RE: Re: Advise needed

[Guest guest]

Alan,

Well said!! Thank you for summing it up so eliquently! I, personally, don't believe it was luck that you stumbled onto LDN. I believe there is a Higher Power (God - as far as I believe) that led you to what is going to work in your case. Hang in there, and stay in control of your health! Starting LDN so soon after diagnosis should be exciting. I was so far progressed before I found out about it that I'm still waiting on a miracle but feel quite certain that the progression has stopped, and I am thankful for that!

Marcie

In a message dated 3/29/2004 7:03:46 PM Central Standard Time, alanms@... writes:

This is the first time I have replied to a post after being diagnosed about a month ago after Optical Neuritis and MRI. I posted questions several times.

After extensive research on the CRAB drugs and ldn (I am an engineer and tend to over study things) I decided to do a phone consult with Dr. Bihari. My insurance would also pay for all treatments (at least for now). I decided to take only LDN based on my consult and reading - including going back many months on this site. The reason I chose LDN only was in part the positive commentary (time and time again) on LDN, plus a most informative and complete consult about LDN and MS with Dr. Bahari. I did consider also using Copaxone (which I understood to be compatible with LDN - not clear on the other's compatibility - didn't think so). Dr. Bahari told me that he has had parients on both LDN and Copaxone but that most, over time, stop Copaxone with no noticable effect on their condition (other than eliminating side effects and itching).

Clearly this is a very personal, and difficult decision. At least it was for me. But I am quite comfortable with it and am just finishing my first week on LDN at 4.5 mg. My advice would be a phone consult with Dr. Bihari before making your "final" choice. I'd also urge you to read the LDN site completely and review past posts on this site in addition to commentary on other sites about the effectiveness and side effects of the crab drugs. What appears to be defined as "WELL TOLERATED" by many neuros, does not appear to be considered as such by many MS'ers.

Hope that helps as I clearly recall how I felt being in your position several short weeks ago. The folks that regularly participate on this site are truely doing a "good" thing (cudos on the petition) as is Dr. Bahari (and some other docs). They certainly have my thanks and admiration, and support with getting LDN recognized as an etremely viable option to the CRAB drugs.

Personally I feel it is borders on criminal that LDN has to be stumble upon, in some cases(as in Mine) by shear luck, rather than being presented (clinical trials or not given the low dosage and approval for other uses) as one of the treatment options by the MS society and all neuros. We all need to take primary responsiilty for our health and health care, and that means we should be told all the facts, including LDN, regardless of liability issues (and yes I recognize - big profits).

Sorry I got carried away - no way not to get mad - Hope this helps

Alan

--- In

[Guest guest]

I thought everyone had been over this just

a little while ago…. Maybe you can look back in the threads? I know on

LDN websites and Bihari even says and Lawrence

too for that matter say Copaxone is fine with LDN and works along the same

lines. It’s the others they feel don’t yet there are many taking

others… it’s up to each person to do their own thing…

From: cheystay

[mailto:c_chey@...]

Sent: Tuesday, March 30, 2004

11:18 AM

low dose naltrexone

Subject: [low dose naltrexone] Re:

Advise needed

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.intersciencewiley.com/cgi-

bin/abstract/107629227/ABSTRACT

Copyright © 2004, All About Multiple Sclerosis

Chey