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Cause of my cfs

Hip

Senior Member
Messages
17,865
My ESR is as good as good can be. How is yours if I may ask? or, better, how was yours at the time of making the photo? Can there be any situation where the ESR is good but there are a lot of rouleaux?

I don't know the answer to you question; but it says here that:
They [rouleaux] occur when the plasma protein concentration is high, and because of them the ESR (erythrocyte sedimentation rate) is also increased.

I don't know if I have had an erythrocyte sedimentation rate (ESR) test in the past. It's possible my doctor ordered one; but I have not seen the results.
 

Hip

Senior Member
Messages
17,865
Wasn't that Ken Lassesen's theory about CFS? He has gone into remission three times over the years.

I just looked it up, and I think Ken Lassesen focuses on hypercoagulation, which is related, but I think slightly different to rouleaux (erythrocyte aggregation).

I mentioned in my earlier post that Dr Berg thinks that in ME/CFS, blood clots too quickly (hypercoagulates), and as a result, the blood becomes more viscous. Blood coagulation involves fibrinogen, but I think the mechanism of increased blood viscosity proposed by Dr Berg relates more to chronic low level production of thrombin, which makes the blood more viscous in a way unrelated to red blood cells, I believe.
 

Lolinda

J'aime nager dans le froid style Wim Hof.. 🏊‍♀️🙃
Messages
420
Location
Geneva, Switzerland
rouleaux would show as a high esr
I put some time into researching this. My conclusion: a good ESR is indeed a valid means to exclude rouleaux.

Details:

The most convincing point I found was this:
Rouleaux formation is a core part of the erythrocyte sedimentation process! So when rouleaux are already preformed, then a part of the sedimentation process is already accomplished:
https://en.wikipedia.org/wiki/Erythrocyte_sedimentation_rate
There are 3 stages in erythrocyte sedimentation
1) Stage 1 : Rouleaux formation - First 10 minutes
2) Stage 2 : Sedimentation or settling stage - 40 mins
3) Stage 3 : Packing stage - 10 minutes (sedimentation slows and cells start to pack at the bottom of the tube)

Clear statements:
http://www.cell.com/biophysj/fulltext/S0006-3495(04)73889-8
" In medical practice, RBC aggregation is usually measured indirectly via the erythrocyte sedimentation rate (ESR),"
https://en.wikipedia.org/wiki/Erythrocyte_aggregation
Erythrocyte sedimentation rate closely reflects the extent of aggregation, therefore can be used as a measure of aggregation.

Unless some further arguments arrive, for me the above settles the question about ESR and rouleaux: A good ESR excludes rouleaux. -> Think no further. Get tested! :)

Additionally, the following might be of interest to the relationship of rouleaux and CFS: Rouleaux (= rbc aggregates) cause high blood pressure:
http://www.sciencedirect.com/science/article/pii/S0026286283710216
But we know that the majority of CFS patients struggle with low BP!
So, this is not a typical rouleaux-like situation, though obviously this argument doesnt exclude it. ESR does. Generally about high viscosity: Imagine you have to press honey (high viscosity) through a small hole. That wont work without using a lot of force... Ever tried this? When I was a child, my parents always bought this lovely honey bear at the right. You see it has a thin tip. When it came from the shop, one needed to cut the tip with a scissor so the honey came out. Now, I sometimes made a mistake: I cut too little, so the hole was very small. In this case it was damn difficult to get out the honey. But at the end of using up the honey, we added some lukewarm water to dissolve the last bits of honey clinging to the bear's inner walls. Now, this water got out easily even if the opening at the tip was cut too small. So I learned this way what viscosity is and that a high viscosity necessitates a big pressure! :D :D
buzasferenc.jpg


Question:
When a person has a good ESR and no elevated fibrinogen like me, then what on earth can be the pleasant improvement effect from fibrinolytic agents such as bromelain or nattokinase? Their action on dismantling biofilms is not likely to make anyone feel well!
As of today, I get horrible chills from nattokinase. This is logical. But earlier, I felt well for several days on it before I had to stop. At no time I had a bad ESR nor CRP. And at all times a lowish BP. My fibrinogen was measured back when I profitted from nattokinase and it was as good as can be: 2.9 (1.5-4.0 g/L).
And I do not at all understand this change in the reaction...
 
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JES

Senior Member
Messages
1,322
Go to scholar.google.com and search for CFS and ESR. I posted the results on the forum a year or so ago, but can never find that post again. From what I recall, no study showed ESR results for patients which were significantly lower than controls. Oxford results were the same, and I think Fukuda/CCC showed higher ESR.

I found plenty of sites that state low ESR is a hallmark of CFS, for example this one. Maybe it all comes from the same source though (Cheney). The logical conclusion as @Lolinda just posted would indeed be the opposite, i.e. that rouleaux and hyperviscoity correlates with ESR positively.

Also, although I read in articles that bromelain can lower fibrinogen, I could not find a study that demonstrated this, apart from this one, but it does not clearly state that bromelain reduces fibrinogen, at least in my cursor reading.

This is the study I read that was mentioned on Lassesen's blog regarding bromelain and fibrin, although the main reason I chose bromelain was that I had it readily stacked at home. Nattokinase would probably be an even more efficient blood thinner, so I'd probably recommend the thread starter to experiment with that rather than bromelain.
 
Messages
30
The foods you sense improve your circulation — asparagus, spinach, cabbage and kale — are all high in iron (see here), but Google says iron may increase blood viscosity.
...
Spinach and kale are very high in vitamin K (see here), which can increase blood coagulation.
At first I thought it might be a high soluble fibre to insoluble fibre ratio in these foods that was helping, with least insoluble fibre being best, after I read humans evolved eating much more soluble fibre and less insoluble fibre and soluble fibre passes through the gut undigested forming a viscous gel attracting water which sounded like what could be helping (thought it might be the stickiness/charge part of those foods I sensed was the factor that helped) like maybe it was drawing something out of the blood that was helping circulation. I've tried soluble fibre supplements and they didn't benefit my circulation but I'm not sure how true they are to pure natural soluble fibre. Also I've come to think it's more complex, like the variety of soluble or insoluble fibre might matter, maybe effects just how much it attracts water and so on.

How do I link within text?
 
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Hip

Senior Member
Messages
17,865
At first I thought it might be a high soluble fibre to insoluble fibre ratio in these foods that was helping

I had a some success using soluble fibre supplements (mainly inulin) to treat my anxiety symptoms, which I think were caused by inflammation in the gut and in the brain (inflammation has been linked to causing mental symptoms). See this thread: The Wonders of Prebiotics

Prebiotics promote friendly bacteria growth in the gut, which can help keep the bad gut bacteria in check and reduce gut inflammation. Since inflammation may cause an increase in blood viscosity, then this might have some bearing on your observations.



How do I link within text?

Select (highlight) the text that you want to insert a link behind, then click on the link icon (it's at the top of the text editor box; it looks like two links of a chain), and paste in your URL.
 
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30
Soluble fibre can also be a prebiotic according to that second link in my last post and I think inulin is a soluble fibre btw
 

Hip

Senior Member
Messages
17,865
Soluble fibre can also be a prebiotic according to that second link in my last post and I think inulin is a soluble fibre btw

In my above post I meant to say "I had a some success using soluble fibre supplements (mainly inulin)". I've correct my post now.

Yes, both soluble and insoluble fibre are prebiotics, but I found soluble more helpful.
 
Messages
30
Has anyone here tried native African fruits? I can't get them in the UK despite searching quite thoroughly online, I'm thinking they might hold the answer to my circulation woes if I'm lucky, although they may be all neutral, the only ones I can get are powdered baobab which is neutral to my circulation and watermelon which is marginally negative probably due to being bred away from its' original form for extra sweetness etc down the years.

Horned melon, if you are in the US, is grown in California and Mississippi.
 
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taniaaust1

Senior Member
Messages
13,054
Location
Sth Australia
Yeah, they're all contradicting the research :p
it may be cause those studies may not have been done on those fitting CCC or the international ME criteria so I dont think we can use the studies to discount what we've read about this unless we are aware of that

With that being said though, my ESR with the ME used to be on the rather high side of things (almost abnormally high). it came down after years of being up when i started supplements (it seemed to have possibly been the vit D i took helped it some)
 

Valentijn

Senior Member
Messages
15,786
it may be cause those studies may not have been done on those fitting CCC or the international ME criteria so I dont think we can use the studies to discount what we've read about this unless we are aware of that
ESR results were higher in the studies with better criteria :p
 
Messages
30
Generally about high viscosity: Imagine you have to press honey (high viscosity) through a small hole. That wont work without using a lot of force... Ever tried this? When I was a child, my parents always bought this lovely honey bear at the right. You see it has a thin tip. When it came from the shop, one needed to cut the tip with a scissor so the honey came out. Now, I sometimes made a mistake: I cut too little, so the hole was very small. In this case it was damn difficult to get out the honey. But at the end of using up the honey, we added some lukewarm water to dissolve the last bits of honey clinging to the bear's inner walls. Now, this water got out easily even if the opening at the tip was cut too small. So I learned this way what viscosity is and that a high viscosity necessitates a big pressure! :D :D
index.php
Compared to the rest of my family, the veins on my hands are thin/small (except when hot when they dilate), which I noticed ever since I had colder extremities than them (their hands always warm, mine always much colder), and I wondered whether I generally have thin veins, which would necessitate more pressure to pump the same amount of blood through them, so perhaps this is a contributing factor to how easily my circulation balance has gone out of whack.

I don't know if there is a test for relative size/thickness of veins?

Anyone else have thin/small hand veins, when they are undilated,?
 
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Messages
30
I mentioned in my earlier post that Dr Berg thinks that in ME/CFS, blood clots too quickly (hypercoagulates), and as a result, the blood becomes more viscous. Blood coagulation involves fibrinogen, but I think the mechanism of increased blood viscosity proposed by Dr Berg relates more to chronic low level production of thrombin, which makes the blood more viscous in a way unrelated to red blood cells, I believe.
That Dr Berg theory fits perfectly (and I would say my circulation reacts to foods/substances outside my African evolution as foreign explaining the thrombin response), has anyone here tried heparin? In the study quoted in that link they used "5000 units of sq heparin BID" for between 3-20 months averaging 8 months with improvement, not sure if that means 5000 per day or what. I am tempted to try it for 3 months and see whether there is any improvement, I want to get dromedary derived heparin if I can.

Were there any follow on studies done since that research does anyone know?
 
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Hip

Senior Member
Messages
17,865
Were there any follow on studies done since that research does anyone know?

I found a couple of good blog articles about heparin for ME/CFS here and here, coincidently both published in the last two weeks. The conclusion of the first article is:
Conclusion
The ME-Hypercoagulation connection was a very promising theory until a small study with Fukuda criteria patients found no coagulation problems in CFS patients. The subsequent coagulation research in ME was then discontinued.

Regardless of the validity of the hypercoagulation theory in ME, heparin has been an effective treatment for many patients. Those in the Berg studies experienced dramatic improvements and Dr. Teitelbaum’s comment that half of those ME patients with the most severe and difficult to treat symptoms “get better” with heparin provides hope.

The double-edged sword with heparin is the potential side effects. This shifts the dynamics of the risk-reward ratio. If an ME patient is severely ill, with cold hands and feet and a low sedimentation rate, it may be worth getting subsequent and specialised coagulation testing done and discussing with their physician about whether heparin treatment is warranted.
 
Messages
30
My first thoughts on that criteria is that it isn't great but nonetheless good enough to diagnose some people so doesn't really dispute the study itself. I'm a little confused by that small study though because platelets weren't mentioned in dr bergs study.
 

Hip

Senior Member
Messages
17,865
I'm a little confused by that small study though because platelets weren't mentioned in dr bergs study

Although the platelets are responsible for blood clotting, I don't think the platelets have any direct affect on blood viscosity.

Dr Berg and others found that in ME/CFS, there is a small but constant production of the the thrombin being released into the blood. Thrombin results in the production of soluble fibrin monomer (SFM), a sticky protein that increases blood viscosity.

So its SFM, not the platelets, that increases blood viscosity. That's my understanding.
 
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30
And I just read this from an interview with Dr David Berg:

"[Kru]:I'm interested in sub groups of CFS
Are you noticing anything about sub groups or sub sets of people that have CFS in relation to when blood thining works and when it doesn't? Or anything else about sub sets for that matter.
[David] The two subgroups that we see are the genetic defects in Thrombin regulation (THROMBOPHILIA) or Fibrinolysis regulation (HYPOFIBRINOLYSIS). HYPOFIB patients are definitely harder to treat, since the process to clean up the vessels is inhibited by high values of Lp(a) or PAI-1. It may take 2-3 months for these patients compared to 2-3 weeks for thrombophilia patients to get to equivalent points in relief." {+from another dr berg source: "Unfortunately, 21% of these patients had a defect in both groups. This means that not only do they form fibrin easily, but also they cannot clean up the fibrin deposition generated."]

And later on he says:

"If I were the patient, I would ask my physician to test me for both a pathogen and coag screens, including HHV6, Mycoplasma, Chlamydia, ISAC, HTRP and the B2GPI panels."

I'm not sure about the pathogen theory personally, I think my body reacts to (most)foods(/any ingestibles) originating outside africa as a threat and changes something in the circulation, kind of like getting an allergic circulation reaction to ingesting stuff not from africa.
 
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30
Regarding rouleaux etc, in another interview dr berg said:

"[BERG] Speaking of thick blood, there are many studies about reduced BLOOD VOLUME. I think we finally have an answer to this also. In looking at microscopic blood samples, we have now seen actual SFM fibers precipitate out on the slides. These are single strands, not cross linked strands as in a clot. This is also what the model predicts. Since this is correlated with high SFM levels in the plasma on these patients, we can say that the levels on the slide are high also. The additional effect seen on the slide is the remarkedly high ROULEUX FORMATION of the RBCs (red blood cells). This looks like a stack of coins, if you can imagine such. Since rouleux formation is NOT normal, it is possible to conclude that the increased SFM is responsible for holding the RBCs together in chains of 3-10 cells long. Since this is what is observed at 1000 power and 8000 power under the microscope, then it is possible that this is happening in the body. If so, then the oxygen delivery will be greatly reduced because the cells stick together and oxygen cannot escape, ie, hypotention. If you are looking at blood volume based on RBCs, then a group of RBCs stuck together would act as one cell, not 3, 8 or 10, etc. Thus you could conclude that there is a low blood volume. This will be interesting experiment to repeat a patient with “low blood volume” after a short period of time on heparin. The blood volume would probably correct, since the cells would not be stuck together by the SFM."

Any other relevant researchers or any researchers who took off where he left off (as he's retired)?
 
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