The difference between MS and ME

[mellster]

I think at some point we have to make a division between the people with cognitive issues (apparently the majority) and those with primarily fatigue or exhaustion or pain symptoms "only". Of course it could be possible that down the road the latter will eventually experience cognitive issues as well (if the source/root problem really is the same), but that yet remains to be proven. When it comes to discussion of cognitive issues I often feel like I might have joined the "wrong" forum as this is something I never experienced, even when I was hit in the past with never severe but at least moderate to significant FM pain and fatigue/exhaustion. Maybe PVFS and CFS/ME and FM are only loosely related or maybe there are just continuations of each other. And maybe early recognition and aggressive therapy will avoid certain symptoms altogether?? It also looks like that thee are quite a few similarities between ME and MS whereas there are hardly any between CFS or FM and MS.

 

[Annesse]

Hi Mellster, I am going to try and address your comment about there not being any similarities between FM and MS.

I posted previously that Dr. Wood, the Scientific Director of the Fibromyalgia Association has discovered that Fibro patients lack dopamine, have low iron and spinal cord changes. Also, another well known and respected resreacher in Fibromyalgia, Dr. Lavin,has demonstrated that fibro patients have dysautonomia. He believes this actually explains " ALL FM FEATURES". Spinal tap studies show low B12 and elevated homocysteine in the cerebrospinal fluid of FM patients. Spinal tap studies also show amyloids as a key feature of fibromyalgia.

Here are the findings in both fibromyalgia and MS.

Spinal Cord Changes- Both
Low dopamine -Both
Amyloids- Both
Dysautonomia- Both
Low B12- Both
High homocysteine-Both

These biological findings in both diseases are what lead to the symptoms of the diseases. Indeed, every symptom of these associated diseases can be traced back to one of these biological findings. (TNF is also involved, I posted a study to show it is dysregulated in CFS, but I believe that based on the identical abnormal protein findings in the spinal tap studies, that CFS and Fibro have already been shown to be one and the same.)

 

[Annesse]

One thing I think I should mention is that each of us can exhibit each of these symptoms to a varying degree. Much like a cold virus that causes similar symptoms. Your primary symptom may be a headache, while your friends could be a runny nose and fever. Someone else may go on to develop a sinus infection. You may not. Someone else could end up with lung involvement that leads to pneumonia. The same is true of the symptoms exhibited in autoimmune disease. If you lack B12 and it frays your myelin sheath, that doesn't mean that your myelin will be damaged in the exact same spot as someone else with B12 deficiency. Different nerves will be affected depending on where the damage was done. And this of course will cause different symptoms. Same with autonomic dysfunction. If your lack of B12 is not as severe, you will be able to produce more acetylcholine (one of the neurotransmitters that regulates the autonomic nervous system). Therefore, your autonomic dysfunction won't be as severe.

 

[Annesse]

Hi Again Enid,

Here is some information on cognitive dysfunction and MS.
http://www.biomedcentral.com/1471-2377/11/17

 

[Annesse]

Also, here is some information on the fatigue in MS. I was diagnosed with lupus, CFS, and fibro nearly 20 years ago. The type of fatigue found in MS is the same type of fatigue I experienced with my illness. If you type in MS and fatigue into yahoo, and read some of the personal accounts, you will see there really is no difference between MS fatigue and CFS fatigue. http://ms.about.com/od/signssymptoms/a/fatigue_over.htm

 

[Enid]

Happily following your findings and reasoning here Annesse - I'm all for the extent of damage done by some original "insult" to the nervous system (and particular degree leaving what appears to be a predominance of certain symptoms one to another). It also occurs that the body has limited ways to respond to illness - pathogen/injury etc. - fatigue is common to all. I just feel the increasing understanding of viruses and biology of the human body's systems and response certainly points us on.

Two years ago I could not write this and know ME has nothing to do with failing intellect and dementia. But we have certainly got to get to bottom of this affecting millions.

 

[searcher]

I am also looking forward to hearing more of your thoughts Annesse. I feel strongly that low Vitamin D are downstream of the illness- I had spent a lot of time in the sun before getting tested, and my levels were 21. I have to supplement a lot to get the levels above 35, and my skin pigmentation can best be described as non-existent so I should theoretically have no problem sustaining high Vitamin D levels without supplementation.

My doctor tested my homocysteine levels after I had a good response to my first B12 sublingual, and it was 5.5 (which I think is considered very good.) But could this have been a temporary response to supplementation? And thus our homocysteine levels go back up after a short while because the root cause has not been addressed?

In regards to mellster's comment-- I don't have pain beyond general soreness in my shoulders and neck (and lymph nodes.) I have a lot of cognitive difficulties, especially when trying to concentrated for more than 20 minutes. But I think there is a similar root cause of MS, ME, and fibromyalgia. It is interesting that similar treatments often seem to help both people with primarily pain issues and people with primarily cognitive difficulties. I have a friend with MS, and she suffers primarily from fatigue and pain, but doesn't have the cognitive difficulties many of us have (as mentioned earlier in the thread.) But I think a lot of her symptoms are too similar to ours to not think there are similar processes going on (and she has the same B12 and Vitamin D issues many or all of us have.)

 

[mellster]

Thanks Annesse & Searcher for your thoughts - it is known that when the body increases pain usually the immune system ramps up (NK cells etc.) so there might be some method or intent to that. I had Vit D & B12 deficiency but brought it back up with supplementation, so I seem to be able to metabolize it ok, but I agree refraining from "mega-doses". My (pure pain and non-cognitive) symptoms have improved (some completely reversed) over time, but I can definitely see some similarities such as tender lymph nodes, shoulder/neck and torso pain (typical for FM) and so on. I also agree with elevated cytokine levels as mentioned by Annesse, such as TNF and IL-8. And looking back the past 8 months starting from the crash in April I definitely experienced more similar symptoms, esp. in the sense that it seems to affect the whole body / every organ to some degree. That being said, another major pillar of recovery/treatment for me is CVAC (www.cvacsystems.com), which has been studied and shown to relieve pain, increase circulation and necessary blood counts as well as testosterone levels and more. It is really good to start for people that cannot exercise at the present and once there is improvement it an be gradually (but not completely) replaced with exercise. cheers!

 

[Annesse]

Thank you so much for both of your comments. One of the ways you will know the answer when you find it is that every finding- low D, low B12, fatigue, sleeplessness,dysautonomia, low iron, low dopamine, the connection to bacteria and viruses etc. will be clearly and completely explained. It might be a good time to clarify why the symptoms are similar though. For instance, the dysautonomia in these diseases is causing many of the symptoms. But what causes dysautonomia? Low B12 for one thing. Acetylcholine is one of the neurotransmitters that regulates the autonomic nervous system. Acteylcholine comes from choline. Choline comes from B12. All of these diseases also show a lack of dopamine and therefore adrenaline.( adrenaline comes from dopamine) Adrenaline is the other neurotransmitter that regulates the autonomic nervous system. As we connect these dots, I want to make sure that we are all on the same page. Then we can move on to what causes the lack of B12 and adrenaline.

Here is a some information on a study that was recently done on B12 and cognition. If all of these diseases have a profound deficiency of B12, (remember in hypothyroidism when patients were tested at even an extremely low level (133 pg/ml) they found that 40% of them were deficient and at 500 to 550 pg/mL you will see dementia) then logically, this deficiency is connected to the cognitive dysfunction also found in these diseases. There is more and we will go there, but lack of B12 most certainly plays a central role.

http://healthland.time.com/2011/09/...nked-to-smaller-brains-and-cognitive-decline/

 

[Annesse]

Hi Mellster, our posts crossed over. Thanks for the link, I will definitely check it out.

One thing that can happen when we supplement with B12 is that we can have a high serum level of B12, but not a sufficient cellular level. B12 is so important to our bodies that it has designed a very specialized transport and delivery system to make sure it arrives at its proper destination. Here is a study that shows degeneration of the spinal cord can still occur even with high serum B12 levels. In the conclusion it states this study, "provides futher evidence that sometimes a serum (blood) level may not be a reliable guide to a vitamin B12 deficiency."

http://www.ncbi.nlm.nih.gov/pubmed/8323478

 

[richvank]

Hi Mellster, our posts crossed over. Thanks for the link, I will definitely check it out.

One thing that can happen when we supplement with B12 is that we can have a high serum level of B12, but not a sufficient cellular level. B12 is so important to our bodies that it has designed a very specialized transport and delivery system to make sure it arrives at its proper destination. Here is a study that shows degeneration of the spinal cord can still occur even with high serum B12 levels. In the conclusion it states this study, "provides futher evidence that sometimes a serum (blood) level may not be a reliable guide to a vitamin B12 deficiency."

http://www.ncbi.nlm.nih.gov/pubmed/8323478

Hi, Annesse.

You are right on about this. Even in a normal, healthy person, most of the B12 in the serum is bound to haptocorrin, not transcobalamin, and it can only be imported by the liver cells. This appears to be a salvage and recycle pathway for B12, which, as you noted, is carefully saved by the body.

What you are referring to here is a "functional deficiency" in B12, rather than an "absolute deficiency." There are several possible causes for a person having a high serum B12 level but still having a functional deficiency of it. These include inherited mutations in one or more of the intracellular B12 processing enzymes, the most common being the CblC or MMACHC protein. In ME/CFS, the cause of the functional B12 deficiency, according to my hypothesis, is glutathione depletion. Glutathione normally works with the CblC complex to remove whatever ligand comes in with it. Glutathione also apparently protects B12 inside the cells by forming glutathionylcobalamin, which is more tightly bound than products of reaction of B12 with xenobiotics. Recent research indicates that CblC is normally capable of retrieving cobalamin from glutathionylcobalamin, and sending it on to form methylcobalamin or adenosylcobalamin, as needed by the cell.

Best regards,

Rich

 

[aprilk1869]

I am also looking forward to hearing more of your thoughts Annesse. I feel strongly that low Vitamin D are downstream of the illness- I had spent a lot of time in the sun before getting tested, and my levels were 21. I have to supplement a lot to get the levels above 35, and my skin pigmentation can best be described as non-existent so I should theoretically have no problem sustaining high Vitamin D levels without supplementation.

Have you considered hyperparathyroidism?

http://parathyroid.com/low-vitamin-d.htm

 

[mellster]

Thanks Annesse & Rich, I will definitely push for another test that can detect functional deficiency as well, especially since I have always been on the low normal side of RBC (with around 4.5), esp. for a male, which I believe is an inherited predisposition from my Italian mother (who despite being pretty healthy otherwise has always had low RBC and some tummy trouble) and has inhibited me somewhat from being more athletic (although I don't have any anemia symptoms) in general. In fact, I had been thinking of something like thalassemia minor (like Pete Sampras) but every doc I brought it up to said "get outta here!" and "there would be more symptoms and also visible abnormalities in the blood tests". But it would explain a certain predisposition to CFS/FM and also the ability to recover with treatment and diet and exercise if it is more of a chronic predisposition that can be worsened with stressors (viral, bacterial, physical and emotional). So many questions

 

[aprilk1869]

Another thing about vitamin d and UV light, here is a couple of paragraphs from Stephanie Seneff article on sulfur.

Hydrogen sulfide (H2S) is consistently found in the blood stream in small amounts. As a gas, it can diffuse into the air from capillaries close to the skins surface. So it is conceivable that we rely on bacteria in the skin to convert sulfide to sulfate. It would not be the first time that humans have struck up a symbiotic relationship with bacteria. If this is true, then washing the skin with antibiotic soap is a bad idea. Phototrophic bacteria, such as Chlorobium tepidum, that can convert H2S to H2SO4 exist in nature for example in sulfur hot springs in Yellowstone Park. These highly specialized bacteria can convert the light energy from the sun into chemical energy in the sulfate ion.

Another possibility is that we have specialized cells in the skin, possibly the keratinocytes, that are able to exploit sunlight to convert sulfide to sulfate, using a similar phototrophic mechanism to C. tepidum. This seems quite plausible, especially considering that both human keratinocytes and C. tepidum can synthesize an interesting UV-B absorbing cofactor, tetrahydrobioptin. This cofactor is found universally in mammalian cells, and one of its roles is to regulate the synthesis of melanin the skin pigment that is associated with a tan and protects the skin from damage by UV-light exposure. However, tetrahydrobiopsin is very rare in the bacterial kingdom, and C. tepidum is one of the very few bacteria that can synthesize it.

From this I gather that certain bacteria on the skin play an important role in utilizing UV light and therefore creating tetrahydrobiopterin (BH4) which is needed for creating neurotransmitters as can be seen on the methylation map here: http://www.heartfixer.com/AMRI-Nutrigenomics.htm

 

[Enid]

Just wonder what trips it all - half my life in Africa half in Europe - why a normally healthy person in both climates suddenly at 65 years succumbs if not a viral.

 

[Annesse]

Sounds like you all need some answers, so lets keep moving forward. Another associated disease to the ones we have been discussing is Sjogren's syndrome. Will we find the same vitamin and mineral deficiencies in Sjogren's that we have seen in the other diseases? How about a connection to these other illnesses?Following is a study that confirms low B12 and low iron (same as fibro) in Sjogren's. Also, 30% had autoimmune thyroid disease and 7% had diabetes.

http://www.ncbi.nlm.nih.gov/pubmed/11495189



All of these diseases are connected. Researchers from the University of Tennessee Health Sciences Center in Memphis have identified a link between hypothyroidism and type 1 diabetes. In the study, 41% of the female patients developed hypothyroidism (Muralidhara Krishna, 2011). Plus, Healthy Divas, a resource center for autoimmune disease states, "An estimated 85% of CFS sufferers also have hypothyroidism,"(Whitaker, 2007) The International Scleroderma Network reports, "About twenty percent of patients with systemic scleroderma also have secondary Sjogren's syndrome." An article in Arthritis Today states, "New research shows that people with diabetes are nearly twice as likely to have arthritis, indicating a diabetes-arthritis connection." (Mann, 2011) The National Institutes of Health reports that, " About 1 of of 3 people who has lupus has Raynaud's." Also, "About 9 out of 10 people who have scleroderma have Raynaud's." WebMD states, "For some people, Raynaud's is the first sign of rheumatoid arthritis."

These statistics are endless. All of these diseases are obviously connected.

 

[Annesse]

And just as in all of the other diseases we have been discussing, autonomic dysfunction is involved. Here is some information that states, "Researchers do not know the exact cause of Sjogren's, but they believe that it may be caused by abnormalities in the autonomic nervous system (ANS) that stimulates these glands.

http://clinicaltrials.gov/ct2/show/NCT00565526

Also, the study entitled:"Autonomic Nervous Symptoms in Primary Sjogren's Syndrome: A Follow-up Study" states in the conclusion, "pss patients showed subjective and objective signs of both a parasympathetic dysfunction."

Both adrenaline and acetylcholine are necessary to regulate the autonomic nervous system. Since Sjogren's patients lack B12, this explains the lack of acetylcholine. The other neurotransmitter, adrenaline is derived from dopamine. Dopamine is derived from tyrosine. Tyrosine is also needed to make both of the thyroid hormones, thyroxine and triiodothyronine. This would explain the connection to hypothyroidism in Sjogren's.

 

[Annesse]

I should have posted above, "pss patients showed subjective and objective signs of both a parasympathetic AND A SYMPATHETIC DYSFUNCTION."

In an additional study done at Malmo University Hospital's Department of Rheumatology in Sweden, researchers concluded, "Both objective and subjective symptoms of parasympathetic dysfunction were seen in primary Sjogren's syndrome patients. Autonomic dysfunction symptoms were significantly associated with fatigue, anxiety, and depression," (Mandl, 2009).

Secretion of salvia is under control of the autonomic nervous system, which controls both the volume and type of saliva secreted. It makes sense that a dysfunction of the salivary glands could be associated with a dysfunction in the autonomic nervous system, by which they are controlled.

Here is another study on Sjogren's and B12.

http://www.ncbi.nlm.nih.gov/pubmed/20144108

 

[Firestormm]

Hi Firestormm, my understanding is that this is not the case, its the common opinion amongst doctors but its wrong. I can't prove this however, as its only based on comments I have read over the years from a number of MS experts. Many ME patients have the same kinds of lesions. There is an overlap with spread and type of lesion in MS and ME. What I understood the difference to be is that ME lesions are transitory, often small, and typically not progressive, but this is not possible to determine from a single MRI scan. Multiple scans over time would be required. MS on the other hand have long term lesions in the same locations, and sometimes it progresses to more and larger lesions. In this context those MS experts were talking about ME as something along a spectrum, as I have said before. I cannot remember who they were, it was many years ago I was reading this.

Bye, Alex

Hi, Alex.

I also believe that there are problems with the myelin in ME/CFS. There are at least three substances in myelin (phos. choline, choline plasmalogen and myelin basic protein) that require methylation for their synthesis. There is good evidence for a partial methylation cycle block in ME/CFS (lab testing and positive results of treatment directed at restoring methionine synthase to normal operation). With low methylation capacity, I think it is reasonable to suspect that myelin repair would suffer. In addition, one of the best documented brain-related problems in ME/CFS is slow processing speed. This would be consistent with myelin damage, because myelin is what makes possible rapid transport of nerve impulses in the axons of the neurons.

Beyond this, I suspect that the electromagnetic radiation sensitivity experienced by some people with ME/CFS is due to myelin damage, because myelin normally acts as electrical insulation on the axons. With damaged myelin, I suspect that currents induced in the body by external em radiation can flow in the nerves, producing neurological symptoms.

In MS, the myelin damage results from an attack on the myelin by the immune system. That is, it is an autoimmune disease. In ME/CFS, I suggest that the myelin damage results from lack of normal maintenance and repair. This may account for the different characteristics of the damage, as viewed by MRI.

Best regards,

Rich

That certainly ties up with everthing my Neurologist tested for and spoke about Rich. And in the end it was all this that so confused him that he gave up - not Parkinsons, not MS but what. (He said could be ME and they think it's viral).

Morning,

Sorry I didn't reply sooner.

I had not heard or read of evidence that myelin in 'CFS/ME' patients was damaged in a similar manner as in patients with MS. This is something new and indeed I had not read (or remembered reading) of its' mention in any criteria including the latest International ME one.

But be that as it may (and I would like to read of any research in this area) the damage to myelin sheathing is observable in MS patients and is the main diagnostic marker for the disease - unlike in 'CFS/ME' - as I understand it and from the links I posted previously.

'A substance called myelin protects the nerve fibres in the central nervous system.

In MS, your immune system, which normally helps to fight off infections, mistakes myelin for a foreign body and attacks it.

This damages the myelin and strips it off the nerve fibres, either partially or completely, leaving scars known as lesions or plaques.'

http://www.mssociety.org.uk/what-is-ms/information-about-ms

The 'lesions' that have been noted previously in research for 'CFS/ME' were not - I don't recall reading - connected or assumed to be connected to myelin. But then again I am not a neurologist or medical professional, though they have ever been referred to simply as 'lesions'.

If myelin damage had been observed in patients with 'CFS/ME' then this would have presented something of a 'breakthrough' surely? And potentially would have enabled trials for the 'disease-modifying-drugs' that are being (not with any great success) trialled on patients with MS.

Before the myelin damage was attributed to MS this disease was in a similar 'boat' to our own (again as I understand it). If you could dig out any research I would be grateful (assuming this layman is able to understand it of course ).

Fire

 

[Annesse]

Hi Fire, Here is one very recent study that shows the presence of white matter lesions in CFS. http://bjp.rcpsych.org/content/167/1/86.abstract

Of course, just as important as their presence is where they come from. Both MS and CFS patients lack B12. In the study entitledlasma Vitamin B12 Status and Cerebral White-matter Lesions it states in the conclusion, "These results indicate that vitamin B12 status in the NORMAL RANGE is associated with severity of white-matter lesions, especially periventricular lesions...it is hypothesised that the association is explained by effects on myelin integrity.." It also states, "Poorer vitamin B12 status was SIGNIFICANTLY associated with greater severity of white-matter lesions....