Research that identified the source of generating gamma brain waves

gettingwell4 2-3 stars Required further work, Acetylcholine, Cerebrum, Neurochemicals , , ,

This 2015 Harvard rodent study found that specific brain neurons trigger cortical band oscillations in the gamma wave length. The cell type:

“Has increased activity during waking and is involved in activating the cerebral cortex and generating gamma oscillations, enabling active cortical processing.

Cortical gamma band oscillations are correlated with conscious awareness.”

1. News coverage of the study misreported the research’s consciousness findings by regurgitating the Harvard press release word-for-word. Several speculations thrown in by the PR staff weren’t supported by the findings regarding:

  • “Awareness of consciousness;
  • Aware of the lower levels of consciousness and their contents.”

2. The researchers used optogenetic stimulation of neurons, similar to the Activation of brainstem neurons induces REM sleep study. The current study took the extra step of lesioning cholinergic neurons to ensure the activity studied was due to the target neurons.

3. The neurons generated gamma waves by simultaneously turning off all receptor neurons, then simultaneously switching them all back on. The researchers said:

“Our results are surprising and novel in indicating that this presumptively inhibitory”

neuron type acted this way.

http://www.pnas.org/content/112/11/3535.full “Cortically projecting basal forebrain parvalbumin neurons regulate cortical gamma band oscillations”

Pulling on the chain of causes and effects with insulin resistance

gettingwell4 0-1 star Wasted resources, Cortisol, Dopamine, Neurochemicals, Stress , , ,

This 2015 Harvard rodent study found multiple undesirable symptoms and attributed the cause to insulin resistance, which is itself a symptom.

Humans most often develop the symptom of insulin resistance due to causes other than genetics, such as a result of abnormal eating behaviors, which are symptoms of other causes.

Use of insulin-resistant-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 develop evidence for how “something” caused symptoms such as abnormal eating behaviors, that in turn caused a symptom of insulin resistance.

The study’s unexamined causes included why genetically insulin-resistant mice developed symptoms of anxiety and depressive-like behaviors between early adulthood and late middle age. Examples of undesirable symptoms described in the supplementary material included:

  • Higher body weight in late middle age, especially in females;
  • Depressive-like behavior in both sexes by late middle age;
  • Higher corticosterone levels in both sexes by late middle age, even when unstressed; and
  • Higher corticosterone levels in late middle age when stressed, especially in males.

It’s remarkable how researchers consistently get caught in a loop of studying only symptoms, paying little attention to studying causes, then suggesting various medications and treatments to suppress the studied symptoms.

It’s not surprising then that there’s no explanation of why and how symptoms develop. The study designs seldom include trying to show causes for the effects in the first place!

http://www.pnas.org/content/112/11/3463.full “Insulin resistance in brain alters dopamine turnover and causes behavioral disorders”

How do we assess “importance” in our lives? An example from scientists’ research choices

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This 2015 Virginia study found that scientists preferred research projects that had the potential to make:

“Deeper vs. broader contributions.

The scientists surveyed considered a hypothetical broader study, compared with an otherwise-comparable deeper study, to be riskier, a less-significant opportunity, and of lower potential importance.”

What were underlying motivations for subject scientists to become the Big Frogs in tiny puddles?

For example, if scientists recognized that there was an opportunity to positively influence a great number of human lives with a “broader” study, such as the hunger research proposed in Do the impacts of early experiences of hunger affect our behavior, thoughts, and feelings today? why would they prefer a “deeper” study such as starving fruit flies?

These researchers said that “scientists’ personal dispositions” accounted for this finding. I agree, but not for any of the specific reasons they stated.

Subjects’ “lower potential importance” judgments were key, and bear closer examination. The study’s supplementary material showed this consideration was made on a sliding scale in response to a question:

“Would you describe Project A (B) as potentially very important?”

The “lower potential importance” finding was an accumulation of each scientist’s personal judgment of a project described as:

“A broad project that spans several topical domains, including at least one that coincides with your area(s) of expertise and interest.

compared with:

“A focused and specialized project that fits your particular interests and leverages your deep expertise in a specific area.”

Weren’t personal judgments of the hypothetical project’s “potentially very important” aspect how each scientist predicted the project would make them feel important?

Given vague project descriptions in above quotations, I assert that their judgments’ contexts were “important to me” rather than “important to science” or “important to society” or important to some other context.

A relevant hypothesis of Dr. Arthur Janov’s Primal Therapy that applies to the “lower potential importance” finding is: the need to feel important is a defense against feeling unimportant due to early experiences of neglect.

Using principles referenced in the hunger post, the need to feel important is:

  1. A derivative need;
  2. A substitute for an unfulfilled need; and
  3. Caused by the impact of an early unmet need.

A corollary is that if an infant didn’t have early experiences of neglect, and their early needs were met, they likely wouldn’t develop derivative needs such as the need to feel important as they progressed through childhood, adolescence, and adulthood.

Are people motivated to act like the scientists who were subjects of this study? Do we make career and personal choices based on whether or not our work and other people make us feel important?

See my Welcome page and Scientific evidence page for further elaborations of this topic.

http://www.pnas.org/content/112/12/3653.full “Different personal propensities among scientists relate to deeper vs. broader knowledge contributions”

New role discovered for a speech area of the human prefrontal cortex

gettingwell4 2-3 stars Required further work, Brain hemispheres, Cerebrum

This 2015 human study found that an area in the left hemisphere of the prefrontal cortex involved with speech has characteristics not previously known:

“Broca’s area coordinates the transformation of information across large-scale cortical networks involved in spoken word production.”

The study found that this area:

“Disengages when we actually start to utter word sequences.”

It was previously thought that the Broca’s area was active during speech.

I looked throughout the study, footnotes and references, and couldn’t find the list of words that were used. The study would have shown more promise if the researchers had made an effort to include words with emotional content. For example, it’s possible that the Broca’s area may have different activation patterns when speaking with emotional content, or that it may account for part of the slowdown that normally occurs when we speak with feeling.

http://www.pnas.org/content/112/9/2871.full “Redefining the role of Broca’s area in speech”

Do the impacts of early experiences of hunger affect our behavior, thoughts, and feelings today?

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This 2015 worldwide human study Hunger promotes acquisition of nonfood objects found that people’s current degree of hungriness affected their propensity to acquire nonfood items.

The researchers admitted that they didn’t demonstrate cause and effect with the five experiments they performed, although the findings had merit. News articles poked good-natured fun at the findings with headlines such as “Why Hungry People Want More Binder Clips.”

The research caught my eye with these statements:

“Hunger’s influence extends beyond food consumption to the acquisition of nonfood items that cannot satisfy the underlying need.

We conclude that a basic biologically based motivation can affect substantively unrelated behaviors that cannot satisfy the motivation.”

The concept of the quotes relates to a principle of Dr. Arthur Janov’s Primal Therapy – symbolic satisfaction of needs.

I stated two fundamentals of Primal Therapy in An agenda-driven study on beliefs, smoking and addiction that found nothing of substance:

  1. The physiological impacts of our early unmet needs drive our behavior, thoughts, and feelings.
  2. The painful impacts of our unfulfilled needs impel us to be constantly vigilant for some way to fulfill them.

Corollary principles of Primal Therapy are:

  • Our present efforts to fulfill our early unmet needs will seldom be satisfying. It’s too late.
  • We acquire substitutes now for what we really needed back then.
  • Acquiring these symbols of our early unmet needs may, at best, temporarily satisfy derivative needs.

But the symbolic satisfaction of derived needs – the symptoms – never resolves the impacts of early unfulfilled needs – the motivating causes:

  • We repeat the acquisition behavior, and get caught in a circle of acting out our feelings and impulses driven by these conditions.
  • The unconscious act-outs become sources of misery both to us and to the people around us.

In his book “Primal Healing” Dr. Arthur Janov gives two examples of critical periods only during which early needs can be satisfied:

  1. Being touched in the first months of life is crucial to a child’s development. The lack of close contact after the age of 5 wouldn’t have the same effect.
  2. Conversely, the need for praise at 6 months of age may not be essential, but it’s crucial for children at age 5.

As this study’s finding showed, there’s every reason for us to want researchers to provide a factual blueprint of causes for our hunger sensation effects, such as “unrelated behaviors that cannot satisfy the motivation.”

Why not start with hunger research? Objectives of the research should include answering:

  • What enduring physiological changes occurred as a result of past hunger?
  • How do these changes affect the subjects’ present behaviors, thoughts, and feelings?

Hunger research that would likely provide causal evidence for the effect of why people acquire “items that cannot satisfy the underlying need” should include studying where to start the timelines for the impacts of hunger. The impacts would potentially go back at least to infancy when we were completely dependent on our caregivers.

Infants can’t get up to go to the refrigerator to satisfy their hunger. All a hungry infant can do is call attention to their need, and feel pain from the deprivation of their need.

Is infancy far back enough, though, to understand the beginnings of potential impacts of hunger? The Non-PC alert: Treating the mother’s obesity symptoms positively affects the post-surgery offspring study referenced an older study of how the hunger of mothers-to-be had lifelong ill effects for the fetuses they carried during the Dutch hunger winter of 1944. The exposed children had epigenetic DNA changes from their mothers’ starvation, which resulted in relative obesity compared with their unexposed siblings.

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

gettingwell4 < 0 Detracted from science, Beliefs, Cerebrum, Primal Therapy ,

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.

http://www.pnas.org/content/112/8/2539.full “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

gettingwell4 0-1 star Wasted resources, Limbic system, Neurochemicals, Serotonin, Stress, Thalamus ,

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:

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?

gettingwell4 < 0 Detracted from science, Brain development, Epigenetics, Hippocampus, Limbic system, Stress , , ,

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.

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

gettingwell4 2-3 stars Required further work, Epigenetics

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:

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

gettingwell4 4-5 stars Advanced knowledge, Brain development, Cerebrum, Cortisol, Epigenetics, Limbic system, Lower brain, Neurochemicals, Primal Therapy, Stress, Telomeres , , , , , ,

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.”

“https://www.youtube.com/watch?v=dbUhjZhpEyct”

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

gettingwell4 2-3 stars Required further work, Amygdala, Beliefs, Brain hemispheres, Cerebrum, Hippocampus, Limbic system, Thalamus ,

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.

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

gettingwell4 2-3 stars Required further work, Primal Therapy , ,

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.”

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

Dr. Arthur Janov Book Expo America 2008 Interview

gettingwell4 4-5 stars Advanced knowledge, Cerebrum, Limbic system, Lower brain, Primal Therapy , ,

“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

gettingwell4 2-3 stars Required further work, Beliefs, Cerebrum, Primal Therapy

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

gettingwell4 4-5 stars Advanced knowledge, Brainstem, Cerebrum, Limbic system, Lower brain, Primal Therapy , , , ,

“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.”