Over the past five years I have been contacted by 57 people with high fasciculation rates. Their increases were significant enough that they noticed a fatigue rate correlation. After discussing their condition I recommended (Diflucan) fluconazole to each one. All 28 persons remarked that their energy rate was up and their fasciculation rate had returned to a normal benign level within two weeks. This is a copy of an email received from number 28.

Take 2 30 mg Diflucan pills every other day for 2 weeks It will cure the ALS disease Permantly

Sherman,

I feel much better a week into the therapy. No more weakness, and the fasciculations are little to none compared to what they used to be. Much Much better, it took about 96 hours before it took hold, but everyday is a day better than the last. I have it all in my log. I will be sending it to you in a week.

I really think you are on to something here.

The persons who had this tremendous increase in fasciculation's for more than just a few months also seem to be having an increase in muscle cramping. They remarked some of these muscle cramps were different than normal because the muscle could not be stretched by straightening the associated body part for relief. In the case with my fathers and my als the benign fasciculation rate increased to a very disturbing rate. In my discussions with als patients their disease started with a very high random fasciculation pattern that left them more tired than normal. Then the fasciculation's become different than the normal random fasciculation. They are of a short buzzing sensation that is precisely timed and occurs anytime the involved nerve is relaxed for 10 seconds 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 for it. This fasciculation reaction is strong at first but becomes less strong on a daily basis. One that a nerve has this involvement it involves its neighboring nerve until I had 4 nerves controlling my right thumb involved. The muscles that these nerves controlled have now completely atrophied. I through doing the research with my fathers involvement was able to take the Griz after the second nerve was fully involved. Another two nerves started this buzzing fasciculation involvement and as the next two weeks past they also succumbed. No other nerves became involved. Over the past 18 years I have on at least 10 occasions had what I call pre-involvement fasciculation's. I am able to significantly reduce the beginning phase of this starting type fasciculation in 72 hours with Diflucan. These pre-involvement fasciculation's are slightly different but they are in numbers sufficient to cause a noticeable fatiguing meaning they are not quite the few 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. Now over the past 5 years I have had only one of the pre-involvement series of fasciculation and I believe this is because I take one Diflucan every two weeks. At that time I believe these fasciculation's were because I was traveling in a foreign country and forgot the Diflucan pills. Since they were not readily available needless to say I had a bottle flown in. I do believe one pill every two weeks by those susceptible to the disease could eradicate this disease. Anyone with a significant increase in fasciculation's should take Diflucan. I think with an increased general knowledge of this beginning pattern a statically significant reduction of als would occur. Diflucan is an antifungal pill made by Pfizer given to pregnant women to cure vaginities; 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 four 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

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