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Visible and near-infrared spectra collected from the thumbs of patients with CFS for diagnosis

SOC

Senior Member
Messages
7,849
Hi, all.

I would say that these results do make sense, but that the authors have interpreted them incorrectly.

The decrease in water content corresponds to the diabetes insipidus (not to be confused with diabetes mellitus) found commonly in ME/CFS. In general. most PWMEs are hypovolemic because of this.

The higher oxyhemoglobin corresponds to the mitochondrial dysfunction in ME/CFS, which produces less of a demand for oxygen, leaving more of it in the blood, bound to hemoglobin.

The increased oxidation of the parts of cytochrome C oxidase, which is in the respiratory chain of the mitochondria, corresponds to the oxidative stress in the mitochondria in ME/CFS.

I think these results fit very well with what we know of ME/CFS.

Best regards,

Rich
Thanks, Rich, that makes sense. That's one less thing niggling at my mind now. :)
 

Guido den Broeder

Senior Member
Messages
278
Location
Rotterdam, The Netherlands
The blood flow acceleration will be linked to the low blood volume.

These are outcomes that can be consistently expected in ME. The others with a diagnosis of CFS are likely to have a different disease.

Is the full text available somewhere?

By the way, I noticed a while ago that when I cut my thumb, the blood drips faster than it used to do.
 
Messages
5,238
Location
Sofa, UK
A few years ago, when I had some food and environmental sensitivity tests, it took us more than half an hour to draw a few drops of blood from my fingers. We had to try all 10 fingers and thumbs, and nothing would flow into the capillary tubes. The nurses said they'd done thousands of these tests and they'd never seen anything like this. Since we're interested in the blood volume and blood flow here, with particular reference to thumbs, I'm just wondering whether anybody else here has had similar difficulties in drawing blood from the thumbs and fingers?
 
Messages
180
The higher oxyhemoglobin corresponds to the mitochondrial dysfunction in ME/CFS, which produces less of a demand for oxygen, leaving more of it in the blood, bound to hemoglobin.

I had an autonomic index done and one of the tests was blood oxygenation level, my p02 at baseline was 43mmHg the reference value being 60mmHg, that seems to contradict these findings as I would expect blood oxygenation to be higher and c02 to be lower, the inverse of which seems to be true for me.
 

SOC

Senior Member
Messages
7,849
A few years ago, when I had some food and environmental sensitivity tests, it took us more than half an hour to draw a few drops of blood from my fingers. We had to try all 10 fingers and thumbs, and nothing would flow into the capillary tubes. The nurses said they'd done thousands of these tests and they'd never seen anything like this. Since we're interested in the blood volume and blood flow here, with particular reference to thumbs, I'm just wondering whether anybody else here has had similar difficulties in drawing blood from the thumbs and fingers?

I've heard of that in reference to antiphospholipid syndrome.
 

richvank

Senior Member
Messages
2,732
Would Les Simpson's work on mis-shaped red blood cells have any bearing on this finding?

http://cfidsreport.com/Articles/researchers/lessimpson.htm

Hi,ukxmrv.

I don't think so. I think Les's observations were a result of elevated oxidative stress, which is also a prominent feature of ME/CFS. Dr. Majid Ali did a study some years back in which he corrected RBC deformation by giving vitamin C.
Les also found that B12 helped, and I think that we can understand that now in view of the link between the partial methylation cycle block and glutathione, which is the basis of the antioxidant enzyme system.

Best regards,

Rich
 

richvank

Senior Member
Messages
2,732
A few years ago, when I had some food and environmental sensitivity tests, it took us more than half an hour to draw a few drops of blood from my fingers. We had to try all 10 fingers and thumbs, and nothing would flow into the capillary tubes. The nurses said they'd done thousands of these tests and they'd never seen anything like this. Since we're interested in the blood volume and blood flow here, with particular reference to thumbs, I'm just wondering whether anybody else here has had similar difficulties in drawing blood from the thumbs and fingers?

Hi, Mark.

Did you happen to have your sed rate measured at that time? If it was less than 5 mm per hour, it suggests hypercoagulation. David Berg found this in many PWMEs, and assigned it the name ISAC (Immune System Activation of Coagulation).

Best regards,

Rich
 

richvank

Senior Member
Messages
2,732
I had an autonomic index done and one of the tests was blood oxygenation level, my p02 at baseline was 43mmHg the reference value being 60mmHg, that seems to contradict these findings as I would expect blood oxygenation to be higher and c02 to be lower, the inverse of which seems to be true for me.

Hi, Vitalic.

I think that the explanation is that there are some countervailing things going on, and the overall results depend on which is dominant. I think it's true that in ME/CFS, several cell types, including the skeletal muscle cells, the heart muscle cells, cells of the immune system, cells in some of the endocrine glands, and cells of the brain and nervous system suffer from mitochondrial dysfunction, and thus use less oxygen and generate less carbon dioxide than normal.

However, the respiratory center in the brain stem works to counter this, by slowing and shallowing the breathing. The effect of that is to raise the CO2 and lower the oxygen content of the blood.

Another thing that apparently happens is that the muscles used in breathing can also suffer mito dysfunction, and this can also cause shallowing of the breathing, also raising CO2 and lowering oxygen in the blood.

Perhaps one or both of these could explain your measurement.

Best regards,

Rich
 
Messages
5,238
Location
Sofa, UK
Thanks to SOC and Rich for the info re: antiphospholipid syndrome and hypercoagulation. Hypercoagulation sounds right as a description of it, I'll mention that term to my GP and see if that suggests any tests to him. I didn't get any other tests at that time, but if I can I'll get the 'sed rate' test done.

It was certainly an odd experience that they couldn't draw the blood, they assured me it had never happened to them before, so although it's obviously not a bothersome thing it might well be a really good clue. Although all my previous blood work had come back normal, thanks to this forum I did get a load of tests done last year that hadn't been tried, and all 4 times during the course of the year my white blood cell count came out a couple of points above the reference range, so it was good to get some kind of significant result under the NHS for a change. Maybe if I follow up that blood work further I might get some further useful clues.
 

Guido den Broeder

Senior Member
Messages
278
Location
Rotterdam, The Netherlands
The thumb may yield different measurements than other locations. I have a low oxygen saturation in general (around 91%), and finding a vessel to draw blood from in my right arm is a fail. But the thumb is no problem.

Note btw that a low saturation outcome can be the consequence of methomoglobin (which gives you a bue skin).
 

richvank

Senior Member
Messages
2,732
Thanks to SOC and Rich for the info re: antiphospholipid syndrome and hypercoagulation. Hypercoagulation sounds right as a description of it, I'll mention that term to my GP and see if that suggests any tests to him. I didn't get any other tests at that time, but if I can I'll get the 'sed rate' test done.

It was certainly an odd experience that they couldn't draw the blood, they assured me it had never happened to them before, so although it's obviously not a bothersome thing it might well be a really good clue. Although all my previous blood work had come back normal, thanks to this forum I did get a load of tests done last year that hadn't been tried, and all 4 times during the course of the year my white blood cell count came out a couple of points above the reference range, so it was good to get some kind of significant result under the NHS for a change. Maybe if I follow up that blood work further I might get some further useful clues.

Hi, Mark.

According to David Berg, if a person has hypercoagulation due to ISAC, as suggested by a low sed rate, what is going on is this:

There is a set of proteins in the blood called the coagulation cascade. It has two branches. One branch deposits fibrin in the capillaries, and the other branch removes it. Normally, they are appropriately balanced so that the blot clots when necessary to prevent hemorrhage, but it doesn't clot when it isn't supposed to, forming blockages in the blood circulation, leading to stroke, heart attack, etc.

According to David, when the immune system becomes activated because of a pathogen, it stimulates some deposition of fibrin to confine the pathogen, and this is normal. However, some people have inherited polymorphisms in one or more of the proteins in the coagulation cascade. The result can be too much fibrin deposition when the immune system responds to infection by a pathogen. This is what he called ISAC (immune system activation of coagulation). The problem with this, according to him, is that it makes it difficult for oxygen to diffuse out of the red blood cells and through the wall of the capillary to supply oxygen to tissue cells.

Conventional physicians usually do not pay attention to low values of the sed rate. They are trained to look for high values, which indicate inflammation or infection. Also, the conventional tests of the coagulation system are directed at detecting hypocoagulation, i.e. hemophilia. Hypercoagulation is not recognized by conventional medicine.

To look for hypercoagulation, it is necessary to run other tests. One of them is to test for soluble fibrin monomer. David Berg developed panels of tests, which are now offered in the U.S. by the Esoterix lab in Phoenix, Arizona, which bought out his old Hemex lab some years ago. Esoterix is now a part of LabCorp. I don't know if these types of tests are offered in the UK.

The treatment for this is either low-dose heparin or one of the proteolytic enzyme products, such as nattokinase or lumbrokinase, combined with something to hold down the viruses, such as a transfer factor or an antiviral. If the latter is not used, removing the fibrin can cause a flare of the infection, and the immune system then activates more, and the hypercoagulation gets worse. This is all according to David Berg.

Best regards,

Rich
 
Messages
5,238
Location
Sofa, UK
Thanks very much Rich, that's a great explanation. Makes total sense to me, and fits well, because my persistently high white cell count does suggest persistent infection, and so does my symptomology.

I'm also now wondering whether some aspects of my 'itching' or allodynia could be related, because my non-medical mind imagines whether small-scale clotting in peripheral veins and/or arteries might cause itchiness in the legs when standing up for a few minutes, and skin sensitivity which fluctuates depending on the level of immune response to the infection.

But I'm in danger of taking this thread off-topic if we continue with this much longer - I guess we're supposed to be talking about thumbs here. :D
 
Messages
180
Hi, Vitalic.

I think that the explanation is that there are some countervailing things going on, and the overall results depend on which is dominant. I think it's true that in ME/CFS, several cell types, including the skeletal muscle cells, the heart muscle cells, cells of the immune system, cells in some of the endocrine glands, and cells of the brain and nervous system suffer from mitochondrial dysfunction, and thus use less oxygen and generate less carbon dioxide than normal.

However, the respiratory center in the brain stem works to counter this, by slowing and shallowing the breathing. The effect of that is to raise the CO2 and lower the oxygen content of the blood.

Another thing that apparently happens is that the muscles used in breathing can also suffer mito dysfunction, and this can also cause shallowing of the breathing, also raising CO2 and lowering oxygen in the blood.

Perhaps one or both of these could explain your measurement.

Best regards,

Rich

Thanks for your input, that does sound plausible, this may explain why perceived shortness of breath or a feeling of being "air hungry" is a prominent trait in ME/CFS.
 

Don Quichotte

Don Quichotte
Messages
97
The PO2 level and the oxygen saturation are two different variables.
Theoretically (if you have no red blood cells) your PO2 level can be normal but the O2 saturation will be 0%.
(That is why the O2 sat. is corrected for the level of hemoglobin, which is only a partial correction because the oxy-hemoglobin saturation curve depends on other variables as well).
see here for further details-http://www.ventworld.com/resources/oxydisso/dissoc.html
The PO2 level is different in arterial, venous and capillary blood, so without knowing where the blood was drawn from it is hard to tell if this a normal or abnormal result.
If your test was done on venous blood the PO2 level you mention is within the normal range.

I had an autonomic index done and one of the tests was blood oxygenation level, my p02 at baseline was 43mmHg the reference value being 60mmHg, that seems to contradict these findings as I would expect blood oxygenation to be higher and c02 to be lower, the inverse of which seems to be true for me.
 

Cort

Phoenix Rising Founder
"RESULTS:

Vis-NIR spectra showed sharp peaks at 694, 970 and 1060 nm and broad peaks in the regions of 740-760 and 830-850 nm. As these peaks are possibly related to oxyhemoglobin, cytochrome c oxidase and water, levels of these factors were compared between the two groups. Statistical analysis of the absorbance of Vis-NIR spectra showed a significant decrease in water content, a significant increase in oxyhemoglobin content, and a significant increase in the oxidation of heme a+a(3) and copper in cytochrome c oxidase in CFS patients."
------------------------------------------
This is a very exciting finding and consistent with what I had predicted.
In my 2008 hypothesis "Chronic fatigue syndrome is caused by dysregulation of hydrogen sulfide metabolism", I specifically mentioned that" hydrogen sulfide binds to the mitochondrial enzyme cytochrome c oxidase, which is part of Complex IV of the electron transport chain, and attenuates oxidative phosphorylation and ATP production". I believe cytochrome c oxidase is a very important part of the puzzle and this research helps to highlight that fact. I hope they will go further in this line of work.


Maybe its time for an update on that theory :)

Is that results section from a different study? (or am I looking at the wrong one?)

The results section that was posted way back i nthe thread is from a 2009 paper. Here is the abstract from the present paper.

Clin Chim Acta. 2012 May 11. [Epub ahead of print]
Visible and near-infrared spectra collected from the thumbs of patients with chronic fatigue syndrome for diagnosis.

Source
Department of Virology, Center for Infectious Disease Control, Research Institute for Microbial Diseases, Osaka University, Yamadaoka, Suita, Osaka 565-0871, Japan; Fatigue Clinical Center, 21st Century COE Program, Osaka City University Graduate School of Medicine, Abeno-ku, Osaka 545-8585, Japan.
Abstract
BACKGROUND:
Currently, diagnosis of chronic fatigue syndrome (CFS) is based on clinical symptoms and therefore relies on the experience and skill of the doctors. Here, we have examined the possible diagnosis of CFS based on spectral information and chemometrics analysis, such as principal component analysis (PCA) and soft modeling of class analogy (SIMCA).
METHODS:
Visible and near-infrared (Vis-NIR) spectroscopy was used to examine possible changes in the region of 600-1100nm in thumbs and assessed.
RESULTS:
The Vis-NIR spectra of thumbs from 57 CFS patients and 74 healthy volunteers were subjected to PCA and SIMCA to develop multivariate models to discriminate between CFS patients and healthy individuals. The model was further assessed by the prediction of 120 determinations (60 in the healthy group and 60 in the CFS patient group). The PCA model predicted a discrimination of the masked samples; specifically the SIMCA model correctly predicted 51 of 60 (83.3%) healthy volunteers and 42 of 60 (70%) CFS patients.
CONCLUSIONS:
Despite the relatively small number of subjects involved in this trial, who were exclusively Japanese, our results imply that Vis-NIR spectroscopy of the thumb combined with chemometrics analysis may provide a valuable tool for diagnosing CFS.
 

Cort

Phoenix Rising Founder
in the paper it says


"(Fig. 3C). The most prominent discriminating power, which represents
independent variables (wavelengths) important in discriminating two
classes (CFS from healthy) were the sharp peak at around 900 nm and
broad peaks at around 700–800 and 1000–1050 nm (Fig. 3C) .

Oxyhemoglobin has greater absorbance at 850 nm than at 760 nm,
whereas deoxyhemoglobin absorbs more at 760 nm than at 850 nm.
In addition, the ratio of absorbance at 605 nm to 620 nm correlates
with the oxidation of heme a + a 3 in cytochrome c oxidase [28]. Similarly, the ratio of absorbance at 830 nm to 780 nm correlates with the oxidation of copper in cytochrome c oxidase [29]. Intriguingly, the absorbance of these wavelengths in thumbs is different between CFS"

if deoxyhemoglobin absorbs more at 760 and the peak was between 7-800 - how could oxyhemoglobin rates be higher in CFS? It sounds like deoxyhemoglobin rates are higher (as well as copper oxidation by cytochrome c oxidase)

deoxyhemoglobin is - hemoglobin not combined with oxygen, formed when oxyhemoglobin releases its oxygen to the tissues. High levels then should relate to high oxygen absorption in the tissues????
 

Cort

Phoenix Rising Founder
later they say "this differentiation may be due to a change in oxyhemoglobin/deoxyhemoglobin and the oxidation of hemea + a3 to cytochrome c oxidase..."

I attached the paper.
 

Attachments

  • Clin chim acta 2012 (2).pdf
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JT1024

Senior Member
Messages
582
Location
Massachusetts
I found this interesting since I recently saw a publication regarding Fibromyalgia and "Skin Response" as mentioned below:

ORIGINAL PAPER
The Correlation of Laboratory Tests and Sympathetic Skin Response Parameters by Using Artificial Neural Networks in Fibromyalgia Patients

Özhan Özkan, Murat Yildiz and Etem Köklükaya

Abstract
Fibromyalgia syndrome (FMS) is a chronic musculoskeletal disease which causes dysfunction of the autonomic nervous system. Sympathetic Skin Response (SSR) is a part of electrical impedance of body which is affected by the autonomic nervous system dysfunctions. In this study, values obtained from the results of the patients diagnosed with fibromyalgia syndrome, and healthy subjects blood samples in the laboratory conditions are recorded in Suleyman Demirel University, Faculty of Medicine, Department of Physical Medicine and Rehabilitation. SSR measurements are recorded from patients and healthy controls. Values of latency time, maximum amplitude and elapsed time between two stimulus parameters are obtained from recorded sympathetic skin response data by using Matlab software. The relationship between SSR parameters and laboratory tests is investigated by using artificial neural networks. As a result SSR seems to be a valid parameter in the classification of FMS.
Keywords Sympathetic skin response – Fibromyalgia syndrome – Laboratory tests – Artificial neural networks – Autonomic nervous system