One Gene Many Disorders: Genetic Finding Could Help Explain POTS, EDS, IBS, FM, ME/CFS and Others
ShyestofFlies
Well-Known Member
The RCCX theory has been around for a little while now and I've read about it recently - I admit a lot of the science stuff goes well beyond my ability to comprehend right now.
I am interested in RCCX and similar theories that include genetic research because I feel strongly thereis a genetic element to many of these illnesses.
I know however many people do not like RCCX because it does make mention of mental illness/psychiatric co-morbidities and the doctor behind it is a psychiatrist. I get that...
Still I think people have not given her enough of a chance to prove herself- she has several of these illnesses herself. The call out to the the psychiatric possibility (related, but she is basically defining a subtype who do have certain psychiatric symptoms- not saying the symptoms are cause by psychaitric illness!)... is simply because of the population she has worked with, observed, and developed this theory from.
The theory is mostly gene and symptom related (physical) with one sub-population which has psychiatric co-morbidities and symptoms. I don't think she thinks it's all psychiatric, that's just her interest in a subset who she encounters in her main practice. She works with an endocrinologist now on the theory as well.
Rccxandillness.com is the site, she's very willing to talk to people too- If you'd be interested Cort it'd be nice to get some mention of her on HR if her theory hasn't been yet. I know she got dis-invited off an ME/CFS community and it'd be interesting to hear how she's addressed those concerns since the early drafts of the theory.
---
This school of thought/idea that many of these diseases co-occur in a statistically and practically apparent way is strikingly relevent.
We tend to notice this unusual pattern of chronically ill people "if you have one illness, you're somehow more likely to have more" - there's plenty of reasons and excuses people will give for this to dismiss it in some way, but the reality is many people who have one of a certain group of illnesses do appear to have another. This has been observed often in auto-immune diseases, which makes me think there is an auto-immune component to ME/CFS for sure.
What the reason for that is is unknown, but to attribute anything other than the benefit of the doubt to these people would be inethical in my opinion. If everyone had all of them it'd make sense to group them as one illness, but that is not the case.
For those who only have one illness I totally understand not spending time researching this line of research/thought if it isn't productive to you. But for those of us with multiple diagnoses, I think it is helpful to at least keep an eye on the study of this pattern.
I am interested in RCCX and similar theories that include genetic research because I feel strongly thereis a genetic element to many of these illnesses.
I know however many people do not like RCCX because it does make mention of mental illness/psychiatric co-morbidities and the doctor behind it is a psychiatrist. I get that...
Still I think people have not given her enough of a chance to prove herself- she has several of these illnesses herself. The call out to the the psychiatric possibility (related, but she is basically defining a subtype who do have certain psychiatric symptoms- not saying the symptoms are cause by psychaitric illness!)... is simply because of the population she has worked with, observed, and developed this theory from.
The theory is mostly gene and symptom related (physical) with one sub-population which has psychiatric co-morbidities and symptoms. I don't think she thinks it's all psychiatric, that's just her interest in a subset who she encounters in her main practice. She works with an endocrinologist now on the theory as well.
Rccxandillness.com is the site, she's very willing to talk to people too- If you'd be interested Cort it'd be nice to get some mention of her on HR if her theory hasn't been yet. I know she got dis-invited off an ME/CFS community and it'd be interesting to hear how she's addressed those concerns since the early drafts of the theory.
---
This school of thought/idea that many of these diseases co-occur in a statistically and practically apparent way is strikingly relevent.
We tend to notice this unusual pattern of chronically ill people "if you have one illness, you're somehow more likely to have more" - there's plenty of reasons and excuses people will give for this to dismiss it in some way, but the reality is many people who have one of a certain group of illnesses do appear to have another. This has been observed often in auto-immune diseases, which makes me think there is an auto-immune component to ME/CFS for sure.
What the reason for that is is unknown, but to attribute anything other than the benefit of the doubt to these people would be inethical in my opinion. If everyone had all of them it'd make sense to group them as one illness, but that is not the case.
For those who only have one illness I totally understand not spending time researching this line of research/thought if it isn't productive to you. But for those of us with multiple diagnoses, I think it is helpful to at least keep an eye on the study of this pattern.
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Cort,
This parasite is very intriguing and has amazingly similar symptoms to CFS. And treatable.
Any thoughts?
http://protomyxzoa.org/wp-content/uploads/2013/05/Protomyxzoa_rheumatica.pdf
This parasite is very intriguing and has amazingly similar symptoms to CFS. And treatable.
Any thoughts?
http://protomyxzoa.org/wp-content/uploads/2013/05/Protomyxzoa_rheumatica.pdf
Merida
Well-Known Member
@Raba
This is an interesting organism. I see it infects red blood cells. Anecdotal information ( (from 13 years of support group leadership) may suggest that we have a higher than usual rate of RH neg blood. Peer -reviewed research on Toxoplasma ( Flegr et al.) suggests that Rh neg individuals have more neurological issues following Toxo infection. So, perhaps this Protomyxzoa can be a factor in our illness?
This is an interesting organism. I see it infects red blood cells. Anecdotal information ( (from 13 years of support group leadership) may suggest that we have a higher than usual rate of RH neg blood. Peer -reviewed research on Toxoplasma ( Flegr et al.) suggests that Rh neg individuals have more neurological issues following Toxo infection. So, perhaps this Protomyxzoa can be a factor in our illness?
Merida
Well-Known Member
This is a important article and I see the 'fit' with my family and me.
Another issue common to many of us is sulfa allergy. I found research that sulfa allergy has developed in people infected with HIV , EBV , and other viruses.
So it seems that certain viruses have the ability to alter immune pathways. And metabolic pathways by hitting the mitochondria.
Oh, geez. Thank goodness we are getting good, young researchers to look closely.
Another issue common to many of us is sulfa allergy. I found research that sulfa allergy has developed in people infected with HIV , EBV , and other viruses.
So it seems that certain viruses have the ability to alter immune pathways. And metabolic pathways by hitting the mitochondria.
Oh, geez. Thank goodness we are getting good, young researchers to look closely.
@Gail C: "But the paper does not really explain why we have too much NE."
I may have a potential answer to that: Norepinephrine is a needed precursor to Epinephrine, the fight-or-flight hormone.
Epinephrine has, according to my completely unproven opinion, some very potent beneficial properties beyond the fight-or-flight response and anaphylaxis it almost solely is linked to.
Mast cells have a very strong link to allergies and the dangerous anaphylaxis (potential deadly allergic reaction): https://en.wikipedia.org/wiki/Mast_cell
And the worldwide number 1 medicine against it is (very) high dose epinephrine: https://en.wikipedia.org/wiki/Anaphylaxis
So far, this is common accepted science.
Now, would this "medicine" called epinephrine not be possible used as a body made medicine? Let's see some arguments:
* MCAS, a mast cell disorder. According to your post, it goes hand in hand with high levels of NE.
* POTS or other OI: According to many sources, it goes hand in hand with high levels of NE.
* Dysautonomia: According to many sources, it goes hand in hand with high levels of NE.
=> In fact, there are subtypes called adrenal POTS and adrenal dysautonomia; they show even up as suggestions in search engines if you enter adrenal PO or adrenal dy.
* 2 out of 3 NIH approved fibromyalgia drugs are SNRI where NRI stands for Norepinephrene Reuptake Inhibitor or medicine that raises Norepinephrene levels in the body a lot.
* Near ALL ME/CFS patients are said to be of the "fight-or-flight" type patients; this fact is often abused to call ME/CFS patients afraid; afraid to move (Wesley and co.); sick because of anxiety thus psychological; obsessive compulsive disorder... and order excuses not to help them...
Now, let me turn cause and effect upside down:
At the start of my university studies I was REALLY stress tolerant. Even after failing a major course and being near guaranteed to have to redo a list of examinations on the second chance thing we have got, I remained calm and continued calmly to finish the two remaining examinations of two other courses that were among the most difficult of the year. When my health went done a lot a few years ago, my mother remembered me that at that time she asked how stressed I was about it and I replied: "What is stress? I don't think I really have got that". I remembered than that I actually said that a few times during university time and I actually felt that way.
Just to say that before I was ill, I had above average stress resilience.
Several years after I have had mononucleosis, haven taken no time to properly recover from it and pushing my body very hard I became nearly the most stressed-up person I did ever met. As the years passed more and more symptoms came up. Doctors attributed all symptoms to me having to much stress.
I did agree my stress levels were much to high. During the following 10 years I put a lot of time in managing my stress and emotions and improved a lot in managing them. I ended up to the point I more and more had stress but failed to find any reasonable explanation as to why I had stress at that moment.
So: does high anxiety makes us sick? I start to doubt so. It does cost plenty of energy and can make us more sick (starting a vicious circle once it gets to high), but it is likely not the cause with many patients. The high anxiety was likely one of the first SYMPTOMS of ME/CFS. Epinephrene has following good properties for us:
* It is likely the best Mast Cell Inhibitor known to mankind.
* Research has indicated that Epinephrene may actually boost immune system: https://www.sciencedaily.com/releases/2012/06/120621223525.htm and https://www.ncbi.nlm.nih.gov/pubmed/6458557/
* The research needs to be repeated, but if correct it works on the T-cells in particular. It "strenghtens" those cells and those are white bloodcells in the bloodstream.
* In comment 23 of http://www.healthrising.org/forums/...rituximab-and-new-drug-for-me-cfs.5004/page-2 I make a hypothetical case that the weakened white blood cells and overactivated mast cells may be a problematic feedback loop keeping Dauer lasting/locked in. Epinephrene reduces both mast cell activation very strongly and may, according to above research, increase white blood cell strength. That may add up to be a perfect anti Dauer medicin in above hypothesis IF IT WERE NOT HAVING THAT EPIC SIDE EFFECTS.
* As an extra, it also redirects blood flow to the core organs, what I see as a plus.
So my hypothesis: our bodies try and find an ideal mix between potentially very beneficial positives of epinehrene and potentially even more devastating side effects.
p.s.: I'll have some more stuff I will add in the future to that other post further trying to strengthen the case for problematic Dauering of white blood cells and how that could possibly explain the different starts of ME/CFS under that hypothesis. My aim is to provide a first "bigger" picture that makes many links and see if others can correct and improve upon it. Having a first model that *could* explain that our disease is theoretical possible would be a big boon to our community I believe. Very unlikely it will be useful, but with enough help it could grow to be so. If value is seen in it, all help would be welcome. I am still quite exhausted.
added: forgot to mention that one of the reason few is known about long term high epinephrine elevated levels (as in "fight-or-flight people" we are called) is likely that it is very hard and expensive to measure it continuously over long periods.
Kind regards,
Jurgen
I may have a potential answer to that: Norepinephrine is a needed precursor to Epinephrine, the fight-or-flight hormone.
Epinephrine has, according to my completely unproven opinion, some very potent beneficial properties beyond the fight-or-flight response and anaphylaxis it almost solely is linked to.
Mast cells have a very strong link to allergies and the dangerous anaphylaxis (potential deadly allergic reaction): https://en.wikipedia.org/wiki/Mast_cell
And the worldwide number 1 medicine against it is (very) high dose epinephrine: https://en.wikipedia.org/wiki/Anaphylaxis
So far, this is common accepted science.
Now, would this "medicine" called epinephrine not be possible used as a body made medicine? Let's see some arguments:
* MCAS, a mast cell disorder. According to your post, it goes hand in hand with high levels of NE.
* POTS or other OI: According to many sources, it goes hand in hand with high levels of NE.
* Dysautonomia: According to many sources, it goes hand in hand with high levels of NE.
=> In fact, there are subtypes called adrenal POTS and adrenal dysautonomia; they show even up as suggestions in search engines if you enter adrenal PO or adrenal dy.
* 2 out of 3 NIH approved fibromyalgia drugs are SNRI where NRI stands for Norepinephrene Reuptake Inhibitor or medicine that raises Norepinephrene levels in the body a lot.
* Near ALL ME/CFS patients are said to be of the "fight-or-flight" type patients; this fact is often abused to call ME/CFS patients afraid; afraid to move (Wesley and co.); sick because of anxiety thus psychological; obsessive compulsive disorder... and order excuses not to help them...
Now, let me turn cause and effect upside down:
At the start of my university studies I was REALLY stress tolerant. Even after failing a major course and being near guaranteed to have to redo a list of examinations on the second chance thing we have got, I remained calm and continued calmly to finish the two remaining examinations of two other courses that were among the most difficult of the year. When my health went done a lot a few years ago, my mother remembered me that at that time she asked how stressed I was about it and I replied: "What is stress? I don't think I really have got that". I remembered than that I actually said that a few times during university time and I actually felt that way.
Just to say that before I was ill, I had above average stress resilience.
Several years after I have had mononucleosis, haven taken no time to properly recover from it and pushing my body very hard I became nearly the most stressed-up person I did ever met. As the years passed more and more symptoms came up. Doctors attributed all symptoms to me having to much stress.
I did agree my stress levels were much to high. During the following 10 years I put a lot of time in managing my stress and emotions and improved a lot in managing them. I ended up to the point I more and more had stress but failed to find any reasonable explanation as to why I had stress at that moment.
So: does high anxiety makes us sick? I start to doubt so. It does cost plenty of energy and can make us more sick (starting a vicious circle once it gets to high), but it is likely not the cause with many patients. The high anxiety was likely one of the first SYMPTOMS of ME/CFS. Epinephrene has following good properties for us:
* It is likely the best Mast Cell Inhibitor known to mankind.
* Research has indicated that Epinephrene may actually boost immune system: https://www.sciencedaily.com/releases/2012/06/120621223525.htm and https://www.ncbi.nlm.nih.gov/pubmed/6458557/
* The research needs to be repeated, but if correct it works on the T-cells in particular. It "strenghtens" those cells and those are white bloodcells in the bloodstream.
* In comment 23 of http://www.healthrising.org/forums/...rituximab-and-new-drug-for-me-cfs.5004/page-2 I make a hypothetical case that the weakened white blood cells and overactivated mast cells may be a problematic feedback loop keeping Dauer lasting/locked in. Epinephrene reduces both mast cell activation very strongly and may, according to above research, increase white blood cell strength. That may add up to be a perfect anti Dauer medicin in above hypothesis IF IT WERE NOT HAVING THAT EPIC SIDE EFFECTS.
* As an extra, it also redirects blood flow to the core organs, what I see as a plus.
So my hypothesis: our bodies try and find an ideal mix between potentially very beneficial positives of epinehrene and potentially even more devastating side effects.
p.s.: I'll have some more stuff I will add in the future to that other post further trying to strengthen the case for problematic Dauering of white blood cells and how that could possibly explain the different starts of ME/CFS under that hypothesis. My aim is to provide a first "bigger" picture that makes many links and see if others can correct and improve upon it. Having a first model that *could* explain that our disease is theoretical possible would be a big boon to our community I believe. Very unlikely it will be useful, but with enough help it could grow to be so. If value is seen in it, all help would be welcome. I am still quite exhausted.
added: forgot to mention that one of the reason few is known about long term high epinephrine elevated levels (as in "fight-or-flight people" we are called) is likely that it is very hard and expensive to measure it continuously over long periods.
Kind regards,
Jurgen
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@dejurgen
I just read your post, and need to read it again. I will also have a look at the other thread you started. But I have some things to do, and it may take awhile. Back later.
I just read your post, and need to read it again. I will also have a look at the other thread you started. But I have some things to do, and it may take awhile. Back later.
kim.der.acquiro
Member
@dejurgen... Ok, let's see how much we can get through here.
I do understand what you have written about NE. I have laughed and said I am a walking talking Epi Pen. I know there is crosstalk between the SNS and the Immune System. If I recall correctly, the SNS and brain are the two main communicators with the Immune System when there is an Immune Response. Where I get stuck is that my NE increases each and every time I stand up and remain on my feet for a few minutes. So does that mean that I have an Immune Reaction each and every time I stand up as well? Why on earth would this happen? Further, it is pretty much assumed (because all have not been tested) that folks with high NE have problems with NE Re-uptake Receptors. This is what we are warned against taking SNRIs.
There is one physician in particular who argues that Mast Cell disease causes POTS, even though he does not have the data to prove it. I believe he thinks that because MCs can store NE. I disputed that position when I first heard it and continue to do so simply because I do not believe it that accounts for all symptoms.
Re POTS and NE...not all POTS patients have high NE. Estimates vary from about 10-12% to about 50%. There are many causes of POTS. However, the type that is considered to be Inherited make up about 10 - 15% of the total and is almost always associated with high NE. It runs in my family, and thus considered genetic for me.
We had a different onset. I have had symptoms for as long as I can remember. I would be very interested in anything that helps explain why some have problems while very young, while others don't see to until there is a triggering event.
I think you could probably make a case for MCA and the Dauer state rather easily. There is something I need to have a look at and simply have not had the time as yet. It was recently found that about 85% of POTS patients have a Dense (Delta) granule storage deficiency. I have a feeling this may be tied to hypometabolism, but need some research time.
Does stress and anxiety make us sick? Absolutely not as far as I am concerned. I discarded that argument long ago. Yes, I ran into the same sort of attitude before I was diagnosed, but it is difficult to argue with Lab results. This is one reason I request Labs any chance I get. Another reason is that I can try to find treatment for some things. I do think we have to remain cognizant of the fact that elevated levels of certain things can do some damage over time however.
If I find anything interesting, I will try to add to your other post.
I do understand what you have written about NE. I have laughed and said I am a walking talking Epi Pen. I know there is crosstalk between the SNS and the Immune System. If I recall correctly, the SNS and brain are the two main communicators with the Immune System when there is an Immune Response. Where I get stuck is that my NE increases each and every time I stand up and remain on my feet for a few minutes. So does that mean that I have an Immune Reaction each and every time I stand up as well? Why on earth would this happen? Further, it is pretty much assumed (because all have not been tested) that folks with high NE have problems with NE Re-uptake Receptors. This is what we are warned against taking SNRIs.
There is one physician in particular who argues that Mast Cell disease causes POTS, even though he does not have the data to prove it. I believe he thinks that because MCs can store NE. I disputed that position when I first heard it and continue to do so simply because I do not believe it that accounts for all symptoms.
Re POTS and NE...not all POTS patients have high NE. Estimates vary from about 10-12% to about 50%. There are many causes of POTS. However, the type that is considered to be Inherited make up about 10 - 15% of the total and is almost always associated with high NE. It runs in my family, and thus considered genetic for me.
We had a different onset. I have had symptoms for as long as I can remember. I would be very interested in anything that helps explain why some have problems while very young, while others don't see to until there is a triggering event.
I think you could probably make a case for MCA and the Dauer state rather easily. There is something I need to have a look at and simply have not had the time as yet. It was recently found that about 85% of POTS patients have a Dense (Delta) granule storage deficiency. I have a feeling this may be tied to hypometabolism, but need some research time.
Does stress and anxiety make us sick? Absolutely not as far as I am concerned. I discarded that argument long ago. Yes, I ran into the same sort of attitude before I was diagnosed, but it is difficult to argue with Lab results. This is one reason I request Labs any chance I get. Another reason is that I can try to find treatment for some things. I do think we have to remain cognizant of the fact that elevated levels of certain things can do some damage over time however.
If I find anything interesting, I will try to add to your other post.
POTS.
The PL dense granules contain ADP, ATP, 5HT, calcium, and
pyrophosphates at different concentrations (e.g., there is 9–10
times as much ADP than ATP in dense granules with the converse
of adenine nucleotide concentrations in the PL cytosol). The
transporters for PL uptake of dense granule constituents are
different for each of these substances; it is not unreasonable to
assume that there could be a PL storage pool deficiency for any of
these substances independent of PL number and function. A
defect of SERT might lead to low levels of 5HT within PL dense
granules but would not affect dense granule number nor ADP
concentration. Studies have defined d-SPD as a condition of
increased PL ATP/ADP ratios exceeding 2.0 directly related to
diminished granular ADP stores and that decreased ADP levels
correlate with reduced numbers of PL dense granules.
[28–30] We and others have found that d-SPD and diminished PL 5HT stores
also correlate with one another. [31,32] Although we have
identified a significant deficiency of the PL dense granules in
these patients, not all of the patients were diagnosed with d-SPD;
19% were found to be within normal limits.
https://www.researchgate.net/public...ociated_with_platelet_storage_pool_deficiency
The PL dense granules contain ADP, ATP, 5HT, calcium, and
pyrophosphates at different concentrations (e.g., there is 9–10
times as much ADP than ATP in dense granules with the converse
of adenine nucleotide concentrations in the PL cytosol). The
transporters for PL uptake of dense granule constituents are
different for each of these substances; it is not unreasonable to
assume that there could be a PL storage pool deficiency for any of
these substances independent of PL number and function. A
defect of SERT might lead to low levels of 5HT within PL dense
granules but would not affect dense granule number nor ADP
concentration. Studies have defined d-SPD as a condition of
increased PL ATP/ADP ratios exceeding 2.0 directly related to
diminished granular ADP stores and that decreased ADP levels
correlate with reduced numbers of PL dense granules.
[28–30] We and others have found that d-SPD and diminished PL 5HT stores
also correlate with one another. [31,32] Although we have
identified a significant deficiency of the PL dense granules in
these patients, not all of the patients were diagnosed with d-SPD;
19% were found to be within normal limits.
https://www.researchgate.net/public...ociated_with_platelet_storage_pool_deficiency
@Gail C:
"Where I get stuck is that my NE increases each and every time I stand up and remain on my feet for a few minutes... ...Why on earth would this happen?"
My reasoning is as follow:
* It is "general knowledge" that epinephrine only kicks in at real and powerful danger. That is repeated time and again as if it were true. Therefore everything that causes arousal or anxiousness must be plain psychological or mental problems... However there is no evidence proving this "general knowledge".
* Epinephrine has however a few more tricks up its sleeve: it causes hypertension or high blood pressure: https://en.wikipedia.org/wiki/Epinephrine. If you have no high average blood pressure and no need too have so or worse would have other new problems if you had average high blood pressure, then a temporal short boost in epinephrine does the job: spiking up blood pressure at times that your cardiac system and arteries are too slow too adjust when you stand up. Remember: gravity forces blood down so standing up without quick adaptation droops blow flow to the brain to dangerously low levels.
Consider my case: When I still had a full-time job (as I so called only had too much stress, no real illness...) I more then once failed to pass trough a door slamming into the wall instead. My brain was that slow. But I still had to commute go and back to my work and do stairs 5 to 10 times a day and cross the street several times a day. At times I couldn't safely walk through a door without a boost to my brain (epinephrine boost my brain very strong for a short period), changes for a car crash (had 1), tumbling down the stairs (did several times, luckily only broke 1 toe) or walking underneath a car were small but real. Let's say there was each time on average a 0.02% change that it ended fatal. I consider that no exaggeration. That is no reason to have an emergency epinephrine boost, isn't it? Or is it?
7 times doing stairs a day, 2 car commutes and on average once crossing a busy street is 10 small risks a day with a tiny change of 0.02% to go awkwardly wrong. Basic chance calculation gives it a daily chance of (1-0.0002)^10=99.8% going fine. So there are no problems here at all. Or maybe there are: doing this every single day of the year makes the change of having no deadly or paralyzing event 0.998^365=48.2%. In plain words: daily small risks end up in less than 50% chance surviving the year.
=> So are daily epinephrine surges irrational, impossible, too idiotic to even consider? No! The danger is small, but too frequent to go uncountered. Individuals with bodies poor at assessing life threatening risks in a statistical way did not live long enough to reproduce. Most people had over 100 epinephrine/adrenaline rushes in their life at age 50 without a single case going terribly wrong. So the notion that epinephrine only kicks in when you face instant chance to die is plain false. Peoples bodies seem to be evolved to assess risk correctly: only kick in epinephrine when there are rare chances of big risk AND when the body notices that there are way to many daily smaller risks that make long term survival highly unlikely. Standing up with far too low blood flow to the brain is one such example. One can risk to feint and fall once with no problem at all, 100 times when lucky but no-one can do so forever.
Is looking at it this way useful or just wasting our poor brains? Be this theory wright or wrong I learned a trick or two from it:
* I learned to use sudden spikes in adrenaline/arousal/anxiety with no obvious reason as an early warning signal that I am overexerting myself. Before I knew I was overexerting hours too late. It saved me many Post Exertion Malaises since I learned it this year. And they tend to be less deep if I get them.
* It may also explain why we again and again and again overexert and crash. If it is true, adrenaline quicks in the strongest when we are at the weakest. But adrenaline is also the hormone that let a frail old woman believe she can lift single handed a car if it can safe here grandchild, no questions asked. So when we are at our weakest we feel as if we can do 5 times as much compared to average. Even if we are smart and learn, we get that estimate down to a smarter and safer factor of 2. In reality our bodies may at that times be at their worst and doing 4 times less than normal may be the best choice.
The 2 above "tricks", among with some other small changes seem to have helped breaking a 15 year ongoing decline in my health. Since 9 months I experience a small and slow recovery. In the past 15 years, the longest period of somewhat recovery lasted 3 months and was less convincing. Time will tell if it keeps going wright. At least my quality of life improved a lot!
That is what I believe: we patients will not "solve" our disease, but we have much knowledge shared among us. This website helps people doing so: thanks Cort!!! If we could find some more potential links and explanations, we community could develop pacing 2.0 or 3.0. http://phoenixrising.me/living-i-th...e-in-chronic-fatigue-syndrome-by-cort-johnson. Pacing is also community developed and is for many of us the best tool in managing our disease. If it could be done and guide many patients to being only half as sick, it would be a little piece of heaven... ...daydreaming...
note1: "Further, it is pretty much assumed (because all have not been tested) that folks with high NE have problems with NE Re-uptake Receptors. This is what we are warned against taking SNRIs."" Yeah, NE seems to be also somewhat in the family here, and taking SNRI is fine most of the times but I had a few humongous surges in epinephrine that were far bigger than what I experienced during armed robbery and made my heart race near out of control. So being careful may be wise.
note2: I will look into those dense granules. Never heard of it before. But that will be next week. My 30 minutes a day having a clear mind are depleted now.
Take care,
Jurgen
"Where I get stuck is that my NE increases each and every time I stand up and remain on my feet for a few minutes... ...Why on earth would this happen?"
My reasoning is as follow:
* It is "general knowledge" that epinephrine only kicks in at real and powerful danger. That is repeated time and again as if it were true. Therefore everything that causes arousal or anxiousness must be plain psychological or mental problems... However there is no evidence proving this "general knowledge".
* Epinephrine has however a few more tricks up its sleeve: it causes hypertension or high blood pressure: https://en.wikipedia.org/wiki/Epinephrine. If you have no high average blood pressure and no need too have so or worse would have other new problems if you had average high blood pressure, then a temporal short boost in epinephrine does the job: spiking up blood pressure at times that your cardiac system and arteries are too slow too adjust when you stand up. Remember: gravity forces blood down so standing up without quick adaptation droops blow flow to the brain to dangerously low levels.
Consider my case: When I still had a full-time job (as I so called only had too much stress, no real illness...) I more then once failed to pass trough a door slamming into the wall instead. My brain was that slow. But I still had to commute go and back to my work and do stairs 5 to 10 times a day and cross the street several times a day. At times I couldn't safely walk through a door without a boost to my brain (epinephrine boost my brain very strong for a short period), changes for a car crash (had 1), tumbling down the stairs (did several times, luckily only broke 1 toe) or walking underneath a car were small but real. Let's say there was each time on average a 0.02% change that it ended fatal. I consider that no exaggeration. That is no reason to have an emergency epinephrine boost, isn't it? Or is it?
7 times doing stairs a day, 2 car commutes and on average once crossing a busy street is 10 small risks a day with a tiny change of 0.02% to go awkwardly wrong. Basic chance calculation gives it a daily chance of (1-0.0002)^10=99.8% going fine. So there are no problems here at all. Or maybe there are: doing this every single day of the year makes the change of having no deadly or paralyzing event 0.998^365=48.2%. In plain words: daily small risks end up in less than 50% chance surviving the year.
=> So are daily epinephrine surges irrational, impossible, too idiotic to even consider? No! The danger is small, but too frequent to go uncountered. Individuals with bodies poor at assessing life threatening risks in a statistical way did not live long enough to reproduce. Most people had over 100 epinephrine/adrenaline rushes in their life at age 50 without a single case going terribly wrong. So the notion that epinephrine only kicks in when you face instant chance to die is plain false. Peoples bodies seem to be evolved to assess risk correctly: only kick in epinephrine when there are rare chances of big risk AND when the body notices that there are way to many daily smaller risks that make long term survival highly unlikely. Standing up with far too low blood flow to the brain is one such example. One can risk to feint and fall once with no problem at all, 100 times when lucky but no-one can do so forever.
Is looking at it this way useful or just wasting our poor brains? Be this theory wright or wrong I learned a trick or two from it:
* I learned to use sudden spikes in adrenaline/arousal/anxiety with no obvious reason as an early warning signal that I am overexerting myself. Before I knew I was overexerting hours too late. It saved me many Post Exertion Malaises since I learned it this year. And they tend to be less deep if I get them.
* It may also explain why we again and again and again overexert and crash. If it is true, adrenaline quicks in the strongest when we are at the weakest. But adrenaline is also the hormone that let a frail old woman believe she can lift single handed a car if it can safe here grandchild, no questions asked. So when we are at our weakest we feel as if we can do 5 times as much compared to average. Even if we are smart and learn, we get that estimate down to a smarter and safer factor of 2. In reality our bodies may at that times be at their worst and doing 4 times less than normal may be the best choice.
The 2 above "tricks", among with some other small changes seem to have helped breaking a 15 year ongoing decline in my health. Since 9 months I experience a small and slow recovery. In the past 15 years, the longest period of somewhat recovery lasted 3 months and was less convincing. Time will tell if it keeps going wright. At least my quality of life improved a lot!
That is what I believe: we patients will not "solve" our disease, but we have much knowledge shared among us. This website helps people doing so: thanks Cort!!! If we could find some more potential links and explanations, we community could develop pacing 2.0 or 3.0. http://phoenixrising.me/living-i-th...e-in-chronic-fatigue-syndrome-by-cort-johnson. Pacing is also community developed and is for many of us the best tool in managing our disease. If it could be done and guide many patients to being only half as sick, it would be a little piece of heaven... ...daydreaming...
note1: "Further, it is pretty much assumed (because all have not been tested) that folks with high NE have problems with NE Re-uptake Receptors. This is what we are warned against taking SNRIs."" Yeah, NE seems to be also somewhat in the family here, and taking SNRI is fine most of the times but I had a few humongous surges in epinephrine that were far bigger than what I experienced during armed robbery and made my heart race near out of control. So being careful may be wise.
note2: I will look into those dense granules. Never heard of it before. But that will be next week. My 30 minutes a day having a clear mind are depleted now.
Take care,
Jurgen
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@dejurgen I have to be very brief just now, but will try to come back. Pacing is absolutely essential for me. If I overextend myself, I am in BIG trouble!
This is just a bit about Primary (Inherited) POTS. There is also Secondary POTS, and treatment can be very different.
http://www.pedneur.com/article/S0887-8994(16)30419-2/abstract
This is just a bit about Primary (Inherited) POTS. There is also Secondary POTS, and treatment can be very different.
http://www.pedneur.com/article/S0887-8994(16)30419-2/abstract
We are different.
My NE spikes each time I stand from sitting. There is no one spike here and one there, but each time day in and day out. I also have the high Tryptase and TGF-Beta to factor in somewhere. We may be comparing apples and oranges. But it wonderful that you have improved! I do hope that improvement continues. Recent research indicates the Vagal nerve lacks tone in H POTS even at rest. I had wondered if the Sympathetic Nerve was just so strong or overactive when we were on our feet that it simply overpowered the Parasympathetic, but that does not seem to be the case.
But going to try to get back to the Tryptase findings Cort posted about. I got a copy of the paper and have been reading that. Will post in a bit.
Paper Title: Elevated basal serum tryptase identifies a multisystem disorder associated with increased TPSAB1 Copy number
Statistically Significant symptoms noted:
Flushing/pruritis, gastrointestinal reflux, congential skeletal abnormality, retained primary dentition, arthralgia, body pain/headache, and sleep disruption.
Overall prevalence of joint hypermobility was 28%., about 2 x higher general population.
46% had elevated autonomic symptom scores. 11 of these had positive TTT.
"How elevated serum tryptase might contribute to the associated multisystem disorder we observed remains unclear"
I think the quote pretty much sums it up. They are not ready to say causative. Reducing tryptase might help some symptoms, but if true, this was not reported. I still welcome any research that helps clarify what is happening with us however.
Statistically Significant symptoms noted:
Flushing/pruritis, gastrointestinal reflux, congential skeletal abnormality, retained primary dentition, arthralgia, body pain/headache, and sleep disruption.
Overall prevalence of joint hypermobility was 28%., about 2 x higher general population.
46% had elevated autonomic symptom scores. 11 of these had positive TTT.
"How elevated serum tryptase might contribute to the associated multisystem disorder we observed remains unclear"
I think the quote pretty much sums it up. They are not ready to say causative. Reducing tryptase might help some symptoms, but if true, this was not reported. I still welcome any research that helps clarify what is happening with us however.
I decided to join this forum because of this thread. I see that it has been a while since there have been any new posts.
Elevated tryptase here. Average 21. My only other family member tested was my late mother, one result - 41.
It was suggested here to Browse Raw Data on 23andme for the TPSAB1 gene. However, when I did so, the answer was No genes or markers found matching "TPSAB1".
Does the that mean none were found for me? Or that somehow the TPSAB1 is not included in 23andme testing?
Thank you.
Elevated tryptase here. Average 21. My only other family member tested was my late mother, one result - 41.
It was suggested here to Browse Raw Data on 23andme for the TPSAB1 gene. However, when I did so, the answer was No genes or markers found matching "TPSAB1".
Does the that mean none were found for me? Or that somehow the TPSAB1 is not included in 23andme testing?
Thank you.
Issie
Well-Known Member
@Cort - I just found this thread. Here is a bit of my background. I'm also HYPERPOTS with high standing NE levels. I have EDS and MCAS. And for those that don't yet know --- there may also be a connection with MCAS and endometriosis. (Of which I also had.) There is a family connection - my mom had MCAS very bad. I haven't had a tryptase test while in a flare and when not in a flare it's not high. GastroCrom has been one of my best meds, not only for MCAS but also POTS. I have a few hypothesis as to why.....one of which is calcium channels (it is not only a mast cell stabilizer but a mild calcium channel blocker - this is a vasodilator.) Unlike those with more OI symptoms who do better to constrict their veins - I do better to vasodilate. NE helps with dilation and also helps carry vital blood and oxygen to heart and brain. I personally don't think blocking that compensation response is wise. Yes, it's very uncomfortable - but our bodies are trying to make needed adjustments to save us.
Here is something for those of you here to look into. I recently had a positive DX of Lupus Anticoagulant antibodies. This indicates Hughes Syndrome or APS - too thick blood. Can lead to blood clots and can definitely affect blood flow. If your blood is too thick, you would need to vasodilate to carry it. You would need the tachycardia of POTS and high NE to carry the blood and oxygen. Probably the muscle pumps are not working correctly with EDS and the speed up of the heart is a compensation for the lack of that pumping action. Therefore, very necessary.
As to the question of stress being a contributor. In the sense of the physiological response - increased adrenal response (epinephrine, NE), mast cell degranulation, tachycardia, autonomic and central nervous system response --- I'd say YES. As for a psychosomatic response due to inability to properly handle the stress of a situation - that too can turn into a physological response based on the above. So it's still a physical dysfunction. We can however moderate that response and change the way we perceive a situation and calm that response. Also another hypothesis as to some of the inappropriate and over exaggerated response issues connected to NMDA (glutamate/GABA dysfunction).
Issie
Here is something for those of you here to look into. I recently had a positive DX of Lupus Anticoagulant antibodies. This indicates Hughes Syndrome or APS - too thick blood. Can lead to blood clots and can definitely affect blood flow. If your blood is too thick, you would need to vasodilate to carry it. You would need the tachycardia of POTS and high NE to carry the blood and oxygen. Probably the muscle pumps are not working correctly with EDS and the speed up of the heart is a compensation for the lack of that pumping action. Therefore, very necessary.
As to the question of stress being a contributor. In the sense of the physiological response - increased adrenal response (epinephrine, NE), mast cell degranulation, tachycardia, autonomic and central nervous system response --- I'd say YES. As for a psychosomatic response due to inability to properly handle the stress of a situation - that too can turn into a physological response based on the above. So it's still a physical dysfunction. We can however moderate that response and change the way we perceive a situation and calm that response. Also another hypothesis as to some of the inappropriate and over exaggerated response issues connected to NMDA (glutamate/GABA dysfunction).
Issie
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Lauren Gordon
Member
HI there, I'm wondering if there has been further progress / any more news re this? Many thanks.
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