Cerebral blood flow is reduced in CFS as assessed by arterial spin labeling

Dolphin

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New research

J Neurol Sci. 2010 Dec 15. [Epub ahead of print]

Cerebral blood flow is reduced in chronic fatigue syndrome as assessed by arterial spin labeling.

Biswal B, Kunwar P, Natelson BH.

Departments of Radiology, UMDNJ-New Jersey Medical School, Newark NJ, United States.

Abstract

BACKGROUND: Chronic fatigue syndrome is diagnosed by a set of clinical criteria and therefore is probably heterogeneous. Earlier reports tested the hypothesis that the syndrome had a neurological substrate by doing studies of cerebral blood flow (CBF) but with discrepant results. One possible reason for the discrepancy was that relative CBF was assessed. We found reduced CBF in an earlier study of absolute CBF using xenon-CT. The purpose of this study was to use a second method of assessing CBF and to look within the study group for heterogeneity of responses.

METHOD: Eleven CFS patients and 10 age matched healthy controls underwent neuroimaging using arterial spin labeling to determine their regional and global absolute CBF. A template was constructed based on the control data, and individual patient montages were compared on a case by case basis to determine if differences in regions of interest occurred.

RESULTS: The patients as a group had significantly lower global CBF than the controls. The reduction in CBF occurred across nearly every region assessed. Nine of the 11 patients showed these reductions compared to the average control data, while two patients showed actual increases relative to the controls.

CONCLUSION: The data extend our earlier observation that CFS patients as a group have broad decreases in CBF compared to healthy controls. However, as expected, the effect was not homogeneous in that 2 of the 11 patients studied showed actual increases in CBF relative to controls.
 

Dolphin

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Could the blood volume abnormalities found in the rest of the body explain this? I've read the full paper but the authors don't mention it.
 

richvank

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Could the blood volume abnormalities found in the rest of the body explain this? I've read the full paper but the authors don't mention it.
Hi, Dolphin.

There are three aspects of CFS that I know of that could contribute to low cerebral blood flow:

1. Low total blood volume, which you mentioned, due to the diabetes insipidus that many PWCs have as part of their illness (not the same as diabetes mellitus)--reported by the late Dr. David Streeten.

2. Low cardiac output, as a result of both the low total blood volume and diastolic dysfunction of the heart, which many PWCs have--reported by Dr. Arnold Peckerman et al. and by Dr. Paul Cheney.

3. Inflammation of the blood vessels in the brain in CFS (actually M.E.)-reported by Dr. Byron Hyde. This causes obstruction and lowers the flow in the blood vessels.

For what it's worth, in the GD-MCB hypothesis for CFS, the first is due to glutathione depletion in the hypothalamus/pituitary, which lowers the secretion of antidiuretic hormone, which in turn causes the kidneys to remove too much water from the blood and excrete it into the urine. The second is due to mitochondrial dysfunction in the heart muscle cells, which in turn is due to both glutathione depletion and the partial methylation cycle block. The third is likely due to an infection as a result of immune system dysfunction, due to the combination of glutathione depletion, the partial methylation cycle block, and draining of folate metabolites from the cells. If this is all true, treating to lift the methylation cycle block should help toward correcting all these problems. Information on this is available at www.cfsresearch.org by clicking on CFS/M.E. and then on my name.

Best regards,

Rich
 

Dolphin

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Thanks Rich.

The paper is a bit disappointing I think in that it doesn't explore much what this might mean or link in with other findings except in the introduction where it basically just links in with other brain scan findings.

Here's the discussion section in case anyone is interested:
4. Discussion

This paper confirms and extends our earlier observation that
patients with chronic fatigue syndrome as a group have diminished
cerebral blood flow relative to matched controls — even when the
data are corrected for volume of brain tissue. Importantly, both this
paper and our earlier one using xenon-CT [9] used a method that
assessed absolute CBF rather than the relative measure used in earlier
studies with other methodologies. The reduction in CBF was quite
diffuse sparing only the right temporal area. Because we have found
diffuse reduction in CBF using two methodologies, we conclude that
CBF is reduced in general in CFS. These data support the previously
done SPECT studies as well as a study using PET technology which also
showed diminished brain blood flow [13].

However, the other reason for our doing this study was to look at
subject-to-subject variability in CBF. When we compared each CFS
patient to a composite map comprised of data from our control
subjects, we found that 9 of the 11 patients showed reduction in CBF.
However, two of the patients showed actual increases in CBF relative
to controls. This result encourages this approach and documents the
idea that CFS is by definition a heterogeneous illness because it is
diagnosed using a clinical case definition and has no specific
diagnostic test. We have hypothesized that some CFS patients have
neurological underpinnings to their illness. An important next step
will be to determine if patients with low CBF have some phenotypic
difference in the presentation of their illness relative to those with
normal CBF: we hypothesize that patients in the group with the
lowest global CBF comprise the same group as those with abnormal
brain neuroimaging results and objective evidence of brain dysfunction
in the form of reduced cognitive testing scores.
 
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Thanks Rich.

The paper is a bit disappointing I think in that it doesn't explore much what this might mean or link in with other findings except in the introduction where it basically just links in with other brain scan findings.

Here's the discussion section in case anyone is interested:
Unfortunately, that's not the way most medical research happens. There are incremental changes that over time help us to get at the truth.

Remember, there are still no recognized biomarkers or physical abnormalities that can be used to diagnose CFS/ME. This is a step in the right direction. It's a test that can differentiate PWCers from healthy people. The more of these we get, the better.
 

Cort

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Thanks Rich.

The paper is a bit disappointing I think in that it doesn't explore much what this might mean or link in with other findings except in the introduction where it basically just links in with other brain scan findings.

Here's the discussion section in case anyone is interested:
They are so darn carefull! Why not speculate? That is just maddening to me...I agree that they need to point out the links; otherwise how will non CFS researchers know???? There is such conservatism in the medical field. I have tried to the get the IACFS/ME to have invited seminars at the Int Conference specifically on what is causing CFS - for researchers to attempt to it wrap and speculate; those would be fascinating seminars to watch....but they just won't do it.
 

Cort

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For what it's worth, in the GD-MCB hypothesis for CFS, the first is due to glutathione depletion in the hypothalamus/pituitary, which lowers the secretion of antidiuretic hormone, which in turn causes the kidneys to remove too much water from the blood and excrete it into the urine. The second is due to mitochondrial dysfunction in the heart muscle cells, which in turn is due to both glutathione depletion and the partial methylation cycle block. The third is likely due to an infection as a result of immune system dysfunction, due to the combination of glutathione depletion, the partial methylation cycle block, and draining of folate metabolites from the cells. If this is all true, treating to lift the methylation cycle block should help toward correcting all these problems. Information on this is available at www.cfsresearch.org by clicking on CFS/M.E. and then on my name.
The thing that scares me about the GSH depletion theory (and mitochondrial theories) is that, it seems to me, that you can apply them to anything - just posit that they happen in whatever organ you are interested in and you have a cause.

But what is the cause of GSH depletion in 3 sentences or less? Is it an internal cellular problem or is it increased oxidative stress outside the cells? If its an internal cellular problem how did that arise and why did it arise in CFS?
 

Sushi

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Hi, Dolphin.

There are three aspects of CFS that I know of that could contribute to low cerebral blood flow:

1. Low total blood volume, which you mentioned, due to the diabetes insipidus that many PWCs have as part of their illness (not the same as diabetes mellitus)--reported by the late Dr. David Streeten.

2. Low cardiac output, as a result of both the low total blood volume and diastolic dysfunction of the heart, which many PWCs have--reported by Dr. Arnold Peckerman et al. and by Dr. Paul Cheney.

3. Inflammation of the blood vessels in the brain in CFS (actually M.E.)-reported by Dr. Byron Hyde. This causes obstruction and lowers the flow in the blood vessels.

Best regards,

Rich
Hi Rich,

What about OI as a contributing cause of low cerebral blood flow? It is known that in some of us blood can pool in the abdomen and the legs. There are several reasons (non-cardiac) why this is thought to happen. One is that the valves in the veins leak in the wrong direction (as in prolapsed heart valves). Collagen is implicated here and it is also known that a subset have a form of Ehlers-Danlos syndrome and the collagen abnormalities that go with it.

Also, my autonomic specialist thought that there was damage to the norepinephrine receptors in peripheral nerves which in turn affected return blood flow. (Hope I got that bit right, but that is what I remember! :rolleyes:)

Thus the combo of low blood volume, plus pooling could be another factor.

I love to hear your thoughts on this.

Best wishes,
Sushi
 

richvank

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Hi, Dolphin, lono and the group.

It's true particularly in CFS research that the researchers usually don't try to interpret their observed results in terms of a comprehensive model for the pathogenesis and pathophysiology. Most of them are specialists in some particular subfield of biomedicine, and they tend to comment only as their results relate to their subfield. Frankly, most of those who are doing CFS research do not have a broad enough scope in their understanding of biochemistry and physiology to have the confidence to attempt to interpret their experimental results in more global terms.

I have interacted with many of the CFS researchers at the IACFS/ME conferences, and have tried to encourage them to look at CFS more globally, but have not had much success. I think there are several other reasons why they don't do that. One is that it is risky. If you are a professional researcher making your living from it, you need to keep the grant money coming in. To do that, you need to be able to show some results each year, and get them published in peer-reviewed journals. To make sure this will happen, it is safer to propose to do something you are sure you can do, and that is familiar to the editors and reviewers of the journals in which you hope to publish, and that often means measuring the same things you have measured before, but using a different method or doing it more precisely. So that is what is commonly done, over and over.

In my research, I have the advantage that I am on a pension and do not have to rely on grants being accepted. I can therefore take more risks and can take a more global view of CFS, to try to see how all the pieces fit together. If I were in their shoes, I would probably not have the courage to try that.

It can be difficult to get a global view published in peer-reviewed journals, because the editors and reviewers are not comfortable with this kind of thinking. Most of them have been trained in the reductionist approach to research, if indeed they have had any specific education in doing research at all. In this approach, one makes only one small step at a time. Hypotheses are one-liners, and the logic does not proceed until that one small step has been tested and proven. This is very slow, but sometimes it is the only thing one can do in a field where not much is known.

My background is in engineering and physics. In these fields, a "systems approach" to research has become more common, because these fields are relatively mature, and there is a large body of accepted theory that one can use to project one's thinking. With this approach, it is possible to develop more comprehensive hypotheses, making several steps at a time. This is what I have been trying to do for CFS, because I think enough is known to do this now. At this point, I think that the GD-MCB hypothesis is a fairly good working hypothesis, in that it appears to be consistent with or capable of incorporating essentially all the published research in CFS. Of course, I need to continue to modify parts of it as more is learned from new research, but I think the main essence of it is pretty solid at this point, though I would not claim that it is "scientifically proven," which is a very high standard.

A difference I've seen in switching fields is that in the physical sciences, when a researcher does something experimentally, and gets some results, it's considered an obligation when publishing them to try to explain them in terms of available theory, or to suggest a hypothesis to do so. In biomedicine, this does not seem to be the case. Researchers do not seem to feel any such obligation, and in fact, if they do suggest an explanation, they run the risk that the journal editors or reviewers will reject it, because they have been trained not to do this.

Another factor is that many of those doing research on CFS were trained as M.D.s, rather than going through a Ph.D. program. These are fundamentally different. M.D.s are trained to diagnose and treat patients, using approaches that are established and accepted as the "standard of care." They mostly memorize a large body of information, and are trained to use it over and over, and not to deviate from the way they have been trained. This produces a uniformity in medical care. If you have certain symptoms, most M.D.s will diagnose and treat you in the same ways. This can be a good thing for well-understood conditions, but it can be maddening if you have an illness such as CFS, which is not well understood and is not dealt with in the curriculum of medical schools.

A Ph.D. program, on the other hand, is designed to educate a person in analytical thinking and to give them experience in actually doing research. The recent interview of Dr. Burt Berkson, who has both Ph.D. education and M.D. training, is very instructive in this regard. There are some M.D.s who are able to make the transition from their training into being good researchers, but many of the M.D.s I have encountered who do research on CFS have very rigid ideas and very narrow scopes of thinking. It can be very frustrating to try to get them to think "outside their box," because they have specifically been trained to stay inside it. In their practice of medicine, if they deviate from the standard of care, they stand to lose their license to practice medicine, as enforced in the U.S. by the state medical boards, and in the UK by the GMC. The FDA, insurance companies, malpractice attorneys, and peer pressure also act to prevent independent thinking and action on the part of M.D.s (Note what Dr. Myhill is currrently going through in the UK.) It is really not fair to expect M.D.s to make this transition on their own, given their training and the regulatory environment in which they must work.

In fairness, let me also say that a person with a Ph.D. degree alone would not be a good choice for diagnosing and treating patients on a routine basis. They have not been trained to do that, and they are usually not aware of all the pitfalls that can be encountered, as well as not having memorized the detailed body of diagnostic and treatment information that M.D.s have available right off the top of their head. Also, of course, they are not licensed to do that. When I have a serious health issue, I go to an M.D., not a Ph.D., at least not first. I also pay a lot of attention to N.D.s, D.O.'s and various alternative practitioners, because I prefer non-drug treatments where possible.

Incidentally, I disagree with the commonly repeated statement that there are no good biomarkers for CFS. In particular, based on quite a bit of experience at this point, I would say that the methylation pathways panel offered by the Health Diagnostics and Research Institute contains a good set of biomarkers for CFS.

Best regards,

Rich
 

richvank

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Hi Rich,

What about OI as a contributing cause of low cerebral blood flow? It is known that in some of us blood can pool in the abdomen and the legs. There are several reasons (non-cardiac) why this is thought to happen. One is that the valves in the veins leak in the wrong direction (as in prolapsed heart valves). Collagen is implicated here and it is also known that a subset have a form of Ehlers-Danlos syndrome and the collagen abnormalities that go with it.

Also, my autonomic specialist thought that there was damage to the norepinephrine receptors in peripheral nerves which in turn affected return blood flow. (Hope I got that bit right, but that is what I remember! :rolleyes:)

Thus the combo of low blood volume, plus pooling could be another factor.

I love to hear your thoughts on this.

Best wishes,
Sushi
Hi, Sushi.

I agree. Sorry that I didn't think to include that in my list. In addition to the possible causes of OI that you mentioned, I think that HPA axis dysfunction can also contribute. Low cortisol can cause low blood pressure, and that can make it difficult to deliver blood to the head against the pull of gravity, especially when standing.

The GD-MCB hypothesis accounts for HPA axis dysfunction by positing that the secretion of CRH and ACTH are affected negatively by glutathione depletion in the hypothalamus and pituitary. I've explained the mechanism in another thread, but basically it involves not keeping the cysteine molecules in their reduced state until the proper stage in the formation of these molecules.

Best regards,

Rich
 

richvank

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They are so darn carefull! Why not speculate? That is just maddening to me...I agree that they need to point out the links; otherwise how will non CFS researchers know???? There is such conservatism in the medical field. I have tried to the get the IACFS/ME to have invited seminars at the Int Conference specifically on what is causing CFS - for researchers to attempt to it wrap and speculate; those would be fascinating seminars to watch....but they just won't do it.
Hi, Cort.

You are right on about this.

I've offered my thoughts on this issue in another post on this thread.

Best regards,

Rich
 

richvank

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Hi, Cort.

Thank you for your willingness to ask the critical questions and attempt to get the heart of the pathogenesis of CFS. Let me just make a few points, and sorry if this runs to more than 3 sentences. Some things in life are a little more complex than can be expressed in three sentences, and I suggest that CFS is one of them! :)-)

1. Generally speaking, glutathione depletion, the partial methylation cycle block, and mitochondrial dysfunction are no longer simply posited in CFS or autism. At one time, that was the case, but at this point, we have what I would consider good lab-based evidence for these phenomena.

2. It's true that back in 2004 I was emphasizing glutathione depletion in CFS. Since then, I have learned that the more fundamental issue is the partial block in the methylation cycle, which is what maintains the depletion of glutathione. So my thinking has moved on since those days, and I would prefer to emphasize the partial methylation cycle block as the more fundamental aspect now, since we have found that if it is corrected, glutathione rises automatically. These two phenomena appear to form a vicious circle together, which is what causes CFS to be a chronic condition, but in treatment, it is the partial methylation cycle block that must be corrrected to break this vicious circle.

3. With regard to applying glutathione depletion and the partial methylation cycle block to a particular organ, there is a basis in biochemistry for judging which organs are likely to suffer these phenomena when they occur in the body as a whole, and which organs are likely to be less affected. This basis is that it is known that the cells in only certain organs have a complete transsulfuration pathway, and are thus able to convert methionine to cysteine. This is important, because cysteine is usually the rate-limiting amino acid for the sythesis of glutathione. The organs that are known to have this capability are the liver, pancreas, kidneys, intestine, lens of the eye, and to a much smaller degree, the cells of the brain. I think it is no accident that these are vital organs for the maintenance of life. When push comes to shove, they can make their own cysteine and hold their glutathione up longer than the other organs, tissues and cells. When glutathione goes down in these vital organs, the person dies. I believe that this is the cause of the socalled "multiple organ failure" which leads to the death of many people in critical care units.

4. Now, what causes depletion of glutathione? First, I believe that there needs to be a genetic predisposition for this to occur in a given person. This genetic predisposition is not completely defined yet. I have encouraged the genetic researchers to focus on looking at the polymorphisms in the antioxidant, B12, and methylation parts of the metabolism, and I hope that that will eventually be done. We do have some information about this, but it is incomplete.

Second, the person has to be subjected to some combination of a variety of stressors (physical, chemical, biological, and/or psychological/emotional), the particular combination varying from one case to another. These stressors are all known to place demands on glutathione, by various biochemical routes, which I discussed in detail in my IACFS/ME poster papers in 2004 and 2007 (these can be found at www.cfsresearch.org). I'm sorry that it would take more than three sentences to describe these mechanisms. The reason is that glutathione normally plays a number of vital roles in the body. If any of these roles demand too much glutathione, as a result of the various stressors, in a person with the appropriate genetic predisposition, glutathione can become depleted, and this can remove the normal protection from B12, thus precipitating a partial methylation cycle block, which then forms a vicious circle with the depletion of glutathione. locking CFS in as a chronic condition, until this vicious circle is broken.

I hope this is helpful.

Best regards,

Rich
 

leela

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A great couple of minutes from Neil DeGrasse Tyson on medical breakthroughs, that coincides exactly with what you are saying, Rich:
[video=youtube;VjY0vqgDMnE]http://www.youtube.com/watch?v=VjY0vqgDMnE[/video]

We really need inter-disciplinary cooperative efforts to look at the big picture here..
 

Cort

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Hi, Cort.

Thank you for your willingness to ask the critical questions and attempt to get the heart of the pathogenesis of CFS. Let me just make a few points, and sorry if this runs to more than 3 sentences. Some things in life are a little more complex than can be expressed in three sentences, and I suggest that CFS is one of them! :)-)

1. Generally speaking, glutathione depletion, the partial methylation cycle block, and mitochondrial dysfunction are no longer simply posited in CFS or autism. At one time, that was the case, but at this point, we have what I would consider good lab-based evidence for these phenomena.

2. It's true that back in 2004 I was emphasizing glutathione depletion in CFS. Since then, I have learned that the more fundamental issue is the partial block in the methylation cycle, which is what maintains the depletion of glutathione. So my thinking has moved on since those days, and I would prefer to emphasize the partial methylation cycle block as the more fundamental aspect now, since we have found that if it is corrected, glutathione rises automatically. These two phenomena appear to form a vicious circle together, which is what causes CFS to be a chronic condition, but in treatment, it is the partial methylation cycle block that must be corrrected to break this vicious circle.

3. With regard to applying glutathione depletion and the partial methylation cycle block to a particular organ, there is a basis in biochemistry for judging which organs are likely to suffer these phenomena when they occur in the body as a whole, and which organs are likely to be less affected. This basis is that it is known that the cells in only certain organs have a complete transsulfuration pathway, and are thus able to convert methionine to cysteine. This is important, because cysteine is usually the rate-limiting amino acid for the sythesis of glutathione. The organs that are known to have this capability are the liver, pancreas, kidneys, intestine, lens of the eye, and to a much smaller degree, the cells of the brain. I think it is no accident that these are vital organs for the maintenance of life. When push comes to shove, they can make their own cysteine and hold their glutathione up longer than the other organs, tissues and cells. When glutathione goes down in these vital organs, the person dies. I believe that this is the cause of the socalled "multiple organ failure" which leads to the death of many people in critical care units.

4. Now, what causes depletion of glutathione? First, I believe that there needs to be a genetic predisposition for this to occur in a given person. This genetic predisposition is not completely defined yet. I have encouraged the genetic researchers to focus on looking at the polymorphisms in the antioxidant, B12, and methylation parts of the metabolism, and I hope that that will eventually be done. We do have some information about this, but it is incomplete.

Second, the person has to be subjected to some combination of a variety of stressors (physical, chemical, biological, and/or psychological/emotional), the particular combination varying from one case to another. These stressors are all known to place demands on glutathione, by various biochemical routes, which I discussed in detail in my IACFS/ME poster papers in 2004 and 2007 (these can be found at www.cfsresearch.org). I'm sorry that it would take more than three sentences to describe these mechanisms. The reason is that glutathione normally plays a number of vital roles in the body. If any of these roles demand too much glutathione, as a result of the various stressors, in a person with the appropriate genetic predisposition, glutathione can become depleted, and this can remove the normal protection from B12, thus precipitating a partial methylation cycle block, which then forms a vicious circle with the depletion of glutathione. locking CFS in as a chronic condition, until this vicious circle is broken.

I hope this is helpful.

Best regards,

Rich
I'm glad you took more than sentences. Thanks for getting that down so I can understand it. :)
 

Dolphin

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It can be difficult to get a global view published in peer-reviewed journals, because the editors and reviewers are not comfortable with this kind of thinking. Most of them have been trained in the reductionist approach to research, if indeed they have had any specific education in doing research at all. In this approach, one makes only one small step at a time. Hypotheses are one-liners, and the logic does not proceed until that one small step has been tested and proven. This is very slow, but sometimes it is the only thing one can do in a field where not much is known.
Just curious have you had any papers turned down? Answer off-list if you prefer.

I submitted an article about a month ago and it is an anxious wait. I'm not a traditional person to be submitting articles nor is it a traditional viewpoint. Although I feel I have backed up my points reasonably well.
 

Dolphin

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Hi Rich,

What about OI as a contributing cause of low cerebral blood flow? It is known that in some of us blood can pool in the abdomen and the legs. There are several reasons (non-cardiac) why this is thought to happen. One is that the valves in the veins leak in the wrong direction (as in prolapsed heart valves). Collagen is implicated here and it is also known that a subset have a form of Ehlers-Danlos syndrome and the collagen abnormalities that go with it.

Also, my autonomic specialist thought that there was damage to the norepinephrine receptors in peripheral nerves which in turn affected return blood flow. (Hope I got that bit right, but that is what I remember! :rolleyes:)

Thus the combo of low blood volume, plus pooling could be another factor.

I love to hear your thoughts on this.

Best wishes,
Sushi
But would that explain this finding? These people were lying supine (i.e. flat or flattish - perhaps the head is slightly elevated? I've never had a brain scan - not sure it would make enough difference?)
 

richvank

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Just curious have you had any papers turned down? Answer off-list if you prefer.

I submitted an article about a month ago and it is an anxious wait. I'm not a traditional person to be submitting articles nor is it a traditional viewpoint. Although I feel I have backed up my points reasonably well.
Hi, Dolphin.

Yes, Dr. Myhill and I wrote a review of all the published work that we believe supports mitochondrial dysfunction being present in CFS. It was rejected by two journals. We may try again.

Best regards,

Rich
 

richvank

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But would that explain this finding? These people were lying supine (i.e. flat or flattish - perhaps the head is slightly elevated? I've never had a brain scan - not sure it would make enough difference?)
Hi, Dolphin.

I think that's a good point with regard to this study. OI can be a factor in lowering blood flow to the brain when people are sitting or standing.

Best regards,

Rich
 
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In following this thread, can see why it has been such a slow process, although unacceptable from a pt perspective. Due to long term cognitive dysfunction, I am grateful to Rich, Cort et al and agree that the difference in PhD and MD is pertinent. My background in Nursing +20 years in hospital venues helped me to understand the analytical theories of Paul Cheney, MD, PhD. Also, he had the broad experience of Air Force, then the Incline Village outbreak. It all adds up to me....even with my comprehension speed. Another frustration is the research, as noted. My experience of late was that to be 'managed' or part of one trial, it was a placebo/antidepressant project. Grant money again partnered with Pharm corp. Told that I could help others by taking part. When I came to my senses, realized in one year my age would eliminate me from the study. Also my track record introducing antidepressants to tx cocktail has proven disasterous. Then am told if bad reaction to just stop the drug....after the panic, rush to local ER, and possible relapse.
It leaves me so discouraged. I do try to update on research such as the recent NJCFSA excellent conference, as I live in Jersey. But financially, psychologically, am continuing on the holistic path of least resistance. Realizing that I am a spiritual being in a physical body. There is hope especially now with such interesting discoveries and researchers who are 'rebels' with a great cause and there do not seem to be any secrets where they are concerned. Enough of my rambling....been quite a spell since posting as the effort can be exhausting. _SueC
 

Dolphin

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2 errors in paper

The authors have confirmed the following error with me:

In Table 1: "whole" for patients #10 and 11 have minus signs in front of them i.e. -16 and -7.

In the discussion section, where it says::
"The reduction in CBF was quite diffuse sparing only the right temporal area."
that should say left rather than right.