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Dr. Anthony G. Payne
E-mail: Biotheoretician@gmail.com
Printable PDF Format, click here
ALS Support Regimen
Methylcobalamin, 20 mgs.,
2-3 x daily (Protects against
glutamate toxicity i.e, excitotoxic damage to motor neurons)
SAMe, 600-1800 mgs. daily
(Take with a B multiple) (Ditto)
Coenzyme Q10, 300-450
mgs. 3 x daily (with or after meals)
Vinpocetine, up to 30
mgs. daily (Protects against excessive
Calcium release intracellularly)
Octacosanol, Viobin 5
mgs. 3 x daily
Use a branched chain
amino acid supplement (But try to avoid taking sulfur-rich aminos such as
cysteine or taurine, unless you have familial amyotrophic lateral sclerosis. If you do have familial ALS, you might want to
discuss use of N-acetylcysteine with your primary care physician. See the
first abstract posted below for the rationale).
Krill Oil, 1 softgel 3
x daily with or after meals (Combats
free radicals that compromise motor nerve function. Has 300 times the
antioxidant power of vitamin E -- ORAC test)
Remilyn (Nerve growth factors. Use 1 bottle daily for 1-2 weeks, then follow
manufacturers suggested dosage regimen) Additional information below.
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Diet: Avoid sulfur and selenium-rich rich foods like
eggs, garlic and onions. ALS patients have elevated sulfur and
selenium levels, both of which contribute to this insidious condition. Calcium
is a sulfur antagonist, so calcium-rich foods should be part & parcel
of the ALS patient’s daily diet (Green vegetables especially. Avoid all
diary products, grains and cereals as these generate compounds that can
fuel inflammation).
The
Paleodiet is high in calcium and potassium, both of which help lower sulfur
and selenium levels.
http://14ushop.com/wizard/living-longer.html
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NOTE: ALS patients appear
to defectively process iron. Lactotransferrin (see the abstract below),
which is generated to deal with excess iron, is elevated in ALS.
This suggests that iron and aluminum levels should be assessed. If they are
elevated, a physician can prescribe desferroxiamine -- a drug that chelates
these metals out of the human body (Use must be monitored and supervised by
an MD or DO).
Also, a subset of ALS
patients appear to have defects in terms of their synthesis of SOD
(Superoxide Dismutase) to protect neurons from cell damaging free radicals. I
am in contact with a firm in Oregon
that has a water soluble form of SOD suitable for consumption by consumers
and patients. This product is absorbed and does get into various bodily
organs and tissues. The website for this firm is www.advantig.net. The
President of this company, Dr. Jerry Schlesser, is a licensed
naturopathic physician who has 25 years experience in R & D, and has been
published in numerous peer reviewed medical and scientific journals including
the LANCET. This tends to underscore the reliability of what he does and
offers.
There are nerve growth
factors that appear to retard the progress of ALS, at least in animal models
(See abstract below). There is a product on the market OTC that is rich in
nerve growth factors -- derived from porcine sources -- called
Remilyn (The various nerve growth factors in pigs are almost identical
to their human counterpart at the molecular level. As such, the porcine stuff
does have a physiological effect. Many MS patients tell me that porcine and
bovine-derived nerve growth factors do make a difference in their
symptomology).
Remilyn is manufactured in a lab up in Canada. You
can get it through Jim Haverlock online by going to his website: www.14ushop.com Jim has progressive MS and has
benefited greatly from the use of Remilyn (He had stem cell therapy also,
which appears to have greatly ameliorated his condition).
Dr. Anthony G. Payne
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Mitochondrial dysfunction due to mutant
copper/zinc superoxide dismutase associated with amyotrophic lateral
sclerosis is reversed by N-acetylcysteine.
Beretta S, Sala G, Mattavelli L, Ceresa C, Casciati A, Ferri A, Carri MT,
Ferrarese C.
Department of Neuroscience and Biomedical Technologies, University of
Milano-Bicocca, San Gerardo Hospital, via Donizetti, 106, 20052, Monza (MI), Italy.
We report that the expression of mutant G93A copper/zinc superoxide dismutase
(SOD1), associated with familial amyotrophic lateral sclerosis, specifically
causes a decrease in MTT reduction rate and ATP levels and an increase in
both cytosolic and mitochondrial reactive oxygen species (ROS) production in
human neuroblastoma SH-SY5Y cells compared to cells overexpressing wild-type
SOD1 and untransfected cells. Exposure to N-acetylcysteine lowers ROS
production and returns mitochondrial functional assays to control levels. No
large aggregates of human SOD1 are detectable under basal growth conditions
in any of the investigated cell lines. After proteasome activity inhibition,
SOD1 aggregates can be detected exclusively in G93A-SOD1 cells, even though
they do not per se enhance cell death compared to control cell lines. Our
findings indicate that mitochondrial homeostasis is affected by mutant
SOD1-generated ROS independently from the formation of aggregates and that
this alteration is reversed by antioxidants.
PMID: 12901835 [PubMed - indexed for MEDLINE]
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Science. 2003 Aug
8;301(5634):839-42.
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Retrograde viral
delivery of IGF-1 prolongs survival in a mouse ALS model.
Kaspar BK, Llado J, Sherkat N, Rothstein JD, Gage FH.
Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, CA
92037, USA.
Amyotrophic lateral sclerosis (ALS) is a progressive, lethal neuromuscular
disease that is associated with the degeneration of spinal and brainstem
motor neurons, leading to atrophy of limb, axial, and respiratory muscles.
The cause of ALS is unknown, and there is no effective therapy. Neurotrophic
factors are candidates for therapeutic evaluation in ALS. Although chronic delivery
of molecules to the central nervous system has proven difficult, we recently
discovered that adeno-associated virus can be retrogradely transported
efficiently from muscle to motor neurons of the spinal cord. We report that
insulin-like growth factor 1 prolongs life and delays disease progression,
even when delivered at the time of overt disease symptoms.
PMID: 12907804 [PubMed - indexed for MEDLINE]
You might also want to
check out this website: www.newhopediscoveries.com (Lorene O'Bryne, Director)
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Brain Res. 1994 Jul
4;650(1):20-31.
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The iron-binding
protein lactotransferrin is present in pathologic lesions in a variety of
neurodegenerative disorders: a comparative immunohistochemical analysis.
Leveugle B, Spik G, Perl DP, Bouras C, Fillit HM, Hof PR.
Department of Geriatrics and Adult Development, Mount Sinai School of Medicine, New York,
NY 10029.
Lactotransferrin is a glycoprotein that specifically binds and transports
iron. This protein is also believed to transport other metals such as
aluminum. Several lines of evidence indicate that iron and aluminum are
involved in the pathogenesis of many dementing diseases. In this context, the
analysis of the iron-binding protein distribution in the brains of patients
affected by neurodegenerative disorders is of particular interest. In the
present study, the distribution of lactotransferrin was analyzed by
immunohistochemistry in the cerebral cortex from patients presenting with
Alzheimer's disease, Down syndrome, amyotrophic lateral
sclerosis/parkinsonism-dementia complex of Guam,
sporadic amyotrophic lateral sclerosis, or Pick's disease. The results show
that lactotransferrin accumulates in the characteristic lesions of the
different pathologic conditions investigated. For instance, in Alzheimer's
disease and Guamanian cases, a subpopulation of neurofibrillary tangles was
intensely labeled in the hippocampal formation and inferior temporal cortex.
Senile plaques and Pick bodies were also consistently labeled. These staining
patterns were comparable to those obtained with antibodies to the
microtubule-associated protein tau and the amyloid beta A4 protein, although
generally fewer neurofibrillary tangles were positive for lactotransferrin
than for tau protein. Neuronal cytoplasmic staining with lactotransferrin
antibodies, was observed in a subpopulation of pyramidal neurons in normal
aging, and was more pronounced in Alzheimer's disease, Guamanian cases,
Pick's disease, and particularly in Down syndrome. Lactotransferrin was also
strongly associated with Betz cells and other motoneurons in the primary
motor cortex of control, Alzheimer's disease, Down syndrome, Guamanian and
Pick's disease cases. These same lactotransferrin-immunoreactive motoneurons
were severely affected in the cases with amyotrophic lateral sclerosis. It is
possible that in these neurodegenerative disorders affected neurons either
take up or synthesize lactotransferrin to an abnormally elevated rate. An
excessive accumulation of lactotransferrin, as well as transported iron and
aluminum, may lead to a cytotoxic effect resulting in the formation of
intracellular lesions and neuronal death.
PMID: 7953673
Other compounds of
possible merit in ameliorating ALS can be found in Dr. Payne's
MS Support Regimen
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© 2003 by Dr. Anthony
G. Payne. All rights reserved.
The information contained in this article is provided for informational
purposes only and should not be construed as medical advice or instruction.
Readers are advised to consult a licensed health care professional
concerning all matters related to their health and well being.
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