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

Information here may help in the treatment or understanding of ALS/MND. It is provided for your information only and I leave you to form your own opinions and conclusions.

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

Poly(ADP-ribose) polymerase-1 (PARP-1) is a member of the PARP enzyme family. PARP-1 is an abundant nuclear protein functioning as a DNA nick-sensor enzyme Poly(ADP-ribosylation) contributes to DNA repair and to the maintenance of genomic stability. On the other hand, oxidative stress-induced overactivation of PARP consumes NAD(+) and consequently ATP, culminating in cell dysfunction or necrosis.

This cellular suicide mechanism has been implicated in numerous pathomechanisms including diabetes, shock, traumatic central nervous system injury, arthritis, colitis, allergic encephalomyelitis and various other forms of inflammation.

I believe this to be a major factor in neurodegeneration in ALS/MND. SS

PARP has also been shown to associate with and regulate the function of several transcription factors that play a central role in the expression of inflammatory cytokines, chemokines, adhesion molecules, and inflammatory mediators.

Efficient three-drug cocktail for disease induced by mutant superoxide dismutase

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 GREDNEY@aol.com Another is "The Over Five Club"

Amyotrophic Lateral Sclerosis (ALS) was first identified a few years after mercury/silver fillings came into common use. The clinical picture is most interesting when considered in light of the documented neurotoxicity of mercury and the potential for neurotoxicity from mercury/silver fillings. Like MS, some people with ALS have found that their condition improved dramatically upon removal of their mercury/silver fillings. The correlation to mercury exposure was first suggested by Brown in 1954.1

A 1961 study of eleven cases of chronic mercurialism from consumption of bread treated with a mercury-containing fungicide presented neurological pictures akin to ALS with some more closely resembling progressive muscular atrophy. The paper concluded:

"1. Since the same causative factor was operative in all these cases, it would appear that amyotrophic lateral sclerosis and progressive muscular atrophy are probably nosologically identical.

2. Amyotrophic lateral sclerosis should not be considered a disease entity but rather a syndrome of variable etiology.

3. Chronic mercurialism is a possible etiologic factor in amyotrophic lateral sclerosis." (emphasis added) 2

Two subsequent reports are noteworthy. A 1978 report by Barber involved two employees in a mercury oxide manufacturing plant who developed neurological changes resembling ALS.3 A JAMA article reports of a 54-year-old man with symptoms resembling ALS after a brief but intense exposure to elemental mercury which resolved afterwards.4

A 1989 Japanese study was done on ALS victims in the vicinity of the biggest mercury mine in Japan. That study found mercury at higher levels in ALS victims than in controls. They followed this with a study in 1990 which compared the mercury and selenium content in the hair of thirteen (13) ALS cases using neutron activated analysis and concluded that mercury with a low content of selenium might be one of the environmental factors.5

In considering the hypothesis that mercury from fillings may contribute to ALS or ALS-like symptoms, a major question is, do silver fillings contribute a significant amount of mercury? Documented scientific research has proven that patients with dental amalgam fillings are constantly exposed to mercury throughout the lifetime of the fillings and that amalgam-derived mercury builds up in the patients' bodies with time.6

A 1990 study in the U.S. also involved neutron activated analysis of brain, spinal cord, blood cells, serum, and nails of ALS victims compared to controls. Imbalances were detected in a number of trace and minor abundance elements in the ALS tissue and more widespread changes were noted in the concentrations of mercury. The authors cautioned that the variation in mercury concentrations need not necessarily indicate active toxicity, as it could merely represent an enlarged pool of detoxified mercury or perhaps a labeling of a specific cellular ligand by mercury in ALS. 7

In 1991 the World Health Organization determined that the vast majority of the average body burden of mercury comes from these fillings.8 A number of studies have shown that the mercury vapor comes off for the life of the fillings and is accentuated by chewing and hot foods. Obviously, bruxism (grinding of the teeth) can also increase the release of mercury and there are other studies showing that the presence of other metals in the mouth cause an increased release.

Anyone considering having his or her fillings removed should be sure that the dentist doing the removal follows the IAOMT protocol or a similar protocol using procedures to minimize exposure to mercury vapor and/or swallowing particles.

Copyright 1998 Robert E Reeves, Lexington, Ky.

1. Brown, I.A. Chronic Mercurialism, a cause of the clinical syndrome of amyotrophic lateral sclerosis. AMA Arch. Neural Psych 72:674-681, 1954.
2. Kantarjiam AD: A syndrome clinically resembling amyotrophic lateral sclerosis following chronic mercurialism. Neurology 11:639-44, 1961.
3. Barber TE: Inorganic mercury intoxication reminiscent of amyotrophic sclerosis. J. Occupat. Med. 20:667-9, 1978.
4. Adams CR, Ziegler DK, Lin JT: Mercury intoxication simulating amyotrophic lateral sclerosis. J. Amer. Med. Assoc. 250:642-3, 1983.
5. Mano Y; Takayanagi T; Abe T; Takizawa Y: Amyotrophic lateral sclerosis and mercury-preliminary report. Department of Neurology, Nara Medical University. Rinsho Shinkeigaku Nov 1990, 30 (11) pl275-7, ISSN 0009-918X Mano ^; Takayanagi T; Ishitani A; Hayride T: Mercury in hair of patients with ALS. Rinsho Shinkeigaku July 1989, 29 (7) p844-8, ISSN 0009-918X.
6. Clarkson TW, Friberg L, Nordberg GF, Sager PR, eds. Biological monitoring of toxic metals. New Yorik: Plenum Press, 1988. National Academy of Sciences, "An Assessment of Mercury in the Environment", Washington, D.C. 1978, p. 84.
Food and Drug Administration Dental Products Panel Meeting Transcript 3/15/91, pp. 67-70, testimony of Lars Friberg, M.D., Ph.D..
Aposhian HV et al. Urinary mercury after administration of 2,3- dimercaptopropane-1 sulfonic acid: Correlation with dental amalgam score. FASEB J 6(6):2472-2476, April 1992.
Zander D. et al. Studies on human exposure to mercury .3. DMPS induced mobilization of mercury in subjects with and without amalgam fillings. Zentralblatt fur Hygiene und Umwelmedizin 192(5):447-454, Feb 1992.
Skare I, Enqvist A. Amalgam restorations - an important source of human exposure to mercury and silver. LAKARTIDNINGEN 15:1299-1301, 1992.
Eggleston, DW; Nylander, M; Suffin, SC; Martinoff, JT; Reiders, MF. (1987):Correlation of Dental Amalgam with Mercury in Brain Tissue. J Prosth Dent. 58:704-7.
Nylander, M; Fribert, L; Birger, L. (1987): Mercury Concentrations in the Human Brain and Kidneys in Relation to Exposure from Dental Amalgam Fillings. Swed Dent J. 11:179-87.
7. Khare SS; Ehmann WD; Kasarskis EJ; Markesbery: Trace element imbalances in amyotrophic lateral sclerosis, Neurotoxicology, Vol. 11, No. 3, pages 521-532, 47 references, 1990
8. World Health Organization (1991) "Environmental Health Criteria 118: Inorganic Mercury", Geneva.

Dr. Martina Berger and colleagues discovered that ALS/MND patients are more likely to have a particular virus in their spinal cords than people without the condition. Findings suggest that the virus may play a role in the development of the disease, although more research is needed to confirm the study results.  If correct, the discovery may lead to a treatment.

Dr. Berger from Centre National de Reference pour les Enterovirus in Lyon, France looked for traces of enteroviruses (a family of viruses that includes the poliovirus) in the spinal cord tissue of 17 patients who died of ALS and 29 people who died of other causes. Previous studies gave inconsistent results when seeking viral particles or products in fluid or cells taken from the spinal cord. Using a more sensitive test, Berger and colleagues were able to detect enteroviruses in 88% of ALS cases. In contrast, the virus was detected in only 3% of patients who died of other causes.

Genetic analysis suggested that the virus most closely resembled echovirus-7 and echovirus-6.  Echovirus-7 is known to cause meningitis, infections of the protective covering of the brain.

"Many researchers have suspected a viral link to ALS, but in this study we were able to identify a virus known for nerve damage in the extract areas of the nervous system that are affected by this disease," said Berger, who is
now at the University of California, Irvine (UCI).  "We think this knowledge will help us finally uncover what causes this disease and may someday lead us to developing a treatment."

"We need to identify the ways this virus causes damage to nerve cells in order to determine how it may play a role in the development of ALS. If this research is successful, we may be able to design new classes of drugs that could be effective against this disease. "SOURCE: Neurology 2000; 54:20-25.

More on the above article: A study was done on 17 ALS patients, post mortem. Scientists, working with Dr Martina Berger and Dr. Darryl See and others at University of California, Irvine have completed genome sequencing of a virus composed of the following: Echo Virus 6 - 91%, Echo Virus 7 - 88%, Coxsackie Virus B3 - 86%, Coxsackie Virus A9 - 68%, Polio Virus 3 - 57%. (Two did not have this sequence but they may not have had ALS - they were misdiagnosed - or the sample was bad).

Below is a paraphrased (and therefore possibly inaccurate) excerpt from the discussion portion of the article:
... A new anti viral drug to treat Herpes from Smith Klein Beecham, generic name Lobucavir, may effect ALS mutant virus. Dr. Martina Berger and the other members of the team believe that this will treat the mutant virus.  An appeal to Smith Kline for advanced use of the drug for ALS has been made.  Until this anti viral drug is available it has been suggested that a Quantitative Immunoglobulin test and IGG subclasses tests be performed. It is possible that if test results are low, treatment with IV Immunoglobulin may positively influence the outcome of the disease.

The paper, published in  Neurology 2000; 54:20-25, describes why previous attempts at uncovering the virus were not successful. Due to development of improved technology they have been able to sequence the virus... There may be a discussion of the samples used and where the samples were taken from and how this relates to other viruses such as diabetes mellitus, chronic fatigue syndrome, idiopathic dilated cardiomyopathy, post polio virus and the detection of entero virus genome sequences in ALS. The studies do not provide an explanation for how the virus arrives at the anterior horn cells but genetic predisposition is possible. Hypo or Hyper oxidative state (in basic terms) can deplete the body and damage the blood brain barrier, thus potentially exposing the Central Nervous System to infection.

Apoptosis is the natural process of cell death that occurs when a cell cannot repair itself.  Neurons are relatively resistant to apoptosis, making viral persistence possible. The discussion moves to free radicals, oxidative protective mechanisms, and the resulting lack of glutamate uptake.

There is a paper entitled "Absence of echovirus sequences in brain and spinal cord of amyotrophic lateral sclerosis patients"  Walker MP, Schlaberg R, Hays AP, Bowser R, Lipkin WI. Dpt of Neurology, UCI. The authors were not able to replicate Dr Berger's findings.  This does not necessarily mean that viruses are not implicated in MND/ALS but it does reopen the debate as to what is the most likely cause of the illness.

Like many of us who have been diagnosed with ALS, one of the coping mechanisms I fell back on was to educate myself about the disease as much as possible.  For a layman, this is a daunting task, requiring excursions into neurophysiology,  cell biology, and biochemistry for which there is little hope of acquiring more than a elementary grasp without the years of training that our doctors and neurologists undergo. Tremendous advances had been made in the understanding of ALS, yet so much more remains a mystery.

The prevailing theory has evolved from auto immunity to the more complex genetic/excitotoxin theories.  I inquired why more research had not been done on the possibility of a viral link but my neurologists stated that studies excluded that possibility long ago. This assertion in itself is a clue to the neglect of the research community to investigate the idea of viral involvement in the pathogenesis of ALS.  Molecular biology and virology in the last few years has caused a revolution in scientific thinking. 

The sensitivity and accuracy of PCR assay techniques have confirmed novel infectious agents like endogenous RNA viruses and prions, little dreamed of a decade ago.  It does not take a medical degree to realize that studies made only a few years ago are not necessarily conclusive. 

Neurologists inevitably tend to dismiss a viral link, while virologists seem to be uniformly open to the possibility. The result is that organizations that fund ALS research have accepted that research on a viral link is a dead end although new discoveries have implicated a virus or multiple virus link in MS and a number of afflictions that were formerly deemed to be psychological ... discoveries that dramatically illustrate why the book should not be closed on a viral-ALS link.

A quick review of Medline will show that little research has been done on the question in recent years, and what little has been published is inconclusive.  While volumes have been generated about the disease process, the vast majority of these have revealed little about the origins of the disease. 

Though we must constantly remind ourselves that the pathogenesis of ALS is almost certainly multi-factorial, the possibility of a viral pathogenesis has not been adequately eliminated to justify the current  dismissive attitude of some sectors of the medical community.

The paucity of research that might eliminate or confirm a viral connection is a cause of concern for PALS who are grasping for rational, credible hope.  We have every right to rebel against a prevailing medical dogma that is based on outdated or inadequate research and maybe more than just a little institutional hubris.

I hope that all PALS and their families will advocate for greater recognition of the yet unexplored potential of viral research.  The availability of new research tools, better understanding of cellular processes and the advent of a whole new era of anti-viral drugs might make the difference between death and survival for many PALS reading this.  It's time for those with the greatest stake in this issue to mobilize and move the medical center of gravity over to a recognition that the viral/ALS link must be seriously examined.

"In summary, it seems appropriate to consider the role of enteroviruses and retroviruses in some forms of motor neuron degeneration. The two mouse models of Mu LV and of age-dependent poliomyelitis illustrate how a virus (or two viruses) can cause noninflammatory neurodegeneration. Thus the involvement of viruses in the pathogenesis of ALS seems to remain a possibility". Gastaut,J.-L: The viral hypothesis. Adv. Neurol. 68 (1995) 135-137.

1 - In the book MOTOR NEURON DISEASE, edited by A.C. Williams (Chapman & Hall Medical; 1994; 755 pages, hard cover), see chapter 27, "Viruses and Motor Neurone Disease: The Viral Hypothesis Lives" written by Dorothy C. Kelley-Geraghty and Burk Jubelt (Department of Neurology; College of Medicine; State University of New York; 750 East Adams Street; Stracuse NY 13210 USA). Here is a quote from the chapter: "We will try to show how the epidemiological evidence, virus infections in MND, latent virus infection in other diseases and finally the immunological findings all support a viral hypothesis." At the end of the chapter is a listing of over 100 references to the topic.

2 - There may also be information to support current research on ALS/MND and Enteroviruses

3 - In June of 1994, Woodall, Riding, Graham and Clements published an article "Sequences Specific for Enterovirus Detected in Spinal Cord from Patients with Motor Neurone Disease."  This study found nucleic acid sequences specific for enterovirus in the spinal cords of 8 of their 11 subjects with motor neuron disease, and in none of the control subjects.

4 - The amino acid Lysine is specifically indicated to treat herpes but does not work for all people (as there are 70 different types of herpes, this is hardly surprising). The herbs Echinacea, Ginseng, Pau D'Arco and Cat's Claw in combination may also assist, although this is untried and should be supervised by a competent naturopathic/herbal practitioner. These may be worth investigating as an interim treatment for ALS/MND if the above research results are correct.

Bacteriophages
An alternative to powerful, broad spectrum antibiotics may be the use of bacteriophages (often simply referred to as phages). A bacteriophage is essentially a virus that will only "eat" one type of bacteria. When the supply of bacteria is used up the phage "dies of starvation".

These phages are cheap and, once isolated, relatively easy to produce and have been used for decades in Georgia (ex USSR). 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.

"I fully agree with your proposal that anti-oxidants and proper liver function are likely to be important for fighting ALS. I would suggest that people also take natural anti-oxidants like drink every day one glass of red beet's juice, tomato juice and carrot juice, for in there are potent ingredients like leucopins, etc. that are good free radical scavengers.

I have worked for many years on the basic research of cellular energy metabolism and creatine kinases (CK). CK and creatine, as well as the energy charged compound phospho-creatine, are very prominent in skeletal and heart muscle as well as in brain and nerve cells. Phosphocreatine is synthesized by CK from creatine by adding a "high-energy phosphate" which, upon hydrolysis, transfers its chemical energy to ATP, the universal energy currency in the cell that can be used for many biologically important functions, like muscle contraction, holding a nerve cell's electrical potential, etc. Thus the proper cellular energy state is very important for functioning of muscle, brain and other cells.

Based on our studies showing beneficial effects of creatine in mdx mice, the animal model of muscular dystrophy (Pulidoet al. 1998, in my publications). Clinicians around Flint Beal in Boston started experiments with FALS mice, the animal model of ALS. This simple and natural body substance had remarkable (beneficial) effects. (Klyvenyiet al. and Flint Beal, Nature Medicine March 5th 1999).

Full clinical trials using creatine are now being set up in several countries but patients with ALS could already take creatine, as long as it is very pure quality. There are many so called pure or purest creatine preparations on the market that are rather poor quality and far from pure. Purity of product is especially important for ALS patients.

Pure creatine is without serious side effects and has been taken extensively by body builders and athletes world wide. It increases the phosphocreatine energy pool, increases muscle performance, lean body mass and appears to prevent muscle wasting from disuse atrophy, the latter being most important for ALS patients, etc.

The strategy of creatine supplementation together with anti-oxidants, etc. as you propose, could possibly improve life quality and expectancy of ALS patients, if taken early enough. (I will have a book chapter in "Guanidino Compounds in Biology and Medicine" on "The Phospho-creatine shuttle and creatine supplementation, both come of age" in English available soon, that maybe helpful for background information).

You may look at my home page and some of the links provided in the signature and hopefully convey this new development to your colleges and ALS/MND patients. This may be a dim light of new hope in delaying the disease and slowing down the neurodegenerative process, as well as its muscle-associated secondary effects"

Update on Creatine Use

Increasingly, PALS are contacting me to say they have discontinued creatine as they felt it was not helping. I used creatine and did not record significant change for better or worse. Some PALS still feel that creatine is helpful but few claim that it has led to significant improvement.

They can detect this protein in CSF from normal healthy volunteers using a combination of nucleotide photoaffinity labelling and two-dimensional gel electrophoresis but not by any other commonly used protein staining methods. 

They are currently attempting to purify and identify this "missing" protein from non-ALS controls.  Once They have done so, they may be able to gain further insight into the disease process.  Possibly this biochemical marker will offer some means of monitoring the progression of the disease or maybe even point to a potential therapeutic target for persons suffering from ALS.

ALS/MND - A Prion Infection?
Stanley B. Prusiner "The Prion Diseases". In the chapter "Striking Similarities" he writes:

Research may determine whether prions consisting of other proteins play a part in common neurodegenerative conditions, including Alzheimer's disease, Parkinson's disease and ALS. There are similarities in all these disorders. As is true of the known prion diseases, the more widespread ills tend to occur sporadically but sometimes run in families. All are usually diseases of middle to later life and are marked by similar pathology: neurons degenerate, protein deposits can accumulate as plaques, and glial cells (which support and nourish nerve cells) grow larger in reaction to damage to neurons.

Strikingly, in none of these disorders do white blood cells - those ever present warriors of the immune system - infiltrate the brain. If a virus were involved in these illnesses, white cells would be expected to appear. Recent findings in yeast encourage speculation that prions unrelated in amino acid sequence to the PrP protein could exist.

Reed B. Wickner of the NIH reports that a protein called Ure2p might sometimes change its conformation, thereby affecting its activity in the cell. In one shape, the protein is active; in the other, it is silent. The collected studies described here argue persuasively that the prion is an entirely new class of infectious pathogen and that prion diseases result from aberrations of protein conformation. Whether changes in protein shape are responsible for common neurodegenerative diseases, such as Alzheimer's, remains unknown, but it is a possibility that should not be ignored.

Findings support previous observations of an increased risk of Alzheimer's disease and ALS among employees occupationally exposed to ELF-MF (Low Frequency Electromagnetic Fields: eg arc welders).

Power Lines Linked to ALS
Pregnant women living near overhead power cables are 10% more likely to lose a baby. A report by the California Public Utilities Commission follows a 4-year review. The findings suggest that as many as 1 in 20 pregnancies end in miscarriage because of electromagentic fields. The results of the most extensive review suggest they can also raise the risk of childhood leukaemia & adult brain cancer & ALS. (Prof Denis Henshaw of Bristol University, UK wants a change in planning laws to stop houses being built close to overhead cables).

PARASITES
This page was reprinted from "The Cure for All Diseases" by Hulda Regehr Clark, Ph.D., N.D.
The Worst Parasite

"Fasciolopsis buskii is the fluke (flatworm) that I find in every case of cancer, HIV infection, Alzheimer's, Crohn's disease, Kaposi's, endometriosis, and in many people without these diseases.  Its life cycle involves six different stages:

Fasciolopsis' Normal Life Cycle
1 Egg expelled with bowel movement onto soil. Washed by rain into ponds.
2 Miracidia Hatches from egg in water.  Has cilia, can swim vigorously and must find intermediate snail host in one to two hours or may be too exhausted to invade.
3 Redia Develop inside miracidia as little balls until expelled.  Those are "mother" redia, and each one bears "daughter" redia for up to 8 months, all still inside the snail, and living on the fluids in the lymphatic spaces. Similarly, daughter redia are continually developing cercaria.
4 Cercaria  Have a tail, use it to exit from snail and swim to a plant.  If the snail is feeding on a plant, cercaria can latch onto plant with sucker mouth and start to encyst (form a "cocoon") within minutes.  Tail breaks off and swims away to dissolve.
5 Metacercaria  Two-walled cyst.  The outer wall is very sticky.  But as you eat the plant it is stuck to, the least pressure will break it, leaving the cyst in the mouth. The "almost unbreakable" inner cyst wall protects it from chewing, and the keratin-like coat prevents digestion by stomach juices.  However when it reaches the duodenum, contact with intestinal juices dissolves away the cyst-wall and frees it. It then fastens itself to the intestinal lining and begins to develop into an adult.
6 Adult Lives in your intestine and can produce 1000 eggs per bowel movement and live many years.

Note that the adult is the only stage that "normally" lives in the human (and then only in the intestines).  Fasciolopsis depends on a snail, called a secondary host, for part of its life cycle. But when your body has solvents in it, the other five stages can develop in you.

If propyl alcohol is the solvent, the intestinal fluke is invited to use another organ as a secondary host ... this organ will become cancerous. If benzene is the solvent, the intestinal fluke uses the thymus for its secondary host, setting the stage for AIDS. Wood alcohol invites pancreatic flukes to use the pancreas as a secondary host. This leads to pancreatic dysfunction which we call diabetes. 

If xylene (or toluene) are the solvents, I typically see any of four flukes using the brain as a secondary host.  If methyl ethyl ketone (MEK) or methylbutyl ketone (MBK) are the solvents, the uterus becomes a secondary host and endometriosis a likely result.

This is a new kind of parasitism, based on pollution.  I call the diseases caused by fluke stages in inappropriate locations "Fluke Disease". Are tapeworms and roundworms affected by solvents this way, too?  This is a fascinating and very important question.  Search for the answer and help others search for the answer.  I do not know yet".

In Australia a pharmacy that sells the Dr Hulda Clarke mixtures: Newtons Pharmacy, 119 York Street, Sydney Telephone: (02) 926 77889. They know about the Hulda Clarke system. They also sell the Minamino Syrup and Lugol's Iodine.

I read "The Cure for All Diseases" and (although Dr Clarke may be correct in her observations) I find it logistically and financially difficult to adhere to the strict regimen she suggests.  Impressive case histories support her ideas so, approached with an open mind and a willingness to make substantial lifestyle changes, you may find Dr Clarke's methods worth considering.

I also tried using the "zapper" for an extended period but found it of little benefit. It could be argued that I was not following the entire regimen whilst using the zapper but, if it works at all, I feel I should have experienced some improvements or changes and I recorded none.

The zapper is cheap and relatively easy to make by following the simple instructions in the book. I would be disinclined to spend a great deal of money on a commercially manufactured model.

The following micronutrients should be taken each day. Although these recommendations do not specifically offer a cure for ALS, because of their sound scientific support they do offer hope - and "that may be the most potent medicine of all."

1. Take the following minerals to enhance production of superoxide dismutase (SOD): zinc (glycine, histidine dipeptide chelate) 5 mg copper (lysine dipeptide chelate) 500mcg manganese (glycine dipeptide chelate) 2 mg
2. Take relatively high dosages of vitamin antioxidants including: ascorbate powder, 2000mg. three times a day vitamin E (natural - containing alpha, beat, gamma & delta tocopherol) 400 IU, increasing to 1000 IU over three to four weeks with food each day. Beta carotene 25,000 IU each day with food. Because of its antioxidant properties, take selenium 100 -150mcg each day.
3. OPC - grape seed/pine bark extract. Start with 50mg each day and after two to three weeks increase to 100mg each day.
4. Take the following amino acids four times each day between meals: L-leucine, 3 grams, L-isoleucine, 2 grams, L-valine, 1.6 grams.
5. If these are unavailable at your health food outlet, contact Meta Metrix Medical Laboratories at: 5000 Peachtree Indus. Blvd., #110 Norcross, GA 30071 (404)446-5483
6. DHEA. Begin with 50mg every other day and after two to three weeks increase to 50mg each day. Dosages as high as 100mg each day may be given under the direction of a physician.  See DHEA.

Using mass spectrometry, researchers identified 10 protein biomarkers that differentiated between the ALS patients and non-ALS patients. Testing for ALS could be completed within a few hours instead of the months now required, allowing possible treatment to commence as soon as possible. This will provide new insight into the biochemical pathways that cause ALS and indicate directions for drug therapy.

Dr. Jeffery Elliott and researchers the University of Texas Southwestern Medical Center at Dallas discovered that aggregates in the mutant protein SOD1 trigger the death of motor neurons in spinal cells. They are now seeking the exact portion of the molecule that induces aggregate formation and how various organs process the mutant SOD1 protein.

When the SOD1 protein mutates, other organs in the body can handle it but not the spinal cord. The liver has a high capacity to get rid of the aggregate but is apparently unaffected, unlike the spinal cord.  

Certain chemicals can remove the aggregates in the mutant protein known to cause ALS in mice, suggesting that it is a reversible process. If these protein inclusions can be removed, the nervous system may be able to repair itself.

 It still has to be shown that the discovery will reverse ALS in humans but if experiments in live mice prove successful, human trials could be under way in less than two years.

VEGF (vascular endothelial growth factor) appears to delay neurodegeneration in ALS Mice. Minoxidil promotes production of VEGF and OPCs provide antioxidant protection but do not inhibit VEGF expression. This may help explain why some PALS seem to benefit from OPC supplementation.

(1) VEGF (vascular endothelial growth factor) has been found to be low in ALS patients.  In addition, low VEGF levels give mice a disease very similar to ALS. Minoxidil (an over the counter hair growth spray approved by the US FDA) directly stimulates VEGF.

(2) A single injection of a VEGF-expressing lentiviral vector into the muscles of mice delayed onset and slowed progression of ALS. VEGF treatment increased the life expectancy of ALS mice by 30 per cent without causing toxic side effects, thereby achieving one of the most effective therapies reported in the field so far. The therapeutic potential of VEGF to treat ALS in humans needs to be assessed. 

(3) Angiogenesis (development of new blood supply) plays a central role in wound healing. Among many known growth factors, VEGF is believed to be the most prevalent, efficacious, and long-term signal known to stimulate angiogenesis in wounds. A wound site is rich in oxidants such as hydrogen peroxide. Grape seed proanthocyanidin extract (GSPE) facilitates oxidant-induced VEGF expression. GSPE upregulated hydrogen peroxide and TNF-alpha-induced VEGF expression and release. Results suggest that GSPE may have beneficial therapeutic effects in promoting dermal wound healing.     

Disrupted vasculature and high energy-demand by regenerating tissue results in wound hypoxia... Oxidants serve as cellular messengers to promote healing. This information is significant to the practice of oxygen therapy but remains largely unexplored. Proanthocyanidins (OPCs) and other tannins facilitate wound healing. A combination of grape seed proanthocyanidin extract and resveratrol facilitates inducible VEGF expression, a key element supporting wound angiogenesis.   

(4) Edible berries may have potent chemopreventive properties. Anti-angiogenic could possibly be used to prevent and treat cancer. (VEGF) plays a crucial role for the vascularization (creation of blood supply) of tumors.

Edible berries impaired angiogenesis. Multiple berry extracts were tested on inducible VEGF expression. Wild bilberry and blueberry extracts had the highest antioxidant values. Strawberry powder and GSPE were higher than cranberry, elderberry and raspberry seed but lower than the other samples. Cranberry, elderberry and raspberry seed samples had similar values but were lower than the other samples. Pure flavonoids, the berry samples, inhibited VEGF expression by the human keratinocytes but alpha-tocopherol (vitamin E) and GSPE did not.      

(5) VEGF Production is Stimulated by Minoxidil
VEGF mRNA is strongly expressed in dermal papilla (hair) cells (DPC) in the anagen phase. DPC stimulated with minoxidil express six times more VEGF than controls and VEGF protein production increases. Minoxidil appears to assist in maintaining good vascularization of hair follicles.

(1) Nature. 2004 May 27;429(6990):413-7. VEGF delivery with retrogradely transported lentivector prolongs survival in a mouse ALS model. Azzouz M, Ralph GS, Storkebaum E, Walmsley LE, Mitrophanous KA, Kingsman SM, Carmeliet P, Mazarakis ND. Oxford BioMedica plc, The Oxford Science Park, Medawar Centre, Oxford OX4 4GA, UK.

(2) Upregulation of oxidant-induced VEGF expression in cultured keratinocytes by a grape seed proanthocyanidin extract. Khanna S, Roy S, Bagchi D, Bagchi M, Sen CK. Laboratory of Molecular Medicine, Department of Surgery, The Ohio State University Medical Center, Columbus, OH, USA. PMID: 15164063 [PubMed - indexed for MEDLINE] Br J Dermatol. 1998 Mar;138(3):407-11.

(3) Oxygen, oxidants, and antioxidants in wound healing: an emerging paradigm. Sen CK, Khanna S, Gordillo G, Bagchi D, Bagchi M, Roy S. Laboratory of Molecular Medicine, Dorothy M. Davis Heart and Lung Research Institute, Department of Surgery (CMIS), The Ohio State University Medical Center, Columbus, Ohio 43210, USA. PMID: 11425488 [PubMed - indexed for MEDLINE] Ann N Y Acad Sci. 2002 May;957:239-49.

 (4) Anti-angiogenic property of edible berries. Roy S, Khanna S, Alessio HM, Vider J, Bagchi D, Bagchi M, Sen CK. Laboratory of Molecular Medicine, Department of Surgery, 512 Heart and Lung Research Institute, Ohio State University Medical Center, 473 W. 12th Avenue, Columbus, OH 43210, USA. PMID: 12074976 [PubMed - indexed for MEDLINE] Free Radic Res. 2002 Sep;36(9):1023-31.

 (5) Minoxidil upregulates the expression of vascular endothelial growth factor in human hair dermal papilla cells. Lachgar S, Charveron M, Gall Y, Bonafe JL. Laboratoire de Biologie Cellulaire Cutanee, Institut de Recherche Pierre Fabre, Faculte de Medecine Rangueil, Toulouse, France. PMID: 9580790 [PubMed - indexed for MEDLINE]  Free Radic Biol Med. 2001 Jul 1;31(1):38-42

Investigations earlier this verified that novel cell damaging agents, termed "stealth adapted" viruses, were present in the blood of ALS patients. A prototype stealth-adapted virus isolated from a patient suffering from severe Chronic Fatigue Syndrome (CFS) has been nearly completely sequenced. The sequence data have confirmed that this prototype originated from an African Green Monkey Simian Cytomegalovirus (SCMV).

The study also confirmed the absence of viral genes that normally code for antigenic proteins targeted by the immune system to identify Cytomegalovirus infected cells. The loss of critical antigen coding genes accounts for the absence of a normal immune response to the presence of the stealth-adapted viruses.

A core property of the stealth virus process is the ability to acquire and to modify useful genes from other viruses, bacteria and host cells. Sequences from all three categories were identified. Of particular interest are bacterial genes that code for transporter proteins, since these could interfere with normal glutamate transport; a leading hypothesis for the malfunction of nerve cells in PALS.

Ongoing sequencing of the many incorporated bacterial genes indicate origins from various types of bacteria including Borrelia, the bacterial cause of Lyme disease. Stealth virus capture of Borrelia genes could easily explain why certain ALS patients surprisingly test positive for Lyme disease in antigen-based assays. Similarly, assimilated bacterial genes can potentially lead to misdiagnoses of Mycoplasma, Chlamydia and/or Rickettsial infections in PALS.

Another striking feature of the stealth virus sequencing study is the marked expansion of chemokine and chemokine-receptor genes of both viral and cellular origins.  These gene sequences are repeated over and over, indicating their importance to the survival of the virus and prompting an adjunct approach to stealth virus therapy based on chemokine blockade. There are some preliminary indications that treatment with anti-chemokine drugs might offer some modest benefit to PALS.

The last but most important characteristic of this virus adaptation process is that it produces the seeds of its own destruction. The gene loss and acquisition process is very sloppy and opportunistic. Virus assembly apparently involves the formation of complex scaffolds of viral segments. This process can seemingly be "sabotaged" by small viral fragments. In sufficient amounts, these fragments will potentially inhibit all viral activity.

In phase one of a twofers project the genes responsible for inhibitor production are being, sequenced and cloned. Positive stealth virus cultures from ALS patients have been used to test inhibitory material. Early results are very promising and the prospects for engineering a bacterial clone for production of sufficient inhibitor to initiate exploratory pre clinical and animal model investigations remain good.

Researchers at CCID are developing treatments based on blocking the chain of subsequent cell-killing events at vulnerable points. By using rapid screening and transgenic animal models, many candidate drugs can be quickly and inexpensively evaluated for possible use in ALS patients.

Many of these drugs are already in established use for other purposes or are natural biochemicals. The work will be conducted at the ALS -Therapy Development Foundation (ALS-TDF) animal laboratory in Boston. Virus effect and inhibitor testing in animals in support of the work at CCID will also be conducted. Details of this collaboration will be announced shortly

For Further Information or to make a donation to their ongoing research
contact Hope for ALS 7822 Santa Elena, Suite 100, Houston, Texas 713-643-2898