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CONTENTS In order of relevance My Study OPCs Diet Stress Talking to Doctors
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MY THEORY If only to save me constantly retyping emails, I offer my opinion here regarding what I think causes ALS/MND. This opinion is based on over a decade of research, observation and plain hard work. I had intended to write a formal paper but the chances of it being published and "peer reviewed" were remote. My opinion has not (yet) be scientifically verified and I make no claim to the contrary, although in one paper it is "now widely accepted that ALS/MND is multi-factoral". Here are my thoughts for your consideration. Steven Shackel 2004 Introduction I further believe that this process is responsible for many other chronic, degenerative illnesses that currently exist as "diagnosable but untreatable". Whether the co-infection specifically attacks the central nervous system or other organs is probably dictated by environmental, lifestyle or genetic factors. This means the same co-infective organisms could be responsible for symptomatically different illnesses. I believe researchers should direct more attention to possible co-infective combinations. If this hypothesis were correct it would explain the relatively low incidence of ALS/MND and why there are many chronic, degenerative but untreatable illnesses that collectively leave a void in medical knowledge. I cannot possibly present all the data I have gathered to support my findings in this short article but I have included some by way of explanation. A Potential Cause of ALS/MND? Some branches of science, epidemiology is an obvious example, first look at the broad picture and systematically eliminate the impossible, improbable and less likely causes of an outbreak of illness. They gradually pare away at the problem until a series of possibilities are revealed. These possibilities are then researched in detail until the cause of the epidemic in question has been isolated. This approach has been used to some extent in an attempt to discover the aetiology of ALS/MND but in my opinion the net cast has not been wide enough. With no medical background, I did not know what questions to ask but more importantly did not know which questions not to ask. Armed with experience in scientific and technical editing and a knowledge of botanical Latin and Greek I slowly ascended the steep learning curve of medical research. I observed a pattern of an entire group of chronic degenerative illnesses that could be described, diagnosed but not adequately explained or treated - ALS/MND among them. As there was little useful information to be gleaned directly from texts on ALS/MND when I started researching its aetiology, I directed my attention to what appeared, from my detached viewpoint, to be a gaping hole in medical knowledge. Comparing the symptoms of diseases including Rheumatoid Arthritis, Lupus, Diabetes, Chronic Fatigue Syndrome/ME, Multiple Sclerosis and even the way neurodegeneration occurs in some cases of AIDS, I found numerous similarities despite the obvious dissimilarities of the illnesses. Liver dysfunction is common to all the chronic illnesses I studied, as are abnormal apoptosis (programmed cell death), mitochondrial changes and a high incidence of toxins (or more correctly "stressors"), throughout the body. Depending on the illness, organisms both benign or infectious were frequently found in places they simply should not be. Infective organisms should find it difficult to cross the blood brain barrier (bbb) but have been found in spinal fluid, inside red blood cells and organs that should have been clear of such "foreign bodies". I have used the words stressors and foreign bodies rather than toxins and infections because some stressors, strictly speaking, are not literally toxic and some organisms are not typically infectious. Organisms implicated included bacteria, viruses, mycoplasmas, spirochetes, parasites, yeast/fungi and prions. In some cases, more than one of these organisms was found in a Person or Persons with ALS (PALS for short). In most cases, if multiple tests were done and multiple organisms were found there was little, if any, attempt made to discover if more than one organism was involved in the degenerative process. The reason these multiple infections have been rarely detected is because it is not yet standard practice to actively seek co-infective organisms. Infective organisms are traditionally sought one at a time. When one is found, the testing usually stops. This changed when a cause was being sought for Gulf War Syndrome because the syndrome could manifest as any one of a number of illnesses. Many of the troops returning from the first Persian Gulf war became ill before or after returning home. The illnesses varied in type, duration and intensity but many were chronic, degenerative, of unknown origin, poorly understood and usually untreatable. The previous sentence more or less describes ALS/MND. Dr's Garth and Nancy Nicolson in California found many Gulf War veterans with a variety of diseases (including ALS/MND) had unexplained mycoplasmal infections. With improving diagnostic techniques, including specialised polymerase chain reaction (PCR) assays, they were finding hitherto hard to detect organisms throughout the body in places they should not have been able to proliferate. If mycoplasmas could set up camp in hostile territory could the same be true of other organisms? On the opposite side of the USA there were similarly disturbing revelations regarding tick borne diseases, particularly Borrelia burgdorferi infections, or Lyme disease (named after a town where infections were common). Lyme disease can manifest in many ways after passing through the acute initial stage. Alarmingly, one of the manifestations of borrelia infection was neuroborreliosis, similar to ALS/MND in everything but name. Of particular interest was the incidence of co-infections including Babesia and Erlichier that were commonly found in patients infected with Lyme/Borrelia. On the other side of the world I had independently concluded from my own research that the single organism/stressor/toxin explanation simply did not fit the aetiology of ALS/MND as I understood it. The questions I had posed myself included the following:
The "single cause" theory does not adequately answer any of these questions but a co-infective or "cascade" theory does. My reasoning is as follows: ALS/MND is a rare disorder, yet most of the research to date implicates relatively common organisms/stressors. This would tend to suggest that a near perfect set of unusual circumstances must exist to enable common organisms/stressors to produce such an uncommon outcome. The outcome, in this case ALS/MND, is so uncommon that simple statistical odds would tend to rule out a "one + two = ALS/MND" formula, hence my use of the word "cascade" or the domino effect. Stand domino's on end, in line and close enough to impact each other as they fall and a single (but possibly relatively inconsequential) event could potentiate a result far enough removed from the causal action to make "cause and effect" difficult to observe and research. One example (but not an explanation for the actual cause of ALS/MND) could be based around a common herpes virus. It can produce extreme ill health but can also exist in or around us and cause no problems. The bbb offers some protection against most infective organisms but herpes zoster causes chicken pox in its initial, acute phase and shingles often decades later because it can cross the bbb and remain dormant in the Central Nervous System (CNS) without ever causing further problems for its host. Given the right circumstances, usually when the host is run-down, stressed or aged, the virus can proliferate once again and cause the excruciating symptoms of shingles. Precisely how run-down or stressed the host needs to be seems to vary. Virtually every adult is host to several herpes viruses yet only some experience "cold sores", shingles or other symptoms of herpes infections. Even run-down and stressed individuals may never experience obvious, symptomatic herpes infections. It therefore seems likely that several "dominos" must fall before herpes symptoms result - and this is a common infection! The domino or cascade theory would explain a number of the "big" questions about ALS/MND. If no obviously unusual organisms have been located we either do not have the technology to find them or, more likely, we have observed known organisms but not the context and particularly the order in which they have affected our bodies. Part of the process may not have been infective. Toxins or trauma may "open the gate" or stressors weaken the body's defences so that common organisms can invade and take hold in uncommon ways. As a starting point again I questioned:
There are so many unknowns that the application of inductive rather than deductive reasoning seemed to be indicated. That would mean that an answer be assumed and the "facts" found to fit the assumption. So I assumed that the cascade theory was correct and therefore had to consider if:
As there was little published research on which to base these conclusions I had to depend largely on empirical and anecdotal evidence. Then I had to sort through seemingly endless research papers to find data to fit the jigsaw puzzle I was piecing together. The big problems were the lack of a "picture on the jigsaw-puzzle box" to refer to and never knowing if I had (a) all the jigsaw pieces (b) any of the correct jigsaw pieces or (c) pieces from entirely different puzzles mixed in. It was rather like picking lottery numbers but not knowing how many numbers to combine and where to register the ticket. This could explain why relatively little progress has been made by ALS/MND researchers in 150 years. One cannot win a lottery if one does not buy a ticket so I decided to reduce the odds a little. What data do we have? What do we know about ALS/MND, in general terms, that we can consider "fact"? We know the following:
In effect we only know a trifling amount about this illness and although this list, like the others is actually longer it only raises more questions than it answers. Fortunately, the situation is improving with current research into neurodegenerative illnesses. We know a great number of ways in which cells in the CNS are being killed but not why. I have communicated with literally thousands of people around the world whose lives have been directly or indirectly affected by ALS/MND. Correspondents have included professors, medical doctors, PhD's, researchers, PALS, carers, students and journalists. Many have expressed opinions or shared information regarding ALS/MND that has helped in supporting my own findings. Much scientific research has been (and by its very nature must be) extremely narrow and has added little to the broad view I have taken of the illness to form my hypothesis. A great deal is now known about how motor neurones die and what kills them. The answer we lack is why is this happening? What mechanism(s) allow neurotoxins to damage or impair motor neurones and other cells of the CNS? What I am left with is a simple theory with extremely complex implications. Chronic, degenerative illnesses, ALS/MND among them, are most likely caused by a co-infection. This co-infection is almost certainly "cascade" dependent. It could be that all PALS have a genetic predisposition to be afflicted with ALS/MND but it could also be argued that environmental stressors can affect us at a genetic level. Strands of DNA can be disrupted by radiation, toxins and, I believe, other factors. Repairing damaged genes may be one way to cure ALS/MND if we are either genetically destined or environmentally battered at the level of our DNA. It is far from an answer because the techniques to effect the appropriate repairs at this level are in their infancy. That said, we should not simply wait and do nothing. If ALS/MND is caused by a co-infection, what process, what set of circumstances allows this to happen? Some of the organisms that could be involved are individually "benign" or at least incapable of causing catastrophic neurodegeneration. Again using herpes zoster as an example: this virus is essentially benign until (a) the virus is stimulated into proliferating or (b) the host's immune system is incapable of suppressing viral replication. It is possible that both (a) and (b) are correct. Herpes viruses have been implicated in neurodegeneration but given that every adult probably has several viable herpes viruses dormant in their body, it seems unlikely that herpes alone causes the neurodegeneration of ALS/MND. Let us allow that herpes could cause catastrophic neurodegeneration. Of the billions of people who carry these viruses why do only 2 - 5 in 100,000 get ALS/MND? The virus does not appear equipped to do that sort of damage unaided. At least one other factor must prompt its proliferation and this would normally result in a known herpes clinical symptom. What if some other organism takes over where herpes (or other viral infection) leaves off? The virus alone causes predictable symptoms and the "other" organism alone causes predictable or subclinical symptoms. What if the two acted together? A particular set of circumstances has allowed (for this example) herpes to proliferate and migrate yet remain asymptomatic. The second organism somehow now has unimpeded access to the CNS. Both organisms may not produce any clinical symptoms but could make several things possible:
These scenarios provoke further speculation. If two known organisms could potentially cause any or all of the above (plus other possibilities I have considered but not included here) imagine what two poorly understood infective agents could do. A spirochete and a mycoplasma would be an example. We are only just beginning to understand the infective and other potentials of either and are barely able to reliably locate and identify these organisms. So far, this hypothesis is more question than answer so I shall use the borrelia (Lyme disease) spirochete and a mycoplasma to further the explanation. Individually, either could cause the symptoms of ALS/MND but once again, both are common (almost certainly more so than conventional medicine currently accepts) so why the low incidence of ALS/MND? Like the various "single organism" hypotheses, we return to "why only 2 - 5 in 100,000?" The neuro-destructive potential of borrelia and a mycoplasma combined could be significant. These (or other) organisms combined could explain why ALS/MND is statistically rare. I will go further and propose that medical statistics would make even more sense if the combined organisms were responsible for several chronic, degenerative illnesses. Depending on where the organisms proliferate, just two in combination could be responsible for many of the currently described, diagnosed but incurable illnesses that (when broadly compared) have certain things in common. Diseases as disparate as Lyme and AIDS can cause neurodegeneration, sometimes resulting in symptoms that bear far more than a passing resemblance to ALS/MND. I expect the preceding statements to provoke cries of derision from neurologists and most conventional researchers. I agree, the statements are not based on solid, irrefutable scientific evidence but that is because much of the necessary data are still unavailable. The reason the data are unavailable is because, as has been unkindly suggested, "PhDs study more and more about less and less". This concentration on and specialisation in minutiae has led to numerous significant scientific breakthroughs but this methodology has its limitations. Often, only when the "minutiae" can be placed into a broader context is their significance appreciated. What I am attempting to do here is to take admittedly limited data and view them in a broader context. The context I propose we explore is that many chronic, degenerative illnesses may be caused by similar processes and possibly even the same organisms - but sequentially and in combination. Because I do not yet have hard data to support this, it must remain hypothetical. The concept of E=mc2 was pure conjecture long before it was mathematically and later empirically proven. I lack the mathematics but believe the empirical evidence may already exist if it is more widely researched. In its early stages ALS/MND is diagnosed by ruling out other illnesses that could cause the neurodegeneration observed. I do not believe that reliable testing for mycoplasmal and borrelia infection is currently part of that reductive, diagnostic process. Reliable testing for borrelia usually reveals the presence of other parasitic organisms, which may include babesia and erlichia. The same may be true of reliable mycoplasmal testing. More than one mycoplasmal species may be present (I believe but cannot confirm that this is often the case). Prions may well be a vector for other infectious organisms to enter the CNS or other organs in the human body. Neurologists diagnosing ALS/MND do not routinely order these tests. The cost of all this "extra" testing, as it would be deemed at present, would be significant but compared to the incalculable cost of suffering from ALS/MND and caring for that person for even two years, it is minimal. If even the potential causal organisms could be agreed upon I believe this testing should be done for all people as soon as they are diagnosed with ALS/MND. The very rarity of the illness statistically makes it a veritable diabolical lottery. I believe this is a major clue. If several potential organisms can cause ALS/MND then the odds of 2 - 5 in 100,000 could point to the number of potential organisms and or stressors involved. I believe the minimum number of factors involved in a cascade illness would be at least three. If correct, it would bear out my hypothesis that a stressor "opens the door" and co-infective organisms are then able to enter the CNS in neurodegenerative illnesses and other organs or systems in other degenerative illnesses. This will be outlined in my conclusion. Environmental Stressors The list of potential environmental toxins (ET's) is long but includes organophosphates (insecticides and fertilisers) heavy metals, some of which are found in dental amalgams (particularly mercury) formaldehyde (from off-gassing of plastics and furnishings, agricultural applications and preservatives) and even aspartame (the sweetener in most "diet" food and drinks) numerous petrochemicals (in paints, solvents, man-made fibres, plastics, furnishings, electrical goods, etc.) food preservatives, aerosol propellants, perfumes, antiperspirants, industrial and household cleaning products, vehicle exhaust fumes, industrial wastes, cigarette smoke, polluted water/air/soil and so on. Entire websites and books are devoted to Environmental Toxins and are worth consulting. There are also mycotoxins produced by fungi/moulds. Mycotoxins are so powerful that they can kill the most virulent bacteria, hence their use as antibiotics. Other mycotoxins are capable of killing much larger organisms, including human beings. Some mycotoxins are among the most powerful of carcinogens. Moulds and other fungi are such an integral part of our lives that we are exposed to them daily via many grain products, damp rooms, mouldy foods and even yeasts in and on our own bodies. Some of these moulds and fungi are potentially beneficial or at least benign but many produce unhealthy mycotoxins. Then there are other environmental stressors, among which are exposure to electromagnetic radiation from power supply lines, industrial and household appliances including the computer that you are probably reading this on. To finalise this far from complete list there are other stressors: the foods we eat, lifestyle choices, excessive alcohol consumption, dental and personal hygiene, physical and psychological trauma, depression, anxiety indeed, chronic stress of any kind. This list should include physical trauma. Depending on the type and severity of the accident or surgery it is relatively easy to extrapolate the potential stresses and stressors that individually or in combination could have long term consequences. Accidents and surgical procedures, especially those that expose cerebrospinal fluid and breach the protective bbb, could be primary stressors. Any surgical procedures could act as stressors in numerous ways: hospitalisation, anaesthesia, post-operative pain and medication are individually and collectively stressful. Accidents could similarly include the stress of shock, pain, medication, rehabilitation and convalescence. Each may lead to stressful loss of income, reduced socialisation and unsettling change of routine. As the majority of people in western societies are occasionally, even frequently exposed to many of the potentially unhealthy toxins and stressors mentioned, if a single factor unaided were responsible for the illness one would expect to see a far higher rate of ALS/MND. Statistics do not support this but, importantly, do not rule out the involvement of ETs in the process of neurodegenerative illnesses. It could be claimed that there is a far higher incidence of neurodegenerative illness in western societies. It could also be argued that neurodegenerative illnesses remain undiagnosed or unrecorded in developing countries. Many scientists believe the incidence of ALS/MND is increasing, though some feel this may be due to improved understanding of the illness and better diagnostic techniques. Even by their reckoning, ALS/MND still only affects about 7 - 8 people out of every 100,000 and statistically that still makes single-factor causality unlikely. A set of statistically rare, sequential circumstances that allow access and damage to the protected CNS of an otherwise healthy human being seems more probable. Another striking anomaly is the number of active, generally healthy and positively athletic people diagnosed with ALS/MND. Dennis Dowd noted this anomaly and has explored the incidence of PALS exposed repeatedly to organophosphates. Athletes figure highly in this category as many train and play on grass that has been maintained with the aid of organophosphates. His research is ongoing and a preliminary paper appears on this website. Ronald J Swanson independently published "E Coli 0157 - The Main Cause of Neurodegenerative Disease", a long overdue statistical evaluation of ALS/MND distribution in the USA. He also noted a possible connection between the bacteria, Escherichia coli and a number of other chronic, degenerative illnesses including lupus, rheumatoid arthritis and several neurodegenerative illnesses. Ronald Swanson presents a cogent argument that, statistically, shiga toxins produced by E. coli, could be the primary cause of neurodegeneration. Particularly interesting to me is that he independently acknowledged that ET's, genetic factors and co-infections could also be implicated. I would recommend that this article be widely read by both researchers and PALS. Dr Martina Berger implicated Echo and Entero viruses as a possible cause of ALS/MND. These viruses should find it difficult to cross the bbb but were found in the CNS of PALS. Antiviral medications may therefore be of use in destroying these viruses but only if these antivirals can also cross the bbb. If echo and entero viruses can infect the CNS and induce the production of neurotoxins or otherwise damage motor neurones, it is my belief that other viruses may be able to do the same. The infective, "misplaced virus" itself may not be as important as its mere presence in the CNS. This alone may be enough to cause production of neurotoxins. It may also explain why the illness can progress in several different ways and at different rates. The presence of entero viruses, normally found in the Gastro Intestinal (GI) tract, in the CNS may be one of the reasons I have so frequently recorded abnormal liver function in PALS. Perhaps an elevated viral load in the digestive system would be required to facilitate CNS infiltration and this would impact liver function? Standard liver function tests may sometimes fail to reveal liver dysfunction until up to 50% of the liver has been affected. Broader, more accurate liver function testing and more holistic observation of symptoms that could be due to liver dysfunction would almost invariably confirm abnormal liver function in all PALS. Proliferation of enteroviruses, E.coli or other infective organisms would stress liver function. If the infective organism alone were less important than the process, or sequence of the infection, this would explain a great deal. Any infective organism in the CNS could potentially cause the production of neurotoxins either directly (example only: E.coli produces shiga toxins) or as a result of the immune response creating neurotoxins as a by-product as infective organisms are destroyed. The type, the potency and the rate at which toxins are produced could be a direct mathematical/logical derivation of the type of organism, the infective load and each person's efficacy of immune response. These variables could explain the differing manifestations and low incidence of ALS/MND, the differing rates of neurodegeneration and more.
Far from suggesting that virtually anything can cause ALS/MND I am proposing that the elements required to facilitate, provoke and maintain a neurodegenerative process can be readily observed and traced if a co-infective or cascade hypothesis were used as the basis for ongoing research. A single drug did not cure AIDS but a drug cocktail has achieved complete remission in many patients. The "cascade" of medications, one enhancing the effect of another, can stop the HIV proliferating and even enable patients to become asymptomatic. This was discovered because standard treatment protocols were not followed. An explanation of why this drug cocktail worked was less important than the overwhelmingly beneficial results. If the same approach could be taken for PALS and several potentially causal factors treated at once we may start to achieve positive results. Dispense with the double blind placebo trials when treating "terminally ill" volunteers (which I believe to be both morally and even scientifically flawed) and observe the efficacy of various "cocktails". A cocktail may differ for various types of PALS. Each PALS should be tested for the presence of heavy metals and environmental toxins, for example (ie immune system inhibitors) then tested for the presence of the most likely infective candidates, be they viral, bacterial, mycoplasmal or parasitic. If the immune system is inhibited or the bbb breached, the presence of two more organisms (particularly in the CNS) could cause neurodegeneration - or other illnesses in cases where the CNS is not involved. Impossible! Is it really? It will certainly be difficult to devise and monitor initially but as more data are gathered from specialists treating the various chronic, degenerative illnesses I am convinced that a pattern will emerge. The habit of compartmentalising and strictly separating what I believe to be a number of related, degenerative illnesses with differing symptoms (but similar causal factors) has stopped western medical science in its tracks. Western medical methodology has failed us so far. The approach taken in holistic, naturopathic, traditional Chinese, Ayurvedic and other "non- traditional" (perhaps I should say "more traditional"?) medicine is to treat the patient, not just the symptoms. These forms of medicine undoubtedly have their limitations but in the case of ALS/MND so does conventional western medicine! Integrative medicine uses the best of both approaches. Naturopathic/holistic and conventional western techniques are used. Informed ALS/MND researchers could take a similar approach. I know, from personal experience, that research funding is difficult to obtain. Often funding is provided to the researchers most likely to produce a profitable end product (ongoing treatments are therefore preferred to permanent cures). Funding for "pure science" is restricted and restrictive. Few branches of research, using the strictly exclusive, reductive protocols of western medical research would expect to be awarded a grant for multi-factoral investigation. AIDS researchers not dependent on this type of funding were therefore able to cast a wider net and within a relatively short time had a working drug cocktail to inhibit the HIV infection. With the infection thus slowed, attention can now be directed to a full cure. I am sure the majority of PALS would be happy with remission until a cure could be found but, as we know, ALS/MND does not have the same public profile as AIDS and therefore lacks that source of funding. It need not lack that type of thinking and open minded approach to research. Current Treatments To further complicate the picture, both known and also unobserved or co-infective organisms may be killed by a high dose, broad-spectrum antibiotic treatment. Also, it has been abserved that amyloid fibres form plaques in the CNS that could potentially protect bacterial and possibly other organisms from antibiotics. Antibiotic therapies are required in relatively high doses and are most effective when administered by injection - intramuscular or intravenous. This requires vigilant supervision because high dose antibiotics may cause unwanted side effects and such treatments can cause severe Jarisch Herxheimer reactions (abbreviated to JH or Herx). JH reactions occur as organisms are killed off en masse. When this occurs the body has trouble clearing the resultant cellular detritus and an acute immune response results. The symptoms can vary but often include symptoms of the original acute infection plus nausea, joint pains, headaches, etc. These symptoms can be severe enough to dissuade patients from continuing the treatment. As the treatment is typically long term it has been recorded that the JH reaction "cycles" and flares-up monthly after commencing treatment - but each JH reaction should be reduced as the infective load decreases. Bacteriophages These phages are cheap and, once isolated, relatively easy to produce and have been used for decades in Georgia (ex USSR). Their successful use even predates that of antibiotics. (Although some bacteria produce restriction enzymes and are therefore resistant). Western drug companies and practitioners have remained suspicious of and unconvinced that bacteriophages work as claimed. This may be due to the drug companies' need to generate substantial profits. Such profits cannot be made from existing phages so their introduction into Western medicine is unlikely to be encouraged - especially as phages will potentially compete with the extremely lucrative antibiotic market. The potential of phages to "seek and destroy" recalcitrant bacterial infections is enormous. If Borrelia/Lyme and/or mycoplasmas are factors in the process that leads to neurodegeneration in ALS/MND, phages may have the potential to help cure the illness. Bacteriophages have been successfully and repeatedly used to combat "golden staph" (staphylococcus aurea) infections that are resistant to all but a single, last resort, antibiotic. When golden staph eventually becomes resistant to even that last line of antibiotic defense, as it almost surely will, we may begin to see bacteriophages routinely used in western hospitals instead of just for the veterinary applications they are restricted to by most western medical governing bodies. There are numerous papers to support the use of bateriophages but because they were not written in English or translated and published in the approved journals they have been unfairly (irrationally?) ignored or even discredited. With any luck, this will soon change and a new weapon added to the slowly growing arsenal of potential treatments for ALS/MND. Flagyl and tinadazole is used to treat babesia and other parasitic organisms. It is believed that these parasitic infections must be eliminated before the mycoplasmas and borrelia can be treated effectively. This type of finding supports my hypothesis. My Regimen A Comment on Stem Cell Therapy Stem cells may be used to repair or slow the effects of neurodegeneration but they do not offer a cure for what causes that degeneration. Perhaps certain stem cell therapies will be developed to outpace the rate of neurodegeneration and thus make a cure, per se, less urgent but I do not believe this will be the case. It is likely that the accepted practise of narrowly studying only motor neurones means that many researchers are overlooking disease or dysfunction of apparently uninvolved surrounding cells. Without healthy cells to constantly communicate with motor neurones, apoptosis (programmed cell death) can occur. To me it seems likely that motor neurones remain relatively healthy until their surrounding cellular environment is compromised. "Turning off" surrounding cells is like breaking an electrical circuit (but not the same as turning off the electrochemical communication that allows neurones to function). With general "cellular conversation" interrupted, the motor neurones simply "rust" through lack of use, as has been observed in the form of neuronal oxidation. [Dr Polly Matzinger's "Danger Theory" as to why transplanted organs are rejected and how apoptosis is involved explains this need for surrounding cellular communication]. It is ultimately better to treat the cause rather than the symptom. With ALS/MND the alarming "symptom" is that motor neurones cease to function, so it is understandable that the focus has been on attempting to correct that symptom as soon as possible. Much conventional western medical research targets treatment of symptoms rather than cause. Drug companies only profit from treating symptoms rather than curing diseases. By actually curing an illness they destroy their own market - yet many neurologists simply wait for drug companies to provide a cure... There are numerous references for the topic of stem cell therapy, many of which can be found via the reference link below. Conclusion This infective agent may exist as a dormant organism within the body or may be acquired and allowed to proliferate unchallenged within the body. Precisely where the organism proliferates is most likely dependent on the concurrent presence of another organism or stressor. The number of variants on this process should be three factorial (ie 3x2x1=6) for example:
Instead, physical trauma, genetic predisposition, genetic damage, unknown organism(s), allergy or other factors may substitute for one or more of the above. The equation would still work but a cascade would still be necessary for a resultant illness to occur and progress as ALS/MND does. Another possibility is that four factors are involved (4x3x2x1 = 24 possible combinations). I do not believe this is the case but it cannot be entirely ruled out. Two causal factors alone (2x1 = 2) would not provide sufficient statistical variation to explain the low incidence of ALS/MND and the differing manner in which it progresses. It would also tend to rule out the idea that other degenerative illnesses are variant results of the same cascade process. A four step cascade starts to provide so many variables that it could apply to an immense number of illnesses: I am proposing that only chronic, degenerative illnesses result and that one of these results is ALS/MND. A three step cascade would facilitate this and a fourth variant (age, general health, free radical load, etc.) would not be causal but could further affect the rate at, or the manner in which the illness progresses. Given the above, it seems most likely that a pair of co-infective organisms trigger (or are triggered into proliferating by) a third factor, be it ET, trauma or something else mentioned. I believe that mycoplasmal, viral or parasitic infection could be the "primary" factor, ET's could "open the door" by weakening or even directly injuring the Immune and/or CNS and a third (but very likely quite common) organism or factor could supply the final domino in the cascade that I think is the cause of ALS/MND. Existing research could provide the data required to isolate the factors involved and possibly even the order in which they interact. Working alone, largely unfunded and limited by injury and illness it is extremely difficult for me to prove or even test my own hypothesis. With sufficient funding and assistance I might be able to do so but I am hoping that by sharing my ideas here, somebody will be able to follow through and use the concept to further ALS/MND research. Steven Shackel References: Numerous scientific references for the majority of what is discussed in this article can be found at or via the ALS Theory and Development Institute Alphabetical Contents List
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