This Is MS Multiple Sclerosis Community: Knowledge & Support

The Three (Yes – Three) Stages of MS

By Ashton Embry

Many people think MS has two stages: relapsing remitting (R-R MS) and
secondary progressive (SPMS). I see the MS disease process as having
three distinct stages. The often-ignored and perhaps most critical stage of MS is the first one which can be called pre-clinical MS (PCMS).

The First Stage of MS - Pre-Clinical MS – A Time Bomb Which Explodes Years Later

The MS disease process usually begins in early childhood and is most likely precipitated in a genetically susceptible child by a cross-reactive, viral infection in combination with a low vitamin D level (i.e. winter to early spring). It would be wonderful if every child was given adequate vitamin D from birth onward. I believe MS would become a very rare disease if this was done. The viral infection results in the activation of immune cells which are sensitised to both the virus and to a protein in myelin, the substance that coats the axons in the central nervous system. The occurrence of a low vitamin D level at this time ensures that the viral infection is not well controlled and this lack of control allows a substantial pool of memory immune cells to develop. These memory immune cells, which are sensitised to the myelin protein as well as the virus, are basically an MS time bomb that most often explodes 20 – 30 years later.

During the long pre-clinical stage of MS various cross-reactive proteins from infectious agents and foods sporadically activate the myelin-sensitive memory cells especially during times when vitamin D levels are low. These immune cells cause minor inflammatory reactions in various areas of the brain, but such inflammation is very diffuse and is not detectable with an MRI scan. The damage associated with these minor inflammatory autoimmune episodes does not cause any noticeable symptoms, but even at this stage nerve axons are damaged and destroyed. With each activation, the pool of problematic memory cells expands and the next episode of autoimmunity is potentially more extensive and damaging.

During the long pre-clinical stage the immune system is gradually altered such that autoimmunity becomes less well controlled and the potential for
more substantial autoimmune reactions increases. Eventually a triggering event such as a cross-reactive viral infection during a time of low vitamin D level will precipitate a large enough autoimmune attack that symptoms become very apparent and the person sees a neurologist. A second, clinically apparent attack plus the appearance of distinct lesions on an MRI scan, usually results in a diagnosis of MS.

The Second Stage of MS – Relapsing/Remitting

In most people with MS (some have Primary Progressive MS), the second stage consists of well-defined attacks separated by periods of remission (R-R MS). New symptoms and disabilities often appear during an attack and many resolve during the following remission as the regulatory side of the immune system regains control. However there is sometimes a small incremental increase in disability by the time the next attack happens. An MS attack is caused by greatly increased, poorly-controlled inflammation in the brain due to amplified autoimmune activity. The inflammation is often focused in distinct lesions, although diffuse inflammation also occurs in the brain. The swelling associated with the inflammation results in most of the new symptoms. The inflammatory action, besides causing demyelination, also damages the nerve axons themselves and this can result in long-term disability.

Axon Damage and Disability

The more frequent and extensive the autoimmune driven inflammatory action, the greater the axon damage and the greater the long-term disability. Inflammation is not the only disease process which is contributing to increased disability during the R-R stage. When the nerve axons are damaged and severed in the lesions and possibly elsewhere in the brain and spinal cord, they degenerate along their entire length. This degeneration of the axons is perhaps the main cause of long-term disability. Thus the R-R stage is characterised by episodes of focal inflammation and by slow, progressive degeneration of nerve
axons. Considerable disability accumulates due to these processes, especially the latter one.

The Third Phase – Secondary Progressive MS

The third and final phase of MS is known as Secondary Progressive MS (SPMS). It is characterised by few if any distinct attacks and by an insidious, slow and steady increase in disability. All the damage that occurred to the demyelinated nerve axons during the first two stages results in a slow and continuous degeneration of the long axon strands. This means fewer and fewer nerve impulses from the brain reach the muscles they are destined for and this translates into increased disability. Autoimmune inflammation continues during this time but is much more diffuse.

Using Diet, Supplements & Exercise To Shut Off The
Inflammatory Process

The long MS disease process which can essentially last a lifetime starts with low level inflammation, progresses to greatly increased inflammation and associated nerve axon degeneration and ends with continual nerve axon degeneration. Most of the accumulated disability is due to the degeneration component of the disease process. To avoid reaching the phase of steady degeneration and experiencing a downward spiral into serious disability, one must shut off the inflammatory process as early as possible. The ideal would be for susceptible persons to use a few nutritional strategies such as adequate vitamin D in childhood. However few do this because most believe that MS will never affect them. More rigorous nutritional strategies and perhaps even one of the MS drugs are needed once MS is diagnosed. The sooner they are instituted the better the chance to short circuit the disease process and the appearance of long-term disability. Because many people do not experience serious symptoms in the early years of R-R MS they often do nothing and falsely believe that MS is no big deal. They do not realise that the disease process and associated damage are continuing. A major attack 5–10 years after diagnosis often results in disabilities which do not resolve. Suddenly they want to “do something” about their MS. Nutrition can still be very helpful at this time but because of the extent of inflammatory damage and ongoing degeneration, the chances of returning to a
disability-free state are low.

Once one is in the SPMS stage it is critical to use the nutritional strategies and to have a good exercise programme with associated mind concentration. The goal of such a programme is to “rewire” the brain and have nerve impulses use new routes and thus restore abilities. Again the chances of halting disease progression at this time are low because of widespread degeneration of the axons. Overall it is important to understand the stages in the evolution of the MS disease process, why disabilities occur and accumulate and what strategies are needed to try to counter the processes going on in each stage. The main lesson learned from this is that the sooner one starts using nutritional strategies the
better the chances of halting disease progression and avoiding any problematic disabilities.


Cheers
Nick

I don't mean to sound critical because I've always admired Ashton's common sense and logic but he really should make it more clear in this article that much of what seems to be portrayed as commonly accepted, is indeed supported only by his common sense and logic.

Not that I haven't done the same thing myself numerous times and without a doubt will do it again
Bob

Nick--As I read your post, I kept looking for a way to explain so many recent pediatric cases (youngest was 2 years old, I believe)--so many that 6 pediatric MS clinics are opening around the country.

They haven't had 20-30 years before the time bomb went off. How do they fit into this scenario?

LC

The use of the phrase time bomb by Ashton refers to the majority of those with MS because most PwMS are diagnosed in adulthood. However there are (as you wrote) examples of children being diagnosed (as there are in the case of MS's sibling, type 1 diabetes).

In IDDM there aren't that many GAD proteins that need to be damaged before sypmtoms arise and in my opinion this accounts for this type of diabetes to prvail mostly in children (hence the term juvenile diabetes). Although there are many more brain neurons than there are GAD proteins that need to affected to become noticeable, I would speculate that juvenile MS could arise from a combination of:

*better detection ability of MRI's
*children with very aggressive imune systems[/list]
*repeaded attacks by the immune system on the same part of the brain
*a dominance of causal elements in the envirnment[/list]
*neurologists trying to put idle MRI scanners to use[/list]


Are these children symptomatic or are they only with lesions?

Cheers
Nick

Nick,

Very interesting article by Ashton and many of his points have been written by other researchers. But despite the apparent common sense in a lot of the article, nobody has been able to prove these theories. Perhaps some day!

Harry