The Causes and Treatments of Spontaneous ALS

The Causes and Treatments

of Spontaneous ALSDavid A. Steenblock, M.S., D.O.

and Donna Hanna, NDPersonalized 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. 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

Lipoteichoic acid (from bacteria outer cell wall) Endotoxins MMP-9 Chemicals, pesticides Diesel fuel Viruses Prions, etc.

Primary Cause of ALS

3. 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.

4. 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

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.

Wijesekera LC, Leigh PN. Amyotrophic lateral sclerosis. Orphanet J Rare Dis 2009; Feb 3; 4:3.

ALS and Genetics

Every ALS patient should have an overall genetic test which can be ordered from www.23andme.com (about $100.00).

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

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

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

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.

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

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

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.

Environmental Risk Factors

The following is a list of environmental risk factors for ALS that may interact with genetic factors: 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

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

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 time-dependent manner.

Li B, et al. The NADPH oxidase is involved in lipopolysaccharide-mediated motor neuron injury. Brain Res 2008; 1226: 199-208.

The Microglia

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

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 (precursor: acetyl-L-cysteine and intravenous glutathione).

MMP-9 and Motoneurons

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: 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: 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

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

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

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.

Candida albicans

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

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

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

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

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 Immuno-pharmacol 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

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

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 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

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

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 necrosisfactor alpha that inhibit glutamatetransport in astrocytes and causeexcitation in synapses (through Calcium ion/AMPA receptors)that then release excess glutamate.

Olmos G, et al. Tumor necrosis factor alpha: a link between neuro- inflammation and excitotoxicity. Mediators Inflamm 2014; 2014: 861231.

Foods High in Tryptophan

Wheat germ Soybeans (organic) Poultry Cowpeas Cocoa (pure) Rice Quinoa Bananas

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

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

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

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

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 thebrain.

Inflammation and Prions

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

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.

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

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

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 MMP-

9), 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

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

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

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

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

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

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

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

Quercetin is a natural plant derivative that works to kill yeast in combination with the humacel, fluconazole and other antifungals. It has anti-allergic properties as well. Dose 1-2 caps, 4 times per day with or without food.

Curcumin phytosome – good intestinal anti-inflammatory – 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

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

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 anti-pain activities.

Supplements

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

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

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 intra-nasally 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

Check out our websites and sign up for our newsletter at:

http://www.stemcellmd.org http://www.stemcelltherapies.org

My clinic toll free number is800-300-1063