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The Inflammatory Reflex - HDW's Learning Log

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#181 HighDesertWizard

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Posted 14 December 2018 - 11:08 AM

Thinking about The Inflammatory Reflex, Bee Products, and my hypothesis from back on 2017-07-03 (that TIR was the Mechanism of Action of TA-65).... Note that the following study supports my hypothesis...

 

I'll describe how and reference this study down thread after a specific slide still to be posted... Posting this now as long as the topic of bees is on the table.

 

2015, The relationship between telomere length and beekeeping among Malaysians

 

The belief that beekeepers live longer than anyone else is present since ages. However, no research has been done to explore the longevity of life in beekeepers. Here, we investigated the telomere length in 30 male beekeepers and 30 male non-beekeepers and associated them with the longevity of life using Southern analysis of terminal restriction fragments (TRFs) generated by Hinf I/Rsa I digestion of human genomic DNA using TeloTAGGG Telomere Length Assay. Interestingly, we found that the telomere length of male beekeepers was significantly longer than those of male non-beekeepers with a p value of less than 0.05, suggesting that beekeepers may have longer life compared to non-beekeepers. We further found that the consumption of bee products for a long period and frequent consumption of bee products per day are associated with telomere length. An increase of year in consuming bee products is associated with a mean increase in telomere length of 0.258 kbp. In addition, an increase in frequency of eating bee products per day was also associated with a mean increase of 2.66 kbp in telomere length. These results suggested that bee products might play some roles in telomere length maintenance.

 


Edited by HighDesertWizard, 14 December 2018 - 11:13 AM.

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#182 QuestforLife

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Posted 14 December 2018 - 02:14 PM

Sounds like there is a link with mitochondrial fusion and telomere elongation if RJ is renewing stem cells. So definitely overlap with Turnbuckles Stem Cell Protocol and my Alternative Methods for Lengthening Telomeres, both of which use this mechanism.
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#183 Nate-2004

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Posted 14 December 2018 - 06:20 PM

Sounds like there is a link with mitochondrial fusion and telomere elongation if RJ is renewing stem cells. So definitely overlap with Turnbuckles Stem Cell Protocol and my Alternative Methods for Lengthening Telomeres, both of which use this mechanism.

 

Guess I should add this to the protocol then. About to do it again after my 5 day fast next week.


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#184 HighDesertWizard

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Posted 08 January 2019 - 02:21 AM

Thinking about The Inflammatory Reflex, Bee Products, and my hypothesis from back on 2017-07-03 (that TIR was the Mechanism of Action of TA-65).... Note that the following study supports my hypothesis...

 

I'll describe how and reference this study down thread after a specific slide still to be posted... Posting this now as long as the topic of bees is on the table.

 

2015, The relationship between telomere length and beekeeping among Malaysians

 

The belief that beekeepers live longer than anyone else is present since ages. However, no research has been done to explore the longevity of life in beekeepers. Here, we investigated the telomere length in 30 male beekeepers and 30 male non-beekeepers and associated them with the longevity of life using Southern analysis of terminal restriction fragments (TRFs) generated by Hinf I/Rsa I digestion of human genomic DNA using TeloTAGGG Telomere Length Assay. Interestingly, we found that the telomere length of male beekeepers was significantly longer than those of male non-beekeepers with a p value of less than 0.05, suggesting that beekeepers may have longer life compared to non-beekeepers. We further found that the consumption of bee products for a long period and frequent consumption of bee products per day are associated with telomere length. An increase of year in consuming bee products is associated with a mean increase in telomere length of 0.258 kbp. In addition, an increase in frequency of eating bee products per day was also associated with a mean increase of 2.66 kbp in telomere length. These results suggested that bee products might play some roles in telomere length maintenance.

 

I've been taking this Royal Jelly product for 6 or 7 days a week since mid-December. Finally hit upon the best way to apportion it from the larger container.

 

It's not bad tasting, not especially greater either. If I dose much larger than 1/2 teaspoon I feel nauseous. Nothing else to report at this point.


Edited by HighDesertWizard, 08 January 2019 - 02:23 AM.

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#185 QuestforLife

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Posted 08 January 2019 - 11:48 AM

I've been taking this Royal Jelly product for 6 or 7 days a week since mid-December. Finally hit upon the best way to apportion it from the larger container.

 

It's not bad tasting, not especially greater either. If I dose much larger than 1/2 teaspoon I feel nauseous. Nothing else to report at this point.

 

I'm quite excited based on this paper (https://www.nature.c...467-018-06256-4) about the potential of Royal Jelly to maintain stemness.

 

I am considering adding it to my next iteration of my statin+sartan protocol, which I'm using to increase progenitor cell numbers and telomere length.



#186 QuestforLife

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Posted 09 January 2019 - 02:02 PM

I've been taking this Royal Jelly product for 6 or 7 days a week since mid-December. Finally hit upon the best way to apportion it from the larger container.

 

It's not bad tasting, not especially greater either. If I dose much larger than 1/2 teaspoon I feel nauseous. Nothing else to report at this point.

 

What dose in grams are you taking, approximately? Very rough calculation you're going to need 15g/day to scale up the actual royal jelly proteins to the level in the Nature in vitro study (and that's not accounting for the fact not all that protein will be royalactin).

 

Good news is the beekeepers in the other study obviously benefited and it's doubtful they ate THAT much honey!



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#187 HighDesertWizard

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Posted 16 January 2019 - 08:31 PM

The (great) Levine et al paper, specifically on Phenotypic Age (and Phenotypic Age Acceleration) based on blood biomarkers (and age) is now out (Dec 31, 2018) validated on the NHANES IV cohort. See:

 

Liu Z, Kuo PL, Horvath S, Crimmins E, Ferrucci L, Levine M. A new aging measure captures morbidity and mortality risk across diverse subpopulations from NHANES IV: A cohort study. PLoS Med. 2018;15(12):e1002718.

https://journals.plo...al.pmed.1002718

 

"...Phenotypic Age was calculated based on a linear combination of chronological age and 9 multi-system clinical chemistry biomarkers in accordance with our previously established method. We also estimated Phenotypic Age Acceleration (PhenoAgeAccel), which represents Phenotypic Age after accounting for chronological age (i.e., whether a person appears older [positive value] or younger [negative value] than expected, physiologically). All analyses were conducted using NHANES IV (1999–2010, an independent sample from that originally used to develop the measure)..."

 

This follows on the previous paper "An epigenetic biomarker of aging for lifespan and healthspan" which is also discussed in this thread as potentially actionable to us, see: https://www.longecit...ndpost&p=862525

 

 

albedo... Thanks for posting this study by Levine / Horvath.

  • I've been on the lookout for this kind of study for a while. That is, I've been looking for solid studies that focus on Survival Probability in the future given some state of health.

I think it's important to highlight a few of the graphic figures of the study.

 

 

yHtGFYe.png

 

 

 

gHrtYYD.png

 

 

ygg5eR4.png

 

 

 

This last pic is especially interesting. The Area Under the Curve (AUC) is a measure of the sensitivity/impact of the independent variable on Survival Probability.

 

It makes clear that fighting specific diseases we find ourselves having is an important objective.

 

 

Yes, and we might add the Table 1 which makes your point more explicit: look e.g. at the importance to have sugar control under check (diabetes) and well functioning kidneys (nephritis/nephrosis) both with a HR of ~20%. We knew this already but what is important here is Phenotypic Age is very well predictive of this, because of its construct, and can possibly guide specific tests and successive treatments in the clinical setting: as the authors write (bold mine):

 

"...we found that Phenotypic Age was predictive of disease-specific mortality including heart disease, cancer, chronic lower respiratory disease, diabetes, influenza/pneumonia, and nephritis/nephrosis, with exception of cerebrovascular disease mortality (HR = 1.03, 95% CI = 0.98–1.09). HRs were the highest for diabetes and nephritis/nephrosis, suggesting that a 1-year increase in Phenotypic Age relative to chronological age increases the risks of death from these causes by about 20%. For the other causes (aside from cerebrovascular disease), a 1-year increase in Phenotypic Age increased risk by between 7% (cancer and chronic lower respiratory disease) and 12% (influenza/pneumonia)..."
 

post-16306-0-86589100-1547632906_thumb.p

 

 

 

The science documented in the comments above highlights the fact that Disease, per se, is a fundamental driver of diminished, personal Survival Probability.

Take a close look, the Survival Curves shown in this post resemble the kinds of Survival Probability curves I've posted upthread that are driven by triggering of The Inflammatory Reflex.

The key point to consider here is a point first made by Kevin Tracey, the premier research scientist of The Inflammatory Reflex, in his 2014 essay, Approaching the Next Revolution? Evolutionary Integration of Neural and Immune Pathogen Sensing and Response.

 

 

 

<SNIP>

Until quite recently, however, the existence of regulatory reflexes exerting control over the immune system had evaded description. Immunological thinking had not viewed immunity as a reflexively regulated response.

 

REFLEX REGULATION OF INNATE IMMUNITY

This began to change following the discovery that cytokines produced in response to infection and injury are necessary and sufficient mediators in disease pathogenesis. This provided experimental tools and strategies that enabled the illumination of neural circuits that regulate innate immunity. Termed “the cytokine theory of disease,” cytokines produced in response to infection and injury mediate cellular, metabolic, and pathological effects underlying the major physiological and clinical manifestations of illness (Tracey 2007). Restated, disease occurs when there is a loss of immunological homeostasis producing an unbalanced or excessive cytokine response. In such cases, inhibiting or modulating the cytokine response to restore immunological homeostasis can prevent or reverse disease, and it should be stressed that the cytokine theory does not state that all cytokines are “bad.” By analogy, the germ theory does not state that all microbes are pathogenic. Rather, the cytokine theory indicates that in some instances of cytokine imbalance or excess, treatment of diseases can be specifically accomplished with targeted therapeutics.

The cytokine theory of disease was validated in mammals, including humans, within a few years after early direct evidence became available that tumor necrosis factor (TNF) is a necessary and sufficient mediator of acute septic shock during infection (Tracey et al. 19861987). The first principles for administering anti-TNF monoclonal antibodies as therapy were established in baboons infected withEscherichia coli (Tracey et al. 1987). Treated animals survived despite the presence of replicating bacteria in their bloodstream, proving that the disease (septic shock) required the activity of TNF. Disease was attributable to the activity of the cytokine, regardless of the status of the pathogen (Tracey et al. 1987). Today it is common to witness this principle being applied to patients receiving monoclonal anti-TNF for the treatment of rheumatoid arthritis, inflammatory bowel disease, and other conditions. From a practical point of view, the earliest underlying or inciting etiological agent can be dissociated from the disease. The physician standing at the patient’s bedside is witness to signs and symptoms of inflammation, organ damage, and toxicity mediated by the direct action of cytokines. In many, if not most, diseases, excessive cytokine activity can be considered as a failure of immunological homeostasis.

 

 

 

There's a new net discovery of all this relatively new science...

  • The fact of the existence of The Inflammatory Reflex itself in humans.
     
  • The fact of the positive impact of Inflammatory Reflex triggering on Survival Probability.
     
  • The fact that the cytokine theory of disease has been validated.
     
  • And, now, just within the last couple of months, the demonstration in the study linked to above by albedo that Disease Count, per se, is an impactful variable on Survival Probability...

 

 

The Inflammatory Cytokine Explanation of Diminished Survival Probability has now been Validated.

 -- Steve Buss, January 2019


Edited by HighDesertWizard, 16 January 2019 - 08:49 PM.


#188 HighDesertWizard

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Posted 23 January 2019 - 04:12 PM

And now for something completely different than anything I've written about The Inflammatory Reflex in the past...
 
The Inflammatory Reflex is a reflex in a way comparable to other sensory and motor reflexes. Among the most often cited examples is the Hand-on-a-Burning Stove example.
 
Put your finger or hand on a hot surface and almost immediately, there is a response to pull it away. The Sensory (aka, Afferent) arm of the Reflex senses the extreme heat and a signal proceeds up this Sensory Neuron to an InterNeuron which, first, processes the signal, and then sends the Pull-It-Away signal via Motor (aka, Efferent) Neurons, and the arm is pulled away. See the figure that illustrates the point.
 
8HucmhBh.png
 
Now, up to this time, I've only been posting about the Motor (Efferent) arm of The Inflammatory Reflex. But there is a Sensory (Afferent) arm and Kevin Tracey and his colleagues have recently published a study about the Afferent arm.
 
I summarize a couple points about this new study below, but you'll need to know a few additional facts as background first...
  • There are 80,000 to 100,000 vagus nerve fibers in our bodies. I'll post a study reference link at some point.
     
  • About 80% of these Vagus Nerve Fibers are Sensory (Afferent) and not Motor (Efferent) fibers.
     
  • A good analogy for how this is architected within our bodies: Imagine the broadband network within a city. Large cables carry thousands of smaller wires from the broadband central location out to individual homes. From one point of view, the connection from the central location to the periphery is singular. From another point of view, it's a profound mistake to think about the wire as a single cable. The same is true about the Vagus Nerve and how its presence within us is architected.
 
 
Significance
 
Evolution conferred animals with molecular sensors that monitor cellular and organ function to detect changes in the environment. These activate sensory neural responses that drive the action of reflexes that maintain cellular and physiological homeostasis. Recent advances reveal that neural reflexes modulate the immune system, but it was previously unknown whether cytokine mediators of immunity mediate specific neural signals. Here we develop methods to isolate and decode specific neural signals recorded from the vagus nerve to discriminate between the cytokines IL-1β and TNF. This methodological waveform successfully detects and discriminates between specific cytokine exposures using neural signals.
 
Abstract
 
The nervous system maintains physiological homeostasis through reflex pathways that modulate organ function. This process begins when changes in the internal milieu (e.g., blood pressure, temperature, or pH) activate visceral sensory neurons that transmit action potentials along the vagus nerve to the brainstem. IL-1β and TNF, inflammatory cytokines produced by immune cells during infection and injury, and other inflammatory mediators have been implicated in activating sensory action potentials in the vagus nerve. However, it remains unclear whether neural responses encode cytokine-specific information. Here we develop methods to isolate and decode specific neural signals to discriminate between two different cytokines. Nerve impulses recorded from the vagus nerve of mice exposed to IL-1β and TNF were sorted into groups based on their shape and amplitude, and their respective firing rates were computed. This revealed sensory neural groups responding specifically to TNF and IL-1β in a dose-dependent manner. These cytokine-mediated responses were subsequently decoded using a Naive Bayes algorithm that discriminated between no exposure and exposures to IL-1β and TNF (mean successful identification rate 82.9 ± 17.8%, chance level 33%). Recordings obtained in IL-1 receptor-KO mice were devoid of IL-1β–related signals but retained their responses to TNF. Genetic ablation of TRPV1 neurons attenuated the vagus neural signals mediated by IL-1β, and distal lidocaine nerve block attenuated all vagus neural signals recorded. The results obtained in this study using the methodological framework suggest that cytokine-specific information is present in sensory neural signals within the vagus nerve.
 
Wow!
 
They put an electrode on an AFFERENT Vagus Nerve fiber and, using Machine Learning techniques, were able to distinguish between two different, key Inflammatory Cytokine Signals, IL-1b and TNF.
 
WEDCAVnh.png
 
Wow!
 
The details of this study are complicated and I haven't (yet) had time to digest all the details.
 
In studies of disorders, disease, death, and healthy longevity, we've been seeing, increasingly, how critical Inflammation Expression Inhibition is for healthy longevity.
 
So, now, understand these two facts together to assess a prediction...
 
--> Someday, it will be possible to identify and monitor specific Inflammatory Cytokine Expression signals in the Periphery of our bodies to provide an appropriate response... 
 
:-)
 

Edited by HighDesertWizard, 23 January 2019 - 04:23 PM.

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#189 HighDesertWizard

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Posted 27 January 2019 - 05:14 PM

I've gotten around to putting together another study slide demonstrating the requirements for Inflammation (TNF) Reduction in the Blood Circulation and in the Spleen.

 

I've posted other slides on this page up thread that Xanomeline increases Survival Probability even in the face of lethal LPS Administration.

 

The experiments described below have been performed multiple times by different study groups around the world.

 

Key Finding...

  • Intact Vagus Nerve and Splenic Nerve functions must exist from Brain to Spleen for the inflammation reduction effect of Xanomeline to be achieved.

 

 

DOlhIjK.png

 

 

 

In the anatomical study diagram below, I've highlighted the Splenic and Vagus nerves in yellow.

 

in2usON.png


Edited by HighDesertWizard, 27 January 2019 - 05:22 PM.

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#190 HighDesertWizard

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Posted 03 February 2019 - 07:23 PM

The following slide highlights one of the most significant findings of the Xanomeline study of The Inflammatory Reflex and Survival Probability...

 

What is the clear implication of the information presented on this slide?

  • It is worthwhile to attempt to trigger The Inflammatory Reflex at multiple times per day.

 

 

 

uP8vkfM.png


Edited by HighDesertWizard, 03 February 2019 - 07:25 PM.


#191 HighDesertWizard

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Posted 03 February 2019 - 07:37 PM

The modern discover and premier scientist of The Inflammatory Reflex (TIR) is Kevin J Tracey, President and CEO of The Feinstein Medical Research Institute. Dr Tracey holds an honorary doctorate from the Karolinska Institute, whose faculty determines who wins the Nobel Prize in Medicine each year.
 
Dr Tracey is the lead author of the Xanomeline study about which I've posted slides above. I haven't done a study count to be certain, but my hunch is that Dr Tracey has led or participated in more studies of the contexts that significantly increase Survival Probability than any other scientist. I'll be happy to change my mind about this point if anyone can point to the studies of some other scientist who has also published studies of the contexts that increase Survival Probability.
 
Dr Tracey has been doing more and longer talks that find their way to youtube in the last few years. I found the latest one, posted just last week. In this one, he covers some ground familiar to those who have seen his previous talks. But he also covers new content I hadn't seen and answers a few questions I've wanted more clarity about.
 
The youtube video of this latest talk appears below. It's a must-see if you want to understand more about the science of The Inflammatory Reflex.
 
Enjoy!
 


#192 HighDesertWizard

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Posted 05 February 2019 - 09:10 PM

 

The youtube video of this latest talk appears below. It's a must-see if you want to understand more about the science of The Inflammatory Reflex.
 

 

 

This week has been exciting for me because I've gotten glimpses of answers to a few key questions I've had about The Inflammatory Reflex for a while now. Here's the most important glimpse...

 

Begin watching the video from 43:40 and watch through 45:50. Here's the money quote I've transcribed and edited a bit without changing the meaning...

 

I'm not proposing optogenetics in clinical studies, there's a big controversy about that. That's not what I'm saying. I am saying the more we understand these specific neurons and their mechanistic roles and specific end-points it will be possible to make devices to control neurons in a highly specific and selective way whether it's surgically implanting them or steering current from outside the head.

 

OMG. And there it is, the answer to an important question...

 

Can we trigger The Inflammatory Reflex to reduce TNF in the serum via an exogenous means close to the Vagal Root in the brain?

 

Tracey says, "it will be possible..." Should we trust that he knows what he's talking about?

 

I'm now on this, to figure out how...

 

:)


Edited by HighDesertWizard, 05 February 2019 - 09:13 PM.

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#193 HighDesertWizard

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Posted 16 February 2019 - 06:34 AM

I haven't posted about the fact that a7 nicotinic acetylcholine Receptors ( a7nAchRs ) have been shown to be required for optimal Inflammatory Reflex Inflammation inhibition. There is at least one study showing that.... If I don't post about it soon, please kick me...

 

I'm trying to establish the basis for a more complex argument/explanation here and I'll make the point that needs making in this thread below, at the bottom of this post... But that point can't really be understood, I don't think if you're unfamiliar with the ways that acetylcholine has profound effects on NF-kB transcription of inflammatory cytokines within cells. Here's a recent Tracey diagram illustrating the multiple ways a7nAcrhRs are implicated in inflammation reduction. There are other diagrams worthwhile to spend time reviewing but I'm not going to bother now to post links to them here.

 

 

Follow the bouncing ball....  # 1....

  • a7nAchR activation, associated with The Inflammatory Reflex, profoundly inhibits inflammation expression in multiple ways...
  • Acetylcholine expression triggers increased NRF2 expression...

:)

 

 

Notice that there are multiple ways that the a7nAcrhR is implicated in inflammation reduction... both within the nucleus and in the mitochondria to inhibit Inflammasome Activation...

 

In that latest Tracey video I posted above I vaguely imagine he mentioned the inflammation reduction was greater in the inflammasome via-the a7nAchR than in the nucleus via NF-kB transcription inhibition.

 

DqoQu0Hh.png

 

 

Ok... Now that I've set that context up... Check this out...

 

Anti-inflammatory effects of astroglial α7 nicotinic acetylcholine receptors are mediated by inhibition of the NF-κB pathway and activation of the Nrf2 pathway

 

 

Abstract

BACKGROUND:

α7 nicotinic acetylcholine receptors (nAChRs) are widely distributed throughout the central nervous system and are reported to have neuroprotective properties. α7 nAChRs are expressed on astrocytes, which are key regulators of neuroinflammation and oxidative stress in several neurodegenerative diseases. However, the anti-inflammatory and antioxidant properties of astroglial α7 nAChRs are not well studied. Therefore, we evaluated the role of astroglial α7 nAChR activation in neuroinflammation.

METHODS:

Anti-inflammatory and antioxidant effects of α7 nAChR activation were evaluated in an in vitro mouse model of neuroinflammation using lipopolysaccharide (LPS) in primary astrocyte cultures. α7 nAChR anti-inflammatory effects on the NF-κB pathway were evaluated using ELISA, gene expression analysis, immunofluorescence, and western blotting. Antioxidant effect of α7 nAChR activation on expression profiles of canonical Nrf2 target genes was examined by quantitative PCR and western blotting. The role of the Nrf2 pathway in α7 nAChR-mediated anti-inflammatory response was evaluated using Nrf2 knockout astrocytes. Brain ex vivo NF-κB luciferase signals were evaluated after treatment with an α7 nAChR agonist in lipopolysaccharide (LPS)-injected NF-κB luciferase reporter mouse model.

RESULTS:

Astrocytes treated with the α7 nAChR partial agonist (GTS21) showed significantly reduced LPS-mediated secretion of inflammatory cytokines and this effect was reversed by the α7 nAChR antagonist methyllycaconitine (MLA) and by knockdown of α7 nAChR expression with a short hairpin RNA. Further, α7 nAChR activation blocked LPS-mediated NF-κB nuclear translocation indicating that the observed anti-inflammatory effect may be mediated through inhibition of the NF-κB pathway. Treatment with GTS21 also upregulated canonical Nrf2 antioxidant genes and proteins suggesting antioxidant properties of α7 nAChR in astrocytes. Using an astrocyte conditioned media approach, we demonstrated reduction in neuronal apoptosis when astrocytes were pretreated with GTS21. Finally, in an in vivo neuroinflammation model using LPS in NF-κB luciferase reporter mice, we demonstrated reduction in LPS-induced NF-κB activity and pro-inflammatory cytokines with GTS21 treatment in brain tissue.

CONCLUSION:

Our results suggest that activating astroglial α7 nAChRs may have a role in neuroprotection by decreasing inflammation and oxidative stress, and therefore could have therapeutic implication for disease modifying treatments of neurodegenerative diseases.

 

There are some other studies showing that acetylcholine expression increases NRF2 expression. Here's another one... You'll recall that the Muscarnic M1 Acetelcholine Receptor is among the primary triggers for activation of The Inflammatory Reflex...

 

The muscarinic M1 receptor activates Nrf2 through a signaling cascade that involves protein kinase C and inhibition of GSK‐3beta: connecting neurotransmission with neuroprotection


Edited by HighDesertWizard, 16 February 2019 - 07:43 AM.


#194 HighDesertWizard

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Posted 03 March 2019 - 04:55 PM

About the opening post conjecture... An Ancient "Heat Shock"/NRF2/Pluripotency Related Epigenetic Turn* Accelerates Human Aging** and These can be Modulated...
 
How Ancient is the "Heat Shock"/NRF2/Pluripotency Related Epigenetic Turn*? From the 2015 Morimoto study, we know that it is almost certainly as old as the common ancestor of c Elegans and Humans.
 
Question: How long ago did c Elegans and Humans have a common ancestor?
 
Answer: 638 million years
 
See the interactive  Tree of Life Explorer ...
 
hywH110h.png

 

We share an ancient, evolutionarily conserved, "Heat Shock" related mechanism with many other species, including c elegans and plants. When triggered, this mechanism has paradoxical effects, including both life-threatening and longevity-promoting effects. (The post at the quote link above includes a pic depicting the 1-billion-years-ago link with mushrooms.)

 

 

"The Inflammatory Reflex" is also an ancient, evolutionarily conserved mechanism, demonstrated to exist within humans and many other mammalian species by multiple experiments, including rodents, dogs, and likely, many other mammals.

 

Most Inflammatory Reflex-related experiments have involved rodents and the pic below suggests that our common ancestor with rodents lived about 90 million years ago. This web page states that "[h]uman, mouse and other mammals shared a common ancestor approximately 80 million years ago. Therefore the genomes of all mammals are comparably similar." A National Geographic page, entitled Meet the Ancestor of Every Human, Bat, Cat, Whale and Mouse suggests this common ancestor only began to Diversify into multiple mammalian species after the extinction event that took out the dinosaurs, an event believed to have taken place 65 million years ago. (See also this study summary, Face-to-face with the earliest ancestor of all placental mammals.)

 

Species diversification from a single species ancestor is an event of a different kind than the arrival on the scene of that ancestor with a specific set of biological functions intact. So these estimated dates of 90 million years and 65 million years can both be taken to be true.

 

For the purpose of grasping the facts of the history of The Inflammatory Reflex and its evolution as a discrete multi-organ mechanism, these nuances of dating aren't especially important.

 

Whatever the case, we can state a belief that is very probably true like this: sometime between 65 and 100 million years ago, an ancestor common to both rodents and humans lived. The ancestor must have had some biological functions operating within it that led to very similar features of The Inflammatory Reflex emerging in humans and in other mammals.

 

GAOIIPGh.png


Edited by HighDesertWizard, 03 March 2019 - 05:23 PM.


#195 Ovidus

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Posted 15 March 2019 - 07:28 PM

This week has been exciting for me because I've gotten glimpses of answers to a few key questions I've had about The Inflammatory Reflex for a while now. Here's the most important glimpse...

 

Begin watching the video from 43:40 and watch through 45:50. Here's the money quote I've transcribed and edited a bit without changing the meaning...

 

I'm not proposing optogenetics in clinical studies, there's a big controversy about that. That's not what I'm saying. I am saying the more we understand these specific neurons and their mechanistic roles and specific end-points it will be possible to make devices to control neurons in a highly specific and selective way whether it's surgically implanting them or steering current from outside the head.

 

OMG. And there it is, the answer to an important question...

 

Can we trigger The Inflammatory Reflex to reduce TNF in the serum via an exogenous means close to the Vagal Root in the brain?

 

Tracey says, "it will be possible..." Should we trust that he knows what he's talking about?

 

I'm now on this, to figure out how...

 

:)

 

Excellent work so far Sir; if we can stimulate the vagus nerve at will, we will hit gold.

 

Are you aware of this device that does exactly that:

 

https://www.migraine...ve-stimulation/

 

 

Also, how about acupuncture with needles hitting the vagus nerve? I read some mentions of it but could not find anything substantial about it. 



#196 HighDesertWizard

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Posted 17 March 2019 - 06:11 PM

Hot off the press--this study doesn't even appear on pubmed yet--here's one of the latest studies by Kevin Tracey's team. Of note, Valentin Pavlov, a Tracey collegue for more than 10 years, has begun to appear as the lead author of what I call "Tracey studies"...

 

The key finding... Cholinergic neurons in the forebrain can be stimulated to trigger TIR (Cholinergic Antiinflammatory Pathway)...

 

March 2019, Forebrain cholinergic signaling regulates innate immune responses and inflammation

 

The brain regulates physiological functions integral to survival. However, the insight into brain neuronal regulation of peripheral immune function and the neuromediator systems and pathways involved remains limited. Here, utilizing selective genetic and pharmacological approaches, we studied the role of forebrain cholinergic signaling in the regulation of peripheral immune function and inflammation. Forebrain-selective genetic ablation of acetylcholine release and vagotomy abolished the suppression of serum TNF by the centrally-acting cholinergic drug galantamine in murine endotoxemia. Selective stimulation of acetylcholine action on the M1 muscarinic acetylcholine receptor (M1mAChR) by central administration of the positive allosteric agonist benzyl quinolone carboxylic acid (BQCA) suppressed serum TNF levels in murine endotoxemia. This effect was recapitulated by peripheral administration of the compound. BQCA also improved survival in murine endotoxemia and these effects were abolished in M1mAChR knockout (KO) mice. Selective optogenetic stimulation of basal forebrain cholinergic neurons innervating brain regions with abundant M1mAChR localization reduced serum TNF in endotoxemic mice. These findings reveal that forebrain cholinergic neurons physiologically regulate innate immune responses and inflammation, suggesting the possibility that in diseases of cholinergic dysfunction this anti-inflammatory regulation can be impaired. These results also suggest novel anti-inflammatory approaches based on targeting forebrain cholinergic signaling in sepsis and other disorders characterized by immune dysregulation.

 

If you've been closely following this thread's content, you know that I've mentioned virtually all the terminology and concepts that appear in the abstract. What's new in this study is the fact that Forebrain Cholinergic Neurons Agonism leads to the kind of Vagus Nerve activation and increased survival probability seen in other studies. (See study pics below.)

 

What I'm puzzled about... In previous studies, the Tracey team noted that Muscarinic-Acetylcholine M1 Receptors (M1mAChRs) in the Hypothalamus could be agonized to trigger the "Efferent, Motor Arm of The Inflammatory Reflex", aka, the "Cholinergic AntiInflammatory Pathway". In the study highlighted in this post, we learn that M1mAChRs in the Forebrain do something comparable. And, in still another study, we learned that activation of the Vagus Nerve at its root in the brain can also trigger the Cholinergic AntiInflammatory Pathway. I don't have the reference link handy at the moment for this last point...

 

==> I take it that this means there are multiple locations in the brain to stimulated CAP.

 

 

 

Some study images below illustrate the same kind of characteristics shown in previous studies: decreased TNF in the spleen and in the serum when CAP is triggered, increased survival probability when CAP is triggered, Vagatomy and M1mAChR knockout decreases survival probability even when the cholinergic pharmacological agonist is applied to the organism.

 

Figure 2 shows impacts on TNF expression in the serum after LPS administration is preceded by Galantamine vs control in the context of both Cholinergic knockout and Vagatomy.

 

fbImuoah.png

 

 

Figure 3 shows the same kind of dose-dependent effects on TNF reduction and how dosing of the cholinergic agonist relates to survival probability that appear upthread. There nothing new here that hasn't been shown upthread except a different cholinergic agonist, BQCA, is used.

 

VuN7cuT.png

 

 

Figure 4 is an important study diagram. It shows that M1 Muscarinic-Acetylcholine Receptors must be intact for Optimal inflammation-(TNF)-reducing-, survival-probability-increasing- effects to be achieved.

 

93SoMSnh.png


Edited by HighDesertWizard, 17 March 2019 - 06:23 PM.


#197 HighDesertWizard

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Posted 17 March 2019 - 06:26 PM

The youtube video of this latest talk appears below. It's a must-see if you want to understand more about the science of The Inflammatory Reflex.
 
Enjoy!
 

 

This week has been exciting for me because I've gotten glimpses of answers to a few key questions I've had about The Inflammatory Reflex for a while now. Here's the most important glimpse...
 
Begin watching the video from 43:40 and watch through 45:50. Here's the money quote I've transcribed and edited a bit without changing the meaning...
 

I'm not proposing optogenetics in clinical studies, there's a big controversy about that. That's not what I'm saying. I am saying the more we understand these specific neurons and their mechanistic roles and specific end-points it will be possible to make devices to control neurons in a highly specific and selective way whether it's surgically implanting them or steering current from outside the head.

 
OMG. And there it is, the answer to an important question...
 
Can we trigger The Inflammatory Reflex to reduce TNF in the serum via an exogenous means close to the Vagal Root in the brain?
 
Tracey says, "it will be possible..." Should we trust that he knows what he's talking about?
 
I'm now on this, to figure out how...
 
:)

 

 

 

 

Another "Tracey study" hot off the press, this time with the full study text more easily available. I anticipated something like this study being published at Longecity not so long ago. This study is a game changer. at least for me...   :)

 

ixfdEXvh.png

 

 

 

March 12, 2019, Noninvasive sub-organ ultrasound stimulation for targeted neuromodulation

 

Tools for noninvasively modulating neural signaling in peripheral organs will advance the study of nerves and their effect on homeostasis and disease. Herein, we demonstrate a noninvasive method to modulate specific signaling pathways within organs using ultrasound (U/S). U/S is first applied to spleen to modulate the cholinergic anti-inflammatory pathway (CAP), and US stimulation is shown to reduce cytokine response to endotoxin to the same levels as implant-based vagus nerve stimulation (VNS). Next, hepatic U/S stimulation is shown to modulate pathways that regulate blood glucose and is as effective as VNS in suppressing the hyperglycemic effect of endotoxin exposure. This response to hepatic U/S is only found when targeting specific sub-organ locations known to contain glucose sensory neurons, and both molecular (i.e. neurotransmitter concentration and cFOS expression) and neuroimaging results indicate US induced signaling to metabolism-related hypothalamic sub-nuclei. These data demonstrate that U/S stimulation within organs provides a new method for site-selective neuromodulation to regulate specific physiological functions.

 

ttYNJYG.png

 

 

Of course, we know what the key substances associated with triggering of TIR/CAP, norepinephrine, acetylcholine, and both, splenic- and serum-TNF. Can and does Focused Pulsed Ultrasound impact those independent-variable substances? Figure 2 of the study addresses that question...

 

6NFXzHBh.png

 

 

 

OMG.

 

A Game Changer Study!


Edited by HighDesertWizard, 17 March 2019 - 06:53 PM.

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#198 Ovidus

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Posted 27 March 2019 - 12:57 PM

Excellent work so far Sir; if we can stimulate the vagus nerve at will, we will hit gold.

 

Are you aware of this device that does exactly that:

 

https://www.migraine...ve-stimulation/

 

 

Also, how about acupuncture with needles hitting the vagus nerve? I read some mentions of it but could not find anything substantial about it. 

 

Anyone found this post of mine interesting at all?

A low-risk, direct Vagus Nerve Activation sounds excellent, no?



#199 Oakman

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Posted 27 March 2019 - 03:40 PM

Anyone found this post of mine interesting at all?

A low-risk, direct Vagus Nerve Activation sounds excellent, no?

 

I've only read some of this lengthy thread, but it might be exciting (sort of), except for the fact it is not available to normal people, and except for under a doctor's care in the UK, not at all (it seems). Show me a device that is available to anyone anywhere and more documented results please.



#200 Ovidus

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Posted 27 March 2019 - 08:11 PM

I've only read some of this lengthy thread, but it might be exciting (sort of), except for the fact it is not available to normal people, and except for under a doctor's care in the UK, not at all (it seems). Show me a device that is available to anyone anywhere and more documented results please.

 

Ah Good Sir, 

I so wish I was able to address your concerns and tell you both where to get this and provide "documented results" as well. 
But, as a respected long-time member on this forum, you know very well that we are swimming upstream; we work with very incomplete data, we speculate and often we take some degree of risk too. 
I am not even mentioning all the money and effort wasted.

 

This particular device is no exception. It is possible that nobody has ever used it for the purpose of reducing inflammation and overall well-being. However, I can speculate on a few things here:

Since patients are provided this and sent home with it, the device should perhaps be fairly foolproof to use and considered very safe.
I also read on a migrane forum that an ex advanced engineer (might even have been a former NASA guy) took it apart and concluded that the device merely send sounds waves and should thus be fairly easy to replicate. I wish I was able to find that post easily; I cannot at the moment, but I can surely try.

 

I'd say that if vagus nerve activation does all that we expect it to -and much more discussion has gone into this than has been covered in this thread- the effort to somehow activate it with a setup like this is well worth it. 
Such on-demand activation would be far superior to medicinal means of activating the vagus nerve; I'd expect drugs to come with way way more side effects than a device like this. 



#201 Oakman

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Posted 27 March 2019 - 10:05 PM

Ah Good Sir, 

I so wish I was able to address your concerns and tell you both where to get this and provide "documented results" as well. 
But, as a respected long-time member on this forum, you know very well that we are swimming upstream; we work with very incomplete data, we speculate and often we take some degree of risk too. 
I am not even mentioning all the money and effort wasted.

 

This particular device is no exception. It is possible that nobody has ever used it for the purpose of reducing inflammation and overall well-being. However, I can speculate on a few things here:

Since patients are provided this and sent home with it, the device should perhaps be fairly foolproof to use and considered very safe.
I also read on a migrane forum that an ex advanced engineer (might even have been a former NASA guy) took it apart and concluded that the device merely send sounds waves and should thus be fairly easy to replicate. I wish I was able to find that post easily; I cannot at the moment, but I can surely try.

 

I'd say that if vagus nerve activation does all that we expect it to -and much more discussion has gone into this than has been covered in this thread- the effort to somehow activate it with a setup like this is well worth it. 
Such on-demand activation would be far superior to medicinal means of activating the vagus nerve; I'd expect drugs to come with way way more side effects than a device like this. 

 

About sending it home, from the website below. It's application is more than a little restrictive. Wonder what are the risks forcing such a policy?

 

"gammaCore Sapphire™ is a rechargeable and reloadable version of the product intended for multi-year use. It is activated on a regular (typically every 3 months) basis through the input of a unique, prescription-only authorization code, delivered via a radio-frequency identification, or RFID, card."

 

Also, the site it's electrical, not sound activation.

 

"gammaCore works by sending a mild electrical stimulation through the skin to activate the vagus nerve from outside your body"

 

Would be informative to know more about it., as it might be fairly simple to replicate for testing.



#202 Ovidus

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Posted 30 March 2019 - 06:58 PM

 

Also, the site it's electrical, not sound activation.

 

"gammaCore works by sending a mild electrical stimulation through the skin to activate the vagus nerve from outside your body"

 

Would be informative to know more about it., as it might be fairly simple to replicate for testing.

 

If so, how hard can it be to replicate?

Could it be that there is some kind of AC/DC type of fluctuation to it?

 

we gotta have engineers here; c'mon people

 

but once again, I am pretty sure that the guy who took it apart concluded it was sound waves; he could have been wrong of course, but just saying



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#203 Mind

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Posted 30 March 2019 - 08:32 PM

 

 

Also, how about acupuncture with needles hitting the vagus nerve? I read some mentions of it but could not find anything substantial about it. 

 

Form what I have read, acupuncture is supposed to work by modulating Qi, not by hitting nerves. Stabbing your vagus nerve with a sharp metal object does not sound like a good idea to me.


Edited by Mind, 30 March 2019 - 11:30 PM.

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#204 Oakman

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Posted 30 March 2019 - 09:07 PM

If so, how hard can it be to replicate?

Could it be that there is some kind of AC/DC type of fluctuation to it?

 

we gotta have engineers here; c'mon people

 

but once again, I am pretty sure that the guy who took it apart concluded it was sound waves; he could have been wrong of course, but just saying

 

Who knows...anyway...I'm not about to electrically stimulate anything (vagus nerve included) on myself as essential to homeostasis as that untested. And esp. not when in reading this thread my main interest was it's discussion of HRV on longevity. I've been tracking mine daily for 9 mos now, and although I see it go up and down for various reasons, I've always wondered if there was a way to help it recover quicker, or just be higher than it is, indicating a return to a younger HRV value. And I found a tantalizing mention of a way to do just that..

 

"I first came across the literature of the Cholinergic Anti-Inflammatory Pathway because I was increasing my Acetylcholine precursor dose while using HeartMath's emWave2 product to practice increasing my Heart Rate Variability. I noticed that it was dramatically easier to raise my HRV while supplementing Acetylcholine than when I wasn't. I didn't understand why that should be. So I began to investigate and that led me to find the work of Kevin Tracey... 8-)"

 

So now I'm on to a treatment method using supplements to increase Acetylcholine and hoping to see results in my observed HRV (rMMSD) going forward. As far as working with the vagus nerve specifically, there are apparently other methods to work with it, YouTube brings up more than a few ways, for example. I have confidence that this thread about the Inflammatory Reflex is much more important than is generally given credit here on the forum, and I intend to learn and experiment more to confirm just that (or not!). So thanks HighDesertWind!


Edited by Oakman, 30 March 2019 - 09:07 PM.


#205 Oakman

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Posted 30 March 2019 - 09:42 PM

I did find this electrical spec for stimulating the Vagus nerve in a reference earlier in the thread. Note it was on an exposed nerve, not skin... and on rats. So could be a starting place at least.

 

"Electrical Stimulation of Intact Vagus Nerve.

 

Where indicated, the vagus nerve was exposed and isolated from surrounding tissue with parafilm. Intact vagus nerves were stimulated with constant voltage at either 1V (2 ms, 5 Hz) or 5V (2 ms, 5 Hz) for 10 min intervals before and after LPS injection, for a total of 20 continuous min, using bipolar platinum electrodes connected to the stimulation module. Rats were subjected to either left vagus stimulation, right vagus stimulation, or sham operation. MABP, HR, and respiratory rate were recorded every 5 min, beginning 30 min before, and ending 150 min after LPS injection."


Edited by Oakman, 30 March 2019 - 09:43 PM.


#206 Ovidus

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Posted 03 April 2019 - 08:09 PM

I did find this electrical spec for stimulating the Vagus nerve in a reference earlier in the thread. Note it was on an exposed nerve, not skin... and on rats. So could be a starting place at least.

 

"Electrical Stimulation of Intact Vagus Nerve.

 

Where indicated, the vagus nerve was exposed and isolated from surrounding tissue with parafilm. Intact vagus nerves were stimulated with constant voltage at either 1V (2 ms, 5 Hz) or 5V (2 ms, 5 Hz) for 10 min intervals before and after LPS injection, for a total of 20 continuous min, using bipolar platinum electrodes connected to the stimulation module. Rats were subjected to either left vagus stimulation, right vagus stimulation, or sham operation. MABP, HR, and respiratory rate were recorded every 5 min, beginning 30 min before, and ending 150 min after LPS injection."

 

Oh sure

very straightforward to stimulate a Vagus Nerve directly; they do this by implanting a device that is in direct contact with the nerve.

Check out the link:
"A stimulator device is implanted under the skin in the chest. A wire from the device is wound around the vagus nerve in the neck."

https://www.epilepsy...stimulation-vns

 

What I am having a hard time understanding is how an electrical current applied to the skin penetrates many layers of tissue and reaches the vagus nerve

 

  • A stimulator device is implanted under the skin in the chest. A wire from the device is wound around the vagus nerve in the neck.


#207 HighDesertWizard

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Posted 05 April 2019 - 11:43 PM

Excellent work so far Sir; if we can stimulate the vagus nerve at will, we will hit gold.

 

Are you aware of this device that does exactly that:

 

https://www.migraine...ve-stimulation/

 

 

Also, how about acupuncture with needles hitting the vagus nerve? I read some mentions of it but could not find anything substantial about it. 

 

 

Anyone found this post of mine interesting at all?

A low-risk, direct Vagus Nerve Activation sounds excellent, no?

 

 

I've only read some of this lengthy thread, but it might be exciting (sort of), except for the fact it is not available to normal people, and except for under a doctor's care in the UK, not at all (it seems). Show me a device that is available to anyone anywhere and more documented results please.

 

I agree with Oakman... Only in the UK. Only by prescription. Not worth considering when there are so many other options out there.



#208 HighDesertWizard

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Posted 05 April 2019 - 11:53 PM

Such on-demand activation would be far superior to medicinal means of activating the vagus nerve; I'd expect drugs to come with way way more side effects than a device like this.

 
Your expectation is mistaken...

 

I just realized I hadn't posted this Galantamine study in this thread... This is a big deal... Take a look at the study, sit down, close your eyes, and reflect on what it means for your life... 
 

 

< SNIP >>
Effects of galantamine in a 2-year, randomized, placebo-controlled study in Alzheimer’s disease

 

They stopped the study after two years because of the statistical variance in the number of elderly dying who were not taking Galantamine, an acetylcholinesterase inhibitor.
  
:)
 
Gi4gJwcl.png


Edited by HighDesertWizard, 05 April 2019 - 11:55 PM.


#209 HighDesertWizard

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Posted 06 April 2019 - 12:19 AM

About sending it home, from the website below. It's application is more than a little restrictive. Wonder what are the risks forcing such a policy?

 

"gammaCore Sapphire™ is a rechargeable and reloadable version of the product intended for multi-year use. It is activated on a regular (typically every 3 months) basis through the input of a unique, prescription-only authorization code, delivered via a radio-frequency identification, or RFID, card."

 

Also, the site it's electrical, not sound activation.

 

"gammaCore works by sending a mild electrical stimulation through the skin to activate the vagus nerve from outside your body"

 

Would be informative to know more about it., as it might be fairly simple to replicate for testing.

 

I recently purchased this TENS device at Amazon. My 85 year old father now uses a cane and sometimes can barely walk and is always skeptical about anything I suggest. But he used that TENS device and experienced almost immediate benefit. I don't know for certain if the effects are cumulative, but I believe they are.

 

--> There is some evidence that the beneficial effects of TENS device are due to the triggering of Heat Shock Proteins.

 

That said... I'll take a look at the Gamma Core device. Perhaps a TENS device can replicate the same effect via a small electrical current...

 

I bought that TENS device because it has an Acupuncture Model, the thought being to use it in one or both of two ways...

  1. At the Hegu acupoint (See the electro-acupuncture survival probability curve related to the Hegu acupuncture point upthread. In rodents, but still....)
  2. At the auricular (within the ear) acupuncture point.

The point is, you've got to hit an acupuncture point that hits the Motor Arm of The Inflammatory Reflex (aka, the Cholinergic Anti-Inflammatory Pathway) because it pings the spleen.

 

In his talks, Tracey says that there are 80,000 to 100,000 vagus nerve fibers in humans, with 80% of them Sensory and 20% of them Motor Arm Fibers. And he's also said in one talk that there are about 50 Vagus Nerve Motor Arm Fibers from Brain to Spleen (evidently passing the electrical signal to the Splenic Nerve at the Celiac Ganglion). See physiology pics above.

 

Question: Why is the Spleen important?

 

Answer: Because the Spleen is the organ that is the most significant "barracks" for the Inflammatory Cytokine "soldiers", especially M1 Macrophages, that are sent out into our bodies' periphery via the blood circulation...

 

I had read that a TENS device should not be used on the neck. But if that's what the Gamma Core device is doing, applying an electrical change to the neck, then, I'm game to try it, and soon...

 

Thanks for continuing to press the point about the Gamma Core device Ovidus!

 

The mechanism is worth investigating if not the device itself.



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#210 HighDesertWizard

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Posted 06 April 2019 - 12:29 AM

Form what I have read, acupuncture is supposed to work by modulating Qi, not by hitting nerves. Stabbing your vagus nerve with a sharp metal object does not sound like a good idea to me.

 

That's not what the evidence suggests is the case. But it can't be just any acupoint. It has to be an acupoint that triggers Vagus Nerve Fibers in the brain that will signal the Spleen via the Splenic Nerve. Evidence below...

 

I've tried using my new TENS device at where I believe my Hegu acupoints are. I couldn't feel anything really. So the real question then becomes...

How do we measure "Effective Enough" Vagus Nerve activation that will result in transformed Splenic Macrophages from an M1 to an M2 phenotype?

 

That's a question I'm thinking a lot about these days...

 

See previous post... Feedback on slide desired...

 

:)

 

gallery_16949_60_363598.jpg







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