Neurochemicals

Assessing a mountain climber’s condition without noticing their empty backpack

gettingwell4 2-3 stars Required further work, Acetylcholine, Cortisol, Neurochemicals, Stress

A metaphor: for a mountain climber, which point has the most influence on their condition during the climb?

  • The path ahead?
  • The current situation?
  • The recent past?
  • The starting point?
  • The preparations?

Hard to say? Once the climb has started and until it’s finished, though, are there any points at which the preparations have no influence?

Let’s imagine that factors beyond the climber’s control ruined their preparations, leaving them with no reserves and a limited capability to adapt to environmental changes.

Let’s imagine further that researchers take initial physical and psychological measurements of the climber’s condition at an arbitrary point of the ascent or descent. Due to the design of their measurement system, however, they don’t discover that this climber has an empty backpack.

When the researchers interpret the results, will they understand how the climber’s measurements were influenced by the ruined preparations?  end metaphor

A 2014 Israeli study primary finding was of:

“Fear of terror-induced annual increases in resting heart rate.”

The researchers took 325 measurements each “of 17,380 apparently healthy volunteers” who had “consistent exposure to terror threats.”

The study was opaque in some areas. For example, what was the content and handling of a 4-item anxiety questionnaire?

The supplementary material showed that the headlined “fear of terror” term involved three disparate factors:

  • feeling unsafe;
  • fear of crowds; and
  • anxiety about future harm.

I’d like to understand the bases of why the researchers and the reviewer felt it was appropriate that:

“The scores on these items were averaged to yield a continuous FOT [fear-of-terror] score.”

The researchers probably had sufficient measurements of the subjects’ current conditions. They didn’t have a frame of reference that incorporated the present data with contextual information from each individual’s history back to the earliest parts of their life.

Lacking the links provided by such a framework, the researchers likely misassessed measurements that were influenced by how the subjects’ backpacks were packed.

http://www.pnas.org/content/112/5/E467.full “Fear and C-reactive protein cosynergize annual pulse increases in healthy adults”

A common dietary supplement that has rapid and lasting antidepressant effects

gettingwell4 4-5 stars Advanced knowledge, Cerebrum, Epigenetics, Glutamate, Hippocampus, Limbic system, Neurochemicals, Stress , , ,

This 2012 Italian rodent study found that a common dietary supplement had rapid and lasting antidepressant effects:

“Remarkably, L-acetylcarnitine displayed a clear-cut antidepressant effect already after 3 and 7 d[ays] of daily dosing. No tolerance was developed to the action of L-acetylcarnitine. The drug was even more effective after 21 d[ays], and the effect persisted for at least 2 w[ee]k[s] after drug withdrawal.”

The researchers studied stressed mice and rats to determine that:

  1. An effect of the stress was to epigenetically change the hippocampus to produce less of an important molecule – type 2 metabotropic glutamate (mGlu2).
  2. A reduction of the mGlu2 molecule decreased the hippocampus’ regulation of the glutamate neurotransmitter.
  3. Under-regulation of glutamate, in turn, caused symptoms of depression.

L-acetylcarnitine reversed the immediate causes of stress-induced symptoms by acetylating histone proteins. These control the transcription of the brain-derived neurotrophic factor (BDNF) and mGlu2 receptors in the hippocampus and prefrontal cortex.

LAC putative action

A commentary on this research, Next generation antidepressants, had the above graphic that showed possible mechanisms for the effects of L-acetylcarnitine. Epigenetic histone modifications seem to be more easily reversible than epigenetic DNA methylation.

“Currently, depression is diagnosed only by its symptoms,” Nasca says. “But these results put us on track to discover molecular signatures in humans that may have the potential to serve as markers for certain types of depression.”

It’s tempting to extrapolate this study to humans and test whether depression symptoms could be effectively treated with some multiple of a normal acetyl-L-carnitine dietary supplement dose of 500 mg at $.25 a day. This dietary supplement is better for depression symptoms than placebo analyzed randomized control trials that tested and demonstrated its efficacy.

To cure stress-induced illnesses in humans, though, ultimate causes of stress should be removed or otherwise addressed.

http://www.pnas.org/content/110/12/4804.full “L-acetylcarnitine causes rapid antidepressant effects through the epigenetic induction of mGlu2 receptors”

The hypothalamus’ role in how calorie restriction delays aging

gettingwell4 4-5 stars Advanced knowledge, Hypothalamus, Limbic system, Neurochemicals

This 2015 Portuguese rodent study showed the underlying mechanism to explain why restricting calories delays aging.

A calorie reduction of 20 to 40% increased production of a normally occurring molecule (neuropeptide Y) in the hypothalamus part of the limbic system. The increased amounts of the molecule stimulated autophagy (the breakdown and recycling of cellular components) in hypothalamic neurons.

“Because both hypothalamic autophagy and neuropeptide Y levels decrease with age..modulation of hypothalamic neuropeptide Y levels may be considered a potential strategy to produce protective effects against hypothalamic impairments associated with age and to delay aging.”

http://www.pnas.org/content/112/13/E1642.full “Neuropeptide Y stimulates autophagy in hypothalamic neurons”

Epigenetic DNA methylation and demethylation with the developing fetus

gettingwell4 5+ stars Premium, Brain development, Cortisol, Epigenetics, Hypothalamus, Limbic system, Neurochemicals, Oxytocin, Serotonin , ,

This extremely dense and informative 2014 UK summary study provided details about genomic imprinting:

“An unusual epigenetic process in that it is heritable and results in autosomal gene expression according to parent of origin.”

Several notes of interest:

  • Figure 3 had a fascinating sketch of how the fetus caused the mother’s hypothalamus to:

    “Determine forward maternal planning by directing/orchestrating maternal physiology and postnatal maternalism to synchronize with development of the fetus.”

  • Figure 4 followed up with a flowchart of how – with a female fetus – coexistence of three matrilineal generations in the pregnant female (her, the fetus, and the grandmother’s influence on the developing fetus’ ovarian oocytes) enabled intergenerational forward planning.
  • The study briefly noted significance of genomic imprinting on male sexual behavior, where, if processes didn’t proceed normally at this early stage of a male fetus’ development, could result in suboptimal adult behavior that didn’t change with experience.

F4.large

I’ll quote a few other unrelated passages that caught my eye.

“Reproductive success of mammals also places a considerable burden on matrilineal time and energy, with some 95% of mammalian female adult life committed to pregnancy, lactation, and maternal care.

Offspring that receive optimal nourishment and improved maternal care will be predisposed to develop a hypothalamus that is both genetically and epigenetically predisposed to this same type of good mothering.

The fetus controls its own destiny in times of acute starvation, especially in the last trimester of pregnancy, by short-term sacrifice of its placenta to preserve resources critical for brain development.”

http://www.pnas.org/content/112/22/6834.full “Genomic imprinting, action, and interaction of maternal and fetal genomes”

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Epigenetic DNA methylation of the oxytocin receptor gene affected the perception of anger and fear

gettingwell4 2-3 stars Required further work, Amygdala, Anterior cingulate cortex, Brain development, Brain hemispheres, Cerebrum, Epigenetics, Hippocampus, Limbic system, Neurochemicals, Oxytocin, Thalamus ,

This 2015 Virginia human study:

“Reveals how epigenetic variability in the endogenous oxytocin system impacts brain systems supporting social cognition and is an important step to better characterize relationships between genes, brain, and behavior.”

The researchers did a lot of things right:

  • They studied a priori selected brain areas, followed by whole brain analyses;
  • Their subjects were carefully selected

    “Because methylation levels have been shown to differ as a function of race, we restricted our sample to Caucasians of European descent”

    but they didn’t restrict subjects to the same gender;

  • They acknowledged as a limitation:

    “A lack of behavioral evidence to reveal how these epigenetic and neural markers impact the overt social phenotype.”

One thing on which I disagree with the researchers is their assessment of what needs to be done next. Their news release stated:

“When imagining the future possibilities and implications this DNA methylation and oxytocin receptor research may have, the investigators think a blood test could be developed in order to predict how an individual may behave in social situations.”

Nice idea, but the next step should be to complete the research. The next step is to develop evidence for how the oxytocin receptor gene became methylated.

The subjects had a wide range of DNA methylation at the studied gene site – from 33% to 72% methylated!

Why?

At the same gene site:

“There was a significant effect of sex such that females have a higher level of methylation than males.”

Why?

Given these significant effects, why was there no research into likely causes?

Aren’t early periods in people’s lives the most likely times when the “Epigenetic modification of the oxytocin receptor gene” that “influences the perception of anger and fear in the human brain” takes place?

Wouldn’t findings from research on the subjects’ histories potentially help other people?

http://www.pnas.org/content/112/11/3308.full “Epigenetic modification of the oxytocin receptor gene influences the perception of anger and fear in the human brain”

Oxytocin blocks alcohol intoxication symptoms

gettingwell4 4-5 stars Advanced knowledge, Neurochemicals, Oxytocin, Vasopressin

This joint 2015 Australian/German rodent study found that oxytocin bound to the brain receptors that cause loss of motor control with alcohol intoxication, and prevented rats from displaying these symptoms:

“While oxytocin might reduce your level of intoxication, it won’t actually change your blood alcohol level,” Dr Bowen said. “This is because the oxytocin is preventing the alcohol from accessing the sites in the brain that make you intoxicated, it is not causing the alcohol to leave your system any faster.”

Vasopressin didn’t have the same effect.

The level of alcohol used to produce this finding was roughly equivalent to a human drinking a bottle of wine over a few hours. Oxytocin didn’t prevent loss of motor control when the equivalent of a bottle of vodka was administered because the excess ethanol found its way into other brain receptors and put the rats to sleep.

The study showed oxytocin acting in its original functionalities such as water regulation rather than with its evolved social functions as described in How oxytocin and vasopressin were repurposed through evolution to serve social functions.

http://www.pnas.org/content/112/10/3104.full “Oxytocin prevents ethanol actions at δ subunit-containing GABA-A receptors and attenuates ethanol-induced motor impairment in rats”

Why do we cut short our decision-making process?

gettingwell4 5+ stars Premium, Beliefs, Cerebrum, Dopamine, Limbic system, Memory, Neurochemicals, Serotonin , , ,

This 2014 Zurich study found that people adapt their goal-directed decision-making processes in certain ways.

First, the researchers found that the subjects usually acted as though the computational cost of evaluating all outcomes became too high once the process expanded to three or more levels. Their approach to a goal involved developing subgoals. For example, for a three-level goal:

“Level 3 was most frequently decomposed into a tree of depth 2 followed by a depth-1 tree.”

A level 3 tree had 24 potential outcomes (24 outcomes = 3*2x2x2) whereas a level 2 tree followed by a level 1 tree had 10 potential outcomes (10 outcomes = 2*2×2 + 1*2).

Second, the subjects memorized and reused subgoals after their initial formation. The researchers found that this practice didn’t produce results significantly different than the optimal solutions, but that could have been due to the study’s particular design. The design also ensured that the subjects’ use of subgoals wasn’t influenced by rewards.

Further:

“It is known that nonhuman primate choices, for instance, depend substantially on their own past choices, above and beyond the rewards associated with the decisions. Similar arguments have been made for human choices in a variety of tasks and settings and have been argued to be under dopaminergic and serotonergic control.”

Third, ALL 37 subjects were unwilling to evaluate decisions that had initial large losses, even if they could see that the path to reach the optimal solution went through this loss outcome! The researchers termed this behavior “pruning” and stated:

“Pruning is a Pavlovian and reflexive response to aversive outcomes.”

The lead author relied on a previous study he coauthored to elaborate on the third finding. One statement in the previous study was:

“This theory predicts excessive pruning to occur in subjects at risk for depression, and reduced pruning to occur during a depressive episode.”

The current study’s subjects were screened out for depressive conditions, though. They were somewhat conditioned by the study design, but not to the extent where their behavior could be characterized as Pavlovian responses.

Fourth, the subjects’ use of larger subgoals wasn’t correlated to their verbal IQ.

So, what can we make of this research?

  1. Are shortcuts to our decision processes strictly a cerebral exercise per the first and second findings?
  2. Do we recycle our decision shortcuts like our primate relatives, uninfluenced by current rewards?
  3. Or is it rewarding to just not fully evaluate all of our alternatives?
  4. Do all of us always back away from decisions involving an initial painful loss, even when we may see the possibility of gaining a better outcome by persevering through the loss?
  5. Is it true that we excessively cut decision processes too short – such that many of our decisions are suboptimal – when we’re on our way to becoming depressed?
  6. Are we overwhelmed when depressed such that we don’t summon up the effort to cut short or otherwise evaluate decisional input?

Let me know your point of view.

http://www.pnas.org/content/112/10/3098.full “Interplay of approximate planning strategies”

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”

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”

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”

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A biologically relevant event can drive long-term memory in a single training session

gettingwell4 2-3 stars Required further work, Brain development, Dopamine, Epigenetics, Memory, Neurochemicals

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

gettingwell4 < 0 Detracted from science, Cortisol, Neurochemicals, Stress

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”

What is the purpose of music? A review of evolutionary and pleasurable research findings

gettingwell4 2-3 stars Required further work, Amygdala, Anterior cingulate cortex, Cerebrum, Dopamine, Hippocampus, Hypothalamus, Limbic system, Lower brain, Neurochemicals

Ever wonder what happens in your brain and body when you get chills from a musical performance?

This 2013 summary review of 126 studies provided details of brain areas that contribute to our enjoyment of music.

Much of the review addressed Darwin’s observation that music had no readily apparent functional consequence and no clear-cut adaptive function. The researchers noted that:

“There is scant evidence that other species possess the mental machinery to decode music in the way humans do, or to derive enjoyment from it.”

The reasons why different types of music affect us differently are similar to the findings of the Reciprocity behaviors differ as to whether we seek cerebral vs. limbic system rewards study.

Here are the “We seek limbic system rewards” similarities:

“The nucleus accumbens played an important role with both familiar and novel music. In the case of familiar music, hemodynamic activity in the nucleus accumbens was associated with increasing pleasure, and maximally expressed during the experience of chills, which represent the peak emotional response; these were the same regions that showed dopamine release. The nucleus accumbens is tightly connected with subcortical limbic areas of the brain, implicated in processing, detecting, and expressing emotions, including the amygdala and hippocampus. It is also connected to the hypothalamus, insula, and anterior cingulate cortex, all of which are implicated in controlling the autonomic nervous system, and may be responsible for the psychophysiological phenomena associated with listening to music and emotional arousal.”

Here is the “We seek cerebral rewards” part.

“Finally, the nucleus accumbens is tightly integrated with cortical areas implicated in “high-level” processing of emotions that integrate information from various sources, including the orbital and ventromedial frontal lobe. These areas are largely implicated in assigning and maintaining reward value to stimuli and may be critical in evaluating the significance of abstract stimuli that we consider pleasurable.”

http://www.pnas.org/content/110/Supplement_2/10430.full “From perception to pleasure: Music and its neural substrates”

Using expectations of oxytocin to induce positive placebo effects of touching

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

This 2013 Scandinavian study detailed which brain structures were involved when fooling oneself about actual sensations in favor of expected sensations.

It was hilarious how the researchers used studies of oxytocin to create expectations in the subjects:

“To induce expectation of intranasal oxytocin’s beneficial effects on painful and pleasant touch experience, participants viewed a 6-min locally developed video documentary about oxytocin’s putative prosocial effects such as involvement in bonding, love, grooming, affective touch, and healing. As all of the material was based on published research, there was no deception. The video concluded that a nasal spray of oxytocin might enhance the pleasantness of:

  • (i) stroking and
  • (ii) warm touch, and
  • (iii) reduce the unpleasantness of pain.”

Other items:

  • Only the placebo effects for the warm and pain-reducing touches were statistically significant, not the stroking touch;
  • The a priori brain areas monitored in the “sensory circuitry” included the thalamus and were all in the right brain hemisphere;
  • The a priori brain areas monitored in the “emotional appraisal circuitry” included the amygdala.

One way the researchers summarized the study was:

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

This finding demonstrated how the thalamus part of the limbic system actively controls and gates information to and from the cerebrum, similar to the Thalamus gating and control of the limbic system and cerebrum is a form of memory study.

There was a terminology problem in the study, evidenced by statements such as:

“We induced placebo improvement of both negative and positive feelings (painful and pleasant touch).”

Touch is a sensation, not a feeling or emotion. This placebo study created expectations of sensations in the subjects’ cerebrums, not expectations of emotions.

Also, including parts of the limbic system such as the amygdala in the “emotional appraisal circuitry” didn’t mean that the researchers studied feelings or emotions. We know from research summarized in the Conscious mental states should not be the first-choice explanation of behavior study that:

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

The current study cast additional light on the dubious Problematic research on human happiness study. Those researchers were fooled by a positive placebo effect!

http://www.pnas.org/content/110/44/17993.full “Placebo improves pleasure and pain through opposite modulation of sensory processing”