is a neuroinflammatory condition where the central nervous system is attacked by a person’s own immune system starting at the myelin sheath. Demyelination, the destruction of the myelin that covers axons leads to a loss of speedy nerve conduction, and over time the destruction of the underlying axons and nerve cells.  After enough myelin, axon and nerve cell loss has occurred plaques or patches of scar tissue form in the white matter of the brain and spinal column. These plaques are what give the condition the name “multiple sclerosis” a term meaning “many scars.”

Once the disease process has fully developed these plaques become large enough to be seen on MRI.  MS is typically given a first diagnosis after MRI is performed to confirm the cause of the multiple signs and symptoms pointing towards MS.  Until recently MRI was the only way to determine disease progression.  After new plaques have grown enough to be visualized and compared to a previous MRI. 

There is another way to monitor disease progression before additional plaques can be visualized.  Neurofilament Light Chain (NFL) is now a readily available blood test.  This test estimates the rate of ongoing axonal destruction by counting tiny pieces of the inner structure of nerve axons in the blood serum. These filaments are first released into cerebrospinal fluid and work their way into the blood stream for clearance from the body.  Before this became a widely available blood serum test, NFL could only be measured in cerebral spinal fluid collected by a spinal tap.

What first triggers the neuroinflammation process driving MS remains an unsettled question. It seems likely there are multiple possible triggers resulting in a heterogeneous causation pattern for this neurodegenerative disease.  We do know women get it more often and men get it worse. 

There are common features in the ongoing pathology in MS no matter how it started.  Chronic demyelinating inflammation that comes in patterns of flares and/or steady progression encompasses all MS cases and their progression. Increasing mitochondrial dysfunction within all the cells of the nervous system is now well documented. A failure to successfully remyelinate and recover nerve function is the common experience of people with MS.  Once lost, a nerve controlled function is expected in conventional thought to never be regained. 

Conventional disease modifying pharmaceutical drugs currently aim at disabling the immune system attack on myelin and nerves by disabling the immune system via one mechanism or another. 

Doctor Clark’s naturopathic strategy for treating MS is to continue using every treatment that has already been tolerated and is viewed as helping.  To this we thoughtfully add trials of additional disease modifying treatments that are safe, and monitored to assure safety.  These additional treatments are aimed to further reduce neuroinflammation, encourage nerve and myelin repair, and to support mitochondrial health and function. All within a supplemented and dietary nutrient environment that supplies the materials needed for nervous system repair.  NFL marker is measured before the start of treatment and then every 2-3 months until the serum score is normal.

This naturopathic approach is accomplished through naturally occurring plant compounds,  nutrients, and off-patent drugs that are available as low cost generics. Near infrared photobiomodulation is a low risk, low cost treatment modality that stimulates mitochondrial function, shifts immune cells to an anti-inflammation state and activates quiescent stem cells already found residing within the nervous system.

Dr. Clark is accepting new patients with multiple sclerosis.

is a neuroinflammatory condition where the peripheral nervous system is attacked by a person’s own immune system starting at the myelin sheath. Demyelination, the destruction of myelin, leads to a loss of speedy nerve conduction, and over time can be followed by axon and neuron cell destruction. 

Guillain-Barre Syndrome (GBS) is a possibly more well known condition that also shares this description. The chief difference between GBS and CIDP is the time course of disease progress. GBS comes on like a freight train over days, and is immediately life threatening. When promptly rescued in the hospital, GBS often resolves in a relatively short course of weeks and months. 

Compared to GBS, CIDP starts slower, over weeks, months and even years. CIDP persists, and without effective treatment continues to slowly progress over months and years leading to ever increasing disability. Some with GBS don’t resolve, and their condition evolves into what looks like CIDP. 

Unlike multiple sclerosis, CIDP has no identifying plaques or lesions that can be visualized to confirm diagnosis. Consequently, some with CIDP languish without proper diagnosis and treatment for years after symptoms first appear.  Diagnosis is primarily a summation of symptoms combined with exclusion of other possible causes of those same symptoms. 

A classic symptom set for CIDP includes sensory, proprioception and motor neuron deficits, sometimes with involvement of autonomic nerves. There are many variants on this classic pattern that are still classified as CIDP.

Symptoms typically start at hands and feet, then over time progress up the limbs towards the torso.  Elevated protein in cerebrospinal fluid without the presence of elevated white cells is a partially confirming objective sign.  Sometimes nerve biopsies are taken to confirm demyelination but is not considered essential to knowledgeable CIDP experts.  A subset of CIDP suffers have specific antibodies driving their disease process. Everyone with a CIDP diagnosis should be screened for neurofascin 155 (NF155), contactin 1, and contactin-associated protein 1 antibodies.  If present, these antibodies indicate use of a biological drug to suppress the B cells that produce these antibodies.

While it is apparent from drug company advertising there is at least one new disease modifying treatment in the works — the current standard of care for this condition comes at a high burden on the patient, their support system, and often finances.

Corticosteroids are said to have helped some to go into complete remission. Others have found temporary and then fading improvements in their disease process and symptoms using these drugs. This drug class has a high risk of causing metabolic problems leading to diabetes and Cushings disease/syndrome. Weight gain, insomnia and irritability being common early side effects.

Plasma exchange is an involved treatment where a person’s entire blood volume is filtered at each treatment. Red and white blood cells are returned to the person while everything else in the blood is discarded and replaced with sterile substitutes added as the returning blood cells are infused. In some geographies, like Portland, Oregon, the treatment can only be received after the person has a dialysis port surgically installed into their superior vena cava of the heart. Plasma exchange has been an effective treatment for some with GBS and CIDP,  but does not work for all.

IVIg is the most common long term therapy that has helped many to slow the disease process and slowly, sometimes very, very slowly regain neurological functions.  But it too doesn’t work for everyone with CIDP. For those who benefit, this treatment has been a godsend.  IVIg infusions can be received at centers and through nurse visits at home depending on insurance coverage and services available near to the patient.  There is also a DIY version of this treatment that can be administered at home—  multi-site subcutaneous injections. 

IVIg has a high burden of time required for each treatment, often not feeling well before, during, and after treatment, and an extremely high expense. A typical maintenance schedule is an infusion every 3 weeks. Some have to take medications to tolerate the treatment, and sometimes need to spread each treatment over several days in order to achieve tolerance.  

After receiving a series of IVIg treatments a person is likely to test positive for any antibody that can be tested. This can include both hepatitis and HIV. That finding doesn’t mean a person has acquired these diseases. Just that they have received pooled blood products from people that have or had those infections. For 100 grams of Ig, somewhere between 1000-7000 pooled blood donations are required to create the dose.  This massive number of blood donations is part of the reason the treatment is so expensive. An example from 2022 is for a man in Portland, Oregon.  The cost of his proposed treatment every 3 weeks was between $180,000 and $200,000 per year.  Most people with CIDP utilizing this treatment are completely dependent on health insurance coverage, and are in great distress when that coverage lapses or is denied for any reason. 

Doctor Clark’s naturopathic strategy for treating CIDP is to continue using every treatment that is already being tolerated and viewed as helping.  To this we thoughtfully add trials of additional disease modifying treatments that are safe,  that are then monitored to assure safety.  These additional treatments are aimed to further reduce neuroinflammation, encourage nerve and myelin repair, and to support mitochondrial health and function. Within a supplemented and dietary nutrient environment that supplies the materials needed for nervous system repair.  

This naturopathic approach is accomplished through naturally occurring plant compounds,  nutrients, and off-patent drugs that are available as low cost generics. Near infrared photobiomodulation is an in office treatment that is a low risk, low cost treatment modality that stimulates mitochondrial function, shifts immune cells to anti-inflammation, and activates stem cells already found in a quiescent state within the nervous system.

Dr. Clark is accepting new patients with CIDP.

is a neurodegenerative disease that is compartmentalized to motor neurons and sometimes also the frontal-temporal executive function area of the brain.  Motor neurons have a major division in each nerve circuit from brain to muscle. Upper motor neurons are within the central nervous system with their cell bodies found inside the brain, and their axons collectively descending the full length of the spinal column to meet peripheral nerves along the way. Along the spinal cord the terminal ends of upper neuron axons form synapses with the cell bodies of lower (peripheral) motor neurons which exit the spinal column and extend throughout the body to form junctions that control the movement of muscle cells.

Neurodegeneration in ALS can originate in either upper or lower neurons eventually spreading to both upper and lower motor neurons affecting all muscles. The disease is progressive, first affecting a single body part before spreading to other motor neurons within the body.  Respiratory failure is the most common cause of death in those suffering from this disease. This happens after full bulbar/brain stem involvement of the disease stops signals to the muscles required for breathing.

The initiating cause of ALS is heterogenous and likely multifactorial. There are multiple genetic markers that correlate with significant risk, and yet are not 100% causal on their own. Genetic variants are thought to be around 10% of all ALS cases with some families having multiple generations acquiring, and then exiting life with the disease.  Most cases of ALS are sporadic, that is, without an identified genetic risk factor or other provable cause.

The most well document environmental cause of ALS is a neurotoxin called b-methylamino-L-alanine (BMAA) produced by cyanobacteria and brought to attention through its causal role in “Guam disease.”  Heavy metals and other environmental stresses have been hypothesized with some evidence to be suspected risk factors for initiating ALS. For most, its just impossible to discern why or how ALS starts. Once the disease has started, the big problem in ALS is the ongoing neuroinflammation causing neuron destruction.

Once the disease process is established there are common features driving the progression. Inclusion bodies of cellular debris, in most cases misfolded proteins and improperly constructed RNA builds up inside ALS cells and are also released into the extracellular environment. These inclusion bodies are thought by some to act as a prion vector of the disease, as these inclusion bodies move from one nerve cell to another. One of these misfolded proteins is the nuclear protein TD43 which is found aggregated in the cytoplasm of the cell of most if not all ALS cases. A toxic buildup of TD43 is being viewed as a common pathological factor in ALS disease progression.  Excitotoxicity, a phenomena where too much glutamate is released and then not recovered at the synapse between upper and lower motor neurons — is another factor contributing to cell stress, weakness and death.

Weakened neurons and an inflammatory, hostile cellular environment produced by phagocytic cells of the central and peripheral nervous system forms a vicious cycle that ultimately drives the loss of both upper and lower motor neurons. Weakened, damaged and failing nerve cells are destroyed by microglia and macrophages. Destroyed nerve cells release their cellular elements into the extracellular environment which increases inflammation, macrophage and microglia activity in response.  This external inflammation further weakens neighboring nerve cells that then die, repeating the cycle. A viscous cycle of cell death and removal leading to more cell death and removal is the driving process of ALS.

Neurofilament Light Chain (NFL) is a potent assessment of the rate of disease progression.  Recent literature has segregated persons with ALS having an NFL score of 40-60 as slow progressing, and those with scores above 100 as fast progressing.  They also note that NFL in an individual ALS patent varies little throughout the duration of their disease. While there are a few examples of individuals spontaneously achieving full remission and recovery, the typical course of ALS is 3-5 years from diagnosis to passing from this life.

There are no recognized disease modifying treatments for ALS outside of a single genetic variant involving SOD enzyme. To the dismay of many with ALS this treatment does not apply to any other variant of the disease. 

In the ongoing research there is considerable effort to identify and prove to the satisfaction of the FDA single factor treatments for this disease.  The more promising approaches include harvesting T-regulatory cells, stem cells and their precursors, growing up a large number and infusing them back into the patient to calm the microglia and macrophage driven inflammatory process. With hopes to support healing and repair. Interfering with, and preventing excitotoxicity is another potentially helpful strategy under research.

Doctor Clark’s naturopathic strategy for treating ALS is to thoughtfully add trials of potentially disease modifying treatments that are safe and monitored to assure safety.  These additional treatments are aimed to reduce neuroinflammation, converting microglia and macrophages from M1 inflammatory state to M2 anti-inflammatory state. To encourage nerve and myelin repair, and to support mitochondrial health and function. All within a supplemented and dietary nutrient environment that supplies the materials needed for nervous system repair.  

This naturopathic approach is accomplished through naturally occurring plant compounds,  nutrients, and off-patent drugs that are available as low cost generics. Near infrared photobiomodulation is a low risk, low cost treatment modality that stimulates mitochondrial function, shifts microglia and macrophages to anti-inflammatory state, and activates stem cells already found within the nervous system.  Potential disease modification is monitored by patient experience, presentation, and serial NFL scores measured every 2-3 months.

Dr. Clark welcomes people with ALS to his practice with limitations.  Patients need to be able to take oral supplements and medications. For photobiomodulation treatments, patients, along with the assistance of their caregivers must be able to get on and off the doctor’s treatment table.