David A. Steenblock, M.S., D.O.
Personalized Regenerative Medicine TM
Mission Viejo, California
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.
My “wholistic” approach has been
- To look at the whole body for clues to determine what the causes are and then
- 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
Acute or chronic damage to spinal nerves.
- Damage to spinal nerves releases toxic cytokines including
- Tumor Necrosis Factor alpha (TNF-α)
- Gamma-interferon (γ-IFN)
- The spinal nerve damage opens the spinal CSF-blood barrier which allows toxins to enter the CSF and spinal cord.
Multiple forms/types of toxins that enter the CSF in ALS
- Metals (mercury, lead, etc.)
- Superoxide (O2-)
- Nitric oxide (S-nitrosylation)
- Intestinal bacteria
- Yeast metabolites
- Clostridial neurotoxins
Primary Causes of ALS
Primary Causes of Als
- Lipoteichoic acid (from bacteria outer cell wall)
- Chemicals, pesticides
- Diesel fuel
- Prions, etc.
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.
5. 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.
Paneth cells (host defense cells in the GI tract mucosa) also secrete TNF-alpha.
Toxic microbial invade the GI Track. Destroying the intestinal wall. Flowing into the bloodstream. See below.
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.
- 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).
- 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
- 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.
- 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.
- 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.
- 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.
- 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.
- 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
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.
Glass CK, et al. Mechanisms Underlying Inflammation in Neurodegeneration, Cell 2010; 140: 918-934.
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.
- 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.
- 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 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
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
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
- 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
- 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 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 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).
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.
- 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.
- 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 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
- Gastrointestinal motility
- Visceral sensitivity
- Pain and sensory perception
- Sexual activity, and
Jing F, et al. Metabolic Kinetics of 5-Hydroxytryptamine. Dig Dis Sci 2014, Jun 12 [Epub ahead of print]
- 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.
- 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.
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)
- Cocoa (pure)
- Broad beans
- Kidney beans
- Adzuki beans
- Dried dates
- Natural cheese
For ALS patients, taking 100mg, 3 times a day of 5-hydroxytryptophan (serotonin) is recommended.
- Avoid foods with monosodium glutamate (MSG) and its substitute hydralized protein names.
- Supplements that reduce glutamate include
- lemon balm,
- Resveratrol, and
Misfiled 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.
- 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 Misfiled 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 the brain.
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.
- 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 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
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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
- 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.
- 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.
- 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).
- 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.
- 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.
- The HDAC inhibitors that are useful and available are
- Butyric acid
- Ketones- See Ketogenic diet under www.stemcellmd.org
- Sulforphane- 3 day old broccoli sprouts, cruciferous vegetables
- 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.
- 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.
- 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.
- 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
My clinic toll free number is 800-300-1063