Download Primary Cause of ALS

The Causes and
Treatments
of Spontaneous ALS
David A. Steenblock, M.S., D.O.
and Donna Hanna, ND
Personalized Regenerative Medicine TM
Mission Viejo, California
26381 Crown Valley Pkwy, St. 130, Mission Viejo, Calif, USA; 800-300-1063
Amyotrophic Lateral Sclerosis
ALS has been quite a mystery!
 Within the spinal cord are certain neurons that
control the muscular movements to a person’s
extremities.
 With ALS, these motor neurons become
irritated, inflamed and over time slowly die,
leaving the person totally paralyzed and
leading to death within a few short years.

Glass CK, et al. Mechanisms Underlying Inflammation in Neurodegeneration,
Cell 2010; 140: 918-934.
Amyotrophic Lateral Sclerosis
My “wholistic” approach has been
 to look at the whole body for clues to
determine what the causes are and then
 to find natural treatments that can remove the
causes and correct the damage that has
already been done by the disease process.
Primary Cause of ALS
1.
Acute or chronic damage to spinal nerves.
Primary Cause of ALS
1. Damage to spinal nerves releases toxic
cytokines including
 Tumor Necrosis Factor alpha (TNF-α)
 Gamma-interferon (γ-IFN)
2. The spinal nerve damage opens the spinal
CSF-blood barrier which allows toxins to enter
the CSF and spinal cord.
Primary Cause of ALS
3.
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Multiple forms/types of toxins that enter the CSF in
ALS
Metals (mercury, lead, etc.)
Superoxide (O2-)
Cytokines
Nitric oxide (S-nitrosylation)
Intestinal bacteria
Yeast metabolites
Clostridial neurotoxins
Primary Cause of ALS
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Lipoteichoic acid (from bacteria outer cell wall)
Endotoxins
MMP-9
Chemicals, pesticides
Diesel fuel
Viruses
Prions, etc.
Primary Cause of ALS
3.
4.
Reactive oxygen species (ROS), endotoxins and
inflammation in the intestinal tract can cause gut
wall permeability (leaky gut syndrome), that allows
the oxidative stress (ROS), endotoxins and
inflammation to oxidize monocytes and T-regulatory
cells.
Biofilm are also formed in the GI tract from E.coli,
yeast, clostridia, etc.
Menozzi A, Ossiprandi MC. Assessment of enteral bacteria. Curr
Protoc Toxicol 2010, Chapter 21: Unit 21.3.
Primary Cause of ALS
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Paneth cells (host defense cells in the GI tract
mucosa) also secrete TNF-alpha.
Paneth cells
Toxic microbials
into the GI tract
Destroying the
intestinal wall
Flowing into the
bloodstream
Genetic Testing
ALS and Genetics
The general consensus is that only about 10% of
ALS patients have the inherited genetic form of
the disease (with SOD1 and/or TDP-43 gene
mutations).
 Most ALS cases are sporadic, having mutations
in other genes.
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Wijesekera LC, Leigh PN. Amyotrophic lateral sclerosis. Orphanet J
Rare Dis 2009; Feb 3; 4:3.
ALS and Genetics
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Every ALS patient should have an overall
genetic test which can be ordered from
www.23andme.com (about $100.00).
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The next step is taking that information to
www.promethease.com and
www.geneticgenie.com for gene-protein
factors (about $15.00 each).
ALS and Genetics
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Knowing a patient’s genetic mutations
may help the physician determine the type
of diet and treatments that will help
promote better overall health.
Spinal Cord Injuries
Spinal Cord Injuries
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Over the past few years, peri-spinal pain,
impingement and avulsion (a forcible tearing away)
of the spinal nerves, especially cervical 4-5 and C5-6,
have been shown to produce increased oxidative
stress through TNF-α and
gamma interferon.
C 4-5
C 5-6
Spinal Cord Injuries
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An early article by Strickland and his research
group (1996) found that ALS patients showed
severe head, neck or back injury compared to
their matched control group.
Strickland D, et al. Physical activity, trauma, and ALS: a case-control
.
study. Acta Neurol Scand 1996; 94(1):45-50
Spinal Cord Injuries
Aminoguanidine has been used in rat studies to
reduce permeability in the blood-spinal cord
barrier.
 In addition, the patient’s bone-marrow stem cells
can be used to heal the injured spinal cord
barrier so that reactive oxygen species (ROS) are
stopped from flowing into the spinal cord.
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Fan ZK, et al. The effect of aminoguanidine on compression spinal cord
injury in rats. Brain Res 2010, 25;1342:1-10.
Spinal Cord Injuries
Degenerative conditions that have impinged the spinal
arteries can lead to marginal oxygenation in the spinal
cord.
 Chronic stimulation of Vascular Endothelial Growth
Factor (VEGF) leads to down-regulation of the VEGF
gene.
Schneeweis C, et al. Chronic CRP-exposure inhibits VEGF-induced
endothelial cell migration. J Atheroscler Thromb 2010; 17(2):203-12.
Spinal Cord Injuries
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A reduction in the VEGF gene leads to a lack of
blood vessel repair and chronic hypoxia.
Chronic hypoxia leads to an increase in cytokines,
oxidative stress, and calcium influx into the motor
neurons.
A test for Nocturnal Oximetry
is recommended for ALS patients.
Spinal Cord Injuries
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If there is an intermittent oxygen deficiency,
breathing oxygen at night will
help to reduce free radical stress in the spine.
de Carvalho M, et al. Percutaneous nocturnal oximetry in
amyotrophic lateral sclerosis: periodic desaturation. Amyotroph Lateral
Scler 2009; 10(3): 154-61.
Spinal Cord Injuries
An ALS patient should have a CT scan of
his/her spine.
 Generally, over the area that has a
degenerative joint disease (DJD), the doctor
can palpate this area for spinal nerve pain.
 This area can then be treated with an injection
of buffy coat from the patient’s bone marrow
aspirate from the iliac crest.
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Environmental Risk Factors
The following is a list of environmental risk factors for
ALS that may interact with genetic factors:
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History of trauma to the brain and spinal cord,
A history of participation in varsity athletics,
A slim physique,
Strenuous physical activity,
Radiation, electrical shocks,
Cigarette smoking,
Heavy metal poisoning, and/or
Pesticide exposure.
The Motor Neuron
Neurotoxicity of the
Motoneurons
Glass CK, et al. Mechanisms Underlying Inflammation in Neurodegeneration,
Cell 2010; 140: 918-934.
TNF-α and The Motoneurons
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Inflammatory TNF-alpha from oxidative stress plays
an important role in the formation and acceleration
of spinal cord damage and motor neuron
degeneration.
Xu L, et al. Oxidative stress in immune-mediated motoneuron
destruction. Brain Res 2009; 1302: 225-32.
TNF-α and The Motoneurons
LPS and Motoneurons
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An endotoxin is a toxic lipopolysaccharide substance
in the outer membrane of gram-negative bacteria.
Endotoxins = Lipopolysaccharides
Exposure to lipopolysaccharide (LPS) leads to the
death of motor neurons in a dose- and timedependent manner.
Li B, et al. The NADPH oxidase is involved in lipopolysaccharidemediated motor neuron injury. Brain Res 2008; 1226: 199-208.
The Microglia
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Nuclear factor-kappa beta (NF-kB) is a master regulator
of inflammation and is upregulated in the spinal cords of
ALS patients.
Activation of NF-kB in microglia induces motor neuron
death in vitro and in vivo.
Frakes AE., et al. Microglia induce motor neuron death via the classical
NF-kB pathway in amyotrophic lateral sclerosis. Neurons 2014; 81(5): 1009-23.
NF-κB, TNF-α and Glutamate
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High levels of pro-inflammatory cytokines such as tumor
necrosis factor-alpha (TNF- α) have been found in ALS
patients.
TNF-α induces NF-κB activation that increases
glutamate excitotoxicity of motoneurons.
Tolosa L, et al. TNF-a potentiates glutamate-induced spinal cord
motoneuron death via NF-κB. Mol Cell Neurosci 2011; 46(1): 176-86.
Microglia
Glutathione is an important detoxifying agent
of the body.
 Therefore, there must be plenty of this
neuroprotector in the ALS patient’s body
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(precursor: acetyl-L-cysteine and intravenous
glutathione).
MMP-9 and Motoneurons
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Matrix metalloproteinases are responsible for the integrity
of the basement membrane by extracellular matrix
degradation.
MMP-9 is involved in the pathology of several neurological
diseases, including ALS.
MMP-9 levels are increased by neurovascular damage and
leads to motor neuron degeneration.
Miyazaki K, et al. Disruption of neurovascular unit prior to motor
neuron degeneration in amyotrophic lateral sclerosis. J Neurosci Res 2011;
89(5):718-28.
MMP-9 Activation
MMP-9 is activated by:
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Candida albicans, Helicobacter pylori
Epstein-Barr virus, rhinovirus, papillomavirus 8,
herpesvirus 6, HIV, cytomegalovirus, hepatitis B
TNF α, NF-kappa B
Mutant SOD1 activates MMP-9 that leads to
endoplasmic reticulum stress (ER stress) that triggers
axonal death.
Kaplan A et al. Neuronal matrix metalloproteinase-9 as a determinant
of selective neurodegeneration. Neuron 2014; 81(2): 333-48.
GI Tract Inflammation
GI Tract Inflammation
Factors that promote inflammation in the GI
tract include:
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Methylmercury, lead, cadmium, etc.
Oxidative stress (ROS)
Tumor Necrosis Factor alpha (TNFα)
Gamma interferon (γ IFN)
Yeast, Candida, Clostridia
Matrix metallopeptidase 9 (MMP-9)
Misfolded superoxide dismutase (SOD)
Superoxide free radical
GI Tract Inflammation
Doctor’s Data has the following tests. If one laboratory does the
tests, it’s easier to compare results from one patient to the next as
well as utilize for research purposes.
 Comprehensive Digestive Stool Test plus ova and parasites
(to determine what “bad” bugs are present in the gut).
 Quantitative Urine Organic Acid Test (to verify and monitor
the neurotoxins present).
 Toxic element challenge test using DMPS to determine heavy
metal poisons.
 Additional tests as needed
Toxic Metals
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There is an increased risk of ALS in people whose
cerebrospinal fluid has higher levels of lead, mercury,
cadmium, manganese, aluminum, cobalt, copper,
zinc, vanadium or uranium.
These metals are directly toxic to neurons.
Roos PM, et al. Metal concentrations in cerebrospinal fluid and
blood plasma from patients with amyotrophic lateral sclerosis. Biol Trace
Elem Res 2013; 151(2): 159-70.
Junas-Morales R, et al. Environmental factors in ALS. Presse Med
2014; 43(5): 549-54.
Methylmercury Health Effects
Nervous system deterioration
Depletes glutathione peroxidase, binds to
thiol groups
Induces mitochondrial dysfunction, reduces
ATP synthesis, increases DNA damage
Hearing, speech, vision and gait impairment
Causes involuntary muscle movements
Disrupts endocrine gland function
Causes difficulty with chewing and
swallowing
Elevated Lead, Mercury
and Cadmium in an ALS patient
Toxic Metals
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A pattern of multiple toxic metals is often seen in the
ALS cerebrospinal fluid.
Chelation therapy is recommended for patients with
these neurotoxic metals.
Mercury needs to be removed either by DMPS IV.
Lead is removed by oral or IV calcium EDTA.
If both are high, use DMPS for the mercury first.
Yeast Biofilm
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Yeast produce a microbial biofilm that promotes gut
inflammation.
A part of the biofilm is gram
negative bacteria which deposit
fragments of their outer cell wall
(endotoxins=lipopolysaccharides)
into the gut wall.
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Candida albicans
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Candida albicans begins as a yeast and then grows
into a fungus, developing hyphae (from the Greek
word: “web” – of long, branching filament
structures of a fungus).
Gut Inflammation
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As the hyphae penetrate into the gut, tumor
necrosis factor alpha (TNF α), gamma
interferon (IFNγ), MMP-9 and other
cytokines (small proteins involved in cell
signaling) are produced in the gut wall,
creating an acute phase inflammatory
condition.
Clostridium difficile
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In 2005, Dr.Longstreth and his research team published
an article hypothesizing that a clostridial species causes
ALS in susceptible individuals.
The bacteria would reside undetected in the gut and
chronically produce a toxin that targets the motor
neurons.
Longstreth WT Jr, et al. Hypothesis: a motor neuron toxin produced by
clostridial species residing in gut causes ALS. Med Hypoth 2005; 64(6): 1153-6.
Costridia Infection
Clostridia infection
in the GI tract
Clostridia Infection
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Clostridium difficile kills 14,000 people a year in America
alone.
Other Clostridium species include:
 Clostridium perfringens (Gangrene, Food poisoning)
 Clostridium tetani (Tetanus)
 Clostridium botulinum (Botulism)
 Clostridium acetobutylicum
 Clostridium haemolyticum
 Clostridium novyi
 Clostridium oedematiens
 Heliobacteria are also in the Clostridia class.
Bugs in the system. The Economist. 3 November 2012.
GI Tract Infections
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Misfolded superoxide dismutase leads to an increase
in the superoxide free radical.
This superoxide free radical can cause Colitis as well
as Crohn’s Disease.
Lactobacillus plantarum increases SOD, reduces
superoxide and reduces Colitis and Crohn’s Disease.
Jang SE, et al. Lactobacillus plantarum CLP-0611 ameliorates
colitis in mice by polarizing M1 to M2-like macrophages. Int Immunopharmacol 2014; 21(1): 186-92.
Smits HH, et al. Selective probiotic bacteria induce IL-10-producing
regulatory T cells. J Allergy Clin Immunol 2005; 115(6): 1260-7.
ALS may be caused by a variant
type of Crohn’s Disease
The Ileum
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The ileum is problematic in ALS because the stool
content from the large intestine can move backwards
through the ileocecal valve back to the terminal
ileum.
This puts fecal bacteria and yeast into an oxygen
deficient part of the body, ripe for growing anaerobic
bacteria, yeast and other noxious endotoxins.
The endotoxins and hypoxia are the two main factors
that are driving this disease, causing oxidized
monocytes.
Overgrowth in the
Distal Ileum
Other Bacterial Overgrowth
Other Markers of Overgrowth
Yeast and fungal overgrowth markers include:
 3-oxyoglutaric acid (high)
 Arabinose (high)
Malabsorption and Bacterial Markers include:
 4-Hydroxyphenylacetic acid (high)– bacterial overgrowth
 3-indoleacetic acid (high) – tryptophan metabolite
 5-hydroxyindoleacetic acid (low) – serotonin deficiency
 4-Creosote (high) – a metabolite of the clostridia species
(Creosote is a dirt mixture of polycyclic aromatic hydrocarbons
that also includes clostridia.)
Oxidative Stress and
Tryptophan
Tryptophan Deficiency
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As the gamma –interferon inflammation increases,
indoleamine 2,3-dioxygenase (IDO) levels also
increase.
The inflammatory cytokines and IDO cause tryptophan
degradation, thereby reducing the amount of
tryptophan that can be used for the synthesis of
serotonin.
The inflammation also leads to intestinal disease.
Serotonin’s Pathways
Through the Brain
Serotonin regulates
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Gastrointestinal motility
Visceral sensitivity
Emotions
Appetite
Pain and sensory perception
Cognition
Sexual activity, and
Sleep
Jing F, et al. Metabolic Kinetics of 5-Hydroxytryptamine. Dig Dis
Sci 2014, Jun 12 [Epub ahead of print]
Serotonin Deficiency
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Platelets deficient in serotonin have been
shown to be correlated with an increased risk
of death in ALS patients, strongly suggesting
that serotonin influences the course of ALS
disease.
Dupuis L et al. Platelet serotonin level predicts survival in
amyotrophic lateral sclerosis. PLoS One 2010; 5(10):e13346.
Serotonin Deficiency
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With little serotonin being absorbed into the body,
motor neurons (i.e., the trigeminal, facial, ambiguus, and
hypoglossal brainstem nuclei that require increased
serotonin) are susceptible to degeneration, especially
with excess glutamate neurotransmission.
Serotonin inhibits glutamate synaptic transmission so
serotonin deficiency causes increased glutamate release.
Sandyk R. Serotonergic mechanisms in amyotrophic lateral sclerosis.
Int J Neurosci 2006; 116(7): 775-826.
TNFα and Excess Glutamate
Activated microglia release
large amounts of tumor necrosis
factor alpha that inhibit glutamate
transport in astrocytes and cause
excitation in synapses (through
Calcium ion/AMPA receptors)
that then release excess glutamate.
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Olmos G, et al. Tumor necrosis factor alpha: a link between neuroinflammation and excitotoxicity. Mediators Inflamm 2014; 2014: 861231.
Foods High in Tryptophan
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Wheat germ
Soybeans (organic)
Poultry
Cowpeas
Cocoa (pure)
Rice
Quinoa
Bananas
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Broad beans
Kidney beans
Adzuki beans
Eggs
Potatoes
Dried dates
Spirulina
Natural cheese
For ALS patients, taking 100mg, 3 times a day of
5-hydroxytryptophan (serotonin) is recommended.
Reducing Glutamate
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Avoid foods with monosodium glutamate (MSG) and
its substitute hydralized protein names.
Supplements that reduce glutamate include
1. lemon balm,
2. N-acetyl-cysteine,
3. Resveratrol, and
4. Saffron
Misfolded Proteins
Oxidative Stress and
Misfolded Proteins
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Oxidative stress as a result of toxins, heavy metals,
etc. in the mitochondria causes calcium cycle
disturbance and the accumulation of misfolded
proteins in the endoplasmic reticulum.
The reactive oxygen species (ROS) affects the sulfur
amino acids in proteins, including cysteine and
methionine, that changes SOD to mutated SOD.
Hawkes WC and Alkan Z. Regulation of Redox Signaling by
Selenoproteins. Biol Trace Elem Res 2010; 134: 235-251.
Mutant SOD-1
ALS and MMP-9
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The misfolding of SOD-1, leaves excess, toxic
superoxide anions (O2-).
Superoxide activates MMP-9, an endopeptidase that
degrades extracellular matrix proteins.
MMP-9 damages the extracellular matrix in the gut
wall, leading to gut permeability.
This damage activates monocytes to migrate to the
injury.
Llzecka J, et al. Matrix metalloproteinase-9 (MMP-9) activity in
cerebrospinal fluid of amyotrophic lateral sclerosis patients.
Prions and Misfolded SOD1
Inflammation and Prions
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Prions are proteins on cell membranes. They can be
normal or infected - having misfolded structures.
Normal prions play important roles in cell-cell
adhesion and intracellular signaling and may therefore
be involved in cell-cell
Communication in the
brain.
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Inflammation and Prions
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Oxidative stress, inflammation and cytokines, first in the
gut, and then in the spinal nerve, damage the prions in the
monocytes and stem cells.
The inflammation causes a misfolding of the prion
proteins, and these “mutated” prions can cause protein
aggregation and misfolding of SOD-1 and perhaps the
propagation from one cell to another of motor neuron
dysfunction.
Kanouchi T, et al. Can regional spreading of amyotrophic lateral sclerosis
motor symptoms be explained by prion-like propagation? J Neurol Neurosurg
Psychiatry 2012; 83(7):739-45.
Prions and Glutamate
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In laboratory studies, mutant prions induce
abnormal ionic currents in neurons that sensitize
them to excitatory glutamate-induced, calcium ion
- mediated death.
E.coli and yeast may also have mutant prions.
Biasini E, et al. A mutant prion protein sensitizes neurons to
glutamate-induced excitotoxicity. J Neurosci 2013; 33(6): 2408-18.
Monocytes
Monocytes
 Protect tissues from foreign substances,
 Important for the formation of the heart and brain,
 Circulate through the bloodstream and tissues,
 During an infection, they differentiate into
macrophages and dendritic cells, and
 Produce inflammatory and anti-inflammatory
cytokines such as Tumor Necrosis Factor (TNF).
Monocytes
Monocytes are white blood cells (leukocytes).
Monocytes
Monocytes and platelets circulate continuously
through the gut wall and can become oxidized
by the endotoxins.
 The oxidized, defective monocytes produce
misfolded superoxide dismutase 1 (SOD-1)
and end up in the spinal cord if there is a spinal
injury.
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Monocytes and the
Endoplasmic Reticulum
Endoplasmic Reticulum
and SOD
A Summary of the Gut-Spinal Cord
Injury-Motoneuron Paradigm
Our Treatment Program
Our ALS Program
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ALS patients suffer from chronic poisoning of their
blood by endotoxins being generated by various
organisms growing in the intestinal tract.
These organisms must be removed, the toxins
removed and
the inflammation and damage repaired by the use of
stem cells in order to return to better health.
Our Treatment Program
Before coming to our clinic:
 Genetic Testing
 CT Scan of spinal cord
 Nocturnal Oximetry
 Gastrointestinal tract tests (Doctor’s Data)
 Heavy metal tests (Doctor’s Data)
Our Treatment Program
Our Treatment Program
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Detoxification with oral supplements, antibiotics, antifungals
and ozone therapy (as needed)
Heavy metal detox with chelation therapy
The ALS diet (on www.stemcellmd.org)
Bone marrow stem cell treatments
Hyperbaric oxygen therapy
Periodic acceleration therapy
Pulsed electromagnetic therapy
External Counterpulsation
Intravenous nutrients
Our Treatment Program
After sufficient detoxification, hyperbaric oxygen
therapy
 Reduces inflammation,
 Strengthens the extracellular matrix (reducing MMP9), and
 Increases vascular endothelial growth factor (VEGF)
that protects motor neurons from degeneration in ALS.
Pronto-Laborinho AC, et al. Roles of VEGF in ALS. Biomed Res Int 2014;
2014: 947513.
ALS Diet
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Avoid foods/drinks with chemicals, sugars, alcohol and toxins.
Avoid nuts, seeds, salt, vinegar and acidic foods, concentrated
juices like orange juice, grape juice, carbonated beverages.
A low protein, ketogenic diet (www.stemcellmd.org),
High amounts of greens, cruciferous vegetables, yellow
vegetables, avocado, fish oil, cod liver oil, vitamin E succinate
(2000 units per day).
Avoid raw foods, popcorn, and caffeine.
Avoid fish, dairy, barley, rye, wheat, oats, sweets.
Supplements
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Coenzyme Q10, 1200 mg per day in divided doses,
i.e. 100 mg capsules = 4 capsules, three times per day.
5-hydroxytryptophan 50 mg, 4 times per day.
Melatonin 3-10 mg, 4 times per day as tolerated. A
great free radical quencher that is able to get into the
CSF (cerebrospinal fluid).
Glutathione 200-500 mg, 4 times per day on an empty
stomach – sublingual is best to use.
N-acetylcysteine – 500 mg, 4 times per day.
Supplements
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Saffron – 1 capsule, 3 times a day. Increases blood
level of serotonin which is missing in ALS patients.
By restoring these levels the nervous system is not
as easily damaged.
Fluconazole – 200 mg once a day indefinitely.
Liquid nystatin – 100,000 units per 5 ml. Swish
and hold one teaspoon in mouth for one minute and
then swallow. Use 4 times per day, preferably
between meals.
Folic acid – 5 mg, twice per day.
Supplements
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B-complex, 100 mg in AM.
Niacin 50 mg, one with each meal (3-4 times per day).
Ginkgo biloba (EGB 761) 60 mg, 4 times per day.
Selenium 200 micrograms, 4 times per day.
Magnesium glycinate – 1 tablespoon 3 times per day
(Magonate) – take up to point of diarrhea and then
decrease dosage.
Get magnesium cream and rub into the muscles at
least once a day.
Supplements
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Broccoli Sprout Extract (Sulforaphane) –
2 capsules, 3 times per day.
Cruciferous vegetables should be used daily.
Humic acid/Fulvic Acid
Diatomaceous earth (food grade). ½ teaspoon each
day for 3 weeks, mix with food or water. Take with
nystatin, if possible.
Supplements
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Humacel – 5 capsules with each meal and at bedtime.
This blocks endotoxins (lipopolysaccharides) and
blocks the production of TNF alpha which is
produced by endotoxins at the terminal ileum
mucosa. It also inhibits yeast, viruses and prions.
If the patient will be in the sun for 30 plus minutes,
take 20 capsules orally 3 hours beforehand and try to
get the abdomen exposed to the sun as much
possible. Don’t use sunblock. Allow the sun to kill
off some of the monocytes.
Supplements
The following can be mixed together and added to
green fresh drinks:
 Sulforaphane – 30 mg, three caps twice per day
 Carnitine fumarate – 500 mg, twice per day
 Stemgevity - 3 to 12 per day. Adjust to what dose
makes the patient feel best.
 L-serine – 500 mg, two capsules, 3 times per day.
 Saffron (LEF) – 1 capsule, three times per day
 Caprylic acid – 3 capsules, 3 times per day for yeast
Supplements
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Avoid raw spinach due to oxalates.
Instead of eating raw foods that can irritate the gut
wall, use a juicer to prepare green drinks.
Small frequent meals are best.
Check out the ketogenic diet for ALS at
www.stemcellmd.org
Start with coconut butter/oil – 1 tablespoon, 3
times per day and gradually work up to 9
tablespoons per day if possible.
Supplements
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Quercetin is a natural plant derivative that works to
kill yeast in combination with the humacel,
fluconazole and other antifungals. It has antiallergic properties as well. Dose 1-2 caps, 4 times
per day with or without food.
Curcumin phytosome – good intestinal antiinflammatory – 2 capsules, 4 times per day.
Supplements
If faciculations (muscle twitching) are present,
add:
 Theanine – 200 mg, 3 times per day.
 Taurine – 500 mg, twice per day.
 Luteomax – 3 tablets, 4 times per day (good
anti-inflammatory).
Supplements
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GABA – 250 mg, 4 times per day on an empty
stomach, if possible.
VSL#3 capsules with each meal (best probiotic to
heal gut inflammation and yeast).
Methylcobalamin – 10,000 micrograms per ml.
Give 1-2 ml per day subcutaneously. Watch for
red colored urine – when you see this within 1-2
hours of getting the shot, you are getting enough,
so stay on that dose everyday. The more of this,
the more nerve regeneration occurs.
Supplements
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Histone Deacetylase Inhibitors- inhibit the histone
deacetylase enzymes which means that histone
acetylases work better. Histone acetyl transferase
acetylates (adds an acetyl molecule) to the lysine
residues in core histones which leads to a less
compact and more transcriptionally active chromatin.
These HDAC inhibitors have anti-cancer effects with
little to no toxicity, have anti-inflammatory and antipain activities.
Supplements
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The HDAC inhibitors that are useful and available
are
Butyric acid
Phenylbutyrate
Nicotinamide
Ketones- See Ketogenic diet under
www.stemcellmd.org
Sulforphane- 3 day old broccoli sprouts,
cruciferous vegetables
Curcumin
ALS Treatment
 If there is spinal nerve compression or pain in any spots in

the back (determine by pushing hard on the areas immediately
next to the vertebral processes) then these areas should be
treated with platelet rich plasma and stem cells by direct
injection.
If all of the first day’s bone marrow is used to treat the spine
then the next day’s bone marrow should be given back to the
patient intravenously in order to help heal the gut and the
injured spine via the blood rather than a direct injection as
was done the day before.
ALS Treatment
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Patients need to find a physician who has
knowledge to do at least one bone marrow treatment
and preferable two immediately.
The spinal nerve injury also needs to be injected
with stem cells immediately and then observed for
two days.
ALS Treatment
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If no improvement, the injection should be repeated
since the physician at times may have a hard time
finding the right location to inject the stem cells.
Once the patient is better then the proper testing
mentioned earlier should be done again and the
patient treated according to the results of the testing.
The use of stem cells into the CSF and/or intranasally should be done ASAP as well.
In Conclusion…

This protocol is bringing patients back from a
previous death march and helping them live
healthy lives again.
Together,
we can make a difference.
For Further Information

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Check out our websites and sign up for our
newsletter at:
http://www.stemcellmd.org
http://www.stemcelltherapies.org
My clinic toll free number is
800-300-1063