In Brief: Mitochondria and ME

October 17, 2013

The third in a series of short articles attempting to explain the science behind fairly common topics and exploring how they relate to ME. This time the topic is Mitochondria – by Andrew Gladman.

A single mitochondrion - hundreds of these exist within each single cell of the body.

A single mitochondrion – hundreds of these organelles exist within each single cell of the body.

Over the years it is fairly safe to say that finding consistent physiological abnormalities in ME has proven difficult for researchers, and that this has likely reinforced the notion that ME is largely a psychological disease – an error which only in recent years is being shaken off.

One area that has shown consistent interest is the mitochondria, with many researchers acknowledging or suspecting mitochondrial dysfunction as a real physiological problem. Some even believe it could play a central role in the pathology of ME.

What are the mitochondria?

The mitochondria are a membrane-bound organelle residing inside the cell. Because the mitochondria themselves have a membrane surrounding them, they could be simply described as a smaller uni-function cell within a larger multi-function cell.

The mitochondria are an integral part of the cell machinery and, to use an analogy, if the cell can be considered a factory then the mitochondria serve as the power generator or engine room – providing the power required for all other cellular processes in the form of a small molecule known as adenosine triphosphate (ATP).

ATP is generally known as the currency of energy within the body, storing energy in the short term and transferring it when required. The majority of energy is produced through a process known as aerobic respiration, and which is based almost entirely within the mitochondria.

The mitochondria consist of two membranes, one inside the other – with the inner one being highly folded in on itself. Within the centre of the mitochondrion (inside both membranes) there exists a circular loop of DNA which codes for the mitochondrial enzymes and proteins which are required for the processes of respiration that occur within the mitochondria.

There also exists some small ribosomes, which are often described as molecular machines that work with the mitochondrial DNA to produce these proteins – if the DNA can be considered the instructions for the protein construction then the ribosomes are the machines in which the construction takes place. 

The mitochondria itself has become a great topic of discussion and debate with regard to its origins and the mechanism by which it produces ATP. Today, it is a commonly held theory that the mitochondria was originally a separate organism hundreds of millions of years ago, solidifying my previous analogy of the mitochondria as a small cell within a larger cell!

By chance a mitochondrion was taken up into the cells of the primordial ancestors of all higher and complex life, and, instead of being destroyed, the two organisms evolved symbiotically, both receiving an advantage from the other, until eventually the mitochondria became fully integrated into the cell and unable to survive outside of it. This is known as the endosymbiont hypothesis. The theory is supported by the similarity of the mitochondria to some bacteria that still exist today and because mitochondria have their own genetic material.

What role does the mitochondrion play in respiration?

Video explaining the process of cellular respiration.

Video explaining the process of cellular respiration.

Prior to the 1960′s it was commonly known that ATP was the currency of energy and that it was produced by the mitochondria, but it was not known how the ATP came into being.

It was initially believed that a simple series of chemical reactions produced ATP as a product – a process known as substrate level-phosphorylation. However in 1961 Dr. Peter Mitchell, a biochemist, proposed the chemiosmotic hypothesis which is the generally accepted theory today. 

However, despite this theory being commonly taught and held in high regard, it was initially met with much criticism and disbelief from his peers, indicating just how much evidence is required before a hypothesis such as this can really become accepted in mainstream science.

To summarise this important theory, it is helpful to have an understanding of the process of respiration, and this can simply be broken down into the following four stages:

  • GlycolysisGlucose, essentially the fuel extracted from our food, in the cell is broken down in numerous stages until two molecules of pyruvate are formed.
  • The Link Reaction – converts the products of glycolysis into the initial reactants required for the krebs cycle.
  • The Krebs Cycle – a multi-stepped reaction that forms a cycle, with the initial reactant being the same as the final product.
  • Oxidative phosphorlyation – the final process and the only one where oxygen is used. Several products of the other three stages are used along with oxygen to produce the vast majority of ATP. 

Each are further divided into many steps however the detail of each step is not required to understand the concept.

The first of these stages, glycolysis, doesn’t occur within any organelle and simply takes place in the liquid filling the cell, known as cytoplasm. During this stage there is in fact some production of ATP, however only a very little amount, and this is used in the absence of oxygen as this stage forms the basis of anaerobic respiration with lactic acid also generated as a by-product.

Glycolysis is thought to be the most ancient method of energy production and is common to all living organisms, evolving long before the mitochondrion entered primordial cells. The end-product of glycolysis, pyruvate, is then transported into the mitochondrion and the new two stages, the link reactions and the Krebs Cycle, both occur within the fluid filling the mitochondrion, often described as the mitochondrial matrix.

The Krebs Cycle, so named after the man who described the process in detail, Dr Hans Krebs, is a step-by-step series of reactions which loop around so that the final product of the process of reaction is the same as the initial reactant hence the cycle keeps going. In a similar fashion to glycolysis a small number of ATP molecules are also produced.

450px-Atp_synthase

ATP synthase enzyme, the enzyme embedded in the inner membrane of the mitochondrion. The upper portion spins when protons flow through the enzyme producing ATP. By Alex.X (enWiki (PDB.org for coordinate)) [GFDL or CC-BY-SA-3.0], via Wikimedia Commons

However, the true purpose of both glycolysis and the Krebs Cycle is to produce a molecule such as NADH and FADH2. These carry energy in the form of electrons and protons to the electron transport chain, a simple series of proteins embedded in the mitochondrial membrane.

These energy carriers are produced as a by-product of many of the reactions involved in both these reaction processes. It appears somewhat difficult to understand why this might be important, however both the electrons and protons become very important in the final stage of respiration, oxidative phosphorylation

Oxidative phosphorylation is the process advanced by Dr Mitchell and he described it quite eloquently:

“It works much like a hydroelectric dam. The energy released by the oxidation of food (via a series of steps) is used to pump protons across a membrane — the dam — creating, in effect, a proton reservoir on one side of the membrane. The flow of protons through amazing protein turbines embedded in this membrane powers the synthesis of ATP in much the same way that the flow of water through mechanized turbines generates electricity.”

For this to work there are two isolated areas within the mitochondria – hence why is has two membranes. An area between the two membrane, known fittingly as the intermembrane space, has a high concentration of H+ molecules and one has a much lower concentration of H+ molecules. This is termed an electro-chemical gradient for the simple reason that one side has more positively charged chemical molecules than the other.

The electron in the energy carrier is transferred into the proteins of the electron transport chain and as the electron is passed from protein to protein, the energy released  is used to pump the protons (H+) into the intermembrane space, forming a lake of protons ready to flow through the dam, thus allowing for the production of ATP. The H+ then flows through the ATP synthase enzyme (the dam) thus spinning the enzyme head and producing the vast majority of ATP. 

Why are the mitochondria important in ME?

In the previous sections I explained the processes involved in respiration and where the mitochondrion fits into this picture. Given this information and the integral role that it plays in this vital process, it is fairly easy to understand why any dysfunction or deregulation within this organelle can spell problems for the patient and how such an occurrence has the potential to explain the symptoms that ME patients suffer on a day to day basis. 

One of researchers most recognised by patients in this area of mitochondria and ME is Dr Sarah Myhill who has published several papers on the topic and also talks about mitochondria on her website. Fundamentally, the hypothesis proposed by Dr. Myhill is best described in her own words:

“The job of mitochondria is to supply energy in the form of ATP (adenosine triphosphate). This is the universal currency of energy. It can be used for all sorts of biochemical jobs from muscle contraction to hormone production. When mitochondria fail, this results in poor supply of ATP, so cells go slow because they do not have the energy supply to function at a normal speed. This means that all bodily functions go slow.”

There are problems with regard to this research however, not least the view that the authors have competing interests, and therefore some patients and other researchers do take the claims made and the treatments prescribed with a pinch of salt, at least until more research can be independently carried out. 

Other researchers such as Professor Julia Newton have shown through their own research that muscles in patients with ME produce much larger volumes of lactic acid upon stimulation than healthy controls. This implies an underlying problem that could be sourced to the mitochondria and might indicate that anaerobic respiration has to ‘pick up the slack’ for the ATP requirements of the cell. 

Dr Chris Snell is renowned for his work with ME patients with regard to exercise ability and subsequent intolerance, specifically with regard to exercise testing. His work has highlighted the post exercise malaise and reduced functional capability exercise can have on patient performance. Dr Snell’s latest research could indicate a possible problem in mitochondrial function.

However, it is worth noting that past studies involving the testing of VO2 MAX and the anaerobic threshold of ME patients have resulted in findings that are dramatically different from results of known diseases involving mitochondrial function, and whilst Dr Snell’s research might indicate there is a problem of exercise intolerance in ME patients, this would appear to contradict the proposed hypothesis of mitochondrial dysfunction as a central mechanism in ME.

Possibly one of the most exciting lines of research is now set to come out of the UK and from a team based in Liverpool and led by Professor Anne McArdle. They are undertaking work using newly developed and ground-breaking mitochondrial analysis techniques in order to better analyse any abnormalities in patient mitochondrial function, and their research will also look at cytokine production in the skeletal muscles of ME patients.

The following quote is taken from the Liverpool University website regarding their ongoing research:

“Scientists have hypothesised that the mitochondria in ME patients could be malfunctioning, significantly reducing the energy supply to the muscle cells that allow the body to carry out its daily activities. The pain and inflammation that follows can cause further mitochondrial abnormalities and so the vicious cycle of events continue.”

Interestingly, both this research and the work by Professor Julia Newton and her team have both been funded in large part by the Medical Research Council.

Given the interest and existing evidence regarding mitochondria and ME, it is clear to me that the mitochondria are very likely to play a role, whether it be directly or indirectly, in the pathology and hence the symptoms of this disease. The evidence however, as in most ME research areas, is somewhat sparse and much of the data has proved unreliable or has not been successfully replicated.

From a personal point of view, it is difficult to place the mitochondria as a central pillar within the pathology of ME, these organelles certainly appear to be adversely affected, hence losing a degree of their function, however it seems likely that this is a downstream result of more widespread dysfunction and dysregulation in other organs and tissues.

Looking ahead, the mitochondria could prove to be one direction for possible symptomatic treatment following further research into the area. However there is much more research to be done and only after each area of interest has been researched thoroughly, can the tangled knot of ME be successfully divided into the numerous strings of which it is composed. 

If anyone has any requests or suggestions of topics for future installments be sure to let me know in the comments below. 

Next time we explore the vascular system; how it works and why it could be one of the most promising areas of research in ME.

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44 comments

{ 44 comments… read them below or add one }

peggy-sue October 17, 2013 at 12:42 pm

I fell very strongly, from my own symptoms, that mitochondrial dysfunction is at the root of what is wrong, not something downstream from it.
My ME is downstream from my mitochondria not working. :p
Every cell, every organ and every system in the body depends on mitochondria working properly.
My every cell, my every organ and (nearly) my every system do not work.o_O

peggy-sue October 17, 2013 at 12:44 pm

Just one wee minor thing of interest missing from this excellent article – which is that the mitochondria are inherited down the female line.

Legendrew October 17, 2013 at 12:57 pm
peggy-sue

Just one wee minor thing of interest missing from this excellent article – which is that the mitochondria are inherited down the female line.

Indeed they are – as an organelle within every cell they are located in the ovum of a mother – the sperm simply serves to combine with the DNA of the ovum and none of its mitochondria are incorporated. Interesting point and one that admittedly I forgot to include although the article was getting pretty long already! Perhaps not entirely relevant but then again we have yet to either confirm or deny whether ME can be passed down through genetic defects etc. The picture is further complicated as despite the mitochondrion having its own DNA, some of the mitochondrial proteins are produced by the normal cell DNA – presumably some of the mitochondrial DNA was incorporated into the cellular DNA millions of years ago.

peggy-sue

I fell very strongly, from my own symptoms, that mitochondrial dysfunction is at the root of what is wrong, not something downstream from it.
My ME is downstream from my mitochondria not working. :p
Every cell, every organ and every system in the body depends on mitochondria working properly.
My every cell, my every organ and (nearly) my every system do not work.o_O

It all comes down to that pesky non-homogeneous grouping of ME. For some mitochondria likely play a much more central role however it appears that for the majority mitochondrial issues aren't as paramount as other areas, the trouble is that mitochondria are indeed central to nearly all cellular activity so even a small degree of dysfunction can cause a wide range of seemingly unconnected symptoms. The reason for my personal view of mitochondria not being central to the pathology is simply the lack of evidence and research to support it, although even if it is a downstream problem that isn't to say it could contribute to or even cause many of the ME symptoms. Another interesting point I didn't include was that there are other energy carrying molecules in the body with very specific function such as GTP which is used primarily in the transfer of proteins and chemicals in and out of the nucleus membrane. It just goes to show that the more we look into these things, the more complex it gets!

Glad you liked the article anyway!

peggy-sue October 17, 2013 at 1:14 pm

The proton pump is is a bit of bio-engineering that never fails to impress me.
Every single one of our cells can strip an electron off a molecule…. and keep it off.

Has physics managed to do that yet?:p

Legendrew October 17, 2013 at 1:22 pm
peggy-sue

The proton pump is is a bit of bio-engineering that never fails to impress me.
Every single one of our cells can strip an electron off a molecule…. and keep it off.

Has physics managed to do that yet?:p

It is pretty amazing, a perfect example of the complexity evolution can achieve through small advantageous steps. I always think that it's amazing that a proton motive force and electrochemical gradient have evolved in perfect harmony with the ATP synthase enzyme to convert chemical and electrical energy into kinetic energy and then back into chemical energy, and how this all occurs simply to phosphorylate ADP. It's easy to see why a single problem could cause the whole system to back up and cause a plethora of seemingly unconnected symptoms.

I couldn't speak for physics unfortunately as I never studied it beyond compulsory levels, other than a little mechanics in maths – I studied biology, chemistry and maths. It always seems that we're a step behind evolution though, everything we come up with is always discovered in nature somewhere.

peggy-sue October 17, 2013 at 1:27 pm

I don't like physics myself.
I don't trust electrons when they're not stuck to molecules, or gently stripped off and put tidily away somewhere else.
Mechanical stuff, levers and pulleys and vetors are fine.

Nature is wonderful and far more amazing than any fiction.

But I don't like that electrickery.

WNM October 17, 2013 at 1:45 pm

Nice article, well written. However I think there is more research to suggest mitochondrial dysfunction occurs in ME/CFS.

http://cellfatigue.blogspot.com/2013/04/mitochondrial-dysfunction-in-cfs.html?utm_source=BP_recent

Legendrew October 17, 2013 at 2:02 pm
WNM

Nice article, well written. However I think there is more research to suggest mitochondrial dysfunction occurs in ME/CFS.

http://cellfatigue.blogspot.com/2013/04/mitochondrial-dysfunction-in-cfs.html?utm_source=BP_recent

nice article there – I particularly like the following comment.

"There is now substantial evidence to suggest systemic mitochondrial dysfunction occurs in ME/CFS and underlies symptoms of fatigue. The causes of this dysfunction could be many but likely include impaired blood flow, cofactor depletion (e.g. Co-Q10), oxidative damage and dysregulation by inflammatory signaling"

It sums up quite eloquently that despite mitochondrial dysfunction appearing to be a downstream problem, the symptoms caused by the dysfunction can be incredibly widespread. The next article in the series relates to the cardiovascular system which links quite nicely with mitochondrial dysfunction. Glad you liked the article.

stridor October 17, 2013 at 3:18 pm

Thank-you for writing this article.
I was wondering if about the proposed incidence of ME/CFS and CCSVI and the purported mitochondrial involvement with loss of patency of the tricuspid valve in the heart with resulting venous congestion in the brain and liver.
Do you have any comments regarding this theory? Would limiting the brain's access to oxygenated blood be the cause of orthostatic intolerance? Could brain-fog be related to this and/or failure to clear catabolites etc?
My brain-fog used to double if I had to stand. Again, thanks….brad

Legendrew October 17, 2013 at 3:48 pm
stridor

Thank-you for writing this article.
I was wondering if about the proposed incidence of ME/CFS and CCSVI and the purported mitochondrial involvement with loss of patency of the tricuspid valve in the heart with resulting venous congestion in the brain and liver.
Do you have any comments regarding this theory? Would limiting the brain's access to oxygenated blood be the cause of orthostatic intolerance? Could brain-fog be related to this and/or failure to clear catabolites etc?
My brain-fog used to double if I had to stand. Again, thanks….brad

I have to admit i'm unfamiliar with CCSVI so i wouldn't feel comfortable answering the question without further research unfortunately. I shall look into it and perhaps post a better researched response tomorrow.

With regard to brain-fog however I think it could well be due to dysregulation clearing catabolites within the brain. Only recently I was reading about the glymphatic system, the specialised lymphatic system in the brain which has only very recently begun to be well understood. It is comprised of many channels within the brain that clear catabolites and waste products from the neurones, especially during sleep when glial cells shrink, hence allowing for increased glymphatic flow. It has been been researched in the context of neuro-degenerative diseases and dementia however I think it could well prove to be an interesting line of research for ME, especially given that one of the most common symptoms is headaches/migraines which could stem from such a waste build-up – not to mention that sleep is often disrupted hence not allowing for the standard 'cleaning' of the brain during sleep.

With regard to orthostatic intolerance, I think it stems from a combination of cardiovascular insufficiency as well as autonomic – that being both sympathetic and parasympathetic – dysfunction. These systems are components of the peripheral nervous system therefore I have to question whether lack of oxygen to the brain is a central cause however given the aforementioned glymphatic system, I think damage in this way could potentially explain certain elements of orthostatic intolerance. There is no doubt that the comorbidity of ME and orthostatic intolerance ought to be telling us something is not working as intended in the circulatory and/or nervous system – both topics I intend to explore in future articles. As with everything further research is vital! Thanks for the good questions and I hope these answers give you interesting things to research and postulate on.

5150 October 17, 2013 at 4:00 pm

Mitochondriae don't "just fail", such as by genetically. Given my 100% certainty that this disease is contagious, it's the stealth pathogen that has so far escaped identification, that is the true causal agent. I don't know the scientific process of "why" the mitochondria are damaged and don't function properly, but it is reasonable that it's associated with the invading pathogen. My best guess: it's a yet undiscovered retrovirus, very difficult to find. But it wreaks havoc by "going viral" ; hence the millions of people now infected, and many more to come if this snail's pace of research isn't sped up. We old-timers are starting to lose the ultimate battle more and more.

Legendrew October 17, 2013 at 4:08 pm
5150

Mitochondriae don't "just fail", such as by genetically. Given my 100% certainty that this disease is contagious, it's the stealth pathogen that has so far escaped identification, that is the true causal agent. I don't know the scientific process of "why" the mitochondria are damaged and don't function properly, but it is reasonable that it's associated with the invading pathogen. My best guess: it's a yet undiscovered retrovirus, very difficult to find. But it wreaks havoc by "going viral" ; hence the millions of people now infected, and many more to come if this snail's pace of research isn't sped up. We old-timers are starting to lose the ultimate battle more and more.

I honestly think the evidence just isn't there for either ME being contagious or a 'stealth pathogen' as you put it. If mitochondrial dysfunction is involved then it is unlikely that such an infectious agent would effect the mitochondria, the sole purpose of a virus at the end of the day is to replicate. I discussed this at some length in my article exploring viruses and I recommend reading that article if viruses are your personal opinion of a causative mechanism – you might enjoy the content. I think that the endless search for viruses has done more harm than good for ME now.

As I've expressed many times previously I believe ME is caused by a genetic defect which could potentially be passed through families. Upon great stress being placed on the immune system the genetic weakness leads to the ongoing diseases process whatever that may be – an analogy I liken it to is spreading petrol in a forest. The spark is the initial virus, infection or stress however once the forest is ablaze there seems little point in searching for the triggering virus which likely plays no role in the ongoing blaze. Whether this blaze is an autoimmune process or otherwise is yet to be seen but I think it's high time that another hypothesis took the lead as the viral hypothesis has proven incorrect for nearly 30 years – if there was something to find, i'm of the opinion that it would have by now.

At the end of the day complex diseases need devious answers and viruses simply do not fit this disease process in my mind, autoimmunity may and I look forward to further research in this area.

aimossy October 17, 2013 at 7:49 pm

Good article Andrew yet again!
Your analogy in the above statement is very good.
I think it is good that we have two areas of research happening. Virus/pathogen and autoimmune.
Both areas will help to form the picture and produce biomarkers and analyse what is happening in our bodies. One area of research can end up helping or supporting another if it is quality research.
I would love to see an article about all the top quality research that's happening right now and an analysis of how they may help support our picture and possibly tie up together.
Not all of us can go searching the net or have the education to see how that might happen.
I could do with that help, analysis and information.
That could also promote more donations or spark more people to join ME organisations.
Just a thought :)

August59 October 17, 2013 at 8:08 pm
WNM

Nice article, well written. However I think there is more research to suggest mitochondrial dysfunction occurs in ME/CFS.

http://cellfatigue.blogspot.com/2013/04/mitochondrial-dysfunction-in-cfs.html?utm_source=BP_recent

They got another $2 million grant to study a larger cohort which is good.

deboruth October 17, 2013 at 8:38 pm

Whose view is it that Myhill et al are not to be considered too seriously because of their "competing" interests? Would like to know whose view and which competing interests, as I am other wise somewhat lost and confused.

Chris October 17, 2013 at 9:35 pm

A helpful essay–many thanks. You probably know the essay from Julia Newton's group, though the first listed author is D.E.J. Jones, "Abnormalities in pH handling by peripheral muscle and potential regulation by the autonomic nervous system in chronic fatigue syndrome", 2009. This suggests various mechanisms by which the ANS might exert control over the mitochondria–the essay does not use the word, but it seems implicit in how it defines "peripheral muscle."

She also has a great little essay, "Home orthostatic training in chronic fatigue syndrome–a randomized, placebo-controlled feasibility study", 2010. I have been doing this for about 3 months now, and my OI is quite substantially improved, and I think slowly my fatigue is improving too–it is good stuff, and I recommend it, though take care–she talks about a "drop-zone" and you have to make sure that you won't get hurt if you pass out! This simple execise has been shown to cure neurocardiogenc syncope, but I think this was the first essay linking it to ME/CFS. Chris

peggy-sue October 18, 2013 at 4:54 am

I think OI might have a lot to do with lack of vasoconstriction, (ie, a smooth muscular problem) as well as low blood volume.

peggy-sue October 18, 2013 at 6:00 am

There isn't one single symptom that cannot be accounted for by the lack of sufficient energy production in the mitochondria.

How much further "downstream" can you get than the mitochondria? :confused:

Legendrew October 18, 2013 at 6:20 am
peggy-sue

I think OI might have a lot to do with lack of vasoconstriction, (ie, a smooth muscular problem) as well as low blood volume.

peggy-sue

There isn't one single symptom that cannot be accounted for by the lack of sufficient energy production in the mitochondria.

How much further "downstream" can you get than the mitochondria? :confused:

From a personal stance I think you're likely getting at something very important in the first quote. Many of the chemicals involved in vasoconstriction and vasodilation have numerous other roles and some influence directly mitochondrial function. As such any dysregulation in the endothelium (the layer of cells that secrete these vasoactive chemicals) could potentially influence mitochondrial function. By downstream, what I mean is that it is likely not the first step of dysfunction occurring – but that is not to say it could be a major part of the disease pathology, to use yet another analogy: If i were to go to the source of a river and pour in gallons of toxins there would be no obersevable problems at that area but downstream all the plants and fish would likely die, the problem started at the very source where i poured in the toxins but the majority of problems occurred much further downstream, you can help the ecosystem by purifying the water downstream but to solve the problem you'd have to stop the pollution at the river source and I think most diseases work like this. I plan to write a lot more in my next article regarding vasoconstriction and vasodilation, the endothelium and the cardiovascular system as a whole which will be worth a read if you're interested in that area of ME research.

peggy-sue October 18, 2013 at 6:42 am

You might be very interested in the work that is currently being carried out in my home town of Dundee, then!

Prof. Chim Lang did his MBChB in the same (very small – my boss, an Hons. student, Chim and me) lab as I worked in, way back in the early '80s.
His project was on trying to discover EDRF. He has had an interest in this area since then, which is how he came to be involved in studying ME now.
He's working with Jill Belch and Faisel Khan.

I bumped into him a while ago. He was shocked that he couldn't get funding from the MRC, but had had to get it from charity, he told me there is ongoing inflammation in ME; that it is absolutely real and physical and not remotely psychological.
That, from a medic who came into the disease and research from an interest outside of it.:thumbsup:

He knew nothing of the politics.

Both studies, one in adults, one in children, showing the ongoing inflammation have been published.

They do infra-red stuff on vasoconstriction in thumbs….

Legendrew October 18, 2013 at 9:29 am
aimossy

Good article Andrew yet again!
Your analogy in the above statement is very good.
I think it is good that we have two areas of research happening. Virus/pathogen and autoimmune.
Both areas will help to form the picture and produce biomarkers and analyse what is happening in our bodies. One area of research can end up helping or supporting another if it is quality research.
I would love to see an article about all the top quality research that's happening right now and an analysis of how they may help support our picture and possibly tie up together.
Not all of us can go searching the net or have the education to see how that might happen.
I could do with that help, analysis and information.
That could also promote more donations or spark more people to join ME organisations.
Just a thought :)

Thanks for the feedback. Good idea for an article too – I did something similar in my first article discussing where rituximab may fit into the current ME research climate, the only trouble with such articles in the sheer amount of work involved researching! It may be something we'll do in the future – that being other writers at phoenix rising or myself. Currently all my effort is going into this series of articles so it won't be anytime soon unfortunately but good suggestion and certainly one that I can see the advantage of!

I cannot urge anyone enough to contact Firestormm if they have any ideas for articles for Phoenix Rising or if they wish to join the content team!

Little Bluestem October 19, 2013 at 12:28 am

Long before I had any idea that I had ME/CFS, I thought that the 'virus from which I never really recovered' must have messed up my mitochondrial function as that was the only thing I could think of that would reduce both physical and mental function.

stridor October 19, 2013 at 4:39 am
Legendrew
stridor

Thank-you for writing this article.
I was wondering if about the proposed incidence of ME/CFS and CCSVI and the purported mitochondrial involvement with loss of patency of the tricuspid valve in the heart with resulting venous congestion in the brain and liver.
Do you have any comments regarding this theory? Would limiting the brain's access to oxygenated blood be the cause of orthostatic intolerance? Could brain-fog be related to this and/or failure to clear catabolites etc?
My brain-fog used to double if I had to stand. Again, thanks….brad

I have to admit i'm unfamiliar with CCSVI so i wouldn't feel comfortable answering the question without further research unfortunately. I shall look into it and perhaps post a better researched response tomorrow.

With regard to brain-fog however I think it could well be due to dysregulation clearing catabolites within the brain. Only recently I was reading about the glymphatic system, the specialised lymphatic system in the brain which has only very recently begun to be well understood. It is comprised of many channels within the brain that clear catabolites and waste products from the neurones, especially during sleep when glial cells shrink, hence allowing for increased glymphatic flow. It has been been researched in the context of neuro-degenerative diseases and dementia however I think it could well prove to be an interesting line of research for ME, especially given that one of the most common symptoms is headaches/migraines which could stem from such a waste build-up – not to mention that sleep is often disrupted hence not allowing for the standard 'cleaning' of the brain during sleep.

With regard to orthostatic intolerance, I think it stems from a combination of cardiovascular insufficiency as well as autonomic – that being both sympathetic and parasympathetic – dysfunction. These systems are components of the peripheral nervous system therefore I have to question whether lack of oxygen to the brain is a central cause however given the aforementioned glymphatic system, I think damage in this way could potentially explain certain elements of orthostatic intolerance. There is no doubt that the comorbidity of ME and orthostatic intolerance ought to be telling us something is not working as intended in the circulatory and/or nervous system – both topics I intend to explore in future articles. As with everything further research is vital! Thanks for the good questions and I hope these answers give you interesting things to research and postulate on.

Thank-you for your reply. You have given me a couple of avenues for further reading and contemplation. Last year, I had read that orthostatic intolerance was related to a "measurable change in circulation" to the brain. I exaggerated symptoms and was tested for MS and using ultrasound, they found the CCSVI. I still am not sure whether this is the "measurable change" that was mentioned….but it will do.
I think that it was Cheney who suggested that most of us have some degree of CCSVI and I was surprised how little this is discussed here on PR. Personally, I think that this could provide a future means of Identifying those with ME from the form of CFS which is on the Major Depressive Disorder continuum.
I look forward to your future endeavours. brad

justy October 20, 2013 at 3:37 am

Hi, thanks for the article – i was really looking forward to this one as i , and many others on this forum have had the Mitochondrial function test done and found it to be useful, especially in convincing others that we are physically ill. Of course the test mainly shows that we are ill, rather than pinpoitning the initial cause, and it is surpirsing how similar the mitochondrial issues are between patients. Given this i was rather surprised how quickly you dismissed the work and research of Myhill et al. Dr Myhill's research work was peer reviewed and published in the same manner as the work of Dr Newton which you appear to hold in higher regard.

Perhaps you could elaborate on your comments about the research of Myhill et al and explain why an exploration of their work was not a part of your article.

All the best,
Justy.

Legendrew October 20, 2013 at 5:20 am
justy

Hi, thanks for the article – i was really looking forward to this one as i , and many others on this forum have had the Mitochondrial function test done and found it to be useful, especially in convincing others that we are physically ill. Of course the test mainly shows that we are ill, rather than pinpoitning the initial cause, and it is surpirsing how similar the mitochondrial issues are between patients. Given this i was rather surprised how quickly you dismissed the work and research of Myhill et al. Dr Myhill's research work was peer reviewed and published in the same manner as the work of Dr Newton which you appear to hold in higher regard.

Perhaps you could elaborate on your comments about the research of Myhill et al and explain why an exploration of their work was not a part of your article.

All the best,
Justy.

My major complaint with the work or Dr. Myhill et al is simply the lack of specificity with regards to why there is mitochondrial dysfunction. I think her initial finding of abnormally functioning mitochondria is very important and she was likely one of the pioneers in this area, however she seems to have done little in depth work to follow this up. For example she recommends the following for treatment.

A basic treatment regime, based on 1) eating the evolutionary correct stone-age diet, 2) ensuring optimum hours of good quality sleep, 3) taking a standard package of nutritional supplements, and 4) getting the right balance between work and rest, was recommended for all patients

From a personal standpoint, this appears of little to no use if a pathological mechanism is targeted towards or indirectly causing major dysfunction within the mitochondria themselves. Certainly it is helpful that she has conducted further studies outlining the commonality of this symptom/sign however I'm not sure I agree with extrapolating that to eating a stone age diet for example.

It appears somewhat that she has been treading water in terms of research for some time and I suspect that could be due to the fact that "Dr Myhill’s income arises from treating patients". Of course this is all personal opinion and everyone is free to use their own judgement for all research published, I suspect the reason people latch onto this somewhat strongly is that it shows an observable problem. Unfortunately I cannot promote the research of a doctor who is also recommending a stone-age diet as a potential treatment for ME, I think it either speaks to her own personal misunderstanding of the pathological mechanisms occurring or she is content to offer the treatment at a cost to patients – neither of which instill me with hope and I don't want to convey that through my articles either.

I think the best question to push science and medicine forward is 'why' and i'm of the opinion that it should be at the root of all research. To me it seems that Dr. Myhill is content with saying there is a dysfunction in the mitochondria and leaving it there whereas Dr. Newton seems to want to make bounds into the field, researching areas that haven't been looked into before – hence why I regard the research of Dr. Newton in higher regard. I'd like to make it clear that i'm not attacking the work of Dr. Myhill here as it's clear she has pioneered the way for mitochondrial issues in ME but i'm always weary when researchers don't follow up promising results.

justy October 20, 2013 at 5:44 am

Legendrew thanks for the clarification of your POV re: Dr Myhill and her work. Unfortunately it seems that you dont have a detailed undertsanding of the position of Dr Myhill on what causes this dysfunction, or the treatments that she uses for her patients. The treatment outline you qouted from in your above post comes from her 'standard for all' package that she believes promotes the bodies ability to heal – she has many patients with varying illnesses and symptoms and M.E/CFS is only one of her patient groups. After testing she then adds other tretaments to the 'standard for all' package, which can include drug tretaments, specific targeted supplements to correct mitochondrial deficiencies, gut programmes, detoxing through FAR suanas etc.

One of the reasons that she uses diet, supplements etc is beacuse she practices environmental medicine as she believes it is less harmful to the body than bombarding it with further assaults and that much disease stems from chemical and environemntal pollution which added to our genes and perhaps viral infections causes the mitochondria to go slow. She does in fact look for and test her patients for CAUSES of mito problems through translocator protein studies, gene adducts etc that may show various toxins (wether exogenous or endogenous) that are binding to the proteins.

I'm afraid i do not have a sicence background and so am not able to do the work of Dr Myhill justice. But you can see for yourself that she has a very extensive (perhaps the most extensive) website available for patients to use and that much of her website contains research by other researchers in the field to back up her hypothesis. From my own personal discussions with her i have seen that she is a voracious reader of research on CFS/M.E and will incorporate them into her tretament and investigation plans if she deems them to be useful for the patient. In my experience she is alos only too fully aware of the lack of real helpful, affordable treatments for her aptients and admits that in many cases, currently recovery is not possible but she seeks to address issues where they lay and stop further tissue damage. She also has a lot of experience in treating very ill patients with MCS/ME and she is more than aware that many patients can tolerate little if any treatments – which is why she advocates the resting, pacing, diet, supplement approach to try and get a very sick population well enough to tolerate treatments such as detoxing, antivirals or in my case just the supplements i needed to stop further damage.

I npotice you mention her paying patients and yes i agree that she may have not been able to carry out further research due to the enormous amount of time she gives to her patients both in appointment time (physical or by phone) andin keeping her webiste up to date and in feilding the thousands of enquires she receives from patients and in ordering tests and writing reports for non patients which i am not aeware of any other M.E/CFS specialist doing. She also runs an office of extremely dedicated staff (and has to pay them too!) As well as spending vast amounts of time and money fending off the GMC at every corner.

All the best,
Justy.

justy October 20, 2013 at 5:46 am

Sorry i forgot to add that you cannot compare Dr Newton with Dr Myhill. Dr Newton is primarily a researcher whilst Dr Myhill is primarily a practicing GP. It is a bit like comapring apples and pears; they are both fruit but not the same fruit.

Justy

Legendrew October 20, 2013 at 5:54 am
justy

Sorry i forgot to add that you cannot compare Dr Newton with Dr Myhill. Dr Newton is primarily a researcher whilst Dr Myhill is primarily a practicing GP. It is a bit like comapring apples and pears; they are both fruit but not the same fruit.

Justy

Indeed you can't however I set out to outline the ongoing research and for this reason I didn't include much about Dr. Myhill as she isn't an ongoing active researcher as you mention. I can see you clearly hold her in high regard as a doctor and i'm sure many share the same feelings – certainly it sounds like she is quite a compassionate doctor who clearly tries her best to help patients for whom there is little other options. I simply set out to outline the ongoing research and it's a little disappointing that she cannot pursue further her personal opinions and hypotheses.

peggy-sue October 20, 2013 at 6:03 am

Her hands are tied by issues with the GMC, she does not have huge research facilities.

If she wants to continue to help people, she has to stay within the rules of the establishment – and that is trying to silence her at every opportunity.

I don't agree with some of her ideas, but she does think "outside the box" – or she wouldn't be taking ME seriously.

I've had more practical, good help from reading her website than from anywhere else.

WNM October 23, 2013 at 3:29 am

Regarding Dr Myhill.

Myhill, Booth and McLaren-Howard have produced 3 papers on mitochondrial dysfunction in ME/CFS. Dr Myhill herself an active doctor practising environmental medicine and major ME/CFS advocate; as nicely expressed by Justy. However Dr McLaren-Howard of acumen lab is the scientist behind the 3 Myhill papers. I think he may have gone further than any other to try and understand what is causing the mitochondrial dysfunction in ME/CFS. Within the mitochondria he has looked at factors such as physical characteristics, functional ATP resynthesis, oxidative stress (MDA levels), TL protein in/out function, toxic gene adducts, cardiolipin synthesis, membrane phoschol/ethano balance and pH amongst others. However some of these findings have not yet been published. Also their testing is still limited to neutrophil mitochondria; the role of neutrophil mitochondria in energy metabolism is slightly controversial (http://www.translational-medicine.com/content/8/1/93/comments). They have also considered basic linkage to systemic factors such as cofactor deficiencies and cell-free DNA. However their research doesn't yet link to the wider ME/CFS pathophysiology such as immunological markers in blood, autonomic function, etc. In this regard they perhaps have a slight environmental medicine bias and hence less interest in all things immunologic or cell signaling orientated.

My opinions only. Interesting topic for sure.

peggy-sue October 23, 2013 at 7:00 am

I do agree, regarding the emphasis on environmental bias. That's what I'm not so sure about.

And "sleep hygeine". That is simply impossible for me. :alien:

I can't even translate or modify it into something managable at different more suitable times.

Esther12 October 24, 2013 at 10:45 am

Thanks for the article and discussion Legendrew

Also, been meaning to mention that I'm a fan of the minish cap avatar – loved that game.

Legendrew October 24, 2013 at 3:18 pm
Esther12

Thanks for the article and discussion Legendrew

Also, been meaning to mention that I'm a fan of the minish cap avatar – loved that game.

No problem – I always like to engage in discussion following these articles as it brings about points that I myself may have not even considered and that's what it's all about really. I've always been a fan of zelda games, I think Wind Waker is my favorite but minish cap is certainly a good one and I liked the style of the artwork best given that minish cap appeared to introduce toon link for the first time.

MeSci October 27, 2013 at 1:35 pm
WNM

Regarding Dr Myhill.

Myhill, Booth and McLaren-Howard have produced 3 papers on mitochondrial dysfunction in ME/CFS. Dr Myhill herself an active doctor practising environmental medicine and major ME/CFS advocate; as nicely expressed by Justy. However Dr McLaren-Howard of acumen lab is the scientist behind the 3 Myhill papers. I think he may have gone further than any other to try and understand what is causing the mitochondrial dysfunction in ME/CFS. Within the mitochondria he has looked at factors such as physical characteristics, functional ATP resynthesis, oxidative stress (MDA levels), TL protein in/out function, toxic gene adducts, cardiolipin synthesis, membrane phoschol/ethano balance and pH amongst others. However some of these findings have not yet been published. Also their testing is still limited to neutrophil mitochondria; the role of neutrophil mitochondria in energy metabolism is slightly controversial (http://www.translational-medicine.com/content/8/1/93/comments). They have also considered basic linkage to systemic factors such as cofactor deficiencies and cell-free DNA. However their research doesn't yet link to the wider ME/CFS pathophysiology such as immunological markers in blood, autonomic function, etc. In this regard they perhaps have a slight environmental medicine bias and hence less interest in all things immunologic or cell signaling orientated.

My opinions only. Interesting topic for sure.

Here is one of the team's recent papers.

Like some others, I very much appreciate the natural approach taken by some ME specialists, but there looks to be some good science there too. I don't necessarily agree with all of it, but it's a damned sight better than anything I have been offered on the NHS!

As a scientist myself, I believe that there are many ways to treat illness other than the reductionist, side-effect-ridden drugs that tend to be thrown at illnesses as a first rather than last resort.

Most illness in the developed world is caused by lifestyle, not least the unhealthy diet that has become the norm over the past few decades.

Let food be your medicine…

Thanks for the articles though, @Legendrew. You are working very hard lately! :)

Legendrew October 27, 2013 at 1:45 pm
MeSci

Here is one of the team's recent papers.

Like some others, I very much appreciate the natural approach taken by some ME specialists, but there looks to be some good science there too. I don't necessarily agree with all of it, but it's a damned sight better than anything I have been offered on the NHS!

As a scientist myself, I believe that there are many ways to treat illness other than the reductionist, side-effect-ridden drugs that tend to be thrown at illnesses as a first rather than last resort.

Most illness in the developed world is caused by lifestyle, not least the unhealthy diet that has become the norm over the past few decades.

Let food be your medicine…

Thanks for the articles though, @Legendrew. You are working very hard lately! :)

I don't think that diet is to be used in the place of conventional medicine but I certainly think it helps in conjunction with it! I for one have cut out all caffeine and carbonated/diet drinks and feel better for it – I like herbal teas anyway so it hasn't really affected me whatsoever. Given the lack of help with ME from the NHS though diet is a simple way to try and help yourself and it's always worth a try, if only to feel that you're doing something.

Glad you like the articles and appreciate the effort I've put into them! I'm having a little break now for a few days at the least and likely a week. I've been experiencing a downturn of late – feeling very jittery with tremors, stomach cramps/IBS, nausea, glassy eyes and ocular headaches – none of which were likely helped by having to get a chipped tooth filled a few days ago and the local anesthetic that was used therein.

I've been referred to an endocrinologist in November as they believe I may have hyperparathyroid issues or perhaps even Graves disease and not ME – they seem pretty convinced that i'm having endocrine problems at the very least so i'm happy to go with it and see what they find – already raised PTH, low Vitamin D and raised ALT have been found so clearly something is not right. I believe next week is IOM week with a few articles on the subject so the article on the nervous system will be November I believe.

peggy-sue October 27, 2013 at 1:58 pm

Time for some aggressive positive inaction, I think. Thank-you for all your hard work. :love:

rosie26 October 27, 2013 at 2:07 pm

Concentrate on resting Andrew. x The lie down kind.

MeSci October 28, 2013 at 3:22 am
Legendrew

I don't think that diet is to be used in the place of conventional medicine but I certainly think it helps in conjunction with it! I for one have cut out all caffeine and carbonated/diet drinks and feel better for it – I like herbal teas anyway so it hasn't really affected me whatsoever. Given the lack of help with ME from the NHS though diet is a simple way to try and help yourself and it's always worth a try, if only to feel that you're doing something.

We will have to differ on whether a natural approach can substitute for an unnatural one. People were cured of illnesses long before 'conventional' medicine came along, and many still are when they can resist the pressure to go down the pharmaceutical route before trying to help themselves. I think you're quite early in your (informal?) study of medical science, and it is very important to keep an open mind, especially at such an early stage. All-too-many scientists lose their open-mindedness later on, when they have invested so much time in a particular line of research and theory that they fear losing respect and status by admitting that they were wrong, but it is essential to do so, as it is how science progresses.

As a medical scientist I assure you that the approach I am taking is very far from being

just to feel that you're (I'm) doing something

I spent months studying scientific papers, using the skills I gained from ten years undergraduate and post-graduate study to analyse, make connections, check, double-check, triple-check (etc.) and then take the plunge.

Results: dramatic improvements in symptoms that doctors have failed to alleviate with a range of pharmaceuticals for decades, e.g. anxiety levels, sleep, gut function, sinuses and dermatitis, plus loss of unwanted fat and gain in muscle. I have lost the excessive hunger followed by nausea when I don't eat very frequently, because my blood glucose seems to be much more stable. I have lost the severe generalised dental pain, and stopped losing fillings and pieces of tooth, which I believe was due to mineral deficiency. All this through a change of diet and addition of certain supplements. I am not on any medication for ME, and never have been – and do not want to be, as drugs so often have side-effects which are worse than the original problem. I do not eschew drugs completely (and never have), and use them carefully for other problems.

Legendrew

I've been experiencing a downturn of late – feeling very jittery with tremors, stomach cramps/IBS, nausea, glassy eyes and ocular headaches – none of which were likely helped by having to get a chipped tooth filled a few days ago and the local anesthetic that was used therein.

Maybe you could put aside your doubts, at least for a while, and try a leaky-gut diet? What have you got to lose?

Also, if you haven't yet read the paper I linked to, why not do so? I'm sure many of us would like to hear your comments on it.

WNM October 30, 2013 at 5:24 pm
MeSci

Here is one of the team's recent papers.

Like some others, I very much appreciate the natural approach taken by some ME specialists, but there looks to be some good science there too. I don't necessarily agree with all of it, but it's a damned sight better than anything I have been offered on the NHS!

As a scientist myself, I believe that there are many ways to treat illness other than the reductionist, side-effect-ridden drugs that tend to be thrown at illnesses as a first rather than last resort.

Most illness in the developed world is caused by lifestyle, not least the unhealthy diet that has become the norm over the past few decades.

Let food be your medicine…

I agree. The role of diet, sleep, exercise and psychology in chronic illness is massively underestimated. These are the foundations of health. Unfortunately the establishment of the current reductionistic pharmacological paradigm in medicine and society has biased and flooded the research literature. I think diet is a particularly complex and changeable factor. It always amazes me how those with a scientific interest can so effortlessly disregard such a deep and complex topic, especially considering your body is constructed from what you eat and your microbiome greatly defined by it!

A random selection of free and interesting papers to inspire healthy lifestyle:

https://www.ibp.ucla.edu/research/GomezPinilla/publications/nrn2421.pdf
http://www.ncbi.nlm.nih.gov/pubmed/23690582

http://www.mdpi.com/2072-6643/4/8/1095/pdf
http://www.ncbi.nlm.nih.gov/pubmed/23305038
http://www.plosone.org/article/info:doi/10.1371/journal.pone.0053867

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2917728/?tool=pmcentrez&rendertype=abstract
http://www.nih.gov/news/health/oct2013/ninds-17.htm

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3160470/?report=classic
http://www.frontiersin.org/Dementia/10.3389/fneur.2011.00028/abstract
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3629142/

peggy-sue October 31, 2013 at 6:22 am

The role of diet is supressed because of the interests of big business in using the nastiest, cheapest ingredients in manufacturing.

How can a woman "build" a healthy baby from hydrogenated fats, fructose syrup and "mechanically recovered meat"?

Leopardtail January 20, 2014 at 8:43 am
Legendrew
justy

Hi, thanks for the article – i was really looking forward to this one as i , and many others on this forum have had the Mitochondrial function test done and found it to be useful, especially in convincing others that we are physically ill. Of course the test mainly shows that we are ill, rather than pinpoitning the initial cause, and it is surpirsing how similar the mitochondrial issues are between patients. Given this i was rather surprised how quickly you dismissed the work and research of Myhill et al. Dr Myhill's research work was peer reviewed and published in the same manner as the work of Dr Newton which you appear to hold in higher regard.

Perhaps you could elaborate on your comments about the research of Myhill et al and explain why an exploration of their work was not a part of your article.

All the best,
Justy.

My major complaint with the work or Dr. Myhill et al is simply the lack of specificity with regards to why there is mitochondrial dysfunction. I think her initial finding of abnormally functioning mitochondria is very important and she was likely one of the pioneers in this area, however she seems to have done little in depth work to follow this up. For example she recommends the following for treatment.

A basic treatment regime, based on 1) eating the evolutionary correct stone-age diet, 2) ensuring optimum hours of good quality sleep, 3) taking a standard package of nutritional supplements, and 4) getting the right balance between work and rest, was recommended for all patients

From a personal standpoint, this appears of little to no use if a pathological mechanism is targeted towards or indirectly causing major dysfunction within the mitochondria themselves. Certainly it is helpful that she has conducted further studies outlining the commonality of this symptom/sign however I'm not sure I agree with extrapolating that to eating a stone age diet for example.

It appears somewhat that she has been treading water in terms of research for some time and I suspect that could be due to the fact that "Dr Myhill’s income arises from treating patients". Of course this is all personal opinion and everyone is free to use their own judgement for all research published, I suspect the reason people latch onto this somewhat strongly is that it shows an observable problem. Unfortunately I cannot promote the research of a doctor who is also recommending a stone-age diet as a potential treatment for ME, I think it either speaks to her own personal misunderstanding of the pathological mechanisms occurring or she is content to offer the treatment at a cost to patients – neither of which instill me with hope and I don't want to convey that through my articles either.

I think the best question to push science and medicine forward is 'why' and i'm of the opinion that it should be at the root of all research. To me it seems that Dr. Myhill is content with saying there is a dysfunction in the mitochondria and leaving it there whereas Dr. Newton seems to want to make bounds into the field, researching areas that haven't been looked into before – hence why I regard the research of Dr. Newton in higher regard. I'd like to make it clear that i'm not attacking the work of Dr. Myhill here as it's clear she has pioneered the way for mitochondrial issues in ME but i'm always weary when researchers don't follow up promising results.

Legendrew,

We need research into treatment and cause.

I fully agree the research needs to be followed up. Myhill is however a doctor first and a researcher second. I would actually like to see others following up and repeating her research – that gives the scientific credibility of repeatability. The problem is funding is short and repeating good research is not as sexy and the novel.

Myhill's view is that food- and environmental- based toxins may be causing the Mitochondrial dysfunction. She sticks to the proven however in her papers. Personally I find the stone age diet a little too extreme, but it is rooted in that view.

I do think it is worth comparing ME to diabetes though. The cause is autoimmune, and genetic – the solution (for now) however is Insulin injection and blood monitoring. Diabetics are still waiting for a better solution, but int he meantime their lives are greatly improved. My view is that research efforts need to be devoted both to what causes it and what can be done to treat it now.

If we can arrest the Mito dysfunction, lives will improve even if it's not the root cause. We are also to prevent the build up of side effects if this is dealt with.

For now the whole picture seems far too complicated to hope for a cause to be found in less than decades. Serious diabetes research took near 100 years to come up with a both a root cause and a clear picture of what's going on. Even now there are doubts amongst some whether those root causes (different types of diabetes) have other upstream causes in and of themselves.

One further point, trying to argue about cause rather than effect too soon causes a lot of academic argument. A shift to a focus in pathophysiology would put the emphasis on what can be agreed better promote working together and improving understanding.

MeSci January 20, 2014 at 8:55 am
Leopardtail

Legendrew,

We need research into treatment and cause.

I fully agree the research needs to be followed up. Myhill is however a doctor first and a researcher second. I would actually like to see others following up and repeating her research – that gives the scientific credibility of repeatability. The problem is funding is short and repeating good research is not as sexy and the novel.

Myhill's view is that food- and environmental- based toxins may be causing the Mitochondrial dysfunction. She sticks to the proven however in her papers. Personally I find the stone age diet a little too extreme, but it is rooted in that view.

I do think it is worth comparing ME to diabetes though. The cause is autoimmune, and genetic – the solution (for now) however is Insulin injection and blood monitoring. Diabetics are still waiting for a better solution, but int he meantime their lives are greatly improved. My view is that research efforts need to be devoted both to what causes it and what can be done to treat it now.

If we can arrest the Mito dysfunction, lives will improve even if it's not the root cause. We are also to prevent the build up of side effects if this is dealt with.

For now the whole picture seems far too complicated to hope for a cause to be found in less than decades. Serious diabetes research took near 100 years to come up with a both a root cause and a clear picture of what's going on. Even now there are doubts amongst some whether those root causes (different types of diabetes) have other upstream causes in and of themselves.

One further point, trying to argue about cause rather than effect too soon causes a lot of academic argument. A shift to a focus in pathophysiology would put the emphasis on what can be agreed better promote working together and improving understanding.

I see you haven't yet participated in the leaky gut forum.

There are threads there that discuss how leaky gut can cause autoimmunity, and I have posted links to papers which postulate, backed by evidence, how this may occur and how it might be treated. You may find the links in my post no. 6 on this page particularly relevant to your stated interests. It includes a study on leaky gut, diabetes and coeliac disease and the autoimmune connections.

Leopardtail January 21, 2014 at 12:42 pm
MeSci

I see you haven't yet participated in the leaky gut forum.

There are threads there that discuss how leaky gut can cause autoimmunity, and I have posted links to papers which postulate, backed by evidence, how this may occur and how it might be treated. You may find the links in my post no. 6 on this page particularly relevant to your stated interests. It includes a study on leaky gut, diabetes and coeliac disease and the autoimmune connections.

Thanks for that MeSci, I will take a look at it.

Leopardtail January 21, 2014 at 2:23 pm
MeSci

I see you haven't yet participated in the leaky gut forum.

There are threads there that discuss how leaky gut can cause autoimmunity, and I have posted links to papers which postulate, backed by evidence, how this may occur and how it might be treated. You may find the links in my post no. 6 on this page particularly relevant to your stated interests. It includes a study on leaky gut, diabetes and coeliac disease and the autoimmune connections.

I have only the briefest outline of the microbial issues relating to ME in the gut. What expertise I have relates more to Neurotransmitters and Hormones and the effect they have on 'flow'.

With immunology likewise I have a good overview of the 'order of failure' and a bit more knowledge of the impact of endocrinology on those systems. As yet my knowledge (I feel) is not rigorous enough to step into that debate.

For now my view of the endocrinology gives me some ideas what might cause the leaky gut, but not it's impact or treatment.

Watching the debate and picking up some views will be interesting though.

;-)

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