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Low Sed Rate = Hyperviscosity?

Discussion in 'Pain and Inflammation' started by Marco, Jan 23, 2012.

  1. Marco

    Marco Old blackguard

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    Hi all.

    I'm posting this here rather than under lab tests as its more of a general point for discussion.

    The sed rate and inflammation

    As you may be aware the erythrocyte sedimentation rate (ESR), often referred to as the sed rate, is a common blood test that serves as a non specific marker of inflammation as might be found in an acute phase infection. A high sed rate is also associated with certain autoimmune diseases and inflammatory conditions such as rheumatoid arthritis.

    http://en.wikipedia.org/wiki/Erythrocyte_sedimentation_rate

    Normal sed rates may be calculated depending on age and gender. One set of ranges defines a normal finding as :

    Less than 15 mm/hr for men under 50 years
    Less than 20mm/hr for women under 50 years.

    A sed rate lower than these cut-off points is rarely given much clinical significance (other than indicating an absence of infection/inflammation) except where a small number of specific diseases are suspected e.g. polycythaemia (a condition where a patient makes too many red blood cells), with extreme leucocytosis (patient has too many white blood cells), and with some protein abnormalities.

    Low sed rates in ME/CFS patients.

    Somewhat paradoxically, given that ME/CFS patients regularly show high levels of c-reactive protein (CRP) and IL6 which are reliable markers of inflammation, there have been a number of threads here and elsewhere in which forum members report low or zero sed rates. Mine tested at 3 last time around.

    Cheney is reputed to have stated that his ME/CFS patients have the lowest sed rates he has ever seen.

    So do we have inflammation or not?

    Hyperviscosity

    It appears that the sed rate is not a particularly reliable measure as it can be affected by a range of factors including the plasma viscosity (thickness or resistance to flow) of the blood where viscosity is negatively correlated with the sed rate (i.e. high viscosity gives a low or zero sed rate). Hyperviscosity may be due to a range of conditions grouped under hyperviscosity syndrome or be a downstream effect of, for example, chronic alcohol abuse .


    High viscosity might be expected to result in reduced blood flow to all organs, and impaired microcirculation to the skin and extremities. Spontaneous bleeding often from mucous membranes results from the viscous blood causing damage due to increased shear stress.

    Has anyone had either or both sed rate and plasma viscosity tested?
  2. biophile

    biophile Places I'd rather be.

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    I think this is the Cheney observation (http://www.dfwcfids.org/medical/cheney/heart04.part2b.htm). I started writing this about ESR last year but didn't post ...

    I haven't had blood tests for years, but in all the tests I did have in the past, ESR was always 1mm/hr except for one occasional when it was 3mm/hr then back to 1mm/hr. I don't think I've been tested for plasma viscosity, I'm aware of most of the tests I've had, there may have been an occasion or two where I didn't have access to the test results eg during a GET program. There are many similar anecdotes from patients and doctors alike that ESR or SED (erythrocyte ie [red blood cell] sedimentation rate) is commonly very low in ME/CFS. I tried to find some sources for this:

    However, I have not been able to find published studies which back these claims up about ME/CFS and low ESR. It is such a common test for routine medical assessment that there should be literally thousands of CFS studies with unpublished data on it. Yes, some ME and CFS patients have repeatedly tested very low ESR (0-3mm/hr), but from the limited amount of studies I have seen which do mention ESR (eg data from p124 of the original Canadian 2003 definition), this does not seem common enough to use as a litmus test, if anything it was slightly higher than healthy controls on average, with a standard deviation which would not suggest that lots of ME/CFS patients with lower ESR are being averaged out by lots of patients with higher ESR.

    And shouldn't many of the possible causes of low ESR be detected in routine medical assessment and exclude one from a CFS diagnosis? Perhaps those of us with very low ESR do not have "CFS" but some underlying but undetected disease and we were dumped in the CFS wastebasket? Or perhaps ME commonly involves low ESR but CFS does not? I have purchased nattokinase and lumbrokinase for the hypothetical hypercoagulation but haven't really tested them yet. I once tried a dose of the former and coincidently noticed a similar sensation in the sinuses that I get from aspirin.
  3. Marco

    Marco Old blackguard

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    Thanks Biophile.

    Interesting stuff.

    I came across an interesting case study of a child with cyanotic congenital heart disease which involves hyperviscosity.

    It lists symptoms that don't usually get a mention when you search for information on hyperviscosity syndrome :

    Easy bruising and petechial haemorrhage (the small red skin dots in another thread in this section) are also mentioned.

    http://journal.nzma.org.nz/journal/123-1312/4072/
  4. Marco

    Marco Old blackguard

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    Hyperviscosity in elite athletes with 'overtraining syndrome'

    Overtraining syndrome in elite athletes shares many symptoms in common with ME/CFS and is similarly characterised by a range of non-specific subjective symptoms and a lack of specific reliable biomarkers.

    This paper correlates subjective questionnaire responses with physiological measures and suggests that early diagnosis is best achieved through a combination of the subjective responses and hemorheological measures - specifically blood viscosity.

    Interestingly low blood viscosity is usually a marker of fitness. The authors argue that 'Overtraining Syndrome' is misnomer as what actually appears to happen is that the capacity to sustain previous levels of performance is lost and the usual hemodilution effect of exercise is reversed.

    They propose that the acquired inability to meet the usual training demands results in increased cytokine release leading to low level systemic inflammation and raised blood viscosity resulting in the common subjective feeling of 'heavy legs' - plus the other associated somatic and psychological symptoms.

    Sounds familiar!



    http://jeanfrederic.brun.free.fr/overheorev.pdf
  5. Marco

    Marco Old blackguard

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    Given the tendency to frequent re-infection and chronic infection, I wonder how this would affect the sed rate even with an underlying condition of hyperviscosity.

    I also wonder, given the range of possible 'triggers' whether a low sed rate might be a characteristic of those whose onset was associated with 'overtraining'.

    While no elite athlete, at the time of onset I was training hard, on a restricted diet and simultaneously under mental pressure (career change etc). I literally collapsed/fainted during a training session an immediately lost the ability to tolerate aerobic exercise.

    In contrast I've read some of the original Royal Free literature and frankly I don't recognise the description despite the fact that I clearly meet the Canadian criteria. While circumstances and symptoms suggest I may have picked up a (entero)virus, I don't recall even a brief period of feeling fluey or feverish (outside of the usual malaise) and certainly didn't spend any time confined to bed because of an acute illness.

    In my case I would suspect overtraining syndrome if there was anything in the literature that suggested that this syndrome could persist over years or decades (come to think of it I did post another French paper that suggested that elite cyclists are at risk of developing CFS even many years after they cease sport!).

    I also wonder if an elite athlete failed to recover in the short term despite the best efforts of their coach and physio, would this be reported or would they be given an alternative diagnosis of ME/CFS?

    If I had been an elite athlete at the time, given my onset, symptoms and blood tests (low sed rate; high cholesterol; high MCH and MCV; depressed T) would I have been diagnosed with overtraining syndrome and told to take it easy for a while rather than shifted from pillar to post only to end up many years later with a diagnosis associated with 'aberrant illness beliefs'

    PS Horses don't have 'illness beliefs'

    http://www.avonvale.plus.com/webfitness.htm
  6. dannybex

    dannybex Senior Member

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    Hi again Marco,

    This is very interesting. My cholesterol is fine, but the 'bad' cholesterol (LDL?) has been too high, and the "good" cholesterol too low for several years now. Also homocysteine, at least on the methylation panel, was too high. MCH, MCV are okay I guess, and haven't had the SED tested.

    I definitely 'overtrained' -- overdid it -- for years and years, as compared to most folks in our local support group, I could walk further, so -- stupid me -- I just took it for granted, plus, I had to walk to the store to buy food (no car) so if I was out of food, I'd have to go anyway, even if my feet were killing me. I still have qualified for the CCC definition diagnosis since 2004, so whlie some might be given a different diagnosis, others may not, after all, exercise, and especially overtraining, can result in severe oxidative stress, adrenal problems, changes in immune function, etc..

    Anyway, thanks for this thread. I'm not sure if I have high blood viscosity or not, but there's definitely some sort of circulation problem from about my knees down -- the exact muscles that are 'overused' too much -- even though I'm way too thin and have lost about 10% of my weight in the last year. Rich says this is due to the methylation block, and another says I'm in adrenal burnout -- erratic cortisol levels -- too low in the AM, then high at noon, and high normal the rest of the day. She counseled me to eat more fat -- but when I do, or when I perhaps add "too much" (which is a comparative thing), then I think that's when my legs feel worse.

    So how do we reduce this inflammation, or decrease blood viscosity? I suppose the answer will be different for everyone.

    When I add fish oil -- even one capsule -- the result is bleeding gums. I've tried nattokinase -- and although I haven't tried it regularily enough, it actually seems to reduce the bleeding gums. I'm not sure how either would affect the parameters you mention above, but natto is supposed to reduce plaque, at least according to some sources.

    Here's a link w/a case history, where 'heaviness' was reduced after 2 weeks of nattokinase:

    http://www.springboard4health.com/notebook/nutrients_natto_case_history.html

    ???

    Thanks again for this thread.
  7. mellster

    mellster Marco

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    Great thread - I remember having a sed rate of 2 when I was tested and was just developing FM and later CFS. Since I am exercising again and the FM pain has also substantially subsided (still somewhat mildly symptomatic though), I might ask for another sed rate test to see whether there is a correlation. However I remember the normal range was given as 0-15 on my sheet, and therefore (as mentioned before) there was no attention paid to low values with a lower threshold of zero ;) Btw. I also used to overtrain (going to 4-5 kickboxing sessions per week) before coming down with the viral trigger and FM although I was never an athlete (meaning I might have overstretched and overestimated my endurance).
  8. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    One way to reduce inflammation is to get good quality sleep(insomnia is known to increasese il6), thats the easy bit, the hard bit is how do we get good quality sleep which helps us to recovery from the days activity etc by producing hormones like growth hormone etc which help the anabolic processes. Inflammation is a sign of injury and the start of the healing process, inflammation is suppose to help attract the immune processes to the area and get the ball rolling. So inflammation isnt bad but chronic inflammation is. The more i read about inflammation, which i think is important, the more i see there are many processes involved in inflammation, too much cortisol, not enough cortisol, not enough sleep/growth hormones, oxidative stress etc etc etc. I think we need to pick them all off one by one, but i truly think sleep should be the first target and i dont think there is one substance that can reduce all the different types of inflammation, although quality sleep i think can get at the biggest majority of them. At the end of the day im chasing my tail, i just hope researchers can work it out for us because i think with our me/cfs brains we wont on our own. Always short term relief from the alcohol rinse protocol i mentioned a few weeks ago, lol.

    cheers!!!
  9. Marco

    Marco Old blackguard

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    Thanks for the responses folks.

    There are a few points I'd like to pick up on for discussion but not right now as I'm feeling crap after exceeding my non-elite energy limits (I might just try the alcohol rinse protocol this evening ;))

    In the meantime here's a little more background on overtraining syndrome.

    Here's a list of overtraining syndrome symptoms. I've found that popular reviews give a much fuller list of symptoms than most of the scientific papers although ideally it would require the references to be followed up :

    http://www.rndsystems.com/cb_detail_objectname_SP01_CytokinesandOvertraining.aspx

    A familiar list and one which begs the question. If localised microtrauma can generate this list of symptoms; systemic inflammation might be expected to generate a similar list and more?
  10. Marco

    Marco Old blackguard

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    You may have seen one of Cort's front page articles which described a 'safe' protocol (from Klimas or Pacific Labs?) based on heart rate etc that might help determine when PWME might be able to exercise and to what degree.

    A similar test has been developed for OTS.

    http://sportsmedicine.about.com/cs/overtraining/a/aa062499a.htm

    It might be interesting to see how PWME do on this simple do at home test.


    PS I definitely had a 'compulsive need to exercise' pre onset to the extent that on days when I couldn't swim my usual 1.5km I became quite anxious and had to go out for a fast run to compensate for the unease.
  11. kaffiend

    kaffiend Senior Member

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    Great thread. Elevated resting and post-exertion (just walking around) heart rate were the best indicators of a PENE day for me.

    I also had an extremely low sed rate and CRP (<0.1) despite inflammatory brain lesions at the time of the blood work.
  12. Marco

    Marco Old blackguard

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    Hi Dannybex. I definitely have an obvious circulation problem also. My veins are rarely visible and when driving, even for a few minutes my hands start to lose feeling. I also have severe problems with heat intolerance which I'd hypothesised might be due to mitochondrial dysfunction (where peripheral circulation is the first system to be sacrificed to protect vital organs) but it may just be simply due to poor skin microcirculation).

    Re the weight loss, I didn't lose weight after onset but found for the first time that I didn't need to diet to maintain a low bodyweight. That lasted for the first 10 years. I do believe though that my body composition changed while my weight stayed constant. It appears that overtraining syndrome is a catabolic state which would tie in with the weight loss.

    That does seem at odds with hyperviscosity. I'm not familiar with nattokinase I'll have to look it up.


    Mellster. One comment that caught my attention when reading up on overtraining syndrome was the question of why some elite athletes succumb to it while others go on to become world champions. Perhaps its a case of individual differences in physiological limits. Elite athletes probably have a much higher limit than most of us with others 'weeded out' through a process of attrition. Like you, I think I overstretched my physiological limit and now that limit is infinitely lower. It could be a mixture of genetic individual differences in physiological potential combined with environmental stressors with perhaps antioxidant status playing a central role?

    Heapsreal. I'm beginning to think the same thing and where best to attempt to 'break the cycle'. I'm not sure about sleep being the 'one' as most of my symptoms preceded sleep disturbances. Obviously sleep is required to repair the microtrauma associated with overtraining but I'm not sure this is the source of inflammation in PWME as psychological effort can have the same effects. Perhaps if we could damp down any inflammation for long enough that might give us time to heal?



    Anecdotally, my experience of ME is not one of 'fatigue' but feeling inflamed. While I do suffer from PEM, on a daily basis, I start off pretty well but as the day goes on my head feels inflamed and progressively 'light' and its this that lands me in bed rather than 'fatigue' (outside of full PEM). I also notice (as does my wife) that my mood deteriorates as this inflamed feeling grows. I haven't had real depression since my physical symptoms worsened in 1997 (weird one that) but I do feel increasingly irritable , angry and 'low'. It isn't just a case of I'm in a bad mood because I don't feel well. The two come from the same source.

    Normally I don't like or tolerate pharmaceuticals but I do get stabbing headaches behind the eyes that I call mini-migraines and Neurofen is the only things that helps. On Thursday, after physically overdoing things, I felt so bad that I took a Neurofen on spec and noticed that not only did the physical symptoms ease but I noticed myself sitting at the computer with a slight smile on my face.

    The overtraining stuff and the sudden mood improvement reminded me of the 'brainflammation'/cytokine theory of depression papers by the likes of Maes and Dantzer.

    Here's an interesting paper to counter those who like to suggest high rates of co-morbid depression in ME/CFS or still cling to the notion that ME/CFS is 'another kind of depression'.

    From inflammation to sickness and depression: when the immune system subjugates the brain


    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2919277/
  13. Valentijn

    Valentijn Activity Level: 3

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    Are you sure this isn't Orthestatic Intolerance?

    The inflammation headache that I get if I don't take fish oil is pretty constant, whereas my neurally mediated hypotension gets steadily worse throughout the day and causes the same symptoms you're attributing to inflammation. It can be checked with a blood pressure monitor at home.
  14. alex3619

    alex3619 Senior Member

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    Just to complicate matters, blood viscosity would be impacted by vascular function, particularly in peripheral blood vessels. There is some kind of disturbance in ME of blood pressure and pressure waves in the vascular system. This is not undestood. So the real impact is a function of blood viscosity and (I suspect) vascular elasticity. Theoretically at least our blood vessels should have reduced elasticity. A further complication is vascular wall damage, either from homocysteine or oxidative stress, both of which can be elevated in ME. Bye, Alex
  15. Marco

    Marco Old blackguard

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    Could be Valentjin, although OI isn't as much of a problem for me now I think compared to the early days. At the start I had regular dizzy spells on standing and was very aware that I couldn't stand for long periods. I don't have this problem now apart from during PEM.
  16. Marco

    Marco Old blackguard

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    Hi Alex.

    Very true but I can't think of a mechanism by which arterial stiffness on is own could lead to a low sed rate.

    I wonder why there haven't been more 'proof of principal' trials of various anti-inflammatories? Inflammation is a pretty reliable finding in ME/CFS studies to the extent that even unrelated papers regularly refer to 'chronic low grade inflammation'.

    There are also a finite number of pro-inflammatory cytokines with IL6 and TNF alpha regularly associated with ME/CFS. Certain biologicals can target specific cytokines (e.g. Etanercept for TNF alpha and one monoclonal antibodt targets IL6). Rituximab downregulates pro-inflammatory cytokines in RA as well as depleting B cells.

    A number of 'nutraceuticals' can target specific or multiple cytokines :


    http://ebm.rsmjournals.com/content/236/6/658.full

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