Health Conditions & Chronic Disease

The Ice Bucket Challenge: ALS & The Media

While the ice budget challenge is not new, as it has been around in one form or another during 2013-2014 it as gained national attention very recently and is now primarily linked to raising money for greater awareness, and “research” in the area of ALS [Amyotrophic Lateral Sclerosis–commonly referred to as Lou Gehrig’s Disease]. There has been criticism from a variety of corners citing the possible dangers of dumping ice-cold water over your head, perhaps leading to a Vagal Nerve response, to taking donations away from other charities.

 

Media awareness is a good thing if then the ALS society and the AMA offer real solutions.  Currently medicine offers NO HOPE, and no cure for ALS.  

The best that Western medicine has to offer is palliative treatments; the drug riluzole, which may slow the progression of the disease, however best case scenario is a 3-6 month increase in life.  This drug acts by slowing down the accumulation of the metabolite Glutamate in the brain. 

Glutamate is a chemical found in the brain that poses a toxic threat to neurons when found in high concentrations.  Dr. Russell Blaylock, MD, as a by-product of the MSG-monosodium glutamate, a flavor enhancer that is found in thousands of processed foods today, has discussed Glutamate extensively. Dr. Blaylock. MD also cites Aspartame as other potential excitotoxins that accumulates within the brain causing damage.   

The most positive thing the media can do is to discuss treatments that have shown to slow the progression of the disease, and improve the quality of life.  The Mayo Clinic recommends the use of Co-Enzyme Q10, an over the counter supplement. The compound Glutathione, another over the counter supplement, helps to reduce the Glutamate load in the brain-which is found in ALL ALS patients. Researchers have found that the artificial sweetener -Aspartame-Nutra–sweet, and the flavor enhancer MSG are contributors to the accumulation to the toxic load on the brain. 

There is hope for better treatment and slowing the disease progression.

The addition of Glutathione offers the potential for a powerful therapeutic intervention. Glutathione’s potential for treating ALS is supported by recently published research from Harvard Medical School. Glutathione is best delivered through IV drip along with Co-Enzyme Q10.  Using a Nebulizer for delivery has also been shown tobe an effective way for Glutathione to reach the brain. 

Not only may glutathione deficiency play a role in the genesis of ALS, but also it’s repletion offers the potential for a powerful therapeutic intervention. Glutathione’s potential for treating ALS is supported by recently published research from Harvard Medical School. 

The authors stated, “Perturbations of free radical homeostasis are proposed to cause ALS. A corollary hypothesis is that antioxidants should slow the disease course. One Strategy for antioxidant therapy is to manipulate levels of glutathione…” BrainRecovery.com, David Perlmutter, MD.

In closing and for futther discussion, around the world, Stem Cell treatment is offering real help, with treatments being conducted in South Korea, Germany, Israel.

References:

Galasko DR, Peskind E, Clark CM, et al. Antioxidants for Alzheimer disease: a randomized clinical trial with cerebrospinal fluid biomarker measures. Arch.Neurol. 2012;69(7):836-841.

Akaike, Akinori; Takada-Takatori, Yuki; Kume, Toshiaki; Izumi, Yasuhiko (2009), “Mechanisms of Neuroprotective Effects of Nicotine and Acetylcholinesterase Inhibitors: Role of α4 and α7 Receptors in Neuroprotection”, Journal of Molecular Neuroscience 40 (1–2): 211–6, doi:10.1007/s12031-009-9236-1, PMID 19714494

Buckingham, S. D.; Jones, A. K.; Brown, L. A.; Sattelle, D. B. (2009), “Nicotinic Acetylcholine Receptor Signaling: Roles in Alzheimer’s Disease and Amyloid Neuroprotection”, Pharmacological Review 61 (1): 39–61, doi:10.1124/pr.108.000562

Burkle, A; Huber, A; Stuchbury, G, et al. (2006), “Neuroprotective Therapies for Alzheimer’s Disease”, Current Pharmaceutical Design 12 (6): 705–717, doi:10.2174/138161206775474251, PMID 16472161

Takada-Takatori, Y; Kume, T; Izumi, Y; Ohgi, Y; Niidome, T; Fujii, T; Sugimoto, H; Akaike, A (2009), “Roles of nicotinic receptors in acetylcholinesterase inhibitor-induced neuroprotection and nicotinic receptor up-regulation”, Biological & pharmaceutical bulletin 32 (3): 318–24, doi:10.1248/bpb.32.318, PMID 19252271

Takada-Takatori, Y; Kume, T; Sugimoto, M; Katsuki, H; Sugimoto, H; Akaike, A (2006), “Acetylcholinesterase inhibitors used in treatment of Alzheimer’s disease prevent glutamate neurotoxicity via nicotinic acetylcholine receptors and phosphatidylinositol 3-kinase cascade”, Neuropharmacology 51 (3): 474–86, doi:10.1016/j.neuropharm.2006.04.007, PMID 16762377

Shimohama, S (2009), “Nicotinic receptor-mediated neuroprotection in neurodegenerative disease models”, Biological & pharmaceutical bulletin 32 (3): 332–6, doi:10.1248/bpb.32.332, PMID 19252273

The pharmacokinetics and pharmacodynamics of procysteine in amyotrophic lateral sclerosis
M. E. Cudkowicz, MD, MSc, P. M. Sexton, BS, T. Ellis, BA, D. L. Hayden, MA, P. R. Gwilt, PhD, J. Whalen, MD and R. H. Brown, Jr., MD, PhD
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Activity and Expression of Glutathione S-transferase Pi in Patients With Amyotrophic Lateral Sclerosis Kuzma M, Jamrozik Z, Baranczyk-Kuzma A Clin Chim Acta. 2006 Feb;364(1-2):217-21. Epub 2005 Aug 18

Increase in Oxidized NO Products and Reduction in Oxidized Glutathione in Cerebrospinal Fluid From Patients With Sporadic Form of Amyotrophic Lateral Sclerosis Tohgi H, Abe T, Yamazaki K, Murata T, Ishizaki E, Isobe C Neurosci Lett. 1999 Feb 5;260(3):204-6

A Study of Glutathione S-transferase pi Expression in Central Nervous System of Subjects with Amyotrophic Lateral Sclerosis Using RNA Extraction from Formalin-Fixed, Paraffin-Embedded Material Ewa Usarek, Beata Gajewska, Beata Kaz´mierczak, Magdalena Kuz’ma, Dorota Dziewulska, Anna Baranczyk-Kuzma Neurochemical Research, Vol. 30, No. 8, August 2005, pp. 1003–1007

Adaptation to G93Asuperoxide dismutase 1 in a motor neuron cell line model of amyotrophic lateral sclerosis: The role of glutathione Tartari S, D’Alessandro G, Babetto E, Rizzardini M, Conforti L, Cantoni L. FEBS J. 2009 May;276(10):2861-74.

Depletion of Reduced Glutathione Enhances Motor Neuron Degeneration in vitro and in vivo Chi L, Ke Y, Luo C, Gozal D, Liu R Neuroscience. 2007 February 9; 144(3): 991–1003.

Dr. Russell Blaylock, MD interview:

http://www.mayoclinic.org/drugs-supplements/coenzyme-q10/evidence/hrb-20059019 

http://aspartamekills.com/blaylock.htm 

http://www.wnho.net/aspartame_potential_danger.htm 

http://www.sweetpoison.com/aspartame-side-effects.html 

http://www.naturalnews.com/027758_aspartame_kidney_failure.html 

http://onlinelibrary.wiley.com 

http://www.uthscsa.edu/hscnews/singleformat2.asp?newID=1539 

http://www.ncbi.nlm.nih.gov/pubmed/20592133 

 http://www.naturalnews.com/035242_aspartame_side_effects_neurological.html#ixzz3CBqKxAQH

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