box that nobody could enter to find causes for the effects of “developing stress-related depression or anxiety?”
- Did things happen in each individual’s history to cause the “preexisting differences” or was each individual born that way?
- Why was the research directed at symptoms with no mention of any underlying causal factors?
It wasn’t sufficient for the researchers to carry on their experiments with assumptions that there weren’t early-life causes for the above symptoms. Such a pretense leads to the follow-on pretense that later-life consequences weren’t effects of causes, but were instead, mysteries due to “preexisting individual differences.”
http://www.pnas.org/content/111/45/16136.full “Individual differences in the peripheral immune system promote resilience versus susceptibility to social stress”
More from the researchers that found people had the same personalities at age 26 that they had at age 3
This 2014 research came from the Dunedin Study in New Zealand that has studied a group of over 1,000 people for 40+ years now. They first came to worldwide fame by finding that the study’s participants at age 26 largely had the same personality that each did at age 3.
The current study linked the participants’ childhood cognitive abilities and self-control to their current cardiac age.
Would a US doctor have the knowledge and foresight to understand that significant factors in a middle-aged patient’s cardiac health came from their early childhood, infancy, or womb life experiences?
http://www.pnas.org/content/111/48/17087.full “Credit scores, cardiovascular disease risk, and human capital”
An example of how we are unaware of some of the unconscious bases of our decisions
This 2014 human study provided details of how we are unaware of some of the unconscious bases of our decisions:
“We show that unconscious information can be accumulated over time and integrated with conscious elements presented either before or after to boost or diminish decision accuracy.
The unconscious information could only be used when some conscious decision-relevant information was also present.
Surprisingly, the unconscious boost in accuracy was not accompanied by corresponding increases in confidence, suggesting that we have poor metacognition for unconscious decisional evidence.”
I wouldn’t agree that these findings apply as broadly as the researchers said they did during interviews.
The first reason is that the researchers restricted the study to the subjects’ cerebrums’ visual processing. In everyday life, though, our limbic systems and lower brains are also very much involved with visual processing.
As an example, have you ever taken a nature walk where you instinctually jumped back from a vague initial impression only to find that the object was a stick? I’ve done that many times, and our shared human instincts operating with the limbic system and lower brain saved me once in childhood from stepping on a copperhead snake.
Secondly, the researchers limited the term “unconscious” to mean below visual perception of the subjects’ cerebrums.
What if, for example, the study’s visual cues included emotional content that involved the subjects’ limbic systems? The researchers may have able to develop a basis for findings that applied to common operations such as making decisions that are influenced by unconscious emotional content.
The third reason to not apply the findings as broadly as the researchers may have desired is that the researchers limited the term “metacognition” to operations of the the subjects’ cerebrums. We know that Task performance and beliefs about task responses are solely cerebral exercises, which accurately describes the metacognition experiment.
As an example of how people’s metacognitions are much broader than just their cerebrums, I take a crowded train to and from work everyday. It’s fairly straightforward to understand people’s actions, body postures, and facial expressions in terms of the combined metacognition operations of their entire brains.
Also, the metacognition finding sample size may have been too small by involving only five subjects.
http://www.pnas.org/content/111/45/16214.full “Unconscious information changes decision accuracy but not confidence”
One way that an infant unconsciously knows the emotions of the humans in their environment
This 2014 human study found one way that an infant unconsciously recognized the emotions of the humans in their environment:
“The current study provides neural evidence for the unconscious detection of emotion and gaze cues from the sclera in 7-mo-old infants.
Wide-open eyes, exposing a lot of white, indicate fear or surprise. A thinner slit of exposed eye, such as when smiling, expresses happiness or joy.”
The basis for finding that the subjects’ responses were unconscious was that the researchers determined that displaying images of eyes for 50 milliseconds fell below the threshold of infants’ conscious awareness.
http://www.pnas.org/content/111/45/16208.full “Unconscious discrimination of social cues from eye whites in infants”
Are you feeling kinda blue? Think your brain cells are too few? Get your fat cells on that bike and ride!
This 2014 rodent study found that fat cells released a certain hormone during exercise that produced two beneficial effects:
- the hormone increased hippocampal neurogenesis;
- it also reduced depression-like behaviors.
So if you’re feeling kinda blue,
Think your brain cells are too few?
Get your fat cells on that bike and ride!
http://www.pnas.org/content/111/44/15810.full “Physical exercise-induced hippocampal neurogenesis and antidepressant effects are mediated by the adipocyte hormone adiponectin”
The degree of epigenetic DNA methylation may be used as a proxy to measure biological age
This fascinating 2014 human study developed the new use of a somewhat intuitive marker of aging. The researchers used the degree of methylation – an epigenetic chemical modification of DNA – as an epigenetic clock to measure biological age.
The researchers found that, on average, the epigenetic age of the liver increased by 3.3 years for every increase in 10 body mass index (BMI) units. Other studied tissue areas weren’t similarly affected.
http://www.pnas.org/content/111/43/15538.full “Obesity accelerates epigenetic aging of human liver”
Fear extinction is the learned inhibition of retrieval of previously acquired responses
This 2014 rodent study showed that fear extinction doesn’t depend on memory retrieval:
“These results show that extinction and retrieval are separate processes and strongly suggest that extinction is triggered or gated by the conditioned stimulus even in the absence of retrieval.”
Key to my understanding this finding came from a definition in another summary study by the authors, The learning of fear extinction, where they stated:
“Extinction is the learned inhibition of retrieval of previously acquired responses.”
These two studies and Hippocampal mechanisms involved in the enhancement of fear extinction caused by exposure to novelty should inform researchers of studies such as If rodent training has beneficial epigenetic effects, how can the next step be human gene therapy? of desirable alternative treatments, rather than proceeding from rodent training directly to human gene therapy.
http://www.pnas.org/content/112/2/E230.full “Extinction learning, which consists of the inhibition of retrieval, can be learned without retrieval”
A biologically relevant event can drive long-term memory in a single training session
This 2014 fruit fly study found:
“A biologically relevant event such as finding food under starvation conditions or being poisoned can drive long-term memory in a single training session.”
I don’t think that we need to discover at these extremes, though, whether or not the finding has human applicability.
We do know from the Dutch hunger winter of 1944 study referenced in the Non-PC alert: Treating the mother’s obesity symptoms positively affects the post-surgery offspring study that prenatal exposure to famine had lifelong ill effects on the children. The exposed children had epigenetic DNA changes – a form of long-term memory – from their mothers’ starvation, which resulted in relative obesity compared with their unexposed siblings.
http://www.pnas.org/content/112/2/578.full “Distinct dopamine neurons mediate reward signals for short- and long-term memories”
Problematic research on stress that will never make a contribution toward advancing science
This 2014 UK human study found:
“Type 2 diabetes is characterized by disruption of stress-related processes across multiple biological systems and increased exposure to life stress.”
HOWEVER, the stress effects weren’t conclusively shown to be either a cause or consequence of type 2 diabetes. Correlation wasn’t causation.
Looking around for clues as to what went wrong, I found this data sample of cortisol in a small table that comprised the total amount of information in the supplementary material:
“Geometric means, adjusted for education, marital status, BMI, smoking status, use of statins, and time of day.”
It’s hubris for the researchers to state that they improved data measurements by averaging them after adjusting for all of the above six factors.
Maybe the problem was elsewhere, maybe in the study design. Wherever the problems were, they guaranteed that the researchers would NEVER find cause and effect.
But maybe that’s the point?
There appeared to be other agendas that ensured studies like these failed to make a contribution toward advancing science. The researchers inevitably used buzzwords such as “allostatic load” and cited the need for further studies (money). Everybody was okay with that, including the reviewer, and everybody kept their safe jobs.
Such studies also had limiting effects on how we “do something” about real problems because the researchers wouldn’t produce findings that weren’t politically correct.
http://www.pnas.org/content/111/44/15693.full “Disruption of multisystem responses to stress in type 2 diabetes: Investigating the dynamics of allostatic load”
We are attuned to perceive what our brains predict will be rewarding
What I got from this 2014 human study is that from the beginnings of our lives, we are attuned to perceive what our brains predict will be rewarding.
The subjects’ whole brains were monitored, but only areas of the cerebrum participated in the findings to a significant degree.
“Sounds associated with high rewards increase the sensitivity of vision.
The same neurons that process sensory information are modulated by reward..and thereby influence perception from the earliest stages of cortical processing.
Reward associations modulated responses in regions associated with multisensory processing in which the strength of modulation was a better predictor of the magnitude of the behavioral effect than the modulation in classical reward regions.”
Sounds a little bit like we all might have a mild case of synesthesia.
http://www.pnas.org/content/111/42/15244.full “Cross-modal effects of value on perceptual acuity and stimulus encoding”
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”
Surface Your Real Self 