(MS - Disease or Condition?) Re: Advise needed - confused!

[Guest guest]

Confusion about MS seems to be the norm rather than the exception.

Based on my reading (including the article below) and discussions in

the last 6 weeks since my diagnosis (and " theories " others have put

forth), I believe what is being called MS is not a disease but a

condition. The condition is the loss of myelin sheath typically

characterized in, and now diagnosed via MRI. It appears on an MRI as

rather specific looking lesions, where myelin should be, and is

often accompanied by several physical and mental " symptoms " .

These " symptoms " come from a rather large potential list.

How and why myelin goes " missing " seems to be unclear. Does it begin

to " die " and gets attacked by the immune system, or does the immune

system attack (for one of various theoretical reasons) healthy

myelin. This apparently remains a one of the key unanswered question.

Many things (based on what I've read) have been theorized to either

directly cause the demyelination characteristic of what is being

generally referred to as MS, or to otehrwise somehow " trigger " it.

They include various viruses (alone or combinations - Herpese and

Epstein Barr as examples), Bacteria, parasites (and the chemicals

they produce and or bacteria often present), envrionmental factors

(mercury and solvents to name a few) and finally a " genetic "

component. Other realted issues also include chronic sinusitus and

gastro - intesinal stuff (Candida, liver and kidney etc.). Not to

mention potential nutritional deficiencies like Vitamin D, Omega3

and enzyme and hormone specific theories.

My conclusions is that what is being called MS is simply when an MRI

picures lesions that look and act a certain way. This makes sense to

me given the general " confusion " over how and why one " gets " MS and

also explains why some people, when trying MS treatments

(traditional and non traditional) seem to get results and others do

not. I suspect that various things (and or combination of things)

can cause the demyelination that is currently being labelled MS. It

makes sense that some people have success and others fail if more

than one set of circumstances can cause a positive " MRI " MS

diagnosis. This is further supported by several reports I've read

that Lyme Disease can have very similiar MRI results and that a

measurable percentage of MSers probably have Lyme. Lyme tests are

not standard protocol and testing is notoriously unreliable (nature

of the infection and tests available), but often treatable with

Antibiotics. I have read some articles talking about treating MS

with Antibiotics and cannot help but wonder if Lyme was definitively

ruled out (if that is reasonably possible) in patients showing

favorable response to antibiotics.

To sum up. It seems clear that no one knows what MS really is, or

how we get it, because no one really knows what causes it. Not

knowing what causes it means curing it is somewhat difficult, to say

the least, and treating it is hit and miss. No doubt putting it into

remission is the current focus. Many MSers would eagerly point out

that the " money " is in the treatment and not the cure. Although this

seems apparent, without a better understanding of cause, which

should be inclusive of all the varied theories rather than exclusive

(focusing only on clinically validated information - which can be

far less impressive and or definitive than we are often lead to

believe) we will all remain very confused (sorry but please recall I

wrote this to address the question of " confusion " about MS and its

treatments).

Because it is so confusing, and if you accept my discussion of why I

believe MS is a condition and not a disease (could be

several " diseases " or one that can be ultimately caused for several

reasons - resulting in the MRI diagnosis) then as someone with MS

you need to take charge or your health and healthcare, don't shy

away from asking anyone anything (even if it is unconventional and

they wear a white coat). Educate yourself until you are comfortable.

No one is as concerned about, or interested in, you and your health

as you are.

Please - fight the confusion - be your own champion and become an

advocate! I guess its clear I have!

Best Regards,

Alan

--- In low dose naltrexone , " cheystay " <c_chey@h...>

wrote:

> I still do not understand. Avonex, Rebif, Betaseron, Copaxone are

> immunesuppressants. LDN is an immunestimulator. In my eyes (I'm no

> doctor) the two cannot combine well. And if you read this I pasted

> below, you wonder who ever came up with suppressants

>

> All about Multiple Sclerose

>

> Prevailing medical wisdom says that multiple sclerosis is an

> autoimmune

> disease - a disease in which the body's immune system turns in on

> itself.

> Specifically, it attacks the myelin sheaths that insulate the nerve

> cells in

> the brain and spinal cord. This immune system activity produces

> inflammation

> similar to what happens in the skin when we get a pimple.

>

> Crucially, the inflammation also kills the cells responsible for

> producing

> and maintaining the myelin. These cells are called oligodendrocytes

> and they

> have long been known to die in large numbers during attacks of MS.

>

> The majority of existing treatments for the disease and a fair

> proportion of

> new treatments currently in research focus on reducing the

> inflammation or

> disabling the immune system cells responsible for it.

>

> However, a dramatic piece of new research published in The ls

of

> Neurology threatens to turn this understanding of multiple

sclerosis

> on its

> head.

>

> The study examined twelve brains of people with multiple sclerosis,

> concentrating on newly forming areas of disease activity called

> lesions. It

> found that the oligodendrocytes in these lesions were dying before

> there

> were any signs of inflammation.

>

> This implies that it is not the inflammation that causes the death

> of the

> oligodendrocytes in multiple sclerosis but the other way around.

The

> inflammation occurs in response to the oligodendrocyte cell death.

>

> The authors, Barnett and Prineas of the Institute of

> Clinical

> Neurosciences at the University of Sydney, Australia don't deny

that

> the

> inflammation might cause some of the damage seen in multiple

> sclerosis but

> they do paint a radically new picture of of the disease.

>

> They suggest that the first stage of the development of a new

> multiple

> sclerosis lesion is mass suicide of the oligodendrocytes over a

> relatively

> small area. This process is called apoptosis or programmed cell

> death and is

> a normal response in the human body during growth and repair. If

> cells were

> allowed to grow and divide without limits, they would form a

cancer.

> Similarily, cells infected by viruses or cells that are no longer

> needed by

> the body will often cell kill themselves.

>

> Barnett and Prineas observed oligodendrocytes in which the central

> nucleus

> was shrivelling up - a typical sign of a cell committing suicide.

> Other

> cells in the brain were also changing. Microglia, another type of

> maintenance cell which can swallow up dead and dying cells, were

> forming

> long extensions ready to engulf the dead and dying

oligodendrocytes.

> Additionally, a group of proteins, called complement, which are

> responsible

> for activating the body's rubbish-collecting cells, had collected

on

> the

> myelin. Crucially, the rubbish-collecting cells of the immune

> system, the

> macrophages, had not yet appeared in the lesion.

>

> Within one or two days of lesion formation, all the

oligodendrocytes

> had

> disappeared. The authors suggest that they had been swallowed up by

> the

> microglia. The spaces that they had once occupied were now full of

> liquid

> forming what is known as edema.

>

> The next stage seems to be the invasion of immune system cells.

> Macrophages

> now start to appear, together with T cells, the orchestrators of

the

> immune

> response. These initiate and take part in inflammation. The

> macrophages

> start to gobble up the myelin left over by the vanished

> oligodendrocytes.

>

> The final stage would appear to be regeneration. Oligodendrocyte

> precursor

> cells, cells that have the ability to develop into new

> oligodendrocytes,

> move in to replace the lost cells. They are fed special chemicals

> called

> trophic factors by the macrophages and the process of remyelination

> can

> begin.

>

> It is important to bear in mind that this was a study of only 12

> brains and

> further work needs to be done to validate the studies findings.

> However, if

> this work reflects what is actually happening in multiple

sclerosis,

> then

> its implications are earth shattering:

>

> a.. Multiple sclerosis will no longer be an autoimmune disease. A

> lot of

> text books are going to have to be rewritten.

> a.. Treatments that target inflammation will not not addressing

> the root

> cause of the diease. This does not mean that they are not effective

> to some

> degree but that they can never be as good as treatments that target

> the

> death of the oligodendrocytes.

> a.. All the animal models of multiple sclerosis are poor

> representations

> of the disease in that they are all primarily autoimmune models.

> Perhaps

> this is why so many treatments that are so effective in mouse

models

> prove

> to make no difference to multiple sclerosis in humans. For animal

> models to

> be valid, they would need to show the kind of disease process

> described by

> Barnett and Prineas.

> a.. Researchers will need to change direction. Whilst work on

> oligodendrocyte precursor cells becomes more important than ever,

> work on

> describing the inflammation process in multiple sclerosis needs to

> take a

> back-seat. Importantly, researchers need to find out why

> oligodendrocytes

> are dying and what can be done to stop them.

> Quite how the world of multiple sclerosis research will react to

> this paper

> is unclear. Thus far, Barnett and Prineas's paper seems to have

been

> met

> with a deafening silence which is why I decided to write this

piece.

> Source:

>

> Relapsing and remitting multiple sclerosis: Pathology of the newly

> forming

> lesion

> H. Barnett, MBBS, W. Prineas, MBBS *

> ls of Neurology, Feb 23, 2004

> http://www3.interscience.wiley.com/cgi-

> bin/abstract/107629227/ABSTRACT

>

> Copyright © 2004, All About Multiple Sclerosis

>

> Chey