CHAPTER SEVEN

SO WHAT DO WE KNOW ABOUT MS?

FIRST THE MECHANICS
I am going to keep away from scientific language as much as possible and use layman’s terms. For anyone who would like a more detailed and precise description, the scientific references are readily available in any medical library.

Multiple sclerosis is a disease that affects the white matter (myelin sheath) of the Central Nervous System (CNS) and/or the stem of the brain. The myelin is made up of mostly fatty acids and one of those in largest concentrations is cholesterol.

The problems of MS start when a plaque of esterfied cholesterol, a chemically different cholesterol, forms in the myelin sheath, which surrounds the CNS. As the plaque enlarges, the myelin is affected in such a way that the nerve impulses are interrupted as they travel from the brain to the muscles, which control some bodily function. The result is the sudden, unexplained inability of the patient to do some task which is normal to him.

Typical early MS symptoms are an unstable, unsteady walk or gate. Blurred vision, many times double vision in one or both eyes. Unexplained numbness in the extremities. The inability to form certain sounds with a resulting slurring of speech reminiscent of a drunk trying to talk. Many times patients lose bladder or bowel control. In short, almost any abnormal body control function could be (but not necessarily is) the result of the onset of multiple sclerosis.

One of the most difficult things about MS has been the inability of medicine to make a quick, sure diagnosis of the problem. Most diseases can be pinpointed by a blood test or urine sample. Not MS. At the present time there is just no simple, standard test, which will tell the physician that any individual patient’s problem is, in fact, multiple sclerosis. There is a new, but very expensive electronic test called an MRI, which is the most conclusive test yet for this problem. It is now finding wider and wider use in diagnosing MS.

Because of medicine’s past inability to make a quick diagnosis, some MS patients went through years of frustration with unexplained problems that continually confronted them. As their problems grew and become more severe, with no explanation forthcoming from their doctors, the fabric of their family life was sometimes torn beyond repair by their reactions to the stresses they face. When the diagnosis was finally made, many times live and relationships had already been ruined through no fault of those involved.

Since there was no “black box” test for MS, the physician had to wait for enough clinical history, which pointed in the direction of MS to make any evaluation. To gain that much clinical evidence might take years of observation. And sometimes that evaluation was delayed even after the doctor had become convinced that he was dealing with MS. Not that the doctor was trying to hide the worst from his patient, but more because the doctor must then admit that he cannot help this particular patient. Remember, MS has been labeled by the orthodox medical profession as an incurable problem. Just as soon as the diagnosis is made, the physician is bound by ethics of this profession to tell the patient there is no hope.

But now with the advent of the MRI there should no longer be excessive delays. The physician no longer needs to make the diagnosis subjectively after a prolonged period of observation. The expense of the MRI can be justified after a fairly short period of observation.

We patients are many times to blame for not getting an earlier diagnosis as well. Americans are used to instant everything, coffee, potatoes, fast food and even medical diagnoses. When we have a problem that is not quickly named and understood by our medical advisor, we are prone to leave that doctor’s care and seek another physician. But when we do that, the new physician must stat the clinical evaluation all over again, so the delay can be even longer. And MRI is not an automatic test to be given without fairly strong indications.

In order to picture what happens with MS to cause our bodies to malfunction, you might compare the human CNS to an electric wire. Not to the rather small wire of a modern lamp cord, but more like the larger, heavier old fashioned wires that used to run through walls of houses to the sockets and had heavy cotton/rubber insulation rather loosely wrapped around them. Call that loosely wrapped insulation the myelin sheath and the heavy wire the CNS and pretend it is made of the neurons. Picture the wire as having some bumps in it at regular intervals. In human nerves, these bumps are called Synapses and are the junctions of the neurons. The nerve impulses (electrons) can’t really run down the nerve fibers (wire), but rather they jump from synapse to synapse along the CNS. From one junction to the next.

A way of visualizing this is to think of the electron stream in a TV picture tube. The electrons come off the cathode (one synapse) and jump to the screen (the second synapse). In order to make sure the electrons go to the screen where they are supposed to go and not off somewhere else within the picture tube and get lost without producing an image on the screen, there are plates that guide the electrons by exerting an electromagnetic force on them. Those focusing plates will not allow the electrons to go anywhere but to the screen.

The plate that keeps the nerve impulses on course from synapse to synapse in our CNS is the “myelin sheath”. Multiple sclerosis attacks this myelin sheath (our wire insulation or TV tube focusing plate), and causes small patches of it to die and wither away as plaque forms in it.

When this happens, the steering pressure on the nerve impulse is interrupted and the impulse can miss the synapse and get “grounded out”. If the same type thing happens to the focusing plate in a TV set, the picture disappears because the electron stream misses its target and does not reach the screen. In MS, we lose the ability to perform some function because the nerve impulse, which controls that particular action, has missed its mark and disappeared.

Make a fist with your left hand. Now stick the index finger of your left hand straight out, away from your fist. That is your nerve (wire) and the knuckles are the synapses.

Now take your right hand and wrap your fingers tightly around your left index finger. That is the myelin sheath (insulation or steering plate). Now, slowly unwrap the fingers of your right hand from around your left index finger without moving your hand away. That is the plaque forming and the myelin dying and withering. Now, in a visual way, you know basically what happens microscopically inside an MS patient’s body.

NOW THE GUESSES

It seems as if there are almost as many theories about what causes MS, as there are researchers.

One of the missing links in all the theories is what triggers an attack. Many things have been found that could cause MS like damage. But just as there are lots of rocks on a mountainside that have been there for thousands of years that could become a landslide, it takes something to cause them to become dislodged or no landslide occurs.

There is a virus theory. According to this theory, a “slow virus,” suspected of lying dormant in the body suddenly becomes active and causes the damage to the myelin. So far, to my knowledge, no virus has been isolated and no activating mechanism has been found to bring the dormant virus to active life. However, a strain of measles virus, which theoretically could cause such a reaction, has been found to be present in a dormant state in some MS patients.

There is the autoimmune theory, in which the body becomes allergic to itself and attacks its own myelin. It has been suggested that an allergic reaction to the ingestion of fat could possibly account for this. There are a couple of pretty good animal models for auto-immune damage, but still no identifiable triggering mechanism has been found which will hold up to scientific investigation.

There is a genetic predisposition theory, in which the victim needs to have an as-yet unidentified genetic error, which will allow the disease to happen. Statistically, people with close relatives who have MS are 5 to 20 times more likely to contract the disease that the general population. (A genetic link?) Perhaps in some people there is a genetic “open door” so to speak that will allow some environmental factor to be expressed in the patient as MS (emotional and/or dietary factor perhaps?). There is as yet no defined trigger mechanism for this idea either.

Then there is a chemical theory. There actually is a toxic chemical material (called Encepholitogenic Antibodies) that is produced in the bodies of some MS patients and which can be identified in the urine of those MS patients. This chemical does cause damage to myelin in a laboratory. It is thought this might be the culprit. The question in this one is which cam first, the chicken or the egg. Is the chemical the base cause of the MS or part of the result?

There is Dr. Swank’s theory, in which the blood platelets become sticky from the mal-utilization of ingested fats and literally plug up some of the small capillaries that feed the myelin cells. Like a cork in a bottle. The cells then die of starvation and also by strangling on their waste. A cholesterol plaque could be encouraged by such an event. This theory has been tied to the chemical theory above as the possible cause for the body to produce the myelin-damaging chemical. But it is far from being a proven or accepted theory. Why, for instance, does this type of capillary blockage and damage only seem to appear in myelin?

There is a theory by Dr. David Horrobin in Canada that an imbalance of prostaglandin, stemming from an inability of the body to correctly process and use essential fatty acids, causes the body to damage itself, kind of in the autoimmune theory way. This theory is also involved with the mal-utilization of fats in the body, this time Essential Fatty Acids. The trigger in this scenario is a lack of some nutrients and blockage of the pathway by too much saturated fat. However, solid proof is lacking in this theory also.

There are a few facts that do point to some type of fat involvement in MS and seem to support the Autoimmune, Swank and Horrobin line of thinking.

Research has determined that the lipid concentrations in the myelin of MS patient’s brain stems and CNS where no lesions were visible is significantly different than in non-MS patients: a ratio of 37.9 to 59.3 percent saturated to unsaturated fatty acids vs. 44 to 48,4 percent in “normal people.” This was chiefly due to a lower concentration of Oleic Acid in the MS patients’ myelin. The absolute significance of this has not yet been determined, but science (Rathbone, 1965) has also shown that fatty acid composition of the brain can be altered by the diet.

The simple fact is that we still don’t know what causes the disease after one hundred and fifty years of searching for an answer. We can’t even really make a good guess as to why I got the disease and the guy next door didn’t. Nor why one twin in a family might contract the disease, but not very often both.

Every theory so far put forth has a thousand different questions that can’t seem to be answered. The only thing that every theory seems to have in common is the search for a single causative factor that cannot seem to be found. What if there is no single cause? What if this modern disease is founded in modern man’s living habits rather than in an outside identifiable factor such as a virus?

MORE QUESTIONS THAN ANSWERS

I certainly don’t claim to have the answers, but I have a few pointed questions of my own. Traditional medicine says nothing known at this time can help MS patients. Other than the 6 percent who seem to have unexplained remission for which, according to some doctors, may have even been misdiagnosed in the first place – no one gets better.

Yet Dr. Swank’s paper on 146 patients who had followed his program for more than twenty years (starting in 1948) shows that, while only a few actually improved from the disability they started with, even those who didn’t show physical improvement did not have the same downward trend as did similar groups followed in VA hospitals or at several prestigious clinics such as the Mayo Clinic, but who did not have any dietary restrictions. In other words, though most of Dr. Swank’s patients didn’t get physically better, many of them didn’t get worse either! In general terms of the disease, no further determination in itself, is an improvement over what could be statistically expected.

After ten years on the diet, Dr. Swank only had 25 percent of his patients unable to continue to work and walk, though some of them had already been moderately disabled when they started on the program. After the same ten years span, 50 percent of the May (no diet restriction) group could not walk or work. The number who had deteriorated to the non-working and wheelchair stage was just half as many in the Swank study! Thus the diet controlled patient rate of deterioration was astonishingly less.

The mortality numbers were even more startling. After 1 year following the Swank program only 6 percent of the diet controlled patients had died, while in four other untreated (non-diet) groups of MS patients between 20 and 28 percent had passed away. Thirty years after being diagnosed, 63 percent of the untreated (non-diet) patients had expired while only 18 percent of the Swank diet controlled group had died. The Swank diet patient mortality rate was almost negligible when compared to all the unrestricted groups.

Something was surely going on! And Dr. Swank only used his low fat diet in these studies, he never used supplements to enhance the program other than a multiple vitamin formula and Cod Liver Oil.

It seems that when someone like Dr. Swank accomplishes an obvious change in the course of a disease by some means he owes it to the rest of us to try and explain how it happened and that seems to be his problem with other scientists. So maybe the mechanics of some of Dr. Swank’s conclusions as to the exact what and how the MS damage occurs, might be off base, but regardless of that the patients who followed his diet DID DO much better than any of those studied who DID NOT follow his diet! The Swank diet did, by itself, modify the progress of the disease!

To me it is totally astonishing that the National Multiple Sclerosis Society and other researchers following their lead totally disregard these findings. Ignoring the facts of what happened, just because Dr. Swank couldn’t explain exactly how they happened, is like denying the existence of radio and TV just because we cannot explaining every facet of the way they work. If we can watch TV and listen to radio, then they do in fact exist. It doesn’t make good sense to me to deny their existence any more than it does to deny the Swank results.

Is the MS Society simply jealous because someone outside their close knit little group made a major breakthrough in overcoming the effects of the disease while they themselves can accomplish absolutely nothing in their research except spending millions of dollars?

Remember how to blunt the opposition in the union election I told you about? How does this scenario sound? Leave Swank way out west in Oregon and simply ignore him. We of the MS society have access to the eastern press where national opinion is formed. If we pretend Swank doesn’t exist and/or that he never really accomplished anything then our millions of dollars in donations will keep pouring in and eventually we will come up with something that can be patented to make even more money instead of allowing a non-patentable thing like diet to kill our golden goose.

The people Dr. Swank studied were all volunteers, not captives, so they had a choice to follow the diet, or to give it up. Some did give up, but the majority stayed with it. Patients are not likely to stay with such a strict diet program for twenty years, or in the case of some of Dr. Swank’s original group, now close to forty years, unless they feel there is a benefit for themselves.

Why does there seem to be such hostility, not only to Dr. Swank’s ideas, buy apparently to any ideas that do not stem from MS Society grants or associating scientists? Regardless of the reasons, any diet theory seems to be immediately discounted by the medical fraternity without ever being impartially investigated.

Yet the only diagnosed MS patients with whom I have ever come in contact that had long standing remissions, or patients who felt that the progress of their disease had been slowed, were following programs that in some way modified their dietary fat intake and presumably, therefore, the lipid balance in the brain and myelin.

I have never met any patient who had gotten any medical treatment, orthodox or unorthodox, from acupuncture to implant surgery, from cortisone injections to snake venom injections that felt they had long-term benefits.

And over the years that I was in the health food business, I was sought out by hundreds of MS patients who wanted to see me, either to seek help and information from me, or to share information on their own good fortune with a program they had been following.

I’ve met people who used the Evers diet and had good results, as long as they were in Europe and were able to get the quality, unsprayed, unprocessed and organically grown things he prescribed. I have met people on the McDougal diet who benefited by abstaining from gluten (a starchy grain protein), along with the modification of fat intake. In recent years there have been several MS patients following macrobiotic diets who were doing much better than just holding their own against the disease. And I am certainly not the only person outside of the original test group who has seen results fro the Swank diet.

There is an old adage, “Where there’s smoke, there’s fire.” It seems it’s time that someone called the fire department with regard to really investigating diet as at least “a” factor in the control of MS, if not “the” factor.

As to the exact whys and wherefores of what causes the problems we have identified as MS, I honestly don’t care! Oh, it would be an interesting exercise in academia to find out, I’m sure. But to tell the truth, I’m a lot more interested in the poor bastards like me who are afflicted with the disease than in the science of why ay of us got it. I believe that maybe instead of spending all of our research resources on trying to find a cause and a magic potion for a cure, it’s time to start working with diet and/or other environmental factors as, at least, a partial control. I believe that the traditional medical approach to MS needs to, at least, be re-evaluated.

I’m not suggesting that we abandon on-going research. Nor am I trying, in any way, to hinder science from maybe finding that elusive cure that will solve the problem once and for all. I’m only asking that diet and lifestyle be really investigated with any eye toward control. I honestly feel that many people, who could overcome the ravages of the disease, are being kept from doing so by he present medical attitudes of disbelief and ridicule. If research does show that changes in diet and lifestyle are helpful, even if it’s in only a few cases, then let them be recognized as a help for those lucky few and be publicized as such.

The present medical policy of total denial without complete investigation is, in my mind, unconscionable.