The man with a new idea is a crank until the idea succeeds.
Mark Twain

In my opinion, the following article is one of the more significant findings in ALS/MND research for many years. Although this has been predicted on this website and elsewhere, this is the first scientific paper supporting the hypothesis.

Cell Environment's Important in ALS
Don Cleveland and Larry Goldstein, The Packard Center for ALS Research at Johns Hopkins Journal: Science 10.2.03

Cells that surround motor neurons, that aren't themselves nerve cells, can play a major role in advancing or limiting the disease.

A principle for extending survival or, perhaps, overcoming ALS, based on how many healthy cells surround an ailing motor nerve cell. Delivery of normal, non-neuronal cells to spinal cords, including stem cell therapies could prove completely protective, even without replacement of motor neurons.

In animal tests, although 75% of the motor neurons in spinal cords carried the mutant gene SOD1 (a known cause of familial ALS) all the motor neurons remained healthy, apparently from having healthy non-neuronal cells nearby.

A small number of normal cells effectively eliminated damage to motor neurons from the ALS-causing genetic error. The opposite effect also appeared: normal motor neurons surrounded by cells carrying an SOD1 mutation showed early signs of disease. Normal neurons can apparently acquire something toxic from at-risk non-neuronal neighboring cells.

A bad cellular environment can damage healthy cells. More importantly, surrounding neurons with healthy adjoining cells can significantly lessen toxic effects. In some cases, having normal cells completely stops motor neuron death.

I believe this is a significant hypothesis that is consistent with my own theories as to what causes ALS/MND.

Hypothesis: A motor neuron toxin produced by a clostridial species residing in gut causes ALS 

We hypothesize that a yet-to-be-identified motor neuron toxin produced by a clostridial species causes sporadic ALS in susceptible individuals. This clostridial species would reside undetected in the gut and chronically produce a toxin that targets the motor system, like the tetanus and botulinum toxins.

After gaining access to the lower motor neuron, the toxin would be transported back to the cell body, as occurs with the tetanus toxin, and destroy the lower motor neuron - the essential feature of ALS. Again like the tetanus toxin, some of the toxin would cross to neighboring cells and to the upper motor neuron and similarly destroy these motor neurons. Weakness would relentlessly progress until not enough motor neurons remained to sustain life. If this hypothesis were correct, treatment with appropriate antibiotics or antitoxins might slow or halt progression of disease, and immunization might prevent disease

Longstreth WT Jr, Meschke JS, Davidson SK, Smoot LM, Smoot JC, Koepsell TD. Department of Neurology, School of Medicine, University of Washington, Seattle, Washington, USA; Department of Medicine, School of Medicine, University of Washington, Seattle, Washington, USA; Department of Epidemiology, School of Public Health and Community Medicine, University of Washington, Seattle, Washington, USA. Med Hypotheses. 2005;64(6):1153-1156.

Increased mitochondrial oxidative damage and oxidative DNA damage contributes to the neurodegenerative process in sporadic ALS.

A study involving 17 patients with sporadic ALS revealed the percentage of oxidized coenzyme Q10 and the concentration of 8-OHdG in the cerebrospinal fluid (csf) of the PALS was significantly greater than that found in 17 age-matched controls. The percentage of oxidized coenzyme Q10 in the csf was inversely associated with the duration of illness and the concentration of 8-OHdG in the csf was positively associated with the duration of illness.

The percentage of oxidized coenzyme Q10 was associated with the concentrations of 8-OHdG in the csf of PALS. The authors, who had set out to investigate whether mitochondrial oxidative damage or oxidative DNA damage contribute to the neurodegenerative process of ALS, conclude, "…both mitochondrial oxidative damage and oxidative DNA damage play important roles in the pathogenesis of sporadic ALS.
Murata T, Ohtsuka C, Terayama Y, Free Radic Res, 2008; 42(3): 221-5. (Address: Department of Neurology, Iwate Prefectural Ninohe Hospital, Iwate, Japan).

Is Inflammation Part of the Neurodegenerative Process?

Inflammation can enable our bodies to fend off various disease-causing bacteria, viruses and parasites but the immunological defence mechanism that causes swelling and turns the tissue around a splinter red can sometimes become chronic and damaging.

When potentially harmful microbes enter the body, inflammation destroys both invader and any tissue it may have infected. The process then subsides and healing begins but sometimes the inflammatory response does not shut down on cue.

A cascade of events is triggered whenever the body is subjected to trauma or injury. When a splinter enters your finger, specialized sentinel cells alert the immune system to the presence of introduced bacteria. Mast cells release histamine to make nearby capillaries leak small amounts of plasma, slowing invading bacteria whilst assisting other immune defenders. Meanwhile, macrophages release cytokines, which call for reinforcements. Soon, immune cells flood the site, destroying pathogens and damaged tissue.

This generalized response to attack is called “innate immunity”. Animals as primitive as starfish defend themselves this way. Higher organisms have a more precision-guided defence system that directs and intensifies the innate response and creates specialized antibodies to target specific bacteria and viruses. Working in tandem, the innate and learned immunological defences fight until invading germs are annihilated. Finally, a wave of cytokines is released, the inflammatory process recedes and healing begins.

A genetic predisposition and things like smoking or high blood pressure may keep the process going so that inflammation becomes chronic rather than transitory. When that occurs, the body turns on itself with after effects that may underlie a wide variety of diseases.

Inflammation destabilizes cholesterol deposits in coronary arteries, and may lead to heart attacks and strokes. It destroys nerve cells in the brains of Alzheimer's victims and may even cause abnormal cells to become cancerous. Chronic inflammation may provoke many illnesses of middle and old age and it is therefore likely that a single, inflammation-reducing remedy may prevent disparate diseases, including colon cancer, Alzheimer’s and possibly ALS/MND.

There is a complex interplay between inflammation, insulin and fat, either in the diet or in large folds under the skin. Fat cells can behave similarly to immune cells, producing inflammatory cytokines if one becomes overweight. Whether inflammation is a cause or an effect remains unclear but the case for a central role is getting stronger. Dr. Steve Shoelson of the Joslin Diabetes Center in Boston, has bred mice with fat cells that cause inflammation. These mice become less efficient at using insulin and develop diabetes following induced inflammation.

Some chronic inflammation may be beneficial but anti-inflammatory drugs are still being tested to see if they have broader benefits.

Celebrex, originally designed to treat inflammation in arthritis, reduces the development of intestinal polyps, precursors to cancer. Dozens of clinical trials of Celebrex have tested if it can also prevent breast cancer, delay memory loss or slow the progression of ALS/MND.

Chronic inflammation indicates that we may have become victims our own success as a species because of our ability to fight off microbial invaders. Now that we live longer, those inflammatory strategies cause problems because the Western lifestyle, typically including a diet high in sugar and saturated fats, coupled with insufficient exercise, make it easier for the body to become overweight and inflamed.

You will see from above that lipid (fat) metabolisation and digestion, stress and diabetes, all identified in my research as potential factors in the neurodegenerative process, are mentioned.

The therapeutic potential of poly (ADP-ribose) polymerase inhibitors.
Source: Pharmacol Rev 2002 Sep;54(3):375-429 Author(s): Virag L, Szabo C. Institute: Inotek Pharmaceutical Corp., Beverly, Massachusetts 01915, USA. Published: 09/01/02

Mitochondrial diseases result from failures of the mitochondria, specialized compartments present in every cell of the body except red blood cells. Mitochondria are responsible for creating more than 90% of the energy needed by the body to sustain life and support growth. When they fail, less and less energy is generated within the cell. Cell injury and even cell death can follow. If this process is repeated throughout the body, whole systems begin to fail, and the life of the person in whom this is happening is severely compromised. The disease primarily affects children, but adult onset is becoming more common.

Mitochondrial defects have been linked to Alzheimer's, Parkinson's, diabetes, autism, and the ageing process.  Diseases of the mitochondria appear to cause the most damage to cells of the brain, heart, liver, skeletal muscles, kidney and the endocrine and respiratory systems.

Depending on which cells are affected, symptoms may include loss of motor control, muscle weakness and pain, gastro-intestinal disorders and swallowing difficulties, poor growth, cardiac disease, liver disease, diabetes, respiratory complications, seizures, visual/hearing problems, lactic acidosis, developmental delays and susceptibility to infection.

Mitochondrial dysfunction and reactive oxygen species in excitotoxicity and apoptosis: implications for the pathogenesis of neurodegenerative diseases. Rego AC, Oliveira CR. Neurochem Res. 2003 Oct;28(10):1563-74.

This is one of the first areas I researched when I started publishing this website. I believe such research is extremely relevant to ALS/MND.

Mitochondria 'Clogged' In ALS/MND

There is evidence that damage to nerve cell powerhouses (mitochondria) is directly responsible for that cells' death. Dysfunctional proteins clog the transport system that brings vital substances into mitochondria, the tiny organelles that provide energy to cells. This mitochondrial damage occurs in muscle-controlling nerve cells, helping explain the selective nature of cell death in (ALS). Mitochondria don't look normal in motor neurons in animal models of ALS and PALS and it was already known that abnormal mitochondria make neurones susceptible to injury from an excess of the chemical transmitter glutamate

Inherited ALS is caused by mutations in the superoxide dismutase (SOD1) gene, an enzyme that cleans toxic molecules from cells. Researchers discovered that the outer mitochondrial surface was clogged with mutant SOD1 protein in spinal cord nerve cells but not in other tissues. It is possible that the way mitochondria work in muscle-controlling nerves might be different from the way they work in other cells.

That could explain why only motor neurones’ mitochondria are damaged and die, even though every cell in an animal or person with inherited ALS carries the instructions for the mutant SOD1. It is possible that mitochondria are also involved in the common forms of ALS and other neurodegenerative diseases. Damaged mitochondria cause many problems and could cause the cell death.

For unedited article: Dr Jeffrey Rothstein, et al journal “Neuron” July 9 2004.

Researchers, led by Dr. Jeffery Elliott at UT Southwestern discovered bright red spots, or aggregates in the mutant protein SOD1, trigger the death of motor neurons in spinal cells of mice.

Isolating the exact portion of the molecule that induces aggregate formation is one of the things that may help find a cure for the disease. When the SOD1 protein mutates, all other organs in the body except the spinal cord can handle it .

The liver has a high capacity to get rid of this thing so researchers are looking into why the liver is not affected and motor neurons are. The research team have focused on how other organs process the mutant SOD1 protein and, after trying chemicals found in other organs and not found in motor neurons, they discovered mice spinal cords growing in the cultures in their labs.

After creating the aggregates in these culture slices they can now remove those aggregates by treating them with chemicals that removed the aggregates in the mutant protein known to cause ALS in mice.

This is an indication that the nervous system can repair itself and can remove these protein inclusions.

There is still much work to do to prove the discovery will reverse ALS in humans. The next step is to test a live animal and see whether it can reverse the aggregates and the disease itself.

If the experiments in live mice prove successful, human trials could be under way in less than two years. In addition to ALS, researchers at UT Southwestern have discovered the mutant SOD1 protein is also found in Parkinson's disease, Huntington's disease and Alzheimer's disease.

n.b. Dr. Elliot's discovery is not specific to the SOD gene. The discovery involves the SOD protein, not the SOD gene. The SOD protein most likely plays a major role in both familial and sporadic ALS. The difference is that in familial ALS, we know that the mutant SOD gene is causing the mutation in the SOD protein. In sporadic ALS, the cause of any protein mutation is unknown, but it is still very likely the SOD protein is mutant.

Oxidative stress plays probably an important role in the etiopathogenesis of ALS. It is known that bilirubin (BR) is an endogenous antioxidant...The study showed that serum BR concentration is significantly decreased in ALS patients with a long duration of ALS compared with patients with a short duration and it is also significantly decreased in ALS patients with a moderate clinical state compared with control group patients...

Results suggest a possibility of endogenous antioxidant system dysfunction in later phase of ALS. A decrease in BR concentration might diminish its protective effect against oxidative injury and could accelerate motor neuron degeneration.

Link to Stem Cell FAQ Website

Use of Adult Stem Cells to Make Neurons

This is one of the most promising areas of research pertaining to neurodegenerative and other chronic illnesses. Human umbilical cord trials to treat ALS are being conducted by Dr. Norman Ende, a faculty member at the UMDNJ - New Jersey Medical School. He is the principal investigator of the studies in this area and his office may be able to offer further details on upcoming trials.

His telephone number is (973) 972-4792 or write a letter to: Dr. Norman Ende, Univ. of Medicine & Dentistry of NJ, 65 Bourbon Street Room, 1528, University Heights Newark, New Jersey 07107-3001.

Dr. Ende said, that most Doctors are afraid to be the first one to start stem cell therapy for ALS patients, but he is not. If PALS and CALS write to support his work and let it be known that we want and need stem cells for PALS it will help in obtaining approval for trials. This support must be in writing - do not telephone.

The Journal of the American Medical Association published a report in which researchers used stem cells to cure an ALS-like disease.

Drs Gearhart and Kerr from Johns Hopkins University cured an ALS-like disease with a stem cell transplant
From The Journal of the American Medical Association JAMA April 4, 2001-Vol 285, 1691-1693

A group of rats were injecting with a virus that killed the spinal cord motor nerve cells that control muscles in the legs. Stem cells were then injected into the spinal fluid that surrounds the spinal cord. These stem cells migrated through several layers of tissue into the injured spinal cord and then replaced the dead nerve cells and began to function like normal nerve cells. The rats were again able to walk.

Stem cell research is in its infancy and many problems must be overcome before it can be used generally but this finding will encourage many scientists in this new field.

Lynn Myers MD is a pathologist and serves as Director of R&D for NuCare. He is also the author of "Creatine Answers for ALS"

Bone Marrow-Derived Stem Cells May Aid in Treating ALS/MND

Four months after transplanting Bone Marrow (BM) stem cells, investigators analyzed the animals' bone marrow, brain, spinal cord, heart, and skeletal muscle tissues for the presence of newly generated neuronal cells and found that the transplanted animals showed high levels of BM stem cell reconstitution.

All tissues derived from the ALS mice contained more newly generated neuronal cells than those derived from their non-transgenic littermates. In the transgenic mice's forebrain and cerebellar cortices, the number of such cells was five times greater than that of the corresponding areas of nontransgenic mice

Based on these findings, it was concluded conclude that BM-derived stem cells contribute to the regeneration of both CNS and striated muscle tissues in certain animal models of ALS/MND and that ALS/MND may therefore affect other organ systems beyond CNS.

These findings are highly preliminary and human trials will not be undertaken for some time (May 2003).

As a patient's own DNA could be used to create the new cells there would be no risk of rejection by the immune system. Transplanting cells grown by this method directly into the brain could replace cells damaged in accidents and many neurodegenerative illnesses, including ALS/MND. This treatment is unlikely to be available for several years. 

Abnormal accumulation of two common lipids in motor nerve cells could play a critical role in the development of ALS, according to investigators at the National Instituteon Aging (NIA. The finding could help scientists develop drugs and other treatments that might one day slow or arrest the disease's progression.

NIA scientists unearthed several new clues through a complex, multi-step investigation. After comparing spinal cord tissue extracted from people who had ALS with those who didn't, the investigators discovered that levels of ceramides, cholesterol esters and several other lipids were significantly elevated in the spinal cords of people with ALS.

To test whether these elevated levels of ceramides, a cell wall component, and cholesterol esters, a form of cholesterol, cause motor neuron degeneration associated with ALS, the investigators studied mice with copper/zinc-superoxide dismutase (Cu/Zn-SOD), incorporated into their genome. As in humans, analysis of the spinal cords of these animals revealed increased levels of ceramides and cholesterol esters.

To determine what might cause these abnormalities in lipid metabolism, investigators exposed mouse motor neurons to free radicals because previous studies suggested that increased production of oxygen free radicals is involved in the onset and progression of ALS. As a result, ceramides and cholesterol esters are increased in the exposed cells, just as was found in motor neurons affected by ALS.

Experiments were conducted to determine if accumulation of ceramides and cholesterol esters in these neurons could be blocked when treated with a drug called ISP-1. The drug prevents the formation of large membrane molecules called sphingolipids, which produce ceramides. When exposed to oxygen free radicals, motor neurons treated with ISP-1 did not accumulate ceramides and cholesterol esters, nor did they degenerate. Untreated motor neurons that were exposed directly to ceramides did deteriorate.

Ceramide accumulation appears to be both necessary and sufficient to explain the degeneration of spinal cord motor neurons in ALS. This knowledge is now being used to develop drugs that potentially could prevent these abnormalities.

In addition to drugs, the NIA scientists are investigating whether changes in dietary intake of cholesterol and lipids involved in the formation of membrane sphingolipids might have an impact on an individual's susceptibility to ALS.

The relevance of this research to ALS/MND is that it further shows that infective organisms can and do penetrate the protective blood brain barrier (bbb) and directly impact nerve function. Dr Martina Berger has found enteroviruses in the Cerebro Spinal Fluid (csf) of a significant number of ALS/MND patients and Prof Garth Nicolson and others believe that mycoplasmas may also pass the bbb and attack the central nervous system (see Mycoplasma and this page for more information on this research).

I believe that many cases of ALS/MND may be the result of chronic infections of one or more organisms - cell wall deficient, bacterial and/or viral - that have passed the blood brain barrier. This could occur due to severe head or spinal trauma, including surgery, and may account for the high incidence of ALS/MND among PALS who have experienced spinal damage/surgery. Unfortunately statistical information on incidence of spinal trauma prior to ALS/MND dx is primarily empirical and varies widely.

Transgenic rats, which carry a human gene, have revealed the important role played by brain cells called astrocytes. The ALS rat moves from onset of symptoms through to ALS-like disability more quickly than ALS mice, making changes in cells in the rats more striking from day to day.

Scientists at Wyeth-Ayerst engineered the rats to carry an abnormal human gene for superoxide dismutase (SOD1), an enzyme that normally breaks down free radicals, highly reactive molecules that quickly damage DNA and kill cells. Faulty SOD1 behaviour, caused by a number of different genetic mutations, is at the root of roughly one-fifth of inherited ALS cases. The SOD1 rats, like the SOD1 mice before them, develop a disease very similar to ALS in humans, which is characterized by the death of motor nerve cells throughout the central nervous system.

So far, the new rat has revealed that specialized brain cells called astrocytes play a key role in the early steps of the disease. Astrocytes, which make up more than 50 percent of the brain's tissue, normally bridge the blood vessels and neurons in the brain. In these rats, before physical symptoms develop and for reasons unknown, the main transporter for the neuron-exciting messenger glutamate begins disappearing from the astrocytes.

Rothstein suggests the loss of the glutamate transporter may be a crucial initial step leading to the death of motor neurons, deaths that directly correspond to symptoms like limb paralysis. Glutamate overexcites neurons. The glutamate transporter in astrocytes helps maintain an appropriate balance of glutamate outside the neurons so these key brain cells aren't over-stimulated. When the transporter in astrocytes begins disappearing, glutamate builds up outside the cells and outside neurons, leading to glutamate toxicity.

"Our idea is that over-stimulation of neurons by glutamate can lead to the neurons' deaths, and we continue to uncover evidence supporting this hypothesis," says Dr Geoffrey Rothstein.

How mutant SOD1 directly injures a cell is still a mystery, but the rat model should help scientists determine how the faulty enzyme leads to disease. In the central nervous system of human patients and SOD1 transgenic mice and rats, globs of faulty SOD1 proteins are found. Scientists know that loss of SOD1 function isn't to blame for the symptoms of ALS; instead, the faulty enzyme picks up a new, still unknown, function. Finding the link between faulty SOD1 and the disappearing glutamate transporter should help clarify why the many SOD1 mutations appear in patients with inherited ALS and even in some non-inherited cases of the disease.

The AIDS virus could cause a type of ALS, which could be treated successfully with anti-retroviral drugs, according to the studies published in the magazine Neurology Magazine Research reinforces the idea that ALS/MND can have a viral origin. Many researchers suspect a virus, but evidence in this direction was merely circumstantial until AIDS related studies revealed a connection. See also Articles on this website.

More information on AIDS, HIV and advances in viral and retroviral research

Microglia are subcomponents of the immune system. They are located in the brain and spinal cord and usually perform beneficial functions such as clearing away dead cells after injury, nutritional support to neurons or attacking 'invaders' such as bacteria. The ALS Therapy Development Foundation believe that in ALS, microglia become altered and then for some reason refuse to shut down. Instead, they deviate from their normal function and go on to attack healthy neurons. A wide range of chemical signalling mechanisms can activate Microglia in the body.

Microglia are mobile and can activate other microglia in adjacent areas, causing the degenerative effect to perpetuate. They kill by releasing oxidants and glutamate, which might explain the finding of excess extracellular glutamate and oxidative stress that are so often mentioned in ALS literature. Conversely, oxidative stress or excitotoxicity could potentially be a triggering mechanism of microglia. Since microglia can be activated through so many pathways, it is imperative to test many different drugs, both individually and in cocktails, to establish the best way to inhibit destructive microglial activity.

Various studies directly or indirectly point toward microglia as the enemy. Specialized testing on SOD1 mice that express the mutated gene yield interesting clues about microglia. For instance, when the mutant gene is present only in neurons, the mice do not get ALS. When the mutant gene is expressed in astrocytes alone the mice also do not get ALS. Though the data are not yet conclusive, it suggests that the mice get ALS only when the SOD1 mutation is present in microglia. The interpretation of these results is open to debate but if these data prove correct a wide range of potential therapies could become available.

There is no question that mercury toxicity can cause neurodegenerative symptoms similar to ALS/MND. A debate as to whether mercury based amalgam dental fillings are the direct or indirect cause of ALS/MND still persists. Some researchers relate the first reported incidence of ALS/MND to the first use of amalgam fillings - both around 150 years ago.

Some advocate the removal of all dental amalgam fillings to prevent the possibility of further leaching of mercury and other toxins from the fillings into the systems of PALS and those suffering other neurodegenerative and chronic illnesses. Some PALS have had amalgam fillings removed and reported minor to miraculous improvement as a result. Other PALS have not improved and have even deteriorated further, and possibly faster, after amalgam removal.

The reasons for such widely differing opinions regarding amalgam fillings and their possible involvement in ALS/MND are many and complex. Removal of amalgam fillings can potentially liberate seriously toxic amounts of mercury as an airborne particulate when drilled from the tooth. This could be inhaled by both patient and dental staff with potentially disastrous results, as mercury is biologically toxic at extremely low levels.

This could explain the worsening of symptoms in some PALS who have had amalgams inexpertly removed. Any lack of improvement can be explained by the argument that mercury has already leached into and concentrated in different bodily organs, including the central nervous system, prior to amalgam removal.

If mercury is not the direct cause of ALS/MND (not everybody with amalgam fillings develops the illness) it can certainly be considered a significant physiological stressor. Anything that chronically stresses one's body must be considered a possible factor in the process of decreasing the body's natural ability to deal with opportunistic infections.

An analogy: A world class athlete may perform poorly when exhausted, stressed, distracted or ill. An average athlete will almost certainly perform poorly. As we age, our bodies are no longer "world class" and when stressed, exhausted, etc. will increasingly fail to fight off infections and neutralize and excrete toxins. Natural barriers and processes that exist to deny admission of pathogens to certain parts of the body may be compromised and become ineffective.

Athletes often become susceptible to infections when "overtrained" - Glandular Fever/Epstein Barre virus commonly infects otherwise healthy, young athletes when they are "stressed" or overtrained for extended periods. It is easy to imagine how long term exposure to a dangerous stressors such as mercury and other heavy metals can "overwork" the immune and central nervous systems. This could invite damage from even normally benign organisms, in addition to the short and long term damage of the mercury itself.

Mercury toxicity and the likelihood that mercury is released from dental amalgams is an incredibly complex and controversial topic.There are many websites, books and research papers that deal with mercury toxicity in depth. Some even deal with the possibility that ALS/MND is directly or indirectly caused by mercury poisoning. Most ALS/MND patients tested for immune reactivity (autoimmunity) using a test like the MELISA blood lymphocyte immune reactivity test are found to be immune reactive to mercury, showing this could be part of their problem.

The International Academy of Oral Medicine and Toxicology has information about mercury toxicity and describes safe protocols for the removal of dental amalgams.

Two opinions, one by Eric Edney and the other by Robert E. Reeves are presented below and there are numerous web pages that can be located by a simple word search on the internet.

Eric Edney's Answer to People With No Mercury Surviving ALS

I have had two inquiries about removal of amalgams. The basic question is "I removed my amalgams, why am I not getting better?" That is the cause of the controversy. Some people have improvement after removal of amalgams, but many don't. For what it is worth, I wish to offer my opinion based on information received from many PALS and from books I have read.

There are two reasons why some people don't improve:

Number one, the amalgams have in almost all cases been in your mouth for many years. During those many years, the mercury has transferred from your mouth into your body tissue where it builds up. Removal of the amalgams does not remove the mercury from your system. You must do everything possible to detox the body. (Read my previous article. If you don't have them, e-mail me and I'll send them.)

Number two, amalgams may or may not be the only contributing cause of your ALS. Even if amalgams were the only cause, you still have a problem. The body has been weakened immeasurably by your ALS condition. As one of my neurologists told me, "you now have sick tissue." Therefore, many other toxins may be harmful to you that were not before.

Basically, you must avoid all toxins; MSG, food preservatives, heavy metals and chlorine in your water, smog, coffee, etc. To emphasize what we are faced with in the way of toxins, let me tell you this story that was in the local newspaper about five days ago. A 16 year old male died from body deodorant spray. Apparently he was spraying his entire body with deodorant spray everyday. According to the article, he died from an accumulation of the gas in the spray.

When I say you have to avoid toxins, I mean you'd better stay away from everything including deodorant spray. You shouldn't even be in the house when someone else uses it. If a lot can kill a young normal person, a little bit could be just as bad for an ALS patient.

The medical doctors and drug companies have not found a cure for ALS because, in my opinion, they're looking for one single cure, or a magic bullet. I don't think that exists. To prevent the continuing progress of ALS and/or cure it, you must do many things. Again, see my previous article.

Basically, avoid all toxins. Detox the body. Help the body heal itself by proper diet and food supplements.

Remember, the first phase is stopping the progression. If you've done the right things and your progression has stopped, be patient because improvement takes a long time.

Eric Edney

Eric Edney has succeded in treating and, to some extent, reversing the symptoms of ALS/MND.

Mercury As One Possible Factor or Cause of ALS
Unlike MS there are not many adverse reaction reports to the FDA involving ALS and the removal of mercury silver fillings. There are some specific cases, one in Nevada one in Sweden and one in New York, where there has been a reversals of the course of the disease. In Nevada a woman had a complete remission from a clearly diagnosed and fast progressing case.

There is also a reported case of complete remission after removal of fillings in Sweden (see Int J Risk & Safety in Med 4:229-236 (1994).

In New York a man had a remission of some symptoms and all progression of the disease for over a year but a remaining paralysis which subsequently began to progress again, but at a slower rate. But it is very important to note there are individuals who have ALS and have never had mercury/silver fillings.

So while mercury may be a cause of ALS as the following discussion suggests, it certainly is not the only one. For those who would debunk this please remember that the first principle of the scientific method is observation.

In addition, there are several individuals who have had considerable success in dealing with and, to some extent, reversing the symptoms of ALS by various methos. One example is "Eric is winning email