ALS or Amyotrophic Lateral Sclerosis (Lou Gehrig's) disease is a motor neuron disease that has been 100% fatal. My father died of ALS in 1974 and he apparently had the familiar form of the disease because I contracted ALS in 1995. I had done considerable research when my father had the disease trying to save his life. As in the old saying "Necessity is the mother of invention," I frantically researched the disease. Did you know Insulin that treats diabetes was discovered by a doctor who's wife had diabetes and by his discovering her bodies insulin shortage as the cause of diabetes he saved her life. In my case I was too late with my discoveries to save my fathers life because he died 18 months after his diagnosis of respiratory failure even with a permanent tracheotomy. In my case I have been able to hold the disease ALS in check. I have been able to arrest the advance of ALS to the beginning stages of the muscle loss controlling my right thumb. This was the beginning stage for both my father and I. My father was the most studied case of ALS at the University of Washington hospital at that time. ALS is a disease that even if you cure the disease the damaged motor neurons will not recover so the condition the patent is in when the disease is arrested is the condition that the patient will retain. That condition reversal becomes another problem. I do believe that ALS changes character after the initial stages and I am especially looking for persons in the beginning stage of their involvement to try my regime. I now feel that all ALS is probably the same form but that it changes character as it progresses. The muscles that have atrophied controlling my right thumb because of the loss of motor neuron stimulation are still gone 17 years later. There was a time when I felt they were coming back but I now feel that it is the other muscles surrounding the ones that have atrophied that are stronger and compensating. I have approached several doctors about my condition and atrophied muscles. The best they can say is they think the diagnosis in my case was wrong. They have talked about testing me with another EMG and a MRI scan to make a study. This has not happened though because they believe my regime was to easy and they hate being upstaged by someone else or they would at least try something this simple. The loss of muscle control in the thumb is one of the easiest to recognize beginning signatures of ALS. I have had 5 GP doctors tell me they recognize the disease ALS from that signature. During the second world war and in every war since there has been an statistically unexplainable percentage of veterans return with the ALS symptoms. Grizeofulvan was invented during the second world war because tremendous outbreaks of fungal infections in the Philippines. None of the soldiers who died of the ALS symptoms they acquired during that war were given Grizeofulvan because their body had dealt with the fungus with another complex chemical reaction. The same relationship was noted in all later conflicts from Korea to Vietnam to Iraq. Several years ago I published some of my findings in different publications including "Bob Broedel" at the ALS Digest. I am published in volume 611- 4 in 1999. A copy can be read by visiting the ALS digest or viewing the ALS Digest 611 page on the left to read of my regime. Copies of all ALS digests can be found at http://www.glnicholas.com/. Bob Broedel can be contacted by email <bro@met.fsu.edu>. I had 2 people who had read the digest while in the beginning stages of ALS try my regime solve their affliction. Their doctors explanation later was that of  misdiagnosis. My studying my fathers fasciculation patterns allowed me to recognize their unique patterns. They are different than the normal random fasciculation. They are of a short buzzing sensation that is precisely timed anytime the involved nerve is relaxed and continues relentlessly without stopping until the nerve is voluntarily stimulated. This nerve is then involved to the point that it is dying and nothing can be done. This fasciculation reaction is strong at first but becomes less strong on a daily basis. One that is involved involves its neighboring nerve until I had 4 controlling my right thumb involved nerves. The muscles that these nerves controlled have completely atrophied. I through doing the research with my fathers involvement was able to take the Griz. after the second nerve was fully involved. The other two nerves had very mild fasciculation involvement and as the next two weeks past succumbed. No other nerves became involved. Over the past 17 years I have on at least 10 occasions had what I call pre-involvement fasciculation's. I am able to stop these fasciculation's now with Diflucan. These pre-involvement fasciculation's are slightly different but not the normal random variety. I used a special probe inside a blood pressure cuff with an oscilloscope to identify these different patterns from the normal on my father.  This was why I could recognize them so rapidly when I became involved. Over the past 5 years I have had only one of the pre-involvement series I believe because I take one Diflucan every two weeks. At that time I believe it was because I was traveling in a foreign country and forgot the Diflucan pills. Since they were not available needless to say I had a bottle flown in . I do believe one pill every two weeks by those susceptible could eradicate the disease. Diflucan is an antifungal pill made by Pfizer given to pregnant women to cure virginities; therefore, anyone who has not killed half their liver with alcohol should try it. I now keep over 4 bottles of 30 pills in reserve because if it ever for some stupid reason is outlawed I will still have a 5 year supply until something better comes along. I even contacted the president of Pfizer to see if he wanted to discuss a research project, and his answer was not at this time. Anyone can contact me at the email address below. Here is a picture of my two thumbs. I am right handed my left thumb is normal. My right thumb lacks three nerves "killed by ALS'' to stimulate the muscle therefore the muscle has atrophied.

On a more technical basis read below. The excerpt was taken From Wikipedia. This research points to mine that I believe makes the motor neurons vulnerable to attack by the specific fungus.

The defining feature of ALS is the death of both upper and lower motor neurons in the motor cortex of the brain, the brain stem, and the spinal cord. Prior to their destruction, motor neurons develop proteinaceous inclusions in their cell bodies and axons. These inclusions often contain ubiquitin, and generally incorporate one of the ALS-associated proteins: SOD1, TAR DNA binding protein (TDP-43, or TARDBP), or FUS. Interestingly, these inclusions do not stain with the dyes Congo Red or Thioflavin S, and are therefore non-amyloid aggregates.^[19][20] This is in contrast to the aggregates and plaques seen in many other neurodegenerative diseases of protein aggregation, including Alzheimer's disease, Parkinson's disease, Huntington's disease, and prion diseases.

Genetic associations include:

SOD1

The cause of ALS is not known, though an important step toward determining the cause came in 1993 when scientists discovered that mutations in the gene that produces the Cu/Zn superoxide dismutase (SOD1) enzyme were associated with some cases (approximately 20%) of familial ALS. This enzyme is a powerful antioxidant that protects the body from damage caused by superoxide, a toxic free radical generated in the mitochondria. Free radicals are highly reactive molecules produced by cells during normal metabolism again largely by the mitochondria. Free radicals can accumulate and cause damage to both mitochondrial and nuclear DNA and proteins within cells. To date, over 110 different mutations in SOD1 have been linked with the disease, some of which have a very long clinical course (e.g. H46R), while others, such as A4V, being exceptionally aggressive. Evidence suggests that failure of defenses against oxidative stress up-regulates programmed cell death (apoptosis), among many other possible consequences. Although it is not yet clear how the SOD1 gene mutation leads to motor neuron degeneration, researchers have theorized that an accumulation of free radicals may result from the faulty functioning of this gene. Current research, however, indicates that motor neuron death is not likely a result of lost or compromised dismutase activity, suggesting mutant SOD1 induces toxicity in some other way (a gain of function).^[21][22]

You can contact me Sherman Smith alsforum@hotmail.com