| @@@STUDY SUGGESTS LOSS OF ZINC FROM SOD1 COMMON TRIGGER FOR ALL ALS
Although genetic defects that affect an enzyme called superoxide dismutase 1 (SOD1) were identified in 1993 as the cause of some cases of familial (inherited) ALS, the way that this mutated enzyme leads to ALS is still not clear. Meanwhile, even less is known about the cause of the disease in the 98 percent of people with ALS who don't have mutations in the SOD1 gene.
Still, many researchers think that the ability of defective SOD1 to cause symptoms indistinguishable from those seen in the sporadic form of the disease provides an important clue to processes that the two forms may have in common.
Now Alvaro Estévez, John Crow and Joseph Beckman of the University of Alabama, Birmingham, have uncovered a plausible role for the malfunction of SOD1 in both sporadic and familial ALS. The work was in the Dec. 24 issue of Science.
SOD1 is an enzyme, a protein that encourages specific chemical reactions to occur. Its normal role in the cell is to help neutralize free radicals, oxidizing molecules that damage cell membranes, proteins and genetic material. In addition to its protein components, SOD1 also contains two atoms each of copper and zinc.
The way in which altered SOD1 leads to the death of motor nerve cells in familial ALS has been the subject of much debate.
A new theory suggests that the loss of zinc from SOD1 may be a common factor in both familial and sporadic ALS.
However, what's become increasingly clear is that problems occur not so much because SOD1 can no longer do its normal job of neutralizing free radicals, but because the mutated version has gained some new and toxic property. Some researchers believe that the mutated form of SOD1 actually creates free radicals.
In an interesting twist to this theory, the UAB researchers found that the mutated SOD1 enzyme was only toxic to cultured nerve cells when it was deprived of its zinc molecule. However, if both the zinc and copper were removed, the resulting enzyme was not toxic, suggesting copper is necessary for the toxic effect of losing zinc. Researchers haven't yet tried removing only the copper, although they say copper is probably not toxic in itself.
Other experiments in test tubes demonstrated that zinc-deficient SOD1 produces more free radicals than it destroys.
These findings are intriguing because earlier results from Beckman's lab suggested that the SOD1mutant in familial ALS can't bind zinc as strongly as normal SOD1.
But the real significance of these results may lie in the finding that normal SOD1 also can be made harmful if it loses its zinc but retains its copper. This means that, even in the absence of a molecule-altering genetic mutation, SOD1 can behave like the mutated version under the right circumstances. Beckman speculates that, in sporadic ALS, the zinc in motor nerve cells may be sopped up by other molecules so that there isn't enough left to bind to SOD1.
This theory dovetails with previous findings by the UAB researchers that a protein called neurofilament, which is known to accumulate in degenerating motor nerve cells, can bind to zinc more strongly than SOD1. The group speculates that, in sporadic ALS, excess neurofilament or some other zinc-binding agent may sop up all of the cells' zinc and be the trigger that converts a helpful SOD1 into a harmful SOD1.
If the loss of zinc from SOD1 is to blame for ALS, it would be expected that the SOD1 in the motor nerve cells of people with familial and sporadic ALS is deficient in zinc. But, Beckman says, there's as yet no evidence that this is true. Part of the difficulty in determining the zinc status of SOD1 in nerve cells affected by ALS is the inability to isolate enough of the enzyme from these particular cells for analysis.
"It's a very challenging problem since motor neurons make up only 2 percent of the cells in the spinal cord," Beckman says. "I don't think it's possible in humans, but we are working on this in mice."
If the loss of zinc from SOD1 could be the trigger for both familial and sporadic ALS, could a person take zinc supplements to boost zinc in the affected motor nerve cells
Unfortunately, zinc isn't very permeable to the brain and Beckman estimates that the amount of zinc needed to be therapeutic would probably approach levels that are toxic in humans. But there are other options.
Because the harmful effects of losing zinc from SOD1 depend on the presence of copper, another approach is to try to shut down SOD1 entirely by removing its copper molecule. Beckman says copper chelators, compounds that bind strongly to copper, have been used to try to remove copper from SOD1 in mice and humans with modest benefit.
But, he adds, "Our results indicate that only certain types of copper chelators can pull the copper out of SOD. We are trying to synthesize better derivatives and are testing existing compounds in mice. However, the existing compounds are too toxic, at present, to try in patients."
Beckman is also looking at specific antioxidants that may counteract the effects of losing zinc from SOD1.
###Zinc-SOD1 interaction abnormality in ALS
*Normal
active SOD1이 Zn와 Cu에 결합하여 유리라디칼을 제거함으로써 신경세포파괴 억제
*Familial ALS
active SOD1에 Cu는 정상적으로 결합하나 Zn은 결합 못함으로써 발생
*sporadic ALS
다른 단백질에 Zn이 붙어버리기 때문에 active SOD1에 붙을 Zn이 결핍되어 발생
@@@THE ALS/VIRUS CONNECTION
New findings may provide the best evidence to date that a viral infection is associated with sporadic ALS
Although mutations in the SOD1 gene have long been the focus of scientific investigation into the causes of ALS, only 2 percent of people with ALS have mutations in this gene, and only 15 percent of people with ALS are likely to have the disease because of any genetic defect.
The vast majority of ALS cases are sporadic, meaning that the cause isn't known. One hypothesis that's been around for years is that ALS is triggered by a virus -- an idea made more plausible by the resemblance of ALS to polio, a disease caused by a virus that destroys the same population of nerve cells that are affected in ALS.
However, unlike in polio, evidence of a viral infection in ALS has been hard to come by. The disease doesn't seem to be contagious and viral particles haven't been detected in tissue samples or spinal fluid. There is also no evidence of an inflammatory reaction, as would be expected if the immune system were fighting off an invader, in tissue samples from people with ALS.
New, more sophisticated techniques for analyzing antibodies and genetic material have confused the matter even more by producing inconclusive or contradictory results that have linked ALS, in turn, to the HIV-1 virus, the herpes simplex I virus, the human T-lymphotropic virus, the hepatitis B virus and various enteroviruses (including the polio virus).
Now, in the January 2000 issue of Neurology, researchers led by Martina Berger, formerly of the National Reference Center for Enterovirus in France, present what may be the most convincing evidence to date demonstrating the association of a virus with sporadic ALS.
Using a very sensitive technique to amplify viral genetic material, the group found evidence for a particular virus in 88 percent of tissue samples taken from people who died of ALS, but in only 3 percent of tissue samples from people who died of other causes. Specifically, the viral material was found in the anterior horns of the spinal cord, a motor-neuron-containing region that's affected in ALS.
The virus is a member of the enterovirus family. This family includes the polio virus and viruses that cause meningitis. The virus identified in the ALS tissue samples most closely resembles a meningitis-causing virus called echovirus-7 and another virus, echovirus-6.
MDA grantee George Karpati, a neurologist at the Montreal Neurological Institute in Canada and the author of a commentary that accompanied the Berger article, is careful to point out that, although these results are intriguing, they show a correlation between the presence of this virus and ALS, not a cause-and-effect relationship. For instance, they don't show whether the virus causes ALS, or whether people with ALS are particularly susceptible to viral infection. More research is needed to determine the role of this virus, if any, in ALS.
But what would be the impact on treatment options if a virus were found to trigger ALS
The scientific community has certainly learned a lot about viral suppression from studies of the AIDS virus (HIV), the flu virus and others. In fact, anti-enteroviral drugs already in existence may be of use in slowing or halting the course of the disease if an enterovirus is to blame. It's less likely that such a hypothetical treatment would reverse advanced symptoms of the disease.
Again, although these new findings make a strong case for the association of an enterovirus with ALS, there is no evidence yet that the virus causes ALS.
If a virus is found to cause sporadic ALS, does that mean all the other theories concerning glutamate excitotoxicity, oxidative stress, misfolded proteins, etc., are wrong
In fact, these theories about the cause of ALS aren't mutually exclusive. It's more likely that several mechanisms play interrelated roles in the disease process. For instance, nerve cells infected with a virus may become susceptible to glutamate toxicity. Or nerve cells already suffering from glutamate toxicity may be more likely to succumb to the effects of a viral infection. Or viral infection may occur as a consequence of glutamate excitotoxicity, but not be, in and of itself, harmful to the nerve cells. More study is necessary to determine if, and how, these processes are related in ALS. (Echo-6, Echo-7 등의 바이러스에 감염된세포는 글루탐산독성에 취약, 또는 글루탐산독성에 노출된 세포가 바이러스에 취약해지고 구리와 함께 SOD1의 활성에 필수적인 아연의 결핍으로 인해 유리라디칼 독성이 제거되지 못한 것이 신경세포 독성을 유발한다고 추정) MMS for viruses, Curcumin, resveratrol, GSE, Goji, Nettle, Ginger root extract, St. John's wort, Quercetine, Apigenin, Schisandra, B12, L-theanine, and IV Glutathione for Glutamate toxicity, Ketogenic diet(MCT oil) such as Coconut oil for Nerve Cell recovery(inc. conversion of glutamin to inhibitory GABA comparative of Glutamate) and neuronal energy source
###Lou Gehrig's Disease --amyotrophic lateral sclerosis (ALS)
Lou Gehrig's disease or amyotrophic lateral sclerosis (ALS) causes progressive degeneration of the nerves within the central nervous system that control muscular activity. The disease generally occurs after age 50 and is more common in males. About 5 to 10 percent of cases run in families.
The first symptoms usually involve weakness and then wasting of the muscles of the hands and arms. Muscular fasciculations (spontaneous irregular contractions of small areas of muscle) and muscle spasms are also common. The throat muscles can be involved making speech difficult and eventually eating difficult as well. The prognosis is usually bleak, with progressive decline and death within 3 to 5 years. However about 20 percent survive more than 5 years and 5 percent more than 10 years.
While ALS is very challenging to treat, a comprehensive programme of natural treatments may prove very helpful and may slow or even stop the progression of the disease. A qualified health practitioner experienced in treating neurological problems is essential. ACAM - American College for Advancement in Medicine
One of the most important aspects of treatment is to check for heavy metal toxicity. Heavy metals, especially mercury, are very toxic to the nervous system. Mercury fillings usually have to be replaced with white fillings. Since mercury is released when the old fillings are removed, intravenous vitamin support, high doses of vitamin-C and homeopathic mercury are recommended after every dental session.
Following the removal of mercury fillings, it is imperative to have 10 to 20 sessions of intravenous chelation therapy to pull out all the heavy metals from the system. Some studies have shown that people with ALS have high levels of manganese, mercury and aluminum in their systems, and low levels of calcium and magnesium. Chelation therapy as well as appropriate mineral supplements will correct this.
A complete nutritional program is vital with particular emphasis on Correct Essential Oils such as Omega 3 and Omega 6 in the correct ratio, a high quality multi-mineral and vitamin supplement and a supergreen drink containing spirulina or other sea algae. Daily injections of vitamin-B-12 and folic acid are often very helpful. Vitamin-B-12 and folic acid are known to improve nerve cell function. Taken orally, these two vitamins are less effective.
Dr. Andrew Eisen of the Neuromuscular Unit at Vancouver General Hospital is conducting a trial in which he is giving men with ALS large doses of DHEA. His previous research indicated that a low level of DHEA or more probably a rapid rate of decline of DHEA may result in a male preponderance of ALS.
Dr. Hans Nieper of Hanover, West Germany has documented excellent results in the long term treatment of ALS with intravenous and oral calcium EAP (calcium 2-aminoethanol). Calcium EAP is the component of the cell membrane needed for the binding and flow of electrical charges. It also inhibits the auto-immune response.
Nieper has treated thousands of MS patients successfully with this compound and it is an officially recognized treatment for MS in Germany. In his book, Dr. Atkin's Health Revolution, (Bantam Books, 1990) New York physician, Dr. Robert Atkins discusses his successful treatment of ALS and MS with the use of calcium EAP, which he believes should be approved by the FDA on compassionate grounds.
In addition to all of the above, all dietary and lifestyle stresses must be eliminated. Food allergies, candida and parasites must also be treated appropriately. Special attention must also be paid to improving digestion and liver function.
In his patient report in the Townsend Newsletter (June, 1997), Peter Ganzel says he believes that ALS is caused by a severe acid base imbalance and outlines a detailed treatment programme. One of the recommendations is the use of Edgar Cayce's wet cell (which sends low voltage electrical impulses into the system) to help restore acid base balance.
http://64.41.99.118/charge/rq065.htm
Mercury: Lou Gehrig's Disease (ALS)
Adams, CR; et al. Mercury intoxication simulating Amyothrophic Lateral Sclerosis. JAMA, 250(5):642-3, 1983. Barber, TE. Inorganic Mercury Intoxication Reminiscent of Amyotrophic Lateral Sclerosis. J Occupat Med, 20(10):667-9, 1978.
Haley, B. Kasarskis, EJ; et al. GTP-binding proteins in amyotrophic lateral sclerosis cerebrospinal fluid. Ann Neurol, 1995.
Khare, SS; et al. Trace Element Imbalances in Amyotrophic Lateral Sclerosis. Toxicol, 11:521-33, 1990.
Pamphlett, R; Waley, P. Motor neuron uptake of low dose inorganic mercury. J Neurologic Sci, 135,:63-7, 1996.
Redhe, P; Pleva, J. Recovery From Amyotrophic Lateral Sclerosis and From Allergy After Removal of Dental Amalgam Fillings. Int J Risk Saf Medicine, 4:229-36, 1994.
http://www.bioprobe.com/reviews.aspreview_id=25
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NOTE:
The fastest known substance to man in raising the body's pH (from acid to alkaline) is Cesium.
The elements in the MoRE formula, work as a natural oral chelation that will rid the body of toxic chemicals and heavy metal materials along with having been proven to restore collogen, strengthen and heal the arterial walls, and much more.
Master Formula II is a full spectrum calcium formula that will raise the body's pH, build and restore the body and allow for a greater electrical charge within the cells.
One of the benefits of the elements in the RAANOW is to allow the cells the ability to build muscle tone.(highCoQ10-300to900mg/day ALA1000mg/day)
CEO (Correct Essential Oils) are available with the correct ratio of Omega 3 and Omega 6 which help oxygenate the cells in the body as well as a great many other benefits.
The above formulas are available at Advanced Scientific Health
RESEARCH the following for more Info:
Cesium Chloride and Cesium Carbonate in raising pH
Toxic Heavy Metals in the Body
The Master Formulas
The Cancer Page
Acidosis
###Amyotrophic Lateral Sclerosis (ALS) can be Treated Naturally
Friday, May 07, 2010 by: Luella May
(NaturalNews) Amyotrophic lateral sclerosis (ALS), otherwise known as Lou Gehrig's Disease, is a rare progressive neurodegenerative disease that affects nerve cells in the brain and spinal cord. This degeneration eventually leads to cell death, making it impossible for the brain to initiate and control muscle movement. As the disease advances to its later stages, it results in total paralysis. The cause of this nerve degeneration is thought to be the muscles not receiving enough nourishment. Therefore, in this article we will look at how we can properly nourish the muscles and delay, if not reverse, the progression of this disease.
When the muscles do not receive the nourishment they need, they waste away. As the muscles degenerate, it leads to scarring or hardening of the spinal cord, disabling the nerve cells that signal and control the muscles.
In addition to malnourished muscles, other factors thought to contribute to ALS include environmental toxins, including aluminum, mercury, and lead.
Early symptoms of ALS include muscle weakness and difficulty in swallowing or breathing. As the illness progresses, it becomes increasingly more difficult to walk, use arms and hands, speak, eat, swallow, and breathe. However, ALS doesn't usually affect the mind. Even in its advanced stages, people with ALS do not lose cognitive function, their memory and the ability to think and reason. Their ability to see, hear, smell, and touch also remain in tact.
Although, a diagnosis of ALS can be devastating, there are constructive steps that a person can take in order to treat this disease.
* Physical therapy can keep the muscles strong.
* Speech therapy can help retain the ability to talk.
* Joining a support group or seeking counseling can help deal with this disease emotionally.
@Supplements that may be beneficial when treating ALS are:
* Vitamin C, which supports many bodily functions. Besides strengthening the immune system, it also strengthens deteriorating connective tissue. Vitamin C is also instrumental in detoxifying the body.
* It is essential to supplement with calcium and magnesium. Calcium and magnesium help stabilize aluminum and mercury, excessive amounts of which have been found in people with ALS. Additionally, ALS sufferers have been found to have low levels of these important minerals. When taking calcium and magnesium it should be done at a ratio of 1:2 or 1:3.
* B-Complex Vitamins and Vitamin E play an important role in muscle and nerve function.
* Creatine has shown to be effective in increasing strength in those suffering from neuromuscular disorders.
* Acupuncture is thought to benefit nervous system function.
* Herbs that counteract sclerosis are: Cayenne, Ginger, Cinnamon, Periwinkle, Butcher's Broom, Manjistha, Chaparral, Goldenseal Root, and Comfrey Root.
* Herbs that repair the nerves are: Lady's Slipper, Kava Kava, Valerian Root, Cinnamon, Chamomile, Blue Vervain, and Passionflower.
* Herbs instrumental in detoxing the liver include milk thistle, turmeric root, and dandelion root.
* Spirulina and chlorella help repair damaged cells, nerves, and muscle tissue.
* Colloidal Gold is also effective, due to its effects on the brain and nervous system.
Lastly, it is thought that people with ALS have too much acid in their system, often due to a poor diet. It is, therefore, recommended that they follow an alkaline diet. This would necessitate eating a mostly raw diet consisting of fruits and vegetables, preferably organic. All meats, dairy products, refined grains, starches, and unhealthy oils should be eliminated, along with processed foods, junk foods, and fast foods.
Learn more: http://www.naturalnews.com/028734_ALS_remedies.html#ixzz1UaP5mg00 |
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