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RichGotsPots

My Theory On What Is Causing Most Dysautonomia And Why There Are Wide Ranging Symptoms- Autonomic Neuropathy

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Hi Everyone, I'm back with my 3rd Dysautonomia updated theory. I hope everyone will take the time to carefully read it over before they dismiss it or think they know aout it already. I will try to write in lay terms as much as possible. I have been researching Dysautonomia on my own without any formal medical or scientific background for just about the last year and a half. I'm well aware of just about every theory out there both in the medical/scientific community as well as on the forums by patients. You name it I've read about it :) please keep that in mind when you comment below. I don't dismiss any theory out there whatsoever, on the contrary I am tying most of them together. I believe all the theories thus far are mainly addressing symptoms rather than underlying causes. I'm speaking in general and prefer not to address any one particular theory so that I do not go off on a tangent or offend anyones set ideas.

As stated this is pure theory and can only be confirmed by diligent clinical and laboratory research.

- Dysmyelination of preganglionic fibers of the Autonomic Nervous System as well as other Small Fiber Autonomic Neuropathies-

I think most of us know and understand that Dysautonomia is a syndrome or dysfunction of the Autonomic Nervous System (ANS) but really when it comes down to it we may know what all the possible symptoms are but we find it hard to get information about how this seemingly automatic system works. I won't bore you with the details but I do want to explain that the ANS is controlled by parts of the lower brain stem as one might expect. Although parts of the ANS for example are believed to operate in autonomy cut off from the control of the brain such as the gastro autonomic system. Also I am not going into detail of the sympathetic vs. parasympathetic system divisions the reason I hope will be apparent at my conclusion.

There is a cascade of ways that the brain communicates with the various parts of the body. But the main way is through biochemical-like receptors that recept or receive messages sent from the brain and launch into action or inaction depending on the messages. Many chemicals are involved such as hormones like cortisol, testosterone or histamines/mast cells and inflammatory T cells or the most important are direct neurotransmitters like catecholamines or even nonadrenic neurotransmitters like GABA. Most theorist zero in on these chemicals to see if they are dysfunctioning and how or why.

The next important detail in how the ANS works is how are those messages from the brain traveling to the receptors that are then acting. Again I won't go into too much detail except on the relevant details pertaining to the ANS. The brain sends electrical signals to the receptors it needs to send messages to via an ingenuously design network of fibers. You can think of it as a fiber optics network in the body. It really is very similar to how fiber optics sends data along glass tubes via light/laser. Again I'm purposely ignoring the great detail of how this happens to make it easier for the general reader here. If you want you can look it up in greater detail and/or msg me in private and I will explain it better.

There are 3 types of Nerve Fibers used as signal conductors and are basically defined by diameter of the tube:

Group A: Large fibers and for the most part send signals to the muscle and have nothing to do with the ANS. These large fibers are large diameter which allows for very fast signals to the muscle. These are mostly all Myelinated fibers (which I define below)

Group B: Small Nerve fibers in this group are myelinated. Generally, they are the preganglionic fibers of the ANS and have much slower signal rates than Group A.

Group C: Also Small fibers but these are unmyelinated and as the Group B fibers they also have a slower signal rate.

These fibers include:

Postganglionic fibers in the ANS

Nerve fibers at the dorsal roots (IV fiber). Which tend to be sensory based

Each Nerve Fiber generally has a Myelin Sheath and an Axon except in the case of unmyelinated ANS small fibers. Think of Myelin as the rubber insulation of an electrical wire and an axon as the actual metal conduction wire inside the rubber tube.

So the two groups I have focused my attention to are Group B and Group C ANS Nerve fibers.

I believe that both these groups are causing 60-80% of our Dysautonomia. The other percentage I believe have other things that mimic or act the same way compared to a true neuropathy. These people are just as ill but their illness is not a direct result of damage to the ANS per se. Meaning damage to the lower brainstem or ANS Nerve fibers. Again there are too many possibilities to list in this group such as B vitamin deficiencies.

In Group B I believe that some of us have what is called Dysmyelination (deformed) as opposed to Demyelination (holes) of the complete myelin sheath. This means, in lay term, that the tubing is deformed but there are not any major holes in it, so the signal still goes through but its very distorted and thus dysfunctions. And that the type of distortion will determine the type of messages that are getting scrambled. Or even that the location of the deformed fiber determines which messages are being transmitter incorrectly. In some that means NE problems, in others it means Mast Cell problems, so in some sympathetic problems and in others parasympathetic problems. dysmyelination is a relatively recent discovery and there are many studies now into how it affect illness of usually mental origins. But those studies are not focused at all of AND dysmyelination at all so don't worry..

In Group C I believe the problem is not with the myelin because there are none in this group. The axons are protected with a special layer of cells instead. And I believe it is already proven that these fibers have been damaged in at least 50% or more of us. There is a simple skin biopsy that can determine with 88% sensitivity just how many fibers are destroyed comparing it to an average. I was found to have only 19% of these cells undamaged.

I believe as time passes and more people get their small fibers tested for damage we will see an increase to 60%+ patients with documented small fiber damage. I believe the 50% number is mostly based on QSART testing which is only 55% sensitive for SFN. and even the skin biopsy test is only 88% sensitive . so some neuropathy is bounded to be overlooked.The question is how we get tested to the Group B Dysmyelination as well. I'm corresponding with a few top Peripheral Neuropathy scientists to help determine the best way to test for this. One possible answer may be with a special MRI test called an MRN the N stands for Nerves..

I'm simply amazed at the little number of people who have gone for a very simple, quick, almost painless skin biopsy to at least test Group C small fiber neuropathy..

Lastly the Peripheral Nervous system contains 2 types of Body Tissue (Muscle and Epithelial are the other ones not included). It contains Nerve tissue (obviously) and Connective Tissues. That's right connective tissue. That's why I believe that so many EDS ppl and autoimmune disease (connective tissue disease really) develop Dysautonomia eventually. If you google causes of SFN you will see almost every cause listed on Dinet for Dysautonomia.

Keep in mind this is where I believe our syndrome is formed for the most part but think about it. If you have wires that are damaged and deformed and signal distortion it can affect the world around the, as well. It can affect different messages, different tissues, different chemicals. Its a cascade that I believe originated with both groups of small fibers. The cause of which are too broad for this post.

There are a few details I'm leaving out for example about the autonomic ganglia nerves, which I believe to be a factor as well, and which I may elaborate on in the future. Hope you enjoyed this long post and I hope it leads to some answers some where down the line.

I wish everyone good health!

RICH

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Rich. I think it is the Vagus nerve primarily. It innervates every single symptomatic expression that those with pots have. Whether it is neuropathy or damage or dysfunction--this is my current target.

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Rich, I didn't test positive for SFN - but, do have some neuropathy and it runs in my family. If they don't take the biopsy in the right place it won't be picked up. Yet, I couldn't feel needle sticks when tested that way. That being said ---I think we have to go deeper then just saying there are issues with nerve fibers and their dysfunction. That would be a side effect of what I think is the under lying problem.

Personally, I think it all comes down to the immune system. The body is attacking itself and CAUSING these issues. Work on the immune system and maybe we will get better. Since I've been doing this - I'm starting to get the feeling back in my feet and lower legs. I used to not be able to feel the bottoms of my shoes - and now I can. It used to be when I'd run my hand up my leg there would be a strange electrical - stinging type feeling (neuropathy) I seldom have this now. There are times when I have more numbness and pain and times where things are near normal. Why is it that the nerves will sometimes - not feel something and other times it will be there?

If we try to get to the core of the problem - correct that - then maybe we will start to get better. I think focusing on autoimmune issues, good healthy diet and maybe genetic mutations of known dysfunctions --- might help us all. This is my focus at the present time.

Rich, you've put an awful lot of thought and research into this. I think maybe you are finding some of your puzzle pieces. Thanks for posting your theories.

Issie

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Rich. I think it is the Vagus nerve primarily. It innervates every single symptomatic expression that those with pots have. Whether it is neuropathy or damage or dysfunction--this is my current target.

Lemon, the vagus nerve is included in my theory. While focusing exclusively on the vague nerve does not tie in a majority of issue for the syndrome as a while. The Vague nerve is located in the autonomic ganglia which I said I would elaborate on in future posts. They completely relate to my theory and the vague nerve is not being discounted at all. I choose to focus here on the bigger picture. There is way more then just innervation of one system involved.

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Rich, I didn't test positive for SFN - but, do have some neuropathy and it runs in my family. If they don't take the biopsy in the right place it won't be picked up. Yet, I couldn't feel needle sticks when tested that way. That being said ---I think we have to go deeper then just saying there are issues with nerve fibers and their dysfunction. That would be a side effect of what I think is the under lying problem.

Personally, I think it all comes down to the immune system. The body is attacking itself and CAUSING these issues. Work on the immune system and maybe we will get better. Since I've been doing this - I'm starting to get the feeling back in my feet and lower legs. I used to not be able to feel the bottoms of my shoes - and now I can. It used to be when I'd run my hand up my leg there would be a strange electrical - stinging type feeling (neuropathy) I seldom have this now. There are times when I have more numbness and pain and times where things are near normal. Why is it that the nerves will sometimes - not feel something and other times it will be there?

If we try to get to the core of the problem - correct that - then maybe we will start to get better. I think focusing on autoimmune issues, good healthy diet and maybe genetic mutations of known dysfunctions --- might help us all. This is my focus at the present time.

Rich, you've put an awful lot of thought and research into this. I think maybe you are finding some of your puzzle pieces. Thanks for posting your theories.

Issie

Issie if you think that you didn't read my theory careful enough. For example you say "The body is attacking itself and CAUSING these issues." Again you are focusing on one type of cause and not seeing the point of my research at all. If the immune system is attacking the body, is it attacking your hair follicles and your hair follicles are causing your dysautonomia? I'm not talking about what is attacking, I'm talking about where. Plus it's a well established fact that not all injuries to fibers both large and small are only due to the immune system. Research if focused right now on developing treatments to protect the nerve fiber from damage and also to regenerate nerves faster. They are still far off. But that means if they can protect nerves from lets say an immune attack then it doesnt matter if it is attacked all day long. Think of a thick walled cable that protects the outside phone and cable wires from storms and harsh weather. Certainly I'm not suggesting to not calm the storm or the cause of the attack. The only point I'm making with my theory is where the damage is and where the focus of the repair should be.

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btw rich. holy guacamole, just ready your post thoroughly. And i think you are spot on mister. Perhaps, though it is not the myelin sheath but the signal itself, either from the brainstem or IMHO somewhere along the vagus nerve as far as damage. Good way to think of it is an electrical cable with a short that works sometimes. Might i add that water is an excellent electrical conductor.

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But, if you can stop the damage in the first place --there won't be a reason to have a repair. There would not be any nerve damage.

I've no doubt at all that there is nerve damage and dysfunction ---but, believe it's a by-product of the core issue.

I agree we have to figure out how to protect the nerves ---but, if we can figure out how to stop the attack in the first place ---there won't be a need for defense - if there isn't any offense.

Like in MS - the sheath is attacked by the immune system and destroyed - causing issues with transmission. There very possibly could be issues like that in POTS. But, as with MS, the focus should be on what caused the destruction in the first place. That would be the Immune System.

Issie

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Issie, is right, that the immune system is a good suspect as far as attacking the nervous system is concerned. Though i also think mehcanical force or abrasion could have the same outcome.

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btw rich. holy guacamole, just ready your post thoroughly. And i think you are spot on mister. Perhaps, though it is not the myelin sheath but the signal itself, either from the brainstem or IMHO somewhere along the vagus nerve as far as damage. Good way to think of it is an electrical cable with a short that works sometimes. Might i add that water is an excellent electrical conductor.

Thanks Lemon :) it could be the original signal message as well but why I think it's not likely is because of where the damage comes from. It's from almost every direction except the brain. Also there is pretty big evidence already of the small fiber neuropathy in group C...

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But, if you can stop the damage in the first place --there won't be a reason to have a repair. There would not be any nerve damage.

I've no doubt at all that there is nerve damage and dysfunction ---but, believe it's a by-product of the core issue.

I agree we have to figure out how to protect the nerves ---but, if we can figure out how to stop the attack in the first place ---there won't be a need for defense - if there isn't any offense.

Like in MS - the sheath is attacked by the immune system and destroyed - causing issues with transmission. There very possibly could be issues like that in POTS. But, as with MS, the focus should be on what caused the destruction in the first place. That would be the Immune System.

Issie

Issie, you are focusing on your own issues while I'm incorporating everyones issues into a bundle that unifies it. Not everyone has the same cause.

For example: The causes of small fiber neuropathy are diverse, and in some cases, the neuropathy is the first manifestation of an underlying systemic disease. The most common cause is diabetes mellitus or glucose intolerance (Polydefkis and McArthur, 2005). Other causes include metabolic syndrome (Zhou et al, 2011), hypothyroidism (Devigli et al, 2008; Penza et al, 2009; Magri et al, 2010), Sjögren’s syndrome (Chai et al, 2005; Chai and Logigian 2010), lupus (Omdal et al, 2002; Goransson et al, 2006), scleroderma (Poncelet and Connolly, 2003), mixed connective tissue disease (Olney, 1998), sarcoid (Holtzman et al, 2005; Bakkers et al, 2010), vasculitis (Lacomis et al, 1997; Zafrir et al, 2004; Lee et al, 2005), inflammatory bowel disease (Gondim et al, 2005), psoriasis (Narayanaswami et al, 2007), unspecified inflammatory conditions (Dabby et al, 2006), Guillain-Barre syndrome (Seneviratne and Gunasekera, 2002), nutritional deficiencies such as B12 deficiency, celiac disease (Brannagan et al, 2005), Lyme disease, HIV-1 infection (polydifkis et al, 2002), Hepatitis C infection (Tembl et al 1999), Fabry disease including in female carriers (Dutsch et al, 2003; Torvin Moller et al, 2009; Liquori et al, 2010), amyloid, alcohol abuse (Zambelis et al, 2005), neurotoxic drugs including statins (Lo et al, 2003), toxins (Kuo et al, 2005), or vaccinations (Souayah et al, 2009).

These all are not unified attacks they aren't all immune attack. Alcohol abuse is not an immune attack. Yes maybe they mostly have to do with inflammation but that is so general it helps no one to focus on it.

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Plausible. Certainly makes sense. It is unclear how basic peripheral small fiber neuropathy could have such wideranging effects - your theory might explain some of that.

Couple of things Id add is that abnormal MIBG uptake in 4 out of 20 POTS patients can also be interpreted to indicate autonomic denervation of the heart as well as NET deficiency, although there is growing evidence for the later.

Some POTSies seem to have just low aldosterone/low flow and hemodynamics that are very unlike the vast majority of POTS.

But its pretty clear at least 50% of POTs patients have associated small fiber neuropathy - how that ultimately fits into the neuropathic POTS paradigm of increased leg or stomach/pelvis blood flow is a little unclear. What you suggest could explain it.

Vagal withdrawal/vagal palsy has been reported in at least one POTS patient and was believed to effect heart rate variability and cerebral blood flow. I believe the vagus is central nervous system so you'd need to use (purely speculatively please dont take this as medical advice) central acting (able to cross the blood brain barrier) acetylcholinesterase inhibitors - mestinon is peripheral only.

What causes the neuropathy? Ultimately it could just be demylenation - which in MS at least is caused by inflammatory cytokines.

In other conditions like Sacroidosis inflammatory cytokines like TNF alpha were definately implicated.

Its also interesting that excessive sympathetic activity leads to increases in other pro inflammatory cytokines like the interleukins.

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its a scary thought though Rich - basically your saying each of us could have random locations of neuropathy or demylination (spelling?).

It is scary but hard to shrug off....even a small lesion/malfunction would be hard to detect. Shoot, in A&P lab i could hardly find the vagus nerve

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Thank you Rich for doing such in debth research and sharing it with us!!! I appreciate you and the rest who research and then share the information or theories they may have. Your theory makes sense. What would be a treatment plan do you think?

I'm not sure if this is the same thing (neuropathy/biopsies/etc) but I had a nerve study where they shocked my legs and arms and put needles as well. It showed a little abnormality but nothing ever became of it.

Thanks again!

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I love all of the theories, so please keep them coming! Thanks, Rich!

I've been going over symptoms and thinking about how this theory would apply to them. I had been thinking that there was a malfunction at the brain level (i.e. feedback messages weren't interpreted properly or brain 'set points' are off), but, as I understand your theory, it could just as easily be that the messages simply aren't getting transmitted properly. It could theoretically explain why we don't always have the same reaction to the same stimuli or situation, right?

How would this account for the people who recover though? Would you consider those people in the other 20-40%? (since you mentioned this could possibly account for 60-80%). I'm thinking that there wouldn't be a way to repair this without some sort of stem cell treatment to repair the sheath/fibers???

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I'm REALLY loving the scientific conversation. I don't have anything to add at the moment, but please keep it up! We have the largest non-study group of POTS patients right here on this forum. No reason we can't discuss possible theories and see how they fit in with the people here!

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Though i also think mehcanical force or abrasion could have the same outcome.

Lemons - just want to get your opinion. I've said this many times before... A lot of my problems began immediately after a chiropractic adjusment. It was quite high in my neck, up near my skull and right after he did this, my heart started to beat really fast. Things went downhill from there, with lots of new symptoms added over the next few weeks. Do you think it's possible to have a vagus nerve "injury" which could cause all the dysautonomic symptoms? Is there anyway to look at this nerve or to test it?

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Oh and I agree with you Rich that small fiber neuropathy is probably the cause of autonomic dysfunction for many with POTS, but it seems pretty challenging to find the root cause of the SFN. I've been tested for sooo many things that can cause it and all has been negative so far. Very frustrating.

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Rich,

Just wanted to say thank you for putting your theory #3 out there.

(have been discouraged about how compartmentalized medicine and treatment are in regards)

Have been hoping to see something show up in forums and discussion regarding this kind of thinking :)

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Nice job : ) Rich!

As my eyes are so so dry tonight and it becomes painful to even read this post. I wonder if we are just so dried out. Our whole wiring system from head to toes, the plumbing, the tummy, the ins and the outs, our eyes, the nose, our joints and our skin. If it's all dried out how can it work right? Then it itches, tingles, hurts, heaves,won't focus, won't move. it might seize, or faint, or freeze,or all those other things that make use feel potsie and so miserable. At least we have each other : ) ( : until they find a cure. Till then I'll buy a round of hugs. (((hugs))) Bellamia

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Demylineation or reductions in small fibers could - potentially - be an autoimmune or inflammatory process. There is strong evidence for both in other conditions.

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Right after I was D/C'd from the hospital in 2012 I started googling my issues of course. I told my Dr that all my symptoms were vagal. I was researching ways to get the vagus nerve healthy. I found the forum and realized that dysaut/POTs best described me. One thing I think I found in my research was the vagus nerve innervates the ear drum. And thru all of this I have always had R ear pain. Not sure this is high level research such as Rich's but it connected for me.

Also, Rich's theory is why I was always so hesitant to try a bunch of meds. I understand on peoples worst functioning days there needs to be meds to get us by but I was never convinced that any of my providers had a clue on what they were treating - just firing off drugs for symptoms was never an answer for me. I did use hydrocortisone and some midrodine in order to survive but the Docs never knew why I needed those drugs. Which is why Rich's work and all the work that forum members provide is so important. Too many docs saying "you may never know why Tracy, but just take these pills to help - the body sometimes just doesn't do what it's supposed to" SO thanks Rich for helping to someday answer my question to my Doc's - Why?

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I totally think your theory is right. I believe my POTS cause was from Craniocervical instability. My symptoms started after doing a Extension and Flexion Xray of the neck. I really went as far as I could forward and backwards.

I had all of the symptoms at first and I kept my neurologist on his toes, he was convinced that I must have a brain tumor. I kept complaining that I felt like my brain was shorting out....like the signals were not getting through. All my tests came back normal except my Xray which showed a 10MM cervical instability between C1 and C2. I had no neck pain or headaches which perplexed the Neurosurgeon. He also didn't think that my symptoms were related to the instability, but did think I needed surgery due to the cervical stenosis it was causing.

I got 4 Neurosurgeon's opinions on my deformity which is called Os Odontoidium. Two out of four thought that the symptoms were caused by it. According to them the craniocervical junction is so complex, and it is like the hard drive of the nervous system. They don't even understand all the functions.

I did have a C1-C2 fusion and just got out of the neck brace last month. I wore it for 3 1/2 months. I am in so much better shape than I was, but not 100%.

Naomi - I think your chiropractor experience could set off the problem. Nerves enter and exit through vertebraes.

Here is a interesting article on EDS, which easily could be related to instability due to connective tissue/hyperflexiblilty.

http://www.upright-health.com/ehlers-danlos.html

One thing that has perplexed me is how would childbirth be related? Maybe vertebraes are misaligned during pregnancy? Love this discussion, thanks Rich!

Another interesting read on Nerves:

http://science.howstuffworks.com/life/human-biology/nerve.htm

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Hi Everyone, Glad most of you agree with my theory :) over time I will develope it even more dig deeper and deeper.

There are a lot of ways that small fibers become injured, each and everyone correlated to list on dinet for causes it would take me way to long to go down the list and explain them all, but they are all inclusive. Whether physical injury or inflammatory or hormonal assaults. The injury is happenning from many angles so a one fits all solution can not be reached by going after the causes.

The key as I see it is either a protection. For example we all need to drive but to minimize risk we have sealbelts and airbags in our cars. So if we could protect the nerves protective cell walls or myelin depending on which type Group B or C, then we wouldn't have to worry so much about the injury.

The other avenue is called Regeneration. There is 2 parts to Regeneration. The 1st part is the natural course of rgeneration of nerves. Just like when we get cuts our body has the ability to regenerate and heal. On cause of Dysmyemilantion could be that our injured nerves are not healing correctly. Schwann cells emit growth factors that attract new axonal sprouts growing from the proximal stump after complete degeneration of the injured distal stump. This leads to possible reinnervation of the target cell or organ. However, the reinnervation is not necessarily perfect, as possible misleading occurs during reinnervation of the proximal axons to target cells. So possibly medicines need to correct this faulty natural process. The other possibility are medicines that add to the natural process. These include stem cells. But there are 3 leading pharma avenues currently the most promising one is NGF or Nerve Growth Factor meds.

i have only just recently started down the avenue of what types of treatments are needed. It is very hard to say at this point and the top researchers in the world are pretty much stumped as well. The most promising research usually comes from Diabetes researchers since a number of those patients have all types of Neuropathy not just small fiber.. I will have new posts in the furture that will discuss some possible treatments.

IVIG is said to contibute to a regrowth in small fiber cells as well. But the mechanism is unknown. Perhaps it acts a little like stem cells.

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