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.

One of the principles 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.

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 ensure that we are on the qui vive, impelled 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.

One 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 behaviors and expressions of thoughts and feelings. Click the Beliefs category or tag 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?

Well, nothing new, really. The study was all about the effects, the symptoms.

I saw:

  • Nothing about impelling physical conditions and causes,
  • Nothing about what primarily drives people’s beliefs and addiction behaviors, and
  • Nothing about 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, and beliefs can 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.


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.”

We know that any therapeutic approach won’t supply the addicting substance, which leaves just the beliefs and their required constant reinforcement. It sounded to me like the research provided details about an approach that wasn’t capable of anything more than temporarily suppressing symptoms.

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 neither contributed to advancing science nor to really helping people.

http://www.pnas.org/content/112/8/2539.full “Belief about nicotine selectively modulates value and reward prediction error signals in smokers”

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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.

So, 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 part of the limbic system) 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.”

So, everything would be fine if the low-serotonin mice would just stop displaying symptoms such as the depression-like behavior? 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.”

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

Which leads me to ask:

  • Will the causes of human problems be found by studying second- and third-order symptoms of serotonin and β-catenin molecules?
  • Will the causes be found by using drugs that turn off or turn on parts of the brain to display fewer symptoms?
  • And as I ask in If research provides evidence for the causes of stress-related disorders, why only focus on treating the symptoms? where is the research on treating the “somethings” – the enduring physiological responses to stress – with goals for reversing them, instead of ignoring the causes and only treating the effects?

http://www.pnas.org/content/112/8/2557.full “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, in my view.

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 are a misallocation of scarce resources. The design and data of such studies 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.

See the Early emotional experiences change our brains: Childhood maltreatment is associated with reduced volume in the hippocampus study as an example of the proper use of the Adverse Childhood Experiences survey. That study contributed to science, and showed causes and effects:

“The strongest associations between maltreatment and volume were observed in the left CA2-CA3 and CA4-DG subfields, and were not mediated by histories of major depression or posttraumatic stress disorder.

These findings support the hypothesis that exposure to early stress in humans, as in other animals, affects hippocampal subfield development.”

http://www.pnas.org/content/112/7/E738.full “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 complicated species don’t retain most of the epigenetic changes between generations.

However:

http://www.pnas.org/content/112/7/2133.full “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.”

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 study may have improved its findings if the researchers 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 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.

http://www.pnas.org/content/111/46/16550.full “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.”

NAC is an inexpensive daily supplement that helps people maintain glutathione levels. Glutathione is one of the two endogenous antioxidants we have, with SOD being the other.

http://www.pnas.org/content/111/8/3176.full “TRPM2 channels mediate acetaminophen-induced liver damage”