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An Ancient "Heat Shock"/NRF2/Pluripotency Related Epigenetic Turn* Accelerates Human Aging** and These can be Modulated

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#181 HighDesertWizard

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Posted 04 May 2019 - 03:46 PM

An interesting study about Pulsed ElectroMagnetic Fields (PEMF) impact on chondrogenesis and dosing with practical significance.
 

Chondrogenesis is the process by which cartilage is developed. - Wikipedia

 

 

2017, Enhancement of mesenchymal stem cell chondrogenesis with short-term low intensity pulsed electromagnetic fields
 

Pulse electromagnetic fields (PEMFs) have been shown to recruit calcium-signaling cascades common to chondrogenesis. Here we document the effects of specified PEMF parameters over mesenchymal stem cells (MSC) chondrogenic differentiation. MSCs undergoing chondrogenesis are preferentially responsive to an electromagnetic efficacy window defined by field amplitude, duration and frequency of exposure. Contrary to conventional practice of administering prolonged and repetitive exposures to PEMFs, optimal chondrogenic outcome is achieved in response to brief (10 minutes), low intensity (2 mT) exposure to 6 ms bursts of magnetic pulses, at 15 Hz, administered only once at the onset of chondrogenic induction. By contrast, repeated exposures diminished chondrogenic outcome and could be attributed to calcium entry after the initial induction. Transient receptor potential (TRP) channels appear to mediate these aspects of PEMF stimulation, serving as a conduit for extracellular calcium. Preventing calcium entry during the repeated PEMF exposure with the co-administration of EGTA or TRP channel antagonists precluded the inhibition of differentiation. This study highlights the intricacies of calcium homeostasis during early chondrogenesis and the constraints that are placed on PEMF-based therapeutic strategies aimed at promoting MSC chondrogenesis. The demonstrated efficacy of our optimized PEMF regimens has clear clinical implications for future regenerative strategies for cartilage.

 

The graphic figures demonstrate the specificity of optimal study parameter values. Here's the one demonstrating differential impacts across 2 key study parameters.
 

x8aIdsjh.png

 

 
Close your eyes and imagine what will be practically important about these (and other) study findings over the longer term...
  • Small Spot Devices to focus on small body areas.
     
  • Devices providing precise control of dosing.
    • From the study, control is needed for ) dosing period [10 minutes], 2) intensity [2 mT], 3) dose size [6 ms bursts], and dose frequency [15 hz].

 

In several posts above, I highlighted study findings I only recently discovered...

 

The healthful effects of several Heat Shock Protein expression promoters appear to be mediated by Transient Receptor Potential (TRP) Channels... Pain Bloc's Capsaicin, Cayenne, and Near Infrared Light...

 

I had never heard of these TRP channels until a couple months ago.

 

But now, OMG, PEMF's healthful effects also appear to be mediated via these same channels. Figure 5 from the study referenced above about stimulating cartilage ...

 

6XkVmDQh.png

 

 

So... What's the obvious question to be asking now? I think it's this...

 

Shall we try to figure out if all or most all known promoters of healthful longevity effects via Heat Shock Protein are mediated via TRP Channels?


Edited by HighDesertWizard, 04 May 2019 - 10:15 PM.


#182 HighDesertWizard

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Posted 04 May 2019 - 04:14 PM

Every once in a while, it's important to recall why we're pushing the peddle to the metal about these nuanced and detailed Heat Shock Protein related topics...
 
They're important because our intention is to learn to Hack Them...
 

People have been thinking about this topic for awhile. I haven't looked at the PDF below in detail, but clearly not a bad find, this PDF, with lots of detail, from 2001...

 

HEAT SHOCK RESPONSE AND AGEING: MECHANISMS AND APPLICATIONS


Ageing is associated with a decrease in the ability of cells to cope with environmental challenges. This is due partly to the attenuation of a primordial stress response, the so-called heat shock (HS) response, which induces the expression of heat shock proteins (HSPs), composed of chaperones and proteases. The attenuation of the HS response during ageing may be responsible for the accumulation of damaged proteins as well as abnormal regulation of cell death. Maintenance of the HS response by repeated mild heat stress causes anti-ageing hormetic effects on cells and organisms. Here, we describe the molecular mechanism and the state of the HS response as well as the role of specific HSPs during ageing, and discuss the possibility of hormetic modulation of ageing and longevity by repeated mild stress.

 

Then, in 2015, we get these two studies in wild-type humans...

Let's sample just two studies, 1 for exercise and 1 for sauna vis-a-vis survival probability. 
2015, Fitness predicts long-term survival after a cardiovascular event: a prospective cohort study

Scgs6Tll.png

2015, Association Between Sauna Bathing and Fatal Cardiovascular and All-Cause Mortality Events

xtaOIKNl.pngj



It's easy to see that deliberate, continuous, and intermittent triggering of the Heat Shock response can make for decades of increased survival probability.

I do not believe there are comparable survival probability findings for ANY other Longevity Science Movement sacred research cow projects currently purported to be important for which ALSO Heat Shock is NOT a confounding variable.

They don't exist.


The NAD+ Survival Probability studies aren't admissible here because, as noted upthread, Heat Shock IS a confounding variable for NAD+'s impact on Survival Probability...

 

It's critical to remember that the studies of Survival Probability shown above were concerned with Wild-Type Humans. That is to say, they were studies of humans who had no knowledge or consciousness that something important in themselves was being studied that might have a profound impact on their health and longevity.

 

We're building on the shoulders of those giants, now having knowledge of what it is that we might try to Hack to increase our health and longevity in some radical way...

 

That's why the details are important...

 

That's why I'm here.


Edited by HighDesertWizard, 04 May 2019 - 04:16 PM.

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#183 HighDesertWizard

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Posted 06 May 2019 - 08:55 AM

I'm working up a list of studies about TRPV Channel intervention techniques. In the meantime, it's useful to begin to grasp how important TRPV is...

 

 

2013, The Membrane-Associated Transient Receptor Potential Vanilloid Channel Is the Central Heat Shock Receptor Controlling the Cellular Heat Shock Response in Epithelial Cells

 

The heat shock response (HSR) is a highly conserved molecular response to various types of stresses, including heat shock, during which heat-shock proteins (Hsps) are produced to prevent and repair damages in labile proteins and membranes. In cells, protein unfolding in the cytoplasm is thought to directly enable the activation of the heat shock factor 1 (HSF-1), however, recent work supports the activation of the HSR via an increase in the fluidity of specific membrane domains, leading to activation of heat-shock genes. Our findings support the existence of a plasma membrane-dependent mechanism of HSF-1 activation in animal cells, which is initiated by a membrane-associated transient receptor potential vanilloid receptor (TRPV). We found in various non-cancerous and cancerous mammalian epithelial cells that the TRPV1 agonists, capsaicin and resiniferatoxin (RTX), upregulated the accumulation of Hsp70, Hsp90 and Hsp27 and Hsp70 and Hsp90 respectively, while the TRPV1 antagonists, capsazepine and AMG-9810, attenuated the accumulation of Hsp70, Hsp90 and Hsp27 and Hsp70, Hsp90, respectively. Capsaicin was also shown to activate HSF-1. These findings suggest that heat-sensing and signaling in mammalian cells is dependent on TRPV channels in the plasma membrane. Thus, TRPV channels may be important drug targets to inhibit or restore the cellular stress response in diseases with defective cellular proteins, such as cancer, inflammation and aging.

 

 

2018, TrpV1 receptor activation rescues neuronal function and network gamma oscillations from Aβ-induced impairment in mouse hippocampus in vitro

 

Amyloid-β peptide (Aβ) forms plaques in Alzheimer’s disease (AD) and is responsible for early cognitive deficits in AD patients. Advancing cognitive decline is accompanied by progressive impairment of cognition-relevant EEG patterns such as gamma oscillations. The endocannabinoid anandamide, a TrpV1-receptor agonist, reverses hippocampal damage and memory impairment in rodents and protects neurons from Aβ-induced cytotoxic effects. Here, we investigate a restorative role of TrpV1-receptor activation against Aβ-induced degradation of hippocampal neuron function and gamma oscillations. We found that the TrpV1-receptor agonist capsaicin rescues Aβ-induced degradation of hippocampal gamma oscillations by reversing both the desynchronization of AP firing in CA3 pyramidal cells and the shift in excitatory/inhibitory current balance. This rescue effect is TrpV1-receptor-dependent since it was absent in TrpV1 knockout mice or in the presence of the TrpV1-receptor antagonist capsazepine. Our findings provide novel insight into the network mechanisms underlying cognitive decline in AD and suggest TrpV1 activation as a novel therapeutic target.

 

 

2016, Shining light on the head: Photobiomodulation for brain disorders (The author is a key scientist and thought leader for photobiomodulation.) 

 

Photobiomodulation (PBM) describes the use of red or near-infrared light to stimulate, heal, regenerate, and protect tissue that has either been injured, is degenerating, or else is at risk of dying. One of the organ systems of the human body that is most necessary to life, and whose optimum functioning is most worried about by humankind in general, is the brain. The brain suffers from many different disorders that can be classified into three broad groupings: traumatic events (stroke, traumatic brain injury, and global ischemia), degenerative diseases (dementia, Alzheimer's and Parkinson's), and psychiatric disorders (depression, anxiety, post traumatic stress disorder). There is some evidence that all these seemingly diverse conditions can be beneficially affected by applying light to the head. There is even the possibility that PBM could be used for cognitive enhancement in normal healthy people. In this transcranial PBM (tPBM) application, near-infrared (NIR) light is often applied to the forehead because of the better penetration (no hair, longer wavelength). Some workers have used lasers, but recently the introduction of inexpensive light emitting diode (LED) arrays has allowed the development of light emitting helmets or “brain caps”. This review will cover the mechanisms of action of photobiomodulation to the brain, and summarize some of the key pre-clinical studies and clinical trials that have been undertaken for diverse brain disorders.

 

Graphic Abstract

 

8CubQpVh.jpg

 

 

 

Figure 1 of the study highlights the fact that TRPV is implicated by Near Infrared photobiomodulation. 

 

gr1.jpg

 

 

 

I believe there's enough evidence now to justify using Near Infrared light for cognitive improvement. So I've begun to shine the Near Infrared bulb I purchased on my head along with other parts of my body.

 

Also, my n = 1 experience is that, when I shine the light of that bulb on my chest for 5 to 10 minutes, my exercise endurance improves for several hours after.

 

I believe my anecdotal experiences are consistent with what one would expect based on the scientific literature.


Edited by HighDesertWizard, 06 May 2019 - 09:10 AM.


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#184 HighDesertWizard

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Posted 06 May 2019 - 09:25 AM

Michael Hamblin, the author of the study posted above about Near Infrared light for cognitive improvement, was the lead author of a review of parameters used in various studies. It amounts to a detailed review of the literature about light and health.

 

I haven't digested it yet, but I will at some point soon...

 

2018, Review of light parameters and photobiomodulation efficacy: dive into complexity

 

Photobiomodulation (PBM) therapy, previously known as low-level laser therapy, was discovered more than 50 years ago, yet there is still no agreement on the parameters and protocols for its clinical application. Some groups have recommended the use of a power density less than 100  mW/cm2 and an energy density of 4 to 10  J/cm2 at the level of the target tissue. Others recommend as much as 50  J/cm2 at the tissue surface. The wide range of parameters that can be applied (wavelength, energy, fluence, power, irradiance, pulse mode, treatment duration, and repetition) in some cases has led to contradictory results. In our review, we attempt to evaluate the range of effective and ineffective parameters in PBM. Studies in vitro with cultured cells or in vivowith different tissues were divided into those with higher numbers of mitochondria (muscle, brain, heart, nerve) or lower numbers of mitochondria (skin, tendon, cartilage). Graphs were plotted of energy density against power density. Although the results showed a high degree of variability, cells/tissues with high numbers of mitochondria tended to respond to lower doses of light than those with lower number of mitochondria. Ineffective studies in cells with high mitochondrial activity appeared to be more often due to over-dosing than to under-dosing.



#185 QuestforLife

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Posted 09 May 2019 - 11:03 AM

Nope. Ain't buying that one after all. I'm virtually convinced that it's a great device. And you can get it for $100 at Amazon. if that currency-value amount is what fits your budget, BUY THAT DEVICE!

 

But after some reflection, and with, regrettably, only recently knowledge I believe is that Red-Light-Related devices trigger Heat Shock Protein, I've been reflecting on this Question...

 

What are the Essential Requirements for Red Light-related Devices for the Serious Longevity Science Enthusiast?

 

-------------

 

Answer

 

After some reflection, I'm thinking that the thing to do is to purchase 2 different Types of devices that do at least 2 different wavelengths of light.

 

Device Types

  • Whole (Half) Body Devices
     
  • Spot Devices

Wavelengths

  • Red Light (generally 630 to 680 nm) provides shallower benefit penetration
     
  • Near Infrared (NIR) - (700 to 1000 nm) provides deeper tissue benefit penetration

 

I've already purchased a spot Red Light Device (650 nm). I purchased this spot NIR Infrared bulb this week.

 

I also purchased this book at Amazon. It recommends this half body device that does both Red and NIR light.

 

Not certain about what I'll do about a whole/half body device yet.

 

Did you make a decision about what red light device to get; whole body or face, and do you have any results to report? The study results are impressive.



#186 HighDesertWizard

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Posted 11 May 2019 - 01:09 AM

Did you make a decision about what red light device to get; whole body or face, and do you have any results to report? The study results are impressive.

 

I did decide on what devices to get me started with these light techniques. My hunch is that these are the early days of Red- and Near InfraRed- Light Therapy devices.

  • There are dozens of studies that already demonstrate significant health, and sometimes fast, even profound, health benefit.
  • Also, a close review of device products available at sites like Amazon shows some with numerous, outstanding reviews describing benefits.

It's the combination of 1) the volume of scientific studies demonstrating benefit, along with 2) the very highly rated product reviews confirming those demonstrated study benefits, that I find compelling.

 

The folks buying and finding benefits in these devices don't know and don't care that we're talking about these devices in the context of some conjectures about a heat shock aging switch in humans. All they know is that they've heard it provides enough benefit for friends or family to recommend, or maybe they've read about it, to buy it, use it, and then recommend it it highly.

 

And for something providing real-deal-like benefits, that's would we all should expect, right?

 

But we don't know close to nothing about the optimal frequencies, wattage, pulsing modalities, etc, etc, etc, and combinations to use for specific purposes. So as we learn more I expect we'll seen improved devices that deliver greater (and more cost effective) benefits.

 

It's early days for the science of Red and NearInfraRed Light and health, IMO...

 

 

 

bMiGjpjh.png

 

Yes. It's not cheap. But as I pondered the science I've already browsed (and posted only a few), I'm convinced that doing light therapy is a demonstrably more effective at triggering the kind of effects I've been paying for with supplements for years. I'm now thinking I won't need to spend so much now...

 

Why would I ever purchase Fullerene C60s again when all the difficult-to-find-in-the-literature benefits of FC60-OO are clearly described in an emerging voluminous literature about the impacts of Near InfraRed Light?

 

This is a no-brainer decision after a bit of time reflecting on the volume and impact significance of the two literatures...

 

I'll try to get to describing how I'm using these spot devices and The-Anecdotal-Positive-Felt-Effects I've experienced in another post soon.

 

:)


Edited by HighDesertWizard, 11 May 2019 - 01:43 AM.


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#187 HighDesertWizard

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Posted 11 May 2019 - 02:22 AM

The following study is much more important for me to spend time on summarizing than to summarize my brief experience at this point...

 

The full text of the study is available on-line and I suggest that the study results support the wildly positive study title. This n = 1 anecdotal report is concerned with the experience of a 64-year old woman who was consciously suffering from a family-related serious early-age alzheimer's-leading-to-dementia condition. Well, that, and she decided to do something about it... Wow!

 

2019-03-14, Rapid Reversal of Cognitive Decline, Olfactory Dysfunction, and Quality of Life Using Multi-Modality Photobiomodulation Therapy: Case Report

 

Abstract

Objective: We present a case report of reversal of cognitive impairment, olfactory dysfunction, and quality of life measures in a patient with cognitive decline after multi-modality photobiomodulation (PBM) therapy.

Background: Transcranial and intranasal PBM has been introduced as a light-based therapeutic technique in which exposure to low levels of red to near-infrared (NIR) light stimulates neuronal function, leading to beneficial neurological effects.

Materials and methods: Patient received twice-daily PBM therapy at home using three different wearable light-emitting diode (LED) devices. For the first week containing a mixture of continuous wave mode red (635 nm) and NIR (810 nm) LEDs, a prototype transcranial light helmet and a body pad were used. The body pad was placed on various areas on the lower back and the helmet was worn while seated. After the first week of treatment, an intranasal LED device, 10-Hz pulsed wave mode NIR (810 nm), was initiated in the left nostril twice daily. All three devices were applied simultaneously for an irradiation time of 25 min per session.

Results: The patient showed a significant improvement in the Montreal Cognitive Assessment score from 18 to 24 and in the Working Memory Questionnaire score from 53 to 10. The cognitive enhancement was accompanied by reversal of olfactory dysfunction as measured by the Alberta Smell Test and peanut butter odor detection test. Quality-of-life measures improved and caregiver stress was reduced. No adverse effects were reported.

Conclusions: PBM therapy may be a promising noninvasive approach for patients with neurodegenerative diseases.

 

n5CVzqSh.png

 

GhKoLjNh.png

 

Don't laugh. That'll sooner or later be you...

 

;)

 

 

 

The great thing about this n = 1 report is that it...

  • begins with a solid review of the literature about the science and health benefits of PhotoBioModulation
  • proceeds to describe the experience a single person who decided to Press-The-Pedal-To-The-Metal to improve her personal health condition
  • ends with detail about why the specific Evaluative Tests done to measure her progress, demonstrated profound, were the right ones.

 

 

I nominate this study as The Most Outstanding Template for all N = 1 reports about health benefit that purports to have larger significance...

 

:)

 

 

 

This study, btw, is another done with Michael Hamblin being involved... He's the person to watch in this space...

 


Edited by HighDesertWizard, 11 May 2019 - 02:46 AM.


#188 HighDesertWizard

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Posted 11 May 2019 - 10:59 AM

Selfhacked.com's Joseph Cohen did an interview of Michael Hamblin last month (April 2019). There is useful commentary on the interview page. As you find yourself irresistibly pulled into the science of healthy longevity hacking with NIR, you'll want to watch this interview and read Cohen's text commentary on the interview page.


Edited by HighDesertWizard, 11 May 2019 - 02:06 PM.

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#189 HighDesertWizard

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Posted 12 May 2019 - 02:32 PM

I might pre-purchase Photobiomodulation in the Brain: Low-Level Laser (Light) Therapy in Neurology and Neuroscience 1st Edition, Michael Hamblin, ed, when it's published on July 15, 2019 at Amazon.
 
It's the first academic textbook about the topic.
 
I've "fast browsed" a couple more Michael Hamblin video interviews. I've inserted the best of them. It's a 90-minute interview by, Ari Whitten, the author of that book I've recommended a couple times up thread...
 

Edited by HighDesertWizard, 12 May 2019 - 02:35 PM.


#190 HighDesertWizard

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Posted 12 May 2019 - 03:25 PM

I took this latest deep dive into Red and Near Infrared Light after realizing that their impact appeared to be mediated by members of the Transient Receptor Potential Superfamily of Receptors.

 

I discovered that the mechanism of action for one of the most beneficial techniques for increasing new artery growth throughout the body, EECP, did so (via "shear stress") via TRP receptors.

It's a complex topic, but one of the most rewarding I've taken on in this thread from the point of view of my personal cardiovascular disease.

 

My anecdotal experience with Near InfraRed light for the last 3 weeks.

  • Near InfraRed light focused on my torso at least once but sometimes multiple times per day significantly increases my exercise endurance and the effect is cumulative.
     
  • Near InfraRed light focused on my torso dramatically reduces appetite.
     
  • Near InfraRed light focused on my forehead has a positive impact on stress level, clarity of thought, and mood.

I'm very clear that the first two effects are not placebo effects.

 

The cognitive impact of Red and NearInfraRed light is more difficult to articulate, but I don't believe it's a placebo effect. I consistently take other cognition improving substances so it's more difficult to assess.

 

I don't post about it because I don't want anyone to know all the kinds of substance combos I'm crazy enough to try, but I'm a big believer in the benefit of combining intervention techniques (substances and, now, light) that impact different dimensions of cognition.

 

I attribute some of the most out-of-the-box-but-still-true insights that have longevity promoting impacts I've posted about in this thread and others to combos of substances I've done (and do).

 

Having NearInfraRed devices on hand to shine on the Forehead is an essential new kind of arrow in my cognition enhancing tools quiver.

 

:)


Edited by HighDesertWizard, 12 May 2019 - 03:36 PM.

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#191 HighDesertWizard

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Posted 13 May 2019 - 01:22 AM

There's a lot more content to post and discuss about Red and NearInfraRed Light. But I want to move on to the larger implications of their impacts (along with those of PEMF, EECP, heat, capsaicin, exercise, sauna, etc.) in the context of the topic of this forum thread.

 

Just one last thing before moving on... I only learned about Transient Receptor Potential Channels in the last many weeks. But it turns out these Channels are important--they are triggered by those interventions above--and I'd like to establish a forum post here that recognizes their importance that I can link to when the time comes to do so... And it will...

 

 

 

Transient Receptor Potential channels: Introduction

 

INTRODUCTION


The superfamily of transient receptor potential (TRP) ion channels consists of 28 distinct genes in mammals. They are grouped into six subfamilies by sequence homology: Canonical (TRPCs), Vanilloid (TRPVs), Melastatin (TRPMs), Mucolipins (TRPMLs), Polycystins (TRPPs), and Ankyrin repeat (TRPA). TRP channels may be generally described as cation permeable channels that function as cellular sensors responding to a broad range of stimuli.

Transient receptor potential (TRP) channels constitute a superfamily of cation permeable ion channels. They integrate multiple stimuli as cellular sensors, are widely expressed, and function in many physiological processes [1, 2]. While a subset of TRP channels primarily spans organellar membranes such as endolysosomes, most TRP channels promote Na+ and Ca2+ flux into cells [3]. In this article, we summarize molecular, structural, and functional properties of TRP ion channels.

 

DISCOVERY AND CLASSIFICATION


The founding member of the TRP channel superfamily was identified as essential component of Drosophila phototransduction [4]. A spontaneous mutation in the trp gene resulted in a transient receptor potential in response to continuous light. Drosophila TRP homologs have been identified in yeast, invertebrates and vertebrates. In mammals, 28 genes are classified as TRP channel subunits that are grouped into six subfamilies: the canonical TRPs (TRPCs), the vanilloid receptor TRPs (TRPVs), the melastatin TRPs (TRPMs), the mucolipins (TRPMLs), the polycystins (TRPPs), and the ankyrin transmembrane protein 1 (TRPA1) [1] (Figure 1). Unlike other ion channels that are classified according to a common ligand, function, or selectivity, TRP channel classification is currently based only on sequence homology [5, 6]. TRPCs, TRPVs, TRPMs, and TRPA1 have the highest homology to Drosophila TRP with TRPCs being the closest homologs. TRPMLs and TRPPs are more distantly related [7].

 

There's more at the link, but that's it for now...

 

Here's a classifying diagram shown at that link...

 

Note that "capsaicin receptor" is either a synonym for the TRPV1 channel or closely related to it...

 

fXPr2Wdh.png


Edited by HighDesertWizard, 13 May 2019 - 03:37 AM.

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#192 HighDesertWizard

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Posted 15 May 2019 - 01:51 PM

Remember this study?
 
2016-12-16, In Vivo Amelioration of Age-Associated Hallmarks by Partial Reprogramming
 

Summary

 

Aging is the major risk factor for many human diseases. In vitro studies have demonstrated that cellular reprogramming to pluripotency reverses cellular age, but alteration of the aging process through reprogramming has not been directly demonstrated in vivo. Here, we report that partial reprogramming by short-term cyclic expression of Oct4, Sox2, Klf4, and c-Myc (OSKM) ameliorates cellular and physiological hallmarks of aging and prolongs lifespan in a mouse model of premature aging. Similarly, expression of OSKM in vivo improves recovery from metabolic disease and muscle injury in older wild-type mice. The amelioration of age-associated phenotypes by epigenetic remodeling during cellular reprogramming highlights the role of epigenetic dysregulation as a driver of mammalian aging. Establishing in vivo platforms to modulate age-associated epigenetic marks may provide further insights into the biology of aging.

 
 
I've resurfaced after that deep dive into the evidence about Near InfraRed (NIR) Light. After catching my breath and some reflection, a question begging to be asked has become clear.
 
Are the beneficial health effects triggered by Near Infrared light exposure mediated by epigenetic reprogramming?
 
Consider the information in the draft chart below. I've provided study links for the first 3 Study Effects by Near Infrared Light exposure up thread. I don't know if a study of NIR and lifespan has been done. We do know that NIR triggers Heat Shock Protein expression and we know that HSP expression can increase survival probability.
 
ZnVk97Th.png
 
 

 

Is there a larger evidence-based explanation of the effects of NIR that suggests epigenetic reprogramming is going on?

 

Yes. There is.

 

The title of this forum thread is...

An Ancient "Heat Shock"/NRF2/Pluripotency Related Epigenetic Turn* Accelerates Human Aging** and These can be Modulated

  • Links to studies demonstrating that Heat Shock Proteins "manage" the induction of pluripotent stem cells were provided in the opening post.
     
  • Links to studies showing that HSP expression can increase survival probability appear upthread.
     
  • And there's this study, among others, showing that NIR triggers HSP expression via TRP Channels.

2015, Role of TRP channels in the induction of heat shock proteins (Hsps) by heating skin

 

Transient receptor potential (TRP) channels in skin are crucial for achieving temperature sensitivity to maintain internal temperature balance and thermal homeostasis, as well as to protect skin cells from environmental stresses such as infrared (IR) or near-infrared (NIR) radiation via heat shock protein (Hsp) production. However, the mechanisms by which IR and NIR activate TRP channels and produce Hsps intracellularly have been independently reported. In this review, we discuss the relationship between TRP channel activation and Hsp production, and introduce the roles of several skin TRP channels in the regulation of HSP production by IR and NIR exposure.

 

A tentative model of Hsp production by heat

 

We discuss the roles of several skin TRP channels in the regulation of Hsps production via increased intracellular calcium induced ROS generation after IR and NIR exposure. Thus, the coexistence of TRPV1 and TRPA1 potentially supports a model to explain how hyperthermia can produce Hsps in the cell. This coexistence fulfills the necessary and sufficient conditions to produce Hsps; for Hsp production in the nucleus, an IP3 signal is needed. For IP3 production, PLC β must be activated; the Nishizuka school has already established that a rapid increase in Ca2+ is enough for PLC β activation in vitro. Also for in vivo study, a conditional tissue specific knockout mice are established, blocking TRPV1 or TRPA1 in skin to further detect the production of Hsps after IR/NIR exposure. Therefore, we hypothesize that the activation of TRP channels induces several types of Hsp proteins via intracellular calcium elevation to protect human skin (the largest organ of the human body) and maintain skin homeostasis from harmful EMW and high temperature.

 

 

 

So... the question is...

 

Are the beneficial health effects triggered by Near Infrared light exposure mediated by epigenetic reprogramming?

 

When a falsifying experiment is performed to determine the answer to the question, I believe the answer will turn out to be yes.

 

:)

 

 

 

Oh... I forgot to remind about one last thing, a difference between the 2016 reprogramming study and the NIR effects studies...

 

The 2016 reprogramming study showed positive In-Vivo effects in mice. The NIR studies showing rapid skin and cognition improvement focused on Wild-Type Humans...

 

I guess that's an important difference, right?

 

:)


Edited by HighDesertWizard, 15 May 2019 - 02:12 PM.


#193 kench

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Posted 15 May 2019 - 11:20 PM

It's important to keep in mind that the direct effects of NIR on cells or tissue will be limited to the skin.

This is because the light does not penetrate, in any strength, through much tissue depth. 

The light could have effects systemically, or beyond the skin, but they would be indirect.

 


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#194 HighDesertWizard

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Posted 16 May 2019 - 12:26 AM

It's important to keep in mind that the direct effects of NIR on cells or tissue will be limited to the skin.

This is because the light does not penetrate, in any strength, through much tissue depth. 

The light could have effects systemically, or beyond the skin, but they would be indirect.

 

No. Not true.

 

I've highlighted the sentences in your post shown to be false per the study below in red. I had linked to that study below up thread. Key passages appear below.

 

 

 

2016, Shining light on the head: Photobiomodulation for brain disorders

 

Abstract

 

Photobiomodulation (PBM) describes the use of red or near-infrared light to stimulate, heal, regenerate, and protect tissue that has either been injured, is degenerating, or else is at risk of dying. One of the organ systems of the human body that is most necessary to life, and whose optimum functioning is most worried about by humankind in general, is the brain. The brain suffers from many different disorders that can be classified into three broad groupings: traumatic events (stroke, traumatic brain injury, and global ischemia), degenerative diseases (dementia, Alzheimer's and Parkinson's), and psychiatric disorders (depression, anxiety, post traumatic stress disorder). There is some evidence that all these seemingly diverse conditions can be beneficially affected by applying light to the head. There is even the possibility that PBM could be used for cognitive enhancement in normal healthy people. In this transcranial PBM (tPBM) application, near-infrared (NIR) light is often applied to the forehead because of the better penetration (no hair, longer wavelength). Some workers have used lasers, but recently the introduction of inexpensive light emitting diode (LED) arrays has allowed the development of light emitting helmets or “brain caps”. This review will cover the mechanisms of action of photobiomodulation to the brain, and summarize some of the key pre-clinical studies and clinical trials that have been undertaken for diverse brain disorders.

 

< SNIP >

 

3.1. Light penetration into the brain

 

Due to the growing interest in PBM of the brain, several tissue optics laboratories have investigated the penetration of light of different wavelengths through the scalp and the skull, and to what depths into the brain this light can penetrate. This is an intriguing question to consider, because at present it is unclear exactly what threshold of power density in mW/cm2 is required in the b5rain to have a biological effect. There clearly must be a minimum value below which the light can be delivered for an infinite time without doing anything, but whether this is in the region of μW/cm2 or mW/cm2 is unknown at present.

Functional near-infrared spectroscopy (fNIRS) using 700–900 nm light has been established as a brain imaging technique that can be compared to functional magnetic resonance imaging (fMRI) [32]. Haeussinger et al. estimated that the mean penetration depth (5% remaining intensity) of NIR light through the scalp and skull was 23.6 + 0.7 mm [33]. Other studies have found comparable results with variations depending on the precise location on the head and wavelength [34][35].

Jagdeo et al. [36] used human cadaver heads (skull with intact soft tissue) to measure penetration of 830 nm light, and found that penetration depended on the anatomical region of the skull (0.9% at the temporal region, 2.1% at the frontal region, and 11.7% at the occipital region). Red light (633 nm) hardly penetrated at all. Tedord et al. [37] also used human cadaver heads to compare penetration of 660 nm, 808 nm, and 940 nm light. They found that 808 nm light was best and could reach a depth in the brain of 40–50 mm. Lapchak et al. compared the transmission of 810 nm light through the skulls of four different species, and found mouse transmitted 40%, while for rat it was 21%, rabbit it was 11.3 and for human skulls it was only 4.2% [38]. Pitzschke and colleagues compared penetration of 670 nm and 810 nm light into the brain when delivered by a transcranial or a transphenoidal approach, and found that the best combination was 810 nm delivered transphenoidally [39]. In a subsequent study these authors compared the effects of storage and processing (frozen or formalin-fixed) on the tissue optical properties of rabbit heads [40]. Yaroslavsky et al. examined light penetration of different wavelengths through different parts of the brain tissue (white brain matter, gray brain matter, cerebellum, and brainstem tissues, pons, thalamus). Best penetration was found with wavelengths between 1000 and 1100 nm [41].

Henderson and Morries found that between 0.45% and 2.90% of 810 nm or 980 nm light penetrated through 3 cm of scalp, skull and brain tissue in ex vivo lamb heads [42].

 

 

 

One of the reasons I like the RubyLux Near Infrared lamp I'm using is that the power density is very high compared to other devices.

 

3e2yYx2h.png

 


Edited by HighDesertWizard, 16 May 2019 - 04:27 AM.

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#195 HighDesertWizard

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Posted 16 May 2019 - 04:58 AM

I realized that, for me to fully grasp the Near InfraRed tissue penetration information in the study referenced in the last post, I needed to reformat the sentences.

 

I won't bother to repost the abstract. What follows below is merely the same study title with link and my reformatting of the complete Section "3.1 Light penetration into the brain" text.

 

2016, Shining light on the head: Photobiomodulation for brain disorders
 

3.1. Light penetration into the brain

 

Due to the growing interest in PBM of the brain, several tissue optics laboratories have investigated the penetration of light of different wavelengths through the scalp and the skull, and to what depths into the brain this light can penetrate. This is an intriguing question to consider, because at present it is unclear exactly what threshold of power density in mW/cm2 is required in the b5rain to have a biological effect. There clearly must be a minimum value below which the light can be delivered for an infinite time without doing anything, but whether this is in the region of μW/cm2 or mW/cm2 is unknown at present.

 

Functional near-infrared spectroscopy (fNIRS) using 700–900 nm light has been established as a brain imaging technique that can be compared to functional magnetic resonance imaging (fMRI) [32].

  • Haeussinger et al. estimated that the mean penetration depth (5% remaining intensity) of NIR light through the scalp and skull was 23.6 + 0.7 mm [33]. Other studies have found comparable results with variations depending on the precise location on the head and wavelength [34][35].
     
  • Jagdeo et al. [36] used human cadaver heads (skull with intact soft tissue) to measure penetration of 830 nm light, and found that penetration depended on the anatomical region of the skull (0.9% at the temporal region, 2.1% at the frontal region, and 11.7% at the occipital region). Red light (633 nm) hardly penetrated at all.
     
  • Tedord et al. [37] also used human cadaver heads to compare penetration of 660 nm, 808 nm, and 940 nm light. They found that 808 nm light was best and could reach a depth in the brain of 40–50 mm.
     
  • Lapchak et al. compared the transmission of 810 nm light through the skulls of four different species, and found mouse transmitted 40%, while for rat it was 21%, rabbit it was 11.3 and for human skulls it was only 4.2% [38].
     
  • Pitzschke and colleagues compared penetration of 670 nm and 810 nm light into the brain when delivered by a transcranial or a transphenoidal approach, and found that the best combination was 810 nm delivered transphenoidally [39].
    • In a subsequent study these authors compared the effects of storage and processing (frozen or formalin-fixed) on the tissue optical properties of rabbit heads [40].
  • Yaroslavsky et al. examined light penetration of different wavelengths through different parts of the brain tissue (white brain matter, gray brain matter, cerebellum, and brainstem tissues, pons, thalamus). Best penetration was found with wavelengths between 1000 and 1100 nm [41].
     
  • Henderson and Morries found that between 0.45% and 2.90% of 810 nm or 980 nm light penetrated through 3 cm of scalp, skull and brain tissue in ex vivo lamb heads [42].

Edited by HighDesertWizard, 16 May 2019 - 05:00 AM.


#196 HighDesertWizard

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Posted 17 May 2019 - 09:04 AM

If you're paying attention to the status of the conjectures animating my posts in this thread, the following may be interesting. If status of the conjectures isn't interesting to you, I suggest you skip this post...

 

It's time again to reevaluate the status of one of the conjectures animating my posts in this thread and that make up the larger scoped conjecture that is this forum thread's title...

 

On November 19, 2018, I made a post suggesting that there were 4 conjectures

 

HighDesertWizard, on 19 Nov 2018 - 02:45 AM, said:snapback.png

It’s worthwhile to review the status of the 4 sub-conjectures of the thread title conjecture in more detail.
 
“Heat Shock” Expression Declines in Humans During Aging but can be Modulated for Benefit
 
“Heat Shock”, OSKM, iPSC, and Epigenetic Reprogramming are Related Biological Processes
 
An Epigenetic Turn Initiates an Aging Process in Humans

See the Seth Grant video in the opening post for what this is about...

4 ... An Ancient, Non-Mammalian “Heat Shock” Related Epigenetic Turn Exists in Mammals
 
This sub-conjecture is that the ancient, heat shock-related gene expression turn in c. elegans Richard Morimoto wrote about in 2015 is an evolutionarily conserved analog to the epigenetic turn mechanism identified by the Grant/Skene/Roy team.. (I'm uncertain that the phrase "evolutionarily conserved analog to the epigenetic turn mechanism" is the right way to phrase what I mean here. If you know the right way to phrase it, please post it.)

 

That last conjecture, #4, contains two distinct conjectures, let's call them #4 and #5... New statements of the conjectures appear below...

 

4... An Ancient, Non-Mammalian, "Heat Shock"-Related Aging Epigenetic Switch Exists in Mammals, Including in Humans
 

This conjecture is intended to state that the Heat Shock-related aging switch Richard Morimoto and his team found in c elegans in 2015 also exists in mammals, including in humans

 

5... The Ancient, Non-Mammalian, "Heat Shock"-Related Aging Epigenetic Switch (of #4) is the same biological process as the #3 conjecture, An Epigenetic Turn Initiates an Aging Process in Humans
 

This conjecture is intended to state that the 2015 c elegans Morimoto Aging Switch, that per #4 exists in humans, is the same biological process as the Epigenetic Turn that Seth Grant epigenetic turn of 2017.

 

 

I understand these details might be confusing to those not following my posts about the distinct conjectures closely.

 

If you look closely, you can spot my earlier error in describing this thread's conjectures...

 

In the prior conjecture list, I was including two conjectures as part of conjecture #4 that should be logically split into two...

  • 1) Morimoto's 2015 aging switch exists in humans and it also 2) is the same biological process as Seth Grant's 2017 "Epigenetic Turn"...

Those two conjectures are now conjectures #4 and #5...

 

Sorry if this is confused and convoluted...

 

:)


Edited by HighDesertWizard, 17 May 2019 - 09:05 AM.


#197 HighDesertWizard

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Posted 17 May 2019 - 09:36 AM

 
[Do] you know what the clinching evidence was that space-time is curved?
It was a photograph, not of space-time, but of an eclipse, with a dot there rather than there.
And the evidence for evolution? Some rocks and some finches.
And parallel universes? Again: dots there, rather than there, on a screen.
What we see, in all these cases, bears no resemblance to the reality that we conclude is responsible
... only a long chain of theoretical reasoning and interpretation connects them.

-- David Deutsch

 

 

 

My friends... It's time to reevaluate the status of (the new) conjecture #4. The argument below has several components. Let's see if I can clearly state them and convince you that new evidence increases the probability that conjecture #4 is true...

 

4... An Ancient, Non-Mammalian, "Heat Shock"-Related Aging Epigenetic Switch Exists in Mammals, Including in Humans

 

This conjecture is intended to mean that the Heat Shock-related aging switch Richard Morimoto and his team found in c elegans in 2015 also exists in mammals, including in humans

 

 

At the outset, we need to remind ourselves of what the 2015 study actually found...

 

2015, Repression of the heat shock response is a programmed event at the onset of reproduction

 

The heat shock response (HSR) is essential for proteostasis and cellular health. In metazoans, aging is associated with a decline in quality control, thus increasing the risk for protein conformational disease. Here, we show that in C. elegans, the HSR declines precipitously over a four hour period in early adulthood coincident with the onset of reproductive maturity. Repression of the HSR occurs due to an increase in H3K27me3 marks at stress gene loci, the timing of which is determined by reduced expression of the H3K27 demethylase jmjd-3.1. This results in a repressed chromatin state that interferes with HSF-1 binding and suppresses transcription initiation in response to stress. The removal of germ line stem cells preserves jmjd-3.1 expression, suppresses the accumulation of H3K27me3 at stress gene loci and maintains the HSR. These findings suggest that competing requirements of the germ line and soma dictate organismal stress resistance as animals begin reproduction.

 

kWA9T32h.png

 

In 2017, Morimoto and his 2015 study co-author Labbadia published another study...

 

2017, Mitochondrial Stress Restores the Heat Shock Response and Prevents Proteostasis Collapse during Aging

 

In Caenorhabditis elegans, the programmed repression of the heat shock response (HSR) accompanies the transition to reproductive maturity, leaving cells vulnerable to environmental stress and protein aggregation with age. To identify the factors driving this event, we performed an unbiased genetic screen for suppressors of stress resistance and identified the mitochondrial electron transport chain (ETC) as a central regulator of the age-related decline of the HSR and cytosolic proteostasis. Mild downregulation of ETC activity, either by genetic modulation or exposure to mitochondria-targeted xenobiotics, maintained the HSR in adulthood by increasing HSF-1 binding and RNA polymerase II recruitment at HSF-1 target genes. This resulted in a robust restoration of cytoplasmic proteostasis and increased vitality later in life, without detrimental effects on fecundity. We propose that low levels of mitochondrial stress regulate cytoplasmic proteostasis and healthspan during aging by coordinating the long-term activity of HSF-1 with conditions preclusive to optimal fitness.

 

 

 

Let's speculate for a moment... Suppose we believed...

  • the Morimoto switch actually does exist in humans....
     
  • the Electron Transport Chain actually is the "central regulator of the age-related decline of the HSR and cytosolic proeostasis".

Suppose, then, that...

  • some technique for "touching" the ETC in something close to an optimal way was found for humans
     
  • use of that technique made for profoundly positive changes in human health, including rejuvenation in some key dimensions of health

I ask myself... if the last two suppositions above turn out to be true, what does that mean for the status of Conjecture #4...

 

 

 

Complex IV of the electron transport chain, also known as cytochrome c oxidase, is a multiunit structure that functions to transfer electrons form cytochrome c to oxygen and in the process form water and help generate a proton gradient.

 

 

 

 

I've seen the light.#1..

 

... some technique for "touching" the ETC in something close to an optimal way was found for humans

 

2018, Inhibitory modulation of cytochrome coxidase activity with specific near-infrared light wavelengths attenuates brain ischemia/reperfusion injury

 

There are many more studies documenting what is now settled science.... Near InfraRed light exposure, in some way, "touches" cytochrome c oxidase, Complex IV of the Electron Transport Chain.

 

I've seen the light.#2..

 

... use of that technique made for profoundly positive changes in human health, including rejuvenation in some key dimensions of health

 

2019-03-14, Rapid Reversal of Cognitive Decline, Olfactory Dysfunction, and Quality of Life Using Multi-Modality Photobiomodulation Therapy: Case Report

 

I posted the abstract and some pics from this study here up thread...

 

2014, A Controlled Trial to Determine the Efficacy of Red and Near-Infrared Light Treatment in Patient Satisfaction, Reduction of Fine Lines, Wrinkles, Skin Roughness, and Intradermal Collagen Density Increase

 

I posted the abstract and some pics from this study here up thread...

 

 

 

4... An Ancient, Non-Mammalian, "Heat Shock"-Related Aging Epigenetic Switch Exists in Mammals, Including in Humans

 

Conjecture #4 must be considered more extremely difficult to falsify when the evidence about Near Infrared light is considered...

 

:)


Edited by HighDesertWizard, 17 May 2019 - 10:34 AM.


#198 HighDesertWizard

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Posted 17 May 2019 - 11:08 PM

 

2018, Inhibitory modulation of cytochrome coxidase activity with specific near-infrared light wavelengths attenuates brain ischemia/reperfusion injury
 
The things to look for in this study, and the reason a first post about the details belongs in this forum thread, are the variable impacts different NIR frequencies have on cytochrome c oxidase expression. Here's the abstract...
 

The interaction of light with biological tissue has been successfully utilized for multiple therapeutic purposes. Previous studies have suggested that near infrared light (NIR) enhances the activity of mitochondria by increasing cytochrome c oxidase (COX) activity, which we confirmed for 810 nm NIR. In contrast, scanning the NIR spectrum between 700 nm and 1000 nm revealed two NIR wavelengths (750 nm and 950 nm) that reduced the activity of isolated COX. COX-inhibitory wavelengths reduced mitochondrial respiration, reduced the mitochondrial membrane potential (ΔΨm), attenuated mitochondrial superoxide production, and attenuated neuronal death following oxygen glucose deprivation, whereas NIR that activates COX provided no benefit. We evaluated COX-inhibitory NIR as a potential therapy for cerebral reperfusion injury using a rat model of global brain ischemia. Untreated animals demonstrated an 86% loss of neurons in the CA1 hippocampus post-reperfusion whereas inhibitory NIR groups were robustly protected, with neuronal loss ranging from 11% to 35%. Moreover, neurologic function, assessed by radial arm maze performance, was preserved at control levels in rats treated with a combination of both COX-inhibitory NIR wavelengths. Taken together, our data suggest that COX-inhibitory NIR may be a viable non-pharmacologic and noninvasive therapy for the treatment of cerebral reperfusion injury.

 
Wow! This is important. The details are worth grasping and I'll explain why in another post in another thread...
 
Keep in mind that most other studies of the benefits of NIR light focus on frequencies between 810 nm and 860 nm...
 
From the Results portion of the paper...
 

Identification of COX-inhibitory NIR

 

We systematically screened the NIR electromagnetic spectrum in the “therapeutic window of opportunity” of 700 nm to 1000 nm, where NIR absorptions by water and blood are minimal, allowing deep tissue penetration of the NIR for possible medical applications. We integrated a light-protected oxygen electrode chamber into a double beam spectrophotometer (see Materials and Methods), which contained regulatory-competent bovine COX purified under conditions preserving the physiological regulatory properties of the enzyme, such as posttranslational modifications (Fig. 1A). While the NIR frequencies were scanned, COX activity was measured simultaneously. In contrast to previous studies concluding that NIR consistently activates COX12,17,18,19,20,21,22, we identified two novel wavelength ranges (750 nm and 950 nm) that inhibit COX activity (Fig. 1B).

 

rIZzOIoh.png

 

Caption

 

NIR modulates COX activity and mitochondrial oxygen consumption rate. (A) Isolated regulatory-competent bovine COX separated into its subunits on a high-resolution urea/SDS-PAGE Coomassie-stained gel. Subunits are indicated in roman numerals. (B) Representative scan of wavelength-dependent COX activity identifying the 750 nm and 950 nm wavelength rages as inhibitory regions. © Effect of NIR emitted by LED diodes confirms that 750 nm and 950 nm NIR inhibit COX in vitro while 810 nm NIR activates the enzyme. Data were obtained over a 3-min interval of irradiation and normalized to non-irradiated samples (n ≥ 4; *p < 0.05). (D) NIR irradiation modulates oxygen consumption rate (OCR) in a wavelength specific manner. 750 nm and 950 nm NIR reduce OCR below the basal respiration rate and 810 nm NIR increase mitochondrial OCR (n ≥ 4; *p < 0.05).

 

 

From the study above we learn that different frequencies of Near InfraRed (NIR) light can either reduce or increase cytochrome c oxidase

  • Combined 750 and 950 nm NIR light exposure maximally inhibited cytochrome c oxidase expression
     
  • 810 nm NIR light exposure maximized cytochrome c oxidase expression

Why is that important?

 

  

2018, The Involvement of Cytochrome c Oxidase in Mitochondrial Fusion in Primary Cultures of Neonatal Rat Cardiomyocytes

 

Cytochrome c oxidase (CCO) is a copper-dependent enzyme of mitochondrial respiratory chain. In pressure overload-induced cardiac hypertrophy, copper level and CCO activity are both depressed, along with disturbance in mitochondrial fusion and fission dynamics. Copper repletion leads to recovery of CCO activity and normalized mitochondrial dynamics. The present study was undertaken to define the link between CCO activity and mitochondrial dynamic changes. Primary cultures of neonatal rat cardiomyocytes were treated with phenylephrine to induce cell hypertrophy. Hypertrophic cardiomyocytes were then treated with copper to reverse hypertrophy. In the hypertrophic cardiomyocytes, CCO activity was depressed and mitochondrial fusion was suppressed. Upon copper repletion, CCO activity was recovered and mitochondrial fusion was reestablished. Depression of CCO activity by siRNA targeting CCO assembly homolog 17 (COX17), a copper chaperone for CCO, led to fragmentation of mitochondria, which was not recoverable by copper supplementation. This study thus demonstrates that copper-dependent CCO is critical for mitochondrial fusion in the regression of cardiomyocyte hypertrophy.

 

There are a few studies already published that suggest NIR light being intimately related to Mitochondrial Fission and Fusion processes via impacts on Cytochrome c Oxidase, in one way or another...

 

More are to be expected...

 

There aren't a lot at this time in which the point is made in the abstract itself and I'm short on time at the moment to carefully select the non-abstract study passages confirming the fact of the importance of cytochrome c oxidase expression for mitochondrial fusion....

 

But I'd like to post about the importance of this fact, so I'm posting with just one study reference in support this evening...

 

:)


Edited by HighDesertWizard, 18 May 2019 - 05:33 AM.


#199 HighDesertWizard

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Posted 18 May 2019 - 05:58 AM

Posted my immediately previous post to Turnbuckle's thread entitled Manipulating mitochondrial dynamics just now...

 

And then I added this comment...
 

At some point soon, no regimen for managing mitochrondrial fission / fusion dynamics will be taken seriously that doesn't include a Near InfraRed Light exposure component...
-- Steve Buss, 2019-05-17
 
:)  :cool:  :)

 

My hope is that Turnbuckle and/or other folks posting to that thread will take up the challenge of figuring out how to incorporate a Near InfraRed light exposure component into their optimal regimen for doing Fission / Fusion dynamics management and then share it with us...

 

:)


Edited by HighDesertWizard, 18 May 2019 - 02:26 PM.

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#200 HighDesertWizard

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Posted 21 May 2019 - 11:41 PM

There are multiple studies showing that specific intra-spectrum (Red, Near Infrared, Far Infrared) frequencies have different effects
 

Evidence
 
2016, Photobiomodulation (blue and green light) encourages osteoblastic-differentiation of human adipose-derived stem cells: role of intracellular calcium and light-gated ion channels
 

Human adipose-derived stem cells (hASCs) have the potential to differentiate into several different cell types including osteoblasts. Photobiomodulation (PBM) or low level laser therapy (LLLT) using red or near-infrared wavelengths has been reported to have effects on both proliferation and osteogenic differentiation of stem cells. We examined the effects of delivering four different wavelengths (420 nm, 540 nm, 660 nm, 810 nm) at the same dose (3 J/cm2) five times (every two days) on hASCs cultured in osteogenic medium over three weeks. We measured expression of the following transcription factors by RT-PCR: RUNX2, osterix, and the osteoblast protein, osteocalcin. The 420 nm and 540 nm wavelengths were more effective in stimulating osteoblast differentiation compared to 660 nm and 810 nm. Intracellular calcium was higher after 420 nm and 540 nm, and could be inhibited by capsazepine and SKF96365, which also inhibited osteogenic differentiation. We hypothesize that activation of light-gated calcium ion channels by blue and green light could explain our results.

 

Study Result #2

 

The activation of 420 nm and 540 nm to promote osteogenic differentiation could be abrogated by TRPV1 and TRPC channel inhibitors

 

We performed Alizarin red (AR-S) staining as a mineralization assay in osteogenic medium with or without addition of TRP channel antagonists CPZ(5 μM) and SKF(5 μM) incubating for 10 minutes before photobiomodulation. There was a significant difference between OM and 420 nm, 540 nm, 810 nm groups. ***(P < 0.001) for 420 nm and 540 nm groups, and *(P < 0.05) for 810 nm group. There was no significant difference between the OM and 660 nm groups. Compared with 810 nm group, 420 nm (#P < 0.05) and 540 nm (###P < 0.001) had better effects in the ARS assay (Fig. 2A–C). The increase in the mineralization level in response to 420 nm and 540 nm groups was abrogated by the TRP channel antagonists CPZ and SKF (Fig. 2A–D). These results imply that TRP calcium channels play a role in blue and green light-enhancement of osteoblast differentiation. The AR staining after red light (660 nm) was partially abrogated by the TRP inhibitors. NIR light-mediated enhancement of osteogenic differentiation was not abrogated by TRP inhibitors, and therefore appears to occur via a different mechanism.

 



... if I'm reading that and other studies correctly...

  • exposure to 750 nm and 950 nm light increases Mitochondrial Fission by inhibiting cytochrome c oxidase.
  • exposure to 810 to 860 nm light increases Mitochondrial Fusion by increasing cytochrome c oxidase
Graphic figure "B" makes clear why those values were selected. See my previous post for the caption.
 
 
rIZzOIoh.png
 
I bought a 940 nm flashlight this morning at Amazon. I'm hoping it will help with damage from an infection injury.injury.

 



#201 HighDesertWizard

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Posted 22 May 2019 - 05:03 AM

Bingo! Maybe...

 

We've seen up thread that applying techniques to increase heat shock provides benefit.

  • Any Heat Shock-related Aging Switch doesn't have to do with the biological benefit of heat shock protein expression.
     
  • The Heat Shock-related Aging Switch I believe exists is about our declining biological capacities for triggering heat shock protein expression.

Keeping that distinction in mind, being on the alert for the biological upstream triggers of heat shock proteins is important...

 

 

First things first...

 

We know that the Transient Receptor Potential (TRP) Vanilinoid 1 (TRPV1) Channel increases heat shock protein.

 

2007, Transient receptor potential vanilloid-1 mediates heat-shock-induced matrix metalloproteinase-1 expression in human epidermal keratinocytes

 

2012, Heat shock factor 1 regulates the expression of the TRPV1 gene in the rat preoptic‐anterior hypothalamus area during lipopolysaccharide‐induced fever

 

Now... I haven't checked this out yet, but this is the kind of upstream trigger-of-heat-shock protein I'm looking for...

 

2012, Aging reverses the role of the transient receptor potential vanilloid-1 channel in systemic inflammation from anti-inflammatory to proinflammatory

 

:)



#202 Nate-2004

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Posted 22 May 2019 - 10:09 PM

 

  • exposure to 750 nm and 950 nm light increases Mitochondrial Fission by inhibiting cytochrome c oxidase.
  • exposure to 810 to 860 nm light increases Mitochondrial Fusion by increasing cytochrome c oxidase

 

The RubyLux bulb I've been using for a while now is a range of 700 nm to 1000 nm wavelength. So I wonder how that affects dynamics?

 

I also have this pad and have been trying it on my belly. It's 660 and 880 nm. Not sure it's enough power.



#203 HighDesertWizard

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Posted 23 May 2019 - 03:00 AM

The RubyLux bulb I've been using for a while now is a range of 700 nm to 1000 nm wavelength. So I wonder how that affects dynamics?

 

I also have this pad and have been trying it on my belly. It's 660 and 880 nm. Not sure it's enough power.

 

Exploring the science of this forum thread's title got me into exploring light frequency techniques. It's a huge topic and not long ago I created another thread for discussing it.

 

I'll post and reply about content related to the Science of Longevity-Promoting, Frequency Sensitive Biological Targets in that thread.

 

Thanks for the reply Nate. I'll reply there.


Edited by HighDesertWizard, 24 May 2019 - 12:16 AM.


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#204 HighDesertWizard

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Posted 24 May 2019 - 08:49 AM

We've been exploring at least 5 conjectures... I've restated and listed them below in a new order...

  • “Heat Shock” Expression Declines in Humans During Aging but can be Modulated for Benefit
    • Posts about practical, healthy longevity benefiting, heat shock protein-related interventions fall into this category.
  • “Heat Shock”, OSKM, iPSC, and Epigenetic Reprogramming are Related Biological Processes
    • study evidence supporting this conjecture was noted in the opening post of this thread
  • An ancient "Heat Shock"-related aging switch exists in c elegans and is triggered in early adulthood
  • A set of genes in mice and humans related to PSD-95 and Schizophrenia can be used to predict biological age and expression of these genes dramatically turns in early adulthood
  • The Ancient "Heat Shock"-Related Aging Switch in c Elegans (conjecture #3) is the Ortholog ("comparable") Biological Process of gene expression turn in mice and humans highlighted in conjecture #4
    • this is a conjecture I've been writing about in this forum thread with varying, hopefully increasing, degrees of clarity

 

I've come across a batch of evidence that supports Conjecture #5 that also might be helpful in configuring an experiment to falsify the conjecture.

 

It's not new evidence, it's evidence I've recently become familiar with.

 

:)


Edited by HighDesertWizard, 26 May 2019 - 05:17 AM.






Also tagged with one or more of these keywords: aging switch, seth grant, psd-95, nf-kb, heat shock protein, senescence, sasp, nrf2, morimoto, survival

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