DECENTRALIZED MEDICINE #17: IS PAIN MANAGEMENT FOR DIABETIC PERIPHERAL NEUROPATHY RELATED TO MKULTRA?

If you understand the science of nnEMF you'd understand why the picture above is an oxymoron. The number one indication for spinal cord stimulation in the USA, according to CMS data, is diabetic peripheral neuropathy (DPM)

The global spinal cord stimulation market size was valued at USD 2.88 billion in 2019 and USD 2.41 billion in 2020 and is projected to grow USD 4.12 billion by 2027, exhibiting a CAGR of 8.0%. North America dominated the global market with a share of 73.96% in 2023.

DO SPINAL CORD STIMULATORS MAKE DECENTRALIZED SENSE FOR CHRONIC PAIN for DPN?

Is "the juice worth the squeeze?  Spinal cord stimulators were conceptualized based on the overly simplistic "gate control theory of pain" proposed by Melzack and Wall. Wall himself later wrote, “The least, and perhaps the best, that can be said for the 1965 paper is that it provoked discussion and experiment.” Is that still true based upon this paper written 10 years ago at the 50th anniversary of this "theory."

Does gate control theory take POMC biology into consideration for pain?  NOPE.  Do you wonder why? 

Who funded the study?  The military did, and so did industrial partner Bell Labs and the Federal agency NASA.  Given what you heard recently on the Danny Jones podcast, does this make any decentralized sense?  If you look at CITE 78 on the original paper written in 1965, you'll see the following funding notes about this "theory":  

"This study was supported in part by contract SD-193 from the Advanced Research Projects Agency, U.S. Department of Defense (to R.M.); and in part by the Joint Services Electronics Program under contract DA36-039- AMC-0320O(E), the Bell Telephone Laboratories, Inc., the Teagle Foundation, Inc., the National Science Foundation (grant GP-2495), the National Institutes of Health (grants MH-04737-05 and NB-04897-02), the National Aeronautics and Space Administration (grant NsG-496), and the U.S. Air Force (ASD contract AF33 (615J-1747)."  

CITE:  

https://pcpr.pitt.edu/wp-content/uploads/2018/01/Melzack-Wall.pdf

Now look at the highlighted part of the picture below again and read it.

HAS IT REALLY REVOLUTIONIZED OUR UNDERSTANDING OF PAIN, OR WAS IT USED TO BLOCK US FROM THE TRUTH ABOUT HOW SUNLIGHT REDUCES PAIN AND DIABETES?

The 1965 gate control theory of pain describes how non-painful sensations can override and reduce painful sensations. A painful, nociceptive stimulus stimulates primary afferent fibers and travels to the brain via transmission cells. Increasing activity of the transmission cells results in increased perceived pain.

So the answer should be a clear no, but we still do them in centralized medicine and CMS data says the market is close to 3 billion dollars. That is a lot of cash for a theory that still has not been proven.  

Many people get stimulators for diabetic peripheral neuropathy.  How many pain specialists or neurosurgeons know about the links between POMC and neuropathy?

Very few. Why? In 1965, two authors, both linked to academic centers with military funding, proposed a new theory about how pain happens.  

Should neurosurgeons and pain specialists know that POMC is critical in DPN and chronic pain?  Why aren't they taught the truth?  

POMC PAIN STORY IS A STORY ABOUT LIGHT = MKULTRA STORY 

The endogenous opioid system is our body’s endogenous line of defense against noxious stimuli. This system is part of the leptin-melanocortin pathway in mammals.  Endogenous opioid precursors are proopiomelanocortin (POMC), pro-dynorphin (PDYN), and pro-enkephalin (PENK)) which are proteolytically cleaved to produce opioid peptides. 

These bind to their cognate opioid receptors and trigger downstream signaling events.  Those ion channels are activated by K+ channels and inhibited by Ca++ channels.  Ironically we know that light and electricity can alter these ion channels.  Blu light and nnEMF were known to cause calcium efflux issues in the 1970s.  When K+ channels are activated or Ca2+ inhibited is usually part of the clinical event one should expect.  These set of circumstances result ultimately in the inhibition of neuronal excitability. Persistent neuropathic pain in DPN = diabetic peripheral neuropathy patients suggests a dysfunction in endogenous opioid-mediated antinociceptive mechanisms.  Blue light exposure is known to drive blood glucose high and drive insulin higher.  See Nora Volkow's papers from NYU circa 2011.  There is a powerful correlation of blue light exposure to diabetic transformation.  Blue light exposure also seems to destroy POMC translation in mammals.

DID YOU KNOW RED LIGHT BY ITSELF LOWERS BLOOD GLUCOSE?

The interesting thing is no one has done a study yet to show that the combination use of UV and IR light might work to reduce pain in the centralized literature.

But did you know that sunlight also reduces the need for insulin for diabetic mammals? It is true, sunlight reduces insulin resistance in all mammals so far tested.

Previous studies have examined the link between the endogenous opioid system and diabetes, and reported that opioid peptide levels are altered in the central nervous system and plasma of diabetic rodent models as well as of diabetic human patients. Today, we now know the opioid levels linked to POMC translation in the peripheral nervous system (PNS) are altered during diabetes.  

In fact, in vivo correction of this deficit can rescue diabetes-induced hyperalgesia and associated behavioral changes, thereby showing the relevance of the dysfunctional POMC-MOR signaling to the increased pain sensitivity observed in diabetes.  So, should DC electric pain stimulators be replaced with light therapy stimulators since POMC responds to UV light?  FYI: Your mitochondria is the UV light generators gone bad in diabetes. This is why all living cells have been shown to liberate ultraweak UV biophotons. Diabetics are no longer capable of this due to their defective mitochondria.

They do not want you to know this because they'd lose 3 billion in generator sales.

GOT IT?

It is well known that UV and IR light reduce blood glucose and decrease pain.  Moreover, it is also well known that UV light raises vitamin D levels, and Vitamin D levels highly correlate with increased pain and higher narcotic use.  Might light stimulators be better than spinal stimulators because the gate theory idea proposed by science linked to the industrial and military complex is entirely flawed?  Better yet, was it really flawed or was it put forth by design by the industrial military complex who paid for Melzack and Walls paper 60 years ago?  

Ask TED what he thinks about the military and truth: https://x.com/ted_macie/status/1842629039682384115

SUMMARY

Your cells capture the light you choose to live under. This was the message distilled from MKULTRA program. Your choices are quantized in your melatonin and insulin levels. You are essentially an electromagnet for light. As a result of electromagnetic capture, the thoughts created in your brain via your retina and skin have a frequency associated with them and that frequency resonates with a select few. That resonance determines whom you collect in your lives. They are essentially antennas in your life and they are linked by the light you choose.

The centralized paradigm in power in healthcare wants people to think it's a type of "lock and key mechanism" but this is factually incorrect. It is more like the electro-magnetic gate control we see in semiconducting light diodes. Melatonin receptors are found to a great degree in the retina, RPE, and the visual pathways of the brain. When light is absent then melatonin activates these "light diode-like" gates. For humans, the absence of light is an optical non-linear signal that indicates that it is the period when redox levels are unstressed by solar radiation. This is how the brain tells time, night from day. Melatonin is an old evolutionary clock that was important before the optical lattice clock that now exists in your visual pathways came along via evolution. Light activation can long before food activation in evolutionary timescales.

The circadian clock in the eye and tissues, however, in humans still controls glucose and insulin metabolism, as the picture above shows. It also is the reason why blue light at night is what is driving insulin resistance and the runaway diabetes we see today. The optical signal of melatonin is a key circadian timing signal that contributes to and is a part of a cascade of other responses that help initiate and maintain sleep when light is not present. Melatonin levels also control the distances between respiratory proteins in our mitochondria. If the level is low anywhere in the system % heteroplasmy rises and the ATPase of that mitochondria begins to spin slower than it should and electron chain transport slows in that tissue and damage occurs that can make that organ disease.  As a result NAD+ drop. This is a result of light not food.

Strangely enough, researchers now know that these receptors are also found in the pancreas, but clinicians have no idea this is what is behind the diabetes epidemic globally. It is related to the amount of deuterium on receptors on alpha and beta cells in the pancreas and a lack of sunlight makes it more likely that you'll get diabetes. Melatonin receptor density is brisk in pancreatic alpha and beta cells. Melatonin controls the mtDNA in the alpha and beta cells in the pancreas. This is how diabetes manifests from getting too much artificial light at night via our eyes or skin. Most people know beta cells release insulin during the day when we are supposed to eat. Beta cells regulate glucose levels in the blood. During daylight blood pools to the surface to absorb specific frequencies of sunlight while releasing nitric oxide. Researchers also know that when melatonin activates these receptors via the blood plasma, insulin secretion is decreased from the pancreas. This mechanism shows your that diabetes is a photo-electric disease. Your government is behind the epidemic.

CITES

https://www.fortunebusinessinsights.com/industry-reports/spinal-cord-stimulation-market-100313#

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4676495/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7814083/

https://pubmed.ncbi.nlm.nih.gov/27727191/

https://x.com/DrJackKruse/status/1842010173910708409