Idioma Espaņol

The key to Controlling Nerve Fascic's

Black Energy Black Matter Explained 

Magnetic North pole Shifts & Flips

Multiple Universes 

Regeneration of Damaged Surface Body Tissues

String Theory Alternative

ALS Forum Treatment and Prevention

Stopping the disease ALS in its first stage and Future Prevention

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. There apparently is genetic susceptibility 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 and have the muscular atrophy or muscle wasting and 3 nerve cells died 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. The doctors that later tested me said you know as much about the disease as we do and with your fathers experience you need to take a six month vacation because as with our experience with your father your health will decline fast at that point. Instead I took it as a challenge, ALS is a disease that even if you cure the disease the damaged nerve cells will not recover so the condition the patent is in when the disease is arrested is the condition in which that the patient will retain. That conditions reversal becomes another problem. I do believe that ALS  metastasizes, 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 muscular atrophy of the muscles controlling my right thumb was because of the loss of motor nerve cells stimulation is still gone 18 years later. There was a time when I felt they were coming back but I now feel that it is the other muscles near the muscle atrophy cells are stronger and doing some 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 tested me with another EMG and a MRI scan to make a study. This was difficult to obtain because they believed 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 in about 30% of the cases. During the second world war and in every war since there has been an statistically unexplainable percentage of veterans return with the ALS. Griseofulvan was invented during the second world war because of the 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 Griseofulvin 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. Bob Broedel can be contacted by email <bro@met.fsu.edu>. I had 17 people who had read the digest while in the beginning stages of diagnosed ALS try my regime solve their affliction. Their doctors explanation later was that there was a misdiagnosis. My studying my fathers fasciculation patterns allowed me to recognize the unique patterns. The disease starts with a very high random fasciculation pattern that actually leaves the patient more tired than normal. Then the twitching muscles or fasciculation's become different than the normal random twitching muscles or 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. These nerve cells are then involved to the point that they are dying and nothing can be done. These twitching muscles feel strong at first but becomes less strong on a daily basis. One that is involved then involves its neighboring nerve cells until I had 4 nerves controlling my right thumb involved. The muscles that these nerve cells controlled now have completed muscular atrophy. 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 the twitching muscles involved as the next two weeks past they also succumbed. No other nerve cells 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. 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 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 the 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 the disease would occur. Diflucan is an antifungal pill made by Pfizer given to pregnant women to cure vaginitis; 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. As a further note I am since 2010 taken one diflucan pill every Sunday with a prayer of thanks to contain the faciculations. Of the 38 people I have helped they are also still taking Diflucan.

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:

Type OMIM Gene Locus
ALS1 105400 SOD1 21q22.1
ALS2 205100 ALS2 2q33
ALS3 606640  ? 18q21
ALS4 602433 SETX 9q34
ALS5 602099  ? 15q15-q21.1
ALS6 608030 FUS 16p11.2
ALS7 608031  ? 20p13
ALS8 608627 VAPB 20q13.3
ALS9 611895 ANG 14q11.2
ALS10 612069 TARDBP 1p36.2
ALS11 612577 FIG4 6q21
ALS12 613435 OPTN 10p15-p14
ALS13 183090 ATXN2 12q24

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

als disease als symptoms, Amyotrophic lateral sclerosis, Lou Gehrigs disease Science Forum, scienceforum, solar, Magnetism, Fusion, Fision, big bang, nerve damage, ALS, muscular atrophy, nerve cells, muscle cell, nerve damage, ALS, muscular atrophy, nerve cells,als disease als symptoms, Amyotrophic lateral sclerosis, Lou Gehrigs disease Science Forum, scienceforum, solar, Magnetism, Fusion, Fision, big bang ALS, twitching muscles, muscular atrophy, nerve cells, muscle twitching causes, muscle wasting, muscle cell, fasciculation, nerve damage, ALS, muscular atrophy, nerve cells, muscle twitching causes, muscle wasting, muscle cell, nerve damage, ALS, twitching muscles, muscular atrophy, nerve cells, muscle wasting,als disease als symptoms, Amyotrophic lateral sclerosis, Lou Gehrigs disease Science Forum, scienceforum, solar, Magnetism, Fusion, Fision, big bang
The Baja Adventure on Blogspot!  The faanct on Facebook!
 copywrite 2004 - Penascowebmaker