An agenda-driven study on beliefs, smoking and addiction that found nothing of substance

The researchers of this 2014 Virginia Tech study said that they found something profound about beliefs and the brain and addiction and smoking.

I’ll assert the short versions of some relevant understandings before assessing the study.

1) A principle of Dr. Arthur Janov’s Primal Therapy is: we all have needs that start at the beginning of our lives. Our needs change as we grow.

If our basic needs aren’t satisfied anywhere along the way, we feel pain.

When the unmet needs are early in our lives and the painful conditions persist, enduring physiological changes may occur.

This basic truth is supported by the findings of much of the recent research I’ve curated on this blog, the references in those studies, and older research elsewhere.

2) Another fundamental of Primal Therapy is that the physiological impacts of these unmet needs drive our behavior, thoughts, and feelings.

The painful impacts of our unfulfilled needs impel us to be constantly vigilant for some way to fulfill them.

This is a richly insightful and truly empathetic method of interpreting people’s behaviors and expressions of thoughts and feelings.

3) A hypothesis of 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 expressions of thoughts and feelings. Click the Beliefs category to view samples of how beliefs, expectations, and predictions are studied using cerebral measurements.

So – what did this study contribute to science about beliefs and the underlying causes of addiction and smoking as found by measuring the subjects’ brains?

Nothing new, really. The study was all about the effects, the symptoms. There was nothing about:

  • Impelling physical conditions and causes,
  • What primarily drives people’s beliefs and addiction behaviors, and
  • What may permanently help someone with their need for the next cigarette.

I wonder what the study’s reviewer saw that factually advanced science.

Everybody already knew that beliefs can temporarily substitute for addicting substances, as well as temporarily change behaviors. It’s a foundation of AA and detox centers.

It’s also a foundation of AA and detox centers that these beliefs have to be constantly reinforced. That fact in and of itself demonstrates that underlying causes aren’t addressed in the AA and detox center approaches. The symptoms always bubble up, and require thought remedies and other interventions in order to stay suppressed.

The research provided details about an approach that wasn’t capable of anything more than temporarily suppressing symptoms. What does the following quote from the Significance statement sound like to you?

“Our findings suggest that subjective beliefs can override the physical presence of a powerful drug like nicotine by modulating learning signals processed in the brain’s reward system.”

Any human therapeutic approach won’t supply the addicting substance. That leaves just beliefs and their required constant reinforcement.

The unsupported overconfidence of the researchers that:

“The implications of these findings may be far ranging”

led to one of the most ridiculous statements I’ve seen in a while:

“Just as drugs micromanage the belief state,” Montague said, “maybe we can micromanage beliefs to better effect behavior change in addiction.”

This hubris just added to the stench of an agenda.

Since smoking isn’t politically correct, I’d guess that it wasn’t that difficult for this study to be funded and promoted. It apparently wasn’t an obstacle that the research DETRACTED from science and didn’t really help people. “Belief about nicotine selectively modulates value and reward prediction error signals in smokers”

Losing track of what are symptoms and what are causes with serotonin and stress

I’m starting to appreciate just how far down the rabbit hole researchers can go when they focus on symptoms and ignore causes.

This 2014 Duke study found that low-serotonin mice were more susceptible to stress than normal mice.

Okay so far, except that the study used transgenic mice that only had 20-40% of normal serotonin.

Humans most often develop low-serotonin symptoms for causes other than genetics, such as a second-order result of being subjected to childhood maltreatment and stress.

Use of the low-serotonin-due-to-genetics mice may have misdirected the researchers to lose focus that their ultimate task was to find ways that their research can help humans. If helping humans was the researchers’ focus, it may have occurred to them to show how stress caused “something” that caused low serotonin.

A second finding was that following exposure to stress, the low-serotonin mice didn’t respond to a standard antidepressant, fluoxetine. SSRI medications usually act to increase serotonin transmission, i.e. treat the symptom of low serotonin.

Stress was again not viewed as a cause of “something” that caused low serotonin. Stress was viewed as the reason that the medication didn’t work.

If helping humans was the researchers’ focus, it may have occurred to them that humans may not need medication to treat the low-serotonin symptom if the “something” that stress caused that keeps the low-serotonin symptom in place was removed.

A third finding was that inhibiting the lateral habenula area (proximal to the thalamus) with a drug relieved some depression-like behavior of the low-serotonin mice.

Okay, but one of the researchers went on to say:

“The next step is to figure out how we can turn off this brain region in a relatively non-invasive way that would have better therapeutic potential.”

Would everything would be fine if the low-serotonin mice just stopped displaying symptoms such as the depression-like behavior? Why no focus on causes, no forward thinking that maybe humans wouldn’t want part of their limbic system that performed many other functions to “turn off” just to suppress a symptom?

The researchers apparently didn’t realize their situation viz-à-viz the rabbit hole, as they circled back to the initial finding to develop a fourth finding – a possible reason that low-serotonin mice were more susceptible to stress was because a signaling molecule, β-catenin, wasn’t produced in a pathway that may be involved in resilience.

The news coverage added one more researcher quote:

“If we can identify what’s both upstream and downstream of β-catenin we might be able to come up with attractive drug targets to activate this pathway and promote resilience.”

If we treat a third-order symptom, the signaling molecule, everything will be alright?

Which leads me to ask: “Brain 5-HT deficiency increases stress vulnerability and impairs antidepressant responses following psychosocial stress”

Is it science, or is it a silly and sad farce when researchers “make up” missing data?

This 2014 French study was a parody of science.

The researchers “made up” missing data on over 50% of the men and over 47% of the women! All to satisfy their model that drove an agenda of the effects of adverse childhood experiences.

As an example of how silly and sad this was:

  • Two of the seven subject ages of interest were 23 and 33 consecutively, and
  • One of the nine factors was education level.

If I was a subject, and wasn’t around to give data at age 33 and later, how would the researchers have extrapolated a measurement of my education level of “high school” at age 23?

I’m pretty sure their imputation method would have “made up” education level data points for me of “high school” for ages 33 and beyond. I doubt that the model would have produced my actual education levels of a Bachelors and two Masters degrees at age 33.

Everything I said about the Problematic research on stress that will never make a contribution toward advancing science study applied to this study, including the “allostatic load” buzzword and the same compliant reviewer.

Studies like this both detract from science and are a misallocation of scarce resources. Their design and data aren’t able to reach levels where they can provide etiologic evidence.

Such studies also have limiting effects on how we “do something” about real problems, because the researchers won’t be permitted to produce findings that aren’t politically correct. “Adverse childhood experiences and physiological wear-and-tear in midlife: Findings from the 1958 British birth cohort”

One possible way that epigenetic DNA changes can pass from one generation to the next generation

This 2015 roundworm study showed one possible way that epigenetic DNA changes could pass from one generation to the next generation:

  • The researchers caused nerve cells to transmit double-stranded RNA to germline cells.
  • The RNA changed the germline cells, and
  • The changes were passed down to the next 25 generations.

This was a new direction that had several known limitations ahead. The researchers didn’t show that this transmission mechanism worked in nature. Also, more complex species don’t retain most epigenetic changes between generations.

However: “Double-stranded RNA made in C. elegans neurons can enter the germline and cause transgenerational gene silencing”

Dr. Arthur Janov interview on his 2011 book Life Before Birth: The hidden script that rules our lives

Dr. Arthur Janov’s 2011 book “Life Before Birth: The hidden script that rules our lives” describes problems that start in the earliest parts of our lives, when epigenetic changes due to trauma in the womb affect our development.

“The science has changed. When I first started out 44 years ago, there was nobody who could understand it, or agree, especially the professionals. Now all, or a great deal of the current research, is backing up everything I say.

I’m saying that this therapy is really a matter of life and death now. I should probably start at the beginning and say that there’s trauma in the womb. We need to set back the clock so that we take account of trauma that occurs while our mother is carrying that has lifelong consequences for how long we live, for example. There’s a current research study that shows that as you get more traumatized in the womb, your life expectancy is much shorter.

When you get rid of the childhood pain that happened way back when – and there are ways to do it – you will live much longer. So truly, a proper therapy now is a matter of life and death. Not only because your life expectancy is shorter when you have trauma, but you get sick earlier, you have diabetes, Alzheimer’s, all kinds of diseases on your way to your death, which makes life very uncomfortable.

But that’s just part of what we do. The idea is that we found a way to take the pain out of the system, going all the way back. And what we’re finding is that pain starts way, way earlier than we thought.

I used to think that the greatest point was the birth trauma. Well that’s no longer true. Way before the birth trauma there are traumas from the smoking mothers, the anxious mothers, the depressed mothers, that have lifelong effects on the baby, the offspring.”

This post has somehow become a target for spammers, and I’ve disabled comments. Readers can comment on other posts and indicate that they want their comment to apply here, and I’ll re-enable comments.

Research on brain areas involved when we imagine people, places, and pleasantness

This highly jargoned 2014 Harvard study was on how people imagine that they’ll feel in the future.

One of the researchers was an author of:

I was surprised that this study also didn’t ignore the limbic system to the point to where the researchers wouldn’t even bother to measure important areas.

Limbic system areas that process people were different than those that process places. For example, the data in Table S4 showed that the subjects’ left amygdala and hippocampus were more activated when simulating future familiar people, whereas their right hippocampus was more activated when simulating future familiar places.

The researchers may have improved the study’s findings if they were informed by studies such as the Hippocampus replays memories and preplays to extend memories into future scenarios, which found that “place” cells in the CA1 segment of the hippocampus preplay events that imagine future scenarios of:

“Novel spatial experiences of similar distinctiveness and complexity.”

Such information may have helped to disambiguate one of the study’s findings in Table S5, that both sides of the subjects’ hippocampus were more activated than other brain regions when simulating both familiar people and places.

The researchers got a little carried away in broadly attributing most of the study’s findings to the ventromedial prefrontal cortex. For example, the data in Table S6 showed that the thalamus was more activated when the subjects anticipated positive pleasantness, but not when negative effects were anticipated.

We know from Thalamus gating and control of the limbic system and cerebrum is a form of memory that this is normally how the thalamus part of the limbic system actively controls and gates information to and from the cerebrum. Their data showed thalamic gating in operation:

  • Active when passing along pleasantness to cerebral areas, and
  • Passive when blocking unpleasantness from cerebral areas.

Also, I didn’t see how the researchers differentiated some of their findings from a placebo effect. For example, Using expectations of oxytocin to induce positive placebo effects of touching is a cerebral exercise found:

“Pain reduction dampened sensory processing in the brain, whereas increased touch pleasantness increased sensory processing.”

This was very similar to the above finding involving the thalamus. “Ventromedial prefrontal cortex supports affective future simulation by integrating distributed knowledge”

Those of us who use painkillers rarely contemplate what pain it is that we’re targeting

Those of us who use painkillers rarely contemplate what pain it is that we’re targeting. For example, alcohol is a painkiller, but when we drink, do we focus on pain?

Detox centers work on the symptoms but seldom address the causes of the patient’s pain. Psychiatrists have no problem dispensing psychoactive medication for symptoms, but do have a problem dealing with the causes of the patient’s pain.

Patients address causes of their pain in Primal Therapy, as explained in the two short videos What is Primal Therapy by Dr. Arthur Janov and Dr. Arthur Janov Book Expo America 2008 Interview.

Painkillers can also kill us. This 2013 rodent study investigated “a potential therapeutic target for treatment of oxidative-stress related liver diseases” especially acetaminophen overdose.

Per one of this study’s references:

“Currently, the only clinically available treatment for acetaminophen overdose is N-acetyl-cysteine, a glutathione precursor, which has to be administered within 15–16 hours after acetaminophen ingestion to be effective.” “TRPM2 channels mediate acetaminophen-induced liver damage”

Dr. Arthur Janov Book Expo America 2008 Interview

“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.”

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.” “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?

  1. 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?
  2. 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.
  3. 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. “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.” “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? “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. “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. “Unconscious discrimination of social cues from eye whites in infants”