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Science to Patients: Talking ME, Exercise and the Mitochondria - with Dr Charles Shepherd

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The latest video release from the Dutch group ME/cvs Vereniging, with Dr Charles Shepherd from the UK ME Association, and announcing a live chat session to be held Thursday, April 10, 2014...


Dutch group ME/cvs Vereniging present their latest video followed by a chat session with Dr Charles Shepherd from the UK ME Association

ME/cvs Vereniging launched a series of broadcasts from expert clinicians and researchers in January 2013, as part of a government subsidized project called, “Science to Patients”.

Each expert has also taken part in Q & A sessions, enabling patients to ask questions on both theoretical and practical aspects of ME/CFS.

The sessions were not meant to be a consultation, but have proven to be a mine of knowledge to many a patient about his/her own condition.

These are all English subtitled broadcasts and have previously featured Dr Kenny De Meirlier, as well as the Dutch cardiologist, Dr Frans Visser.

Dutch international project: Science to Patients

This current year kicked off with a series of interviews from paediatrician Dr Nigel Speight, Medical Adviser to the 25% ME Group for severely affected patients and Honorary Paediatric Medical Adviser to the ME Association, who spoke in some detail about how the condition affects children.

Announcing the latest broadcast: Dr. Charles Shepherd on ME, Exercise and the Mitochondria


Dr Charles Shepherd.
Click Image to Watch Latest Video

Dr Charles Shepherd MB BS, is Honorary Medical Adviser of the ME Association, and a private physician with a longstanding personal interest in ME/CFS - having developed the condition following an episode of chickenpox encephalitis that he caught from one of his hospital patients.

He has been involved with all aspects of the illness - benefits, education, management, media, politics, research, services - for over 30 years and was a member of the Chief Medical Officer's Working Group on ME/CFS and the Medical Research Council's Expert Group on ME/CFS research.

He is currently a member of the Department of Work and Pensions Fluctuating Conditions Group, whose recommendations regarding changes to the way eligibility for work-related sickness benefits (ie ESA) are assessed has recently been tested in an evidence based review.

Dr Shepherd is also involved with parliamentary work - including forming part of Secretariat for the All Party Parliamentary Group on ME at Westminster.

His research involvement includes supervising all the research that is currently being funded by the ME Association - in particular the establishment of an ME Biobank for blood samples at the Royal Free Hospital in London - and he is an executive board member of the UK ME/CFS Research Collaborative.

“...so we know there seems to be a problem with mitochondrial function in ME and this may play a very important part in explaining why people have this very characteristic symptom of exercise-induced muscle fatigue and sometimes pain in this illness.”

Research interests include the role of vaccines as trigger factors for ME/CFS, post-mortem tissue collection and analysis, and muscle/mitochondrial abnormalities in ME/CFS.

He has written a self-help guide for people with ME/CFS ('Living with ME') and a 52-page guideline for health professionals ('ME/CFS/PVFS: An Exploration of the Key Clinical Issues'), written with Consultant Neurologist, Dr Abhijit Chaudhuri; as well as having made numerous contributions to the medical literature.

Dr Shepherd is married with three children and lives in Gloucestershire.

The video broadcast - available to watch now - will be followed by a Q & A session in English, on Thursday 10 April, from 17:00-17:45 Central European Time. Please visit HERE on the day to watch, or to take part.

Please be advised that further interviews will be broadcast and chat sessions held over the summer and autumn with Professor Julia Newton and Professor Lenny Jason.


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There is quite a lot of anecdotal (= patient) evidence, and some research evidence, to show that vitamin D deficiency can occur in people with moderate and severe ME/CFS - because they are seldom (or not at all) outside in the sunshine. The MEA guidelines for doctors therefore recommends that groups at risk should be tested (a simple blood test for 25-hydroxyvitamin D) for vitamin D levels and that vitamin D supplements should be taken by those at risk, and appropriate supplementation should be given to people with a proven vitamin D deficiency. The role of vitamin D, and vitamin D deficiency, is covered in the research and treatment sections of the MEA purple booklet. We also have an MEA information leaflet on vitamin D assessment, deficient, prevention. and treatment.
 
There is quite a lot of anecdotal (= patient) evidence, and some research evidence, to show that vitamin D deficiency can occur in people with moderate and severe ME/CFS - because they are seldom (or not at all) outside in the sunshine. The MEA guidelines for doctors therefore recommends that groups at risk should be tested (a simple blood test for 25-hydroxyvitamin D) for vitamin D levels and that vitamin D supplements should be taken by those at risk, and appropriate supplementation should be given to people with a proven vitamin D deficiency. The role of vitamin D, and vitamin D deficiency, is covered in the research and treatment sections of the MEA purple booklet. We also have an MEA information leaflet on vitamin D assessment, deficient, prevention. and treatment.
Vitamin D levels in ME/CFS - this paper could be used if a doctor is unwilling to investigate the possibility of vitamin D deficiency in someone with ME/CFS who falls into an at risk group.

Int J Vitam Nutr Res. 2009 Jul;79(4):250-4. doi: 10.1024/0300-9831.79.4.250.
Serum 25-hydroxy vitamin D levels in chronic fatigue syndrome: a retrospective survey.
Berkovitz S1, Ambler G, Jenkins M, Thurgood S.
Author information

Abstract
INTRODUCTION:
Patients with chronic fatigue syndrome (CFS) may be at risk of osteoporosis due to their relative lack of physical activity and excessive time spent indoors, leading to reduced vitamin D synthesis. We hypothesized that serum 25-OH vitamin D levels are lower in CFS patients than in the general British population.
SUBJECTS AND METHODS:
We performed a retrospective survey of serum 25-OH vitamin D levels in 221 CFS patients. We compared this to a group of patients attending the hospital for other chronic conditions and to a large British longitudinal survey of 45-year old women, using a variety of appropriate statistical approaches.
RESULTS:
25-OH vitamin D levels are moderately to severely suboptimal in CFS patients, with a mean of 44.4 nmol/L (optimal levels >75 nmol/L). These levels are lower and the difference is statistically significant (p<0.0004) than those of the general British population from a recent national survey, but similar to those in patients with other chronic conditions.
CONCLUSIONS:
This data supports the recommendation made in recent NICE guidelines that all patients with moderate to severe CFS should be encouraged to obtain adequate sun exposure and eat foods high in vitamin D. Oral or intramuscular vitamin D supplementation should be considered for those whose levels remain suboptimal.
 
@charles shepherd thank you so much for all the support here, your time is much appreciated.

What some are over looking is that vitamin D deficiency in ME may be from lack of sun exposure (for sure), but also low Magnesium levels which is an issue for us. I took magnesium and taurine injections for years and my D levels went right up. This text states, "magnesium depletion may impair vit D metabolism".

Low serum concentrations of 1,25-dihydroxyvitamin D in human magnesium deficiency.
Rude RK, Adams JS, Ryzen E, Endres DB, Niimi H, Horst RL, Haddad JG Jr, Singer FR.
Abstract
The effect of magnesium deficiency on vitamin D metabolism was assessed in 23 hypocalcemic magnesium-deficient patients by measuring the serum concentrations of 25-hydroxyvitamin D (25OHD) and 1,25-dihydroxyvitamin D [1,25-(OH)2D] before, during, and after 5-13 days of parenteral magnesium therapy. Magnesium therapy raised mean basal serum magnesium [1.0 +/- 0.1 (mean +/- SEM) mg/dl] and calcium levels (7.2 +/- 0.2 mg/dl) into the normal range (2.2 +/- 0.1 and 9.3 +/- 0.1 mg/dl, respectively; P less than 0.001). The mean serum 25OHD concentration was in the low normal range (13.2 +/- 1.5 ng/ml) before magnesium administration and did not significantly change after this therapy (14.8 +/- 1.5 ng/ml). Sixteen of the 23 patients had low serum 1,25-(OH)2D levels (less than 30 pg/ml). After magnesium therapy, only 5 of the patients had a rise in the serum 1,25-(OH)2D concentration into or above the normal range despite elevated levels of serum immunoreactive PTH. An additional normocalcemic hypomagnesemic patient had low 1,25-(OH)2D levels which did not rise after 5 days of magnesium therapy. The serum vitamin D-binding protein concentration, assessed in 11 patients, was low (273 +/- 86 micrograms/ml) before magnesium therapy, but normalized (346 +/- 86 micrograms/ml) after magnesium repletion. No correlation with serum 1,25-(OH)2D levels was found. The functional capacity of vitamin D-binding protein to bind hormone, assessed by the internalization of [3H]1,25-(OH)2D3 by intestinal epithelial cells in the presence of serum was not significantly different from normal (11.42 +/- 1.45 vs. 10.27 +/- 1.27 fmol/2 X 10(6) cells, respectively). These data show that serum 1,25-(OH)2D concentrations are frequently low in patients with magnesium deficiency and may remain low even after 5-13 days of parenteral magnesium administration. The data also suggest that a normal 1,25-(OH)2D level is not required for the PTH-mediated calcemic response to magnesium administration. We conclude that magnesium depletion may impair vitamin D metabolism.

PMID:
3840173
[PubMed - indexed for MEDLINE]
 
@charles shepherd thank you so much for all the support here, your time is much appreciated.

What some are over looking is that vitamin D deficiency in ME may be from lack of sun exposure (for sure), but also low Magnesium levels which is an issue for us. I took magnesium and taurine injections for years and my D levels went right up. This text states, "magnesium depletion may impair vit D metabolism".

Low serum concentrations of 1,25-dihydroxyvitamin D in human magnesium deficiency.
Rude RK, Adams JS, Ryzen E, Endres DB, Niimi H, Horst RL, Haddad JG Jr, Singer FR.
Abstract
The effect of magnesium deficiency on vitamin D metabolism was assessed in 23 hypocalcemic magnesium-deficient patients by measuring the serum concentrations of 25-hydroxyvitamin D (25OHD) and 1,25-dihydroxyvitamin D [1,25-(OH)2D] before, during, and after 5-13 days of parenteral magnesium therapy. Magnesium therapy raised mean basal serum magnesium [1.0 +/- 0.1 (mean +/- SEM) mg/dl] and calcium levels (7.2 +/- 0.2 mg/dl) into the normal range (2.2 +/- 0.1 and 9.3 +/- 0.1 mg/dl, respectively; P less than 0.001). The mean serum 25OHD concentration was in the low normal range (13.2 +/- 1.5 ng/ml) before magnesium administration and did not significantly change after this therapy (14.8 +/- 1.5 ng/ml). Sixteen of the 23 patients had low serum 1,25-(OH)2D levels (less than 30 pg/ml). After magnesium therapy, only 5 of the patients had a rise in the serum 1,25-(OH)2D concentration into or above the normal range despite elevated levels of serum immunoreactive PTH. An additional normocalcemic hypomagnesemic patient had low 1,25-(OH)2D levels which did not rise after 5 days of magnesium therapy. The serum vitamin D-binding protein concentration, assessed in 11 patients, was low (273 +/- 86 micrograms/ml) before magnesium therapy, but normalized (346 +/- 86 micrograms/ml) after magnesium repletion. No correlation with serum 1,25-(OH)2D levels was found. The functional capacity of vitamin D-binding protein to bind hormone, assessed by the internalization of [3H]1,25-(OH)2D3 by intestinal epithelial cells in the presence of serum was not significantly different from normal (11.42 +/- 1.45 vs. 10.27 +/- 1.27 fmol/2 X 10(6) cells, respectively). These data show that serum 1,25-(OH)2D concentrations are frequently low in patients with magnesium deficiency and may remain low even after 5-13 days of parenteral magnesium administration. The data also suggest that a normal 1,25-(OH)2D level is not required for the PTH-mediated calcemic response to magnesium administration. We conclude that magnesium depletion may impair vitamin D metabolism.

PMID:
3840173
[PubMed - indexed for MEDLINE]

Just found the full text pdf here.
 
The repeat cardiopulmonary exercise test developed by Prof Mark VanNess et al cannot yet be described as a diagnostic test for ME/CFS but it does produce sound objective evidence of post-exertional malaise, which is a very characteristic clinical feature of ME/CFS. It is not highly expensive to do if the equipment is available. I suggest you take abstracts (readily available via google) from the two most recent papers from this group that have been published and show them to your GP.

There are certainly anecdotal reports of people benefitting from vitamin B12 injections but no sound evidence in the literature of B12 deficiency in ME/CFS or proven benefits from B12 injections in properly controlled clinical trials. So most UK doctors are reluctant to prescribe this vitamin. In addition, vitamin B12 is not a form of treatment endorsed by NICE.
You might also find this video of a presentation by Prof Mark VanNess in Bristol useful:

https://www.youtube.com/watch?v=q_cnva7zyKM

I attended a half day physicians workshop with Mark and his team at the IACFS conference in San Francisco last month and am currently writing up a detailed report (7,600 words so far) of what was a very interesting clinical and research meeting.
 
Anecdotal evidence indicates that a number of vaccinations, including flu vaccine, are capable of either triggering ME/CFS, or causing an exacerbation of pre-existing symptoms

But there hasn't been any really robust research carried out to investigate the role of this other type of immune system stressor in ME/CFS

I have a research interest in the role of vaccinations and my patient data on the subject, which is now quite substantial and includes a lot of health workers who are vaccinated almost as a condition of employment, indicates that hepatitis B vaccine plays an unusual and significant role here

This is supported by the resultrs of the MEA website poll on the roll of vaccinations as trigger factors for ME/CFS:

MEA WEBSITE POLL:



  • If your ME/CFS was triggered by a vaccination, which vaccine was involved?
    • Hepatitis B (57%, 338 Votes)

    • Flu (9%, 51 Votes)

    • Other (7%, 41 Votes)

    • BCG (6%, 33 Votes)

    • Cannot remember (5%, 31 Votes)

    • Combination (5%, 27 Votes)

    • Tetanus (3%, 18 Votes)

    • Meningitis (3%, 17 Votes)

    • MMR (2%, 14 Votes)

    • Polio (2%, 10 Votes)

    • Hepatitis A (1%, 7 Votes)

    • Typhoid (0%, 4 Votes)


      Total Voters: 591
Start Date: April 30, 2010 @ 3:20 pm
End Date: June 2, 2010 @ 3:20 pm
Dear Dr. Shepard, My physiology changed after the Hep B vaccine in 1999. I got very sick after each shot. When the series was done, the first symptoms of physiologic change was "leaden legs" when exercising. Exercise tolerance diminished remarkably (I was very athletic). I had an MMR a few months before. I don't think that helped matters much. Thank you for somewhat validating my theory re: what really, really got the ball rolling. I'm not sure if this helps your research, I don't remember doing a survey at any time about this.
 
Science to Patients, video # 40: Dr Charles Shepherd--ME & possible treatments.

Questions of patients Dr. Charles Shepherd answers in this video are:

- What are the most common symptoms in ME?
- Which symptoms can be treated?
- What other treatment suggestions can you give?
- What help can be given to very severe ME-patients?

 
Getting back to B12, briefly, because somebody has just posted a link to this paper in another thread.
http://jrs.sagepub.com/content/92/4/183

It would appear that simon wesseley himself found evidence of B12 deficiency in '99.
But he appears to have conveniently "forgotten" this.
Nah, he believes we're psychogenically making ourselves physically ill. So any objective measures are still explained away by our supposed ability to create physical illness by just thinking wrongly. :rolleyes:
From Wikipedia -- Psychogenic Disease
Psychogenic diseases are physical illnesses that stem from emotional or mental stresses.[1]
 
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You're using big words, @SOC :eek:;)

Are you saying that he's excusing the low B12, on the grounds that we managed to supress it with "mind control".

Actually, shouldn't the CIA be interested in us if we have such amazing mind control? :whistle:
After all, they did try to train men to kill goats by staring at them. :p
 
On April 21, the next webinar of dr. Charles Shepherd has been broadcast, in which he talks about ME, its most significant symptoms and possible treatments:

http://youtu.be/R7JtNImePlY
http://youtu.be/DmyR33LeUPs is the right link, tho' Llewellyn King's video is worthwhile watching as well :D

this broadcast was followed by a very noteable chatwingsession with dr. Shepherd on Thursday 24th April.

if you would wish to receive all transcripts of both webinars and chatsessions, simply send your request to wvp@me-cvsvereniging.nl

Next webinar within the Dutch porject Science to Patients will be broadcast on May 5th,
on promising discoveries & researches.

Next inernational chatsession with dr. Charles Shepherd will be on Thursday 15th May, from 5 pm cet onward. (logging in with http://chatwing.com/mecvsvereniging.wvp)
 
Great article and a very interesting video, a lot of people are very critical of Dr. Shepherd for one reason or another but it has to be said his commitment to ME/CFS is very admirable, as is his willingness to aid research and exposure of the condition where he can.

I'm very interested in the mitochondrial problems that may arise in relation to ME/CFS. From a personal perspective, following my sudden onset, PEM was never a major issue earlier in my disease however as time has progressed it appears to play a larger role where other symptoms and problems have diminished. It makes me wonder whether mitochondrial problems may arise later as a result of something else. My mind immediately turns to recent studies displaying vascular problems in ME/CFS patients, particularly endothelial dysfunction, a problem very closely related to autonomic dysfunction which appears to have quite an important role in the pathophysiology of ME.

To me the build up of lactate, alongside evidence of damaged mitochondria, imply an insufficient blood supply is reaching the muscle cells. This would mean waste products would build up quickly as their production will vastly outpace the removal which normally takes place via the blood stream. A build up of lactate is well documented to cause cellular damage, I think this would be best termed a type of ischemia which is well known to cause mitochondrial damage alongside a plethora of other problems for cells.

While I don't think mitochondrial abnormalities are therefore the primary disease driving force for ME/CFS, I do believe that they are the cause of one of its most discerning feature - post exercise malaise.
I feel you made a good point here I consider very strongly that once Mito dysfunction occurs one must deal with it, it becomes central in the same way that lack of Insulin does in Type I diabetes even though immunology create the disease. However remains difficult to know the extent to which it's an Etiology or a symptom with certainty. We need to test people very early in the disease process and while at low severity. It is attractive in that it can explain pretty much every feature of the disease.
 
You make a very valid point about the role of blood flow to skeletal muscle - because this could link in with the autonomic nervous system, which helps to control blood flow, and ANS dysfunction is a well recognised feature of ME/CFS.

The MEA Ramsay Research Fund has been funding more research at the University of Newcastle (Prof Julia Newton et al) into abnormal muscle energy metabolism in ME/CFS and the possible underlying pathophysiology behind the abnormalitity involving lactic acid production.

I would refer you in particular to the findings from Newcastle that have been reported in this paper:
Dr Shepperd,

when discussing blood flow - why is volume always ignored by medics? A very small scale experiment showed that restoring blood volume (with saline) caused the nervous system of ME patients to normalise. The nervous system (in that limited number of patients) was prioritising the core (heart and lungs) and reducing peripheral blood flow. Similar issues are known in other diseases causing marked reduction in blood volume. I find it quite scandalous that none of our national charities have repeated this and verified it (either way).

I have personally experienced complete restoration of mental function with administration of Saline.

Vis-a-vis Mitochondria in the circumstance - blood cells also show mitochondrial under-performance (various papers by Howard and MyHill) hence their issue would not be 'blood supply'. I do however agree that blood supply seems likely to aggravate issues in peripheral skeletal muscle - there does seem to be tendency to forget we have mitochondria outside muscle however :). Those of us for whom mental dysfunction is our biggest issue would quite like some focus there!

Also Myhill has identified two groups of patients. One produces more lactic acid under when 'going anaerobic' the other uses the very destructive process in which two molecules of ADP become one of ATP. Given these two groups, just how reliable is lactic acid as an indicator of Mito dysfunction rather than pain?