A few thoughts for Deb and others.

[raven]

During recent months I haven't really been looking into the science behind MS. AS I continue to improve on my treatment I have spent less time musing on the whys and wherefores.

However, a conversation with Alasdair Coles and a chance conversation elsewhere got me thinking again. The upshot of the conversation with Alasdair was that MS is actually a group of diseases, not just one. The other conversation forced me to revisit my investigations into mitochondrial disease.

Excuse the rambling nature of the thoughts below but I'm trying to get things straight in my head and hopefully by just jotting a few things down others will come along and either tear down, or help me build on my thoughts.

Firstly if we examine the classic RRMS we know that demyelination occurs. This may be as a result of an auto-immune reaction. Following DeMyelination there is redistribution of Sodium Channels along the Axon and Mitochondria are recruited to the DeMyelinated regions, to meet the increased energy requirements necessary to maintain Conduction. The Mitochondria present within the chronically DeMyelinated Axons will be functioning at full capacity. The Axon may well be able to function for many years due to these adaptive mechanisms. But, eventually, despite AntiOxidant defences, free radical damage will accumulate and Mitochondrial function will become compromised. The actual cause of cell death could be due to a number of mechanisms related to Mitochondrial dysfunction including failure of Ionic homeostasis, Calcium influx, Mitochondrial mediated cell death or impaired Axonal Transport.

The switch from the RRMS stage to the progressive phases can be caused by an induced mitochondrial dysfunction.

We all know that the classic model doesn't really fit the cases that present as progressive from the outset. We also know from the work of Luchinetti et. al. that there are perhaps four different and distinct lesion patterns. Perhaps we can argue that these cases are mitochondrial diseases that present without the auto-immune component.

One of the things that has baffled me, and I suspect many others is the variety of treatments that appear to work for some yet not for others.

For starters we have the CPn / ABX regimen. Many may think that I am against this regimen given some of my recent postings. That actually isn't the case. I do believe that the ABX regimen will help a subset of MS patients. I just don't believe in the one size fits all. It is known that CPn can affect mitochondrial function, even to the point of inducing apoptosis. Perhaps for those that initially present with a progressive course trying the ABX regimen would be a good start.

Then of course we have the diet regimens.

In other mitochondrial diseases, some researchers are trying very low carbohydrate diets to reduce the workload for mitochondria. Perhaps evidence for the paeleolithic diet being effective in some cases.

In addition vitamins such as thiamine (B1), riboflavin (B12), vitamin C, and vitamin E. Lipoic acid and coenzyme Q-10 are useful supplements in other mitochondrial diseases. They also appear to be effective for some MS patients. The recent posts on leptin brought up another area. Leptin is known to be the primary mitochondrial signalling mechanism.

I would bet that statins have a role in regulating the mitochondria as well.

I haven't really studied LDN but I suspect that there may be something to that as well for the more progressive forms.

It is known that Alzheimers and Parkinsons are mitochondrial diseases. Can we add at least some patterns of MS to that list as well?

Just a few thoughts... Feel free to scribble all over them

Robin.

[bromley]

Robin,

From my own research I consider that there is a strong case to suggest that MS is probably a group of diseases, maybe with different triggers. I believe that a virus may be the trigger for some cases of MS - maybe as as the trigger which kicks off the immune response or it lays dormant in the CNS, reactivating at a later stage. In the cases of PML, in the Tysabri trials, the JC virus was identified as the culprit.

I have seen a number of types of MS described - RR, SP, PP, Relapsing Progressive, and malignant. Devics disease (NMO) was considered an aggressive form of MS, but has recently been classified as a separate disease.

De-myeliantion, as you say, is a feature of RR but I've still seen no definitive answer as to whether this results from an attack by the immune system or something going on under the myelin.

If the immune sytem is involved, T cells and or B cells may be involved. We have seen treatments such as Tovaxin which erradicate the 'bad' T cells and have produced good results. However, other treatments such as B cells are being targeted by treatments such as Rituximab and are showing good results in some. As usual a confused and mixed picture suggesting different mechanisms at play.

In recent years it has been recognised that it is damage to the axon that causes the permanent disability - this can take place in the RR stage as well as the SP.

The relationship between RR and SP is also confusing - I have seen data showing that the time between the two can vary between 2 and 33 years.

There is also the gender difference - females getting MS 2-3 times as much as men (although PP is more 50:50!)

At least for the RR immune involvement there are some heavy duty drugs that can put a stop to the attacks and hopefully limit the damage to myelin (if it is caused by the immune attack). Re-myelination is being examined in labs and might, if successful, protect the axons left.

Many researchers are recognising the mechanisms which are destroying de-myelinated axons and trials of channel blockers are starting. We should start hearing about results in the next couple of years.

You have raised many issues which I will leave to those more knowledgeable to comment on. But as a layman with this disease, the evidence certainly points to different diseases under the umbrella of MS. In the future one would hope that they can identify the sub-sets and tailor treatment to these.

Ian


PS I met Robin for a coffee last week and he looked very well (apart from the eye patch, slurred speech and limp).

[raven]

You forgot to mention the parrot on one shoulder....... ;)

[mrhodes40]

I so wholeheartedly agree that I thank you for the chance to say that a group of diseases is likely in my mind also. Not only is it likely that there are possibly several kinds of MS but also that differential diagnosis is not as good as it might be.

Take lyme disease. It can cause neuro symptoms and can be devilishly hard to find, even in cases where it is known to be there. On pubmed there's a case study of a woman who was known to have had lyme and developed psychiatric symptoms. She tested negative but was cured of her problem after being treated with antibiotics empirically, suggesting a cryptic infection.

another example, the ataxias. Ataxia means discoordination due to nerve problems of some kind or another. MS is an ataxic disease obviously. This is however a symptom and not a diagnosis as any number of things cause ataxia. There are over a hundred kinds of ataxia, a number of them mitochondrial, as you guessed. There are "allergic" ataxias like gluten ataxia. This is a disease in which the person is sensitive and reacts to gluten making antibodies that damage the brain though the usual target for those particular antibodies is the intestines in that case diagnosed as "celiac disease". Gluten ataxia differs from MS a little clinically in that it usually has headaches and is slowly progressive, but the MRI looks the same. Simply avoiding gluten will fix this problem, and interestingly enough it is simple to diagnose; all you need is a blood test for celiac including the full panel while you are eating gluten in your diet. Problem is no one tests for this.

in my OPINION this is what people who swear by avoiding gluten have, and it IS molecular mimicry in that case. They were misdiagnosed in the beginning, probably because it is a newer diagnosis, a disease only recently described, or if it happens today simply because the MD in question does not know of this possibility and simply does not check. But not everyone has this if they''ve been told "ms"

CO Q 10 ataxia is a metabolic ataxia. Without enough coq you get ataxic. I've never met anyone with an MS diagnosis who was tested for this. Yet should this be your issue potentially you could supplement and do much better. Also you may well then be a member of the diet police and place less demand on your body by eating less allergic foods and processed things thus allowing the body more ability to use the co q you do have for the necessary processes rather than detoxifying free radicals created by an unhealthy diet. Actually, I think everyone can benefit some from this anyway no matter the neuro diagnosis because free radical damage is a feature of all of them.

Some ataxias are genetic like frederichs (adrenoleukodystrophy-Like Lorenzo Odone) and are the result of an inborn error of metabolism, in that case the use of fatty acids resulting in a buildup. This is usually easy to distinguish from MS because of the age of the person and the genetic component in those ones already described, but are there others we do not know of? something that builds up slowly or depletes slowly? Look at pernicious anemia, a diseases which has a genetic component that manifests inthe 3-4th decade or even later. The intrinsic factor is lacking so b12 is not absorbed as it should be. Yet most people have such a good supply in the liver that they only then get short of needs. As a result neuro problems

And then as you say some of us may well have a germ that's been missed. I have been on abx for 4 months and only this week finally know for sure it is helping me. I am a good candidate for this because I got both severe seronegative arthritis and MS in the same week 15 years ago. This happened a couple months after a long long backpack in the backwoods with many bites (think lyme) and also immediately after a severe respiratory illness. I also have adult onset asthma. Now is it likely that my immune system lost it's mind and suddenly started creating antibodies to brain cells and cartiledge all in that week? Nope it never made much sense. I was forever saying this must be a germ like lyme and the neuro and rheumatologist both said, no bad karma. You just got unlucky. When a single germ can cause both problems it's more likely I got a double whammy of autoimmunity in the week I got a terrible URI? When terrible URI's can be caused a CPn a germ that can cause both symptoms?
Geez GIMME A BREAK. I am so thankful that Sarah came out with her story so we can evaluate it's possibility for ourselves.

In my opinion CPn ought to be a differential diagnosis. The lifecycle of the germ and how it invades and misappropriates the cells it invades, as well as how it evades detection is absolutely unbelieveable in terms of what we used to know about germs. Problem is we cannot detect persistent CPn well yet, so we are now still empirically treating as it is an unproven connection to "MS" like symptoms. But if you have gluten ataxia and have been told you have MS, abx will not help you at all, though once you try the gluten free diet you'll think you solved the MS mystery including possibly thinking that people inland eat more wheat that seaside (gee, I live seaside and we have wheat at the store as well as milk...)and this proves the link to "MS" because of epidemiology. OR perhaps the paleolithic angle becomes very key in your mind.

It doesn't matter that we've been told we have MS. All that means is tha we have the set of symptoms that matches that and that no better explanation came up. That other diseases have matching symptoms means potentially any other thing that can cause the same symptoms could be "IT" in your case. Doesn't mean that's it in my case.

I heartily agree that there are likely several causes of MS, not least of which is weak diagnostics and a loyalty to a pradigm that is at best limited.
Marie

[Melody]

I can't believe everyone here hasn't tested for Celiac right off the bat. I had John tested stat it is not his problem but it did remove the guess work as well as IMO a unnecessary restriction in his diet. I also believe we have many different trigger's to MS. John's I believe were allergies and a nasty episode of anaphylactic shock. Diet seems to be his controlling factor at this time. Supplements are a given IMO for
John as we need to rebuild. Right now it is working for us and I can only pray it holds in the long run. I also think anyone with a DX of MS should immediately seek out an allergist and have the E.L.I.S.A. test done as well as the usual skin scratch test.I realize your Doctor might fight the E.L.I.S.A. test as ours did but went over his head. I had the allergist order it as well as the Celiac. You need to remove all the toxins from your system(each system is different). No aspartame,no smoking and no caffeine. As well as other's. The better your system is dealing with what is incoming the less likely it is to rebel. Once again my opinion not law.

[mrhodes40]

Melody I so agree with you. Everyone should be tested for celiac and hughes (antiphospholipid antibodies) syndrome also though many Md's or DO's do not do this. It's a shame. Both are easily treatable but if untreated progressive and indistinguishable from ms progression. After years who questions your downhill slide? Don't we get "married" to MS?

In the US celiac testing has a shockingly low rate given how our genetic makeup makes us prime candidates for it. the last figures I saw were that it is diagnosed in the US in about 1 in 4500 people. In a large study on red cross blood, it turned out that something close to 1 in 240 has it!!!! And since they tend to have anemia by nature and these people are excluded from donating, the actual incidence is assumed to be 1 in 120!! How many of those have gluten ataxia?

Since there is such a thing as gluten ataxia every person ought to be tested if diagnosed with MS for celiac antibodies IMHO.
Marie

[Melody]

hughes (antiphospholipid antibodies) syndrome.

Had never heard of this one will need to check with our GP to see if it was run in Aug 2004 when John spent 3 days in the hospital due to what they thought might be a heart attack. They ran so many test at that time I have no idea what test were actually run. His supposed heart attack ended up of course being a MS attack.

[raven]

As if by magic this popped up on pubmed today

HYPOTHESIS: A mitochondrial mechanism contributes to neurodegeneration in multiple sclerosis (MS)

<shortened url>

EDIT: whoops, the date on this is Jan 15 2005 I had just not seen it before. One hundred lines for me.. It is now 2006, It is now 2006, It is now 2006....... ;)

[bromley]

Robin,

Your initial post mentined the possibility of MS being a number of diseases. I haven't really followed the findings from the Lesion Projects so looked at the NMSS website. Apologies to those who have seen this before:

The MS Lesion Project. Is MS More Than One Disease?

Disease activity and symptoms vary greatly among people with MS. In response to a recommendation from its volunteer Research Programs Advisory Committee, a senior panel of MS experts, in 1998 the National MS Society convened a task force to discuss whether looking at lesions—that is, areas of brain tissue where myelin has been stripped from nerve fibers—would reveal why people experience the disease so differently. The task force noted that this issue was of prime importance, and ripe for development, and recommended a targeted research initiative to investigate it. Understanding lesion patterns can provide more information about differences in disease between individuals, which will enable doctors to make more accurate diagnoses, prognoses, and treatment decisions.


Early Findings

Claudia F. Lucchinetti, MD (Mayo Clinic and Foundation) and collaborators from the U.S., Germany and Austria were chosen to conduct this study for their groundbreaking contributions in this area. They have amassed a large collection of tissue samples from people with MS—a painstaking effort, because these are obtained through brain biopsies (a rare procedure) or autopsy. The group has reported promising findings on samples from 83 cases. They found four types of lesions, which differed in immune system activity. Within each person, all lesions were the same, but lesions differed from person to person. The researchers believe that this may be correlated with differences in disease type and prognosis, and perhaps with different responses to treatment. This report suggests that there may be several types of MS with different immune-related causes (possibly different than the recognized four courses that MS can take, such as relapsing-remitting), and that MS may be a “syndrome” of several diseases.

Follow Up: The MS Lesion Project

The MS Lesion Project has just been renewed with a commitment of $1.2 million for three years. The investigators are analyzing MS lesions in brain tissues from biopsies and autopsies to identify the types of immune cells and other immune factors involved with tissue destruction. The investigators are also examining clinical characteristics of the individuals from whom these tissues were taken, including clinical symptoms and stages of disease, response to therapy, magnetic resonance images, and immune characteristics of blood samples.

The researchers are attempting to correlate the clinical manifestations of the disease and findings from brain imaging (magnetic resonance) with the brain pathology seen directly in brain tissue. They are trying to confirm their initial findings of different patterns of immune pathology and any evidence of possible disease “sub-types” that involve different, definable underlying pathologies. It is possible that such “sub-types” of MS may evolve differently over time and may respond differently to the same therapies. Ultimately investigators could identify which individuals would do best with which treatments.

This study is pathbreaking because of the access to brain tissue being made available for study, its international scope, and the painstaking clinical and imaging follow-up involved. It will greatly increase our knowledge of the pathology underlying MS and should lead to therapeutic trials targeted to specific subgroups of people with MS.


__________________________________________________________


While I had heard that four lesion types had been identified, I hadn't realised that an individual only has one lesion type. I'm sure other researcher will challenge this findings, but such a finding would certainly suggest perhaps different diseases / causes / treatments? I suppose the issue to be addressed is how they identify your lesion type without drilling a hole in your head. I suppose the other option would be to prescribe treatment and if there was no effect it would eliminate one of the types (a bit like the old mastermind game with the colour pegs).

I'm not sure how long this project is funded for or when the next installment is due, but it seems a better approach than keep injecting mice with different chemicals.

Ian

[raven]

In my conversation with Prof Coles when he said the current opinion was that MS was a group of related conditions I said "Oh, you mean the work of Claudia lucchinetti?" (Deb and I had bounced her initial findings around a year or so ago) He looked a little surprised for a moment and then said "Yes, that's the one".

Viewing MS as a group of related but distinct conditions answers an awful lot of questions and inconsistancies.

Robin

[OddDuck]

Hi, Robin (and all)!

Sorry I haven't joined in before this.

I'm chuckling over what you just said about your conversation with Prof Coles.

I do still ascribe to the theory that MS is a group of related but distinct conditions.

Like you, I have also gotten away from keeping tabs on MS progress, but now that I have taken a few moments to update myself,...........man, I see that nothing much that is "new" has been learned or discovered. Not really, anyway.

Speaking of mitochondria, though, I'll paste here my portions of two conversations I had with Vanderbilt this past October, 2005.

Robin (and others).......note the connection between HD and MS. The only difference is that HD primarily takes place in the striatum, whereas MS does not. We have held discussions here previously with regard to how close most neurological diseases are.......the only difference between them being logistical, is all. That presents an interesting paradox, doesn't it?

(Forgive the "desipramine" connection again, but most of my best discoveries still come from that avenue of research!)

Deb

Ok..............just a real quick substantiation via another avenue that desipramine may help protect the oligodendrocytes (OLG) in MS. As I noted before, desipramine decreases "DNA fragmentation and caspase 9 and 3 activation", in addition to inhibiting TNFa. Now add that knowledge to the following:

Found out via the recent Huntington's research:

"....Because the signals that lead cells to die can come from multiple pathways, the researchers then determined which cell death pathway affected the nerve cells carrying mutant huntingtin. They found that the nerve cells' mitochondria, the parts of the cell that create energy, released a protein called cytochrome c through a pore just before dying. From other studies, it was known the drugs nortriptyline and desipramine, which are antidepressants, and trifluoperazine, an antipsychotic, block the mitochondrial pore through which cytochrome c and other death signals are released. By treating the mouse nerve cells containing the mutant huntingtin protein with these drugs, the team was able to block the nerve cells from dying. ...."
*******************************************

http://www.jimmunol.org/cgi/content/full/167/4/2305

...."Therefore, factors that rescue OLG from apoptosis may increase the survival and remyelinating potential of OLG. ...."

....Apoptosis of OLG is associated with an increase in cyto-c release and caspase-9 activation
We have measured the release of cyto-c and the activation of caspase-9 in OPC in defined medium. We have detected cytoplasmic cyto-c after 24 h, and the released cyto-c level was increased significantly at 72 h. Increased cyto-c in supernatants was associated with decreased cyto-c in pellet fractions (Fig. 2A). The supernatant was free of mitochondrial contamination, as shown by the absence of cox IV in digitonin-treated samples. The absence of cyto-c in digitonin-permeabilized supernatant of the control cells (Fig. 2A, t = 0 point) also indicated that the cyto-c was released from the mitochondria affected by apoptosis, not mitochondria permeabilized by digitonin. The mitochondrial involvement was further supported by the activation of caspase-9, as shown by the generation of a 37-kDa caspase-9 cleavage fragment (Fig. 2B), a process requiring cyto-c release (50).

....We showed for the first time that apoptosis of OLG and their progenitor cells is associated with cyto-c release and caspase-9 activation. ...."

I just did a simple comparison between HD and MS. What the HD research found desipramine does as far as rescuing cells is great (and proves my point), but the problem in HD may be that in vivo desipramine does its "work" in the dentate gyrus, not the striatum, and HD appears to mainly be a disease of the striatum. Levetiracetam, though, DOES bind in the striatum and is neuroprotective (they should take a look at that one for HD, also.)

BUT, now take MS!! That rarely involves lesions in the striatum (sometimes, but pretty rare), so let's take a look again at which disease desipramine's actions will more likely assist.

I did some research a while back about logistics in MS, where the O's, axons and neurons are regenerated, etc. Take a quick look at this thread (what can I tell ya, it's easier to direct you to my online postings). Combine this with what I said the other day with regard to protection from apoptosis of the O's.

Nerve and Axonal Regeneration:

http://www.thisisms.com/modules.php?nam ... 54&start=0

Skim until you get like halfway down the page, where I start to really talk scientifically. My discussion also gets into the genetic influences. It will only take a second to look at. Interesting, huh?

[Shayk]

Here are a couple of abstracts on the topic that might be of interest.

Molecular Pathogenesis of Progression in MS

..we still lack a consensus regarding the causes, pathogenesis, and mechanisms of disease progression. Current evidence indicates that multiple sclerosis is an inflammatory neurodegenerative disorder in which both adaptive and innate immunity play important roles in initiation and maintenance of the disease. Recent evidence supports the notion of molecular pathologic abnormalities beyond the plaques and dysfunction of neurons in normal appearing areas, in addition to the multifocal demyelination and axonal loss, as important features that may underlie early reversible changes in the disease. Chronic failure of remyelination, axonal regeneration, and neuronal dysfunction may contribute to disease progression….

Another "medical hypothesis" abstract specifically addresses the mitochondrial issue: Mitchondrial Dysfunction Plays A Key Role in Progressive Axonal Loss in MS

There has been relatively little attention given to investigation of the mechanisms involved in chronic axonal loss in the progressive stages of MS. We propose a hypothesis that mitochondria play a key role in this chronic axonal loss.

So Robin and Deb….your deliberation about mitochondria definitely seems to be on target.

Sharon

[Shayk]

Sorry Robin

Just saw you'd posted the Mitchondrial Hypothesis.

Sharon

[mrhodes40]

Here is the abstract for the original lucchinetti research. It was always earthshaking from the fact that it indicates one type of lesion in each person and only one type while distinct 4 types were found. The thing I have kept in my mind is the part that notes that only two types were autoimmune appearing. The other two were looking infective "reminiscent of a virus" and or toxic.

Ann Neurol. 2000 Jun;47(6):707-17. Related Articles, Links


Comment in:
Ann Neurol. 2000 Jun;47(6):691-3.

Heterogeneity of multiple sclerosis lesions: implications for the pathogenesis of demyelination.

Lucchinetti C, Bruck W, Parisi J, Scheithauer B, Rodriguez M, Lassmann H.

Department of Neurology, Mayo Clinic, Rochester, MN, USA.

Multiple sclerosis (MS) is a disease with profound heterogeneity in clinical course, neuroradiological appearance of the lesions, involvement of susceptibility gene loci, and response to therapy. These features are supported by experimental evidence, which demonstrates that fundamentally different processes, such as autoimmunity or virus infection, may induce MS-like inflammatory demyelinating plaques and suggest that MS may be a disease with heterogeneous pathogenetic mechanisms. From a large pathology sample of MS, collected in three international centers, we selected 51 biopsies and 32 autopsies that contained actively demyelinating lesions defined by stringent criteria. The pathology of the lesions was analyzed using a broad spectrum of immunological and neurobiological markers. Four fundamentally different patterns of demyelination were found, defined on the basis of myelin protein loss, the geography and extension of plaques, the patterns of oligodendrocyte destruction, and the immunopathological evidence of complement activation. Two patterns (I and II) showed close similarities to T-cell-mediated or T-cell plus antibody-mediated autoimmune encephalomyelitis, respectively. The other patterns (III and IV) were highly suggestive of a primary oligodendrocyte dystrophy, reminiscent of virus- or toxin-induced demyelination rather than autoimmunity. At a given time point of the disease--as reflected in autopsy cases--the patterns of demyelination were heterogeneous between patients, but were homogenous within multiple active lesions from the same patient. This pathogenetic heterogeneity of plaques from different MS patients may have fundamental implications for the diagnosis and therapy of this disease.

Publication Types:

"reminiscent of Viral or toxin induced oligodendrocyte death." I knew this, and this background is what made me interested in the abx approach. Later when I learned that endotoxin specifically can cause demyelination I felt another kind of Aha! Certainly we would be talking about this subset of MS patients. I have referred to this research often. It is part of the overall circumstantial picture that makes it a plausible idea. It's clear that there is a lot of support for the idea that MS is heterogenous but also note that the authors here suggest only two types are autoimmune.

Another brief comment in this year's look at the lesions by Claudia L. it is clear that type 2 with complement is well treated by plasma exchange while type 1 and 3 are not helped at all by that approach. More assurance that it is not one thing. Now, if only instead of, as Ian says, people would stop checking ot see if "copaxone plus garlic plus bubble gum" (I LOVE this it's so perfectly funny Ian) is better for ms than copaxone alone and instead try to figure out which type of MS patient is best helped by copaxone we'd all be better off. (link here :<shortened url> )

Deb, the desiprimine and it's interaction with the immune system are well supported in psychoneuroimmunology. The immune system and the brain use the same signaling systems so there is a lot of research into the psychoactive drugs being useful in immune problems. I first heard of desiprimine and ms here after reading your post and have thought it a brilliant bit of investigation. I'd have taken it myself but for retention.

Blssings
Marie
edited to add link to complemet research

[OddDuck]

Thanks, Marie!

And you know what was hilarious (and somewhat frightening)? The neurologists I spoke with here in Nashville (and they are pretty high profile) had no IDEA that desipramine affected the immune system, etc., at all! That is the original argument I had with them and set out to prove them incorrect. And I hate to say it, but I (and many others here) was correct. Now, how could we know that, but they didn't?

And the point of all this being, the researchers know enough about the various possible pathogeneses of MS, but they don't seem to try any drugs nor combinations of drugs that are KNOWN to affect any (and sometimes many) of those particular degenerative mechanisms! (Nor even test people to see exactly what is going on more precisely.)

Desipramine can't be the only one, ya know? It's just a perfect example, I guess, of how they are ignoring the obvious "connections" between what some drugs will do with what they are finding over and over needs to be done for treatment of MS! That just makes me wild!

Not to mention everything all of us has found with regard to diet, etc. I can't tell you how many times I have heard from neuros that diet (fish oil, CoQ10, etc.) won't help. Come on, we all know they do! They don't "cure", but they do help!

I just don't get it sometimes, ya know? Even at those big conferences that are held...........what is your best guess that a bunch of MS neuros and researchers all sit around TOGETHER and brainstorm like we do? Not really. They couldn't be. Otherwise, why does it take US to make such a stink about things? They would already be where we are at with their findings, but they aren't.

MS research is too divided. Nobody compiles it all together to see where and how it all shakes out.



Deb