• Closing In On Amyotrophic Lateral Sclerosis (ALS)

    Posted March 13, 2018: by Bill Sardi

    In the land of the blind,
    a one-eyed man is king.

    Over 130 years ago modern medicine began chasing down the cause of amyotrophic lateral sclerosis (ALS) and has come up empty handed.  No one knows what causes ALS let alone what might successfully treat it.  But recent discoveries explain why.  Maybe ALS doesn’t originate in motor neuron cells but in the environmental surrounding nerve cells.

    The current predicament of ALS patients is next to hopeless. This motor neuron disease is without a known cause and there is no meaningfully effective treatment.  ALS affects 5000 newly diagnosed patients annually in the U.S.  However, published research on the origin(s) of amyotrophic lateral sclerosis (ALS – aka Lou Gehrig’s disease) is mounting at a rapid pace and may portend a therapeutic change of course.

    First described in the 1800s, modern medicine has almost run out of ideas where to search for the cause of this destructive motor neuron disease.  ALS may have many causes, which further obfuscates a cure.

    Motor neurons are nerve cells that send electrical signals to muscles.  (A video presentation that explains motor neurons can be viewed online.)  Survival for most ALS patients is 3-5 years and most ALS sufferers die due to inability to expand their lungs to breathe.

    Most ALS patients are over 40 years old at diagnosis. It affects men more than women.

    One of the problems in searching for answers to this devastating mortal disease is that an investigator will be led in different directions, many which have little application for the majority of ALS patients.

    For example, recently there has been discovery that a genetic mutation of a copper-dependent antioxidant gene (superoxide dismutase 1 or SOD1) may be at the root of ALS.  But over 100 different gene mutations for SOD1 have been linked to the inherited (familial) form of ALS that only comprises 5-10% of all cases.   So even if genetic testing confirms inherited ALS, discoveries involving SOD1 and copper have little application to the vast majority of ALS patients.

    Demand for treatment

    Ah, yes, desperate ALS patients and their loved ones demand something be done, so there is drug treatment, but it is not a cure.

    The drug Rilutek (riluzole) is FDA approved and costs ~$110 for 60 tablets.  Rilutek only addresses symptoms that emanate from toxic levels of glutamate, a nerve transmitter, and was shown to increase survival by just 8 months among older adult ALS patients.

    A new ALS drug Radicava (edaravone) has recently been approved but it costs $145,524 a year and requires onerous 1-hour infusions for 14 straight days.  Edaravone does not benefit the general ALS population and only modestly slows the decline in nerve function and comes with unwanted side effects (skin bruising, headaches, walking problems).

    Environmental factors

    Environmental factors are involved in ALS.  For example, men whose jobs frequently exposed them to formaldehyde (like funeral directors) are three times more likely to develop ALS.  But most cases of ALS do not involve people who are exposed to formaldehyde.

    Personal interest in ALS

    A reason why I chase down the origins of ALS is I lost a best friend to this disease.  My friend had a liking for Dr. Pepper as his beverage of choice.  He was raised by his grandmother and was given Dr. Pepper from when he was in a highchair.  His diet, which he had no control over as a child, produced obvious intellectual deficits that he physically compensated for (he was a world-class guitar player and he once sank twelve 3-point shots in a single basketball league game – only recently bested by Stephen Curry of the Golden State Warriors by the way).

    Did the Dr. Pepper habit have something to do with my friend’s ALS?  Soda pop is sweetened with high fructose corn syrup and that sugar is also used to enhance the growth of a nasty gut bacterium – Clostridium difficile — in laboratory experiments.

    Germ theory of ALS

    In 2005 researchers proposed that Clostridium, a soil organism that induces chronic diarrhea and colitis, is THE nerve toxin that targets ALS-susceptible individuals.  C-diff. can reside undetected in the human digestive tract and produce a toxic nerve attack similar to tetanus.  Antibiotics were proposed as treatment.

    But sadly, antibiotic trials have been met with failure.  However, direct online reports from ALS patients indicate antibiotics often work in spite of medical trials that deny that. A doctor published an online report how he successfully treated his ALS with antibiotics.  This suggests these patients have a variant form of ALS.

    But some antibiotics may be worse than the disease.  Serious toxic side effects or psychiatric events have plagued the use of some antibiotics for ALS.

    Ironically, antibiotics may bring on Clostridium difficile colitis that in turn may result in ALS.

    My friend who succumbed to ALS was also exposed to herbicides at work and noticed onset of symptoms after he was vaccinated after a mild work injury (probably for tetanus, another nerve paralyzing disease.)


    It’s not like modern medicine is dragging its feet over an orphan disease that only strikes 3.9 per 100,000 persons (17 per 100,000 in the age 70-79 group).  There are numerous studies where many natural and synthetic molecules have been screened for their potential effectiveness in treating ALS.

    Researchers have found mis-folded proteins that pass through nerve cells (through a convoluted protein-transport pathway inside living cells called the endoplasmic reticulum) in ALS patients.  But these mis-folded proteins are not unique to ALS and are observed in many other nerve and non-nervous system diseases.


    A report of a young teenage girl who succumbed to the aftereffects of the Papilloma virus vaccine, upon tissue examination it was suspected the vaccine acted as a trigger to induce ALS.  The subject of vaccination and ALS is not covered adequately in the medical literature.

    Cholesterol and ALS

    A striking new revelation is an association between statin cholesterol-lowering drug use and ALS.  The relative increased risk for ALS jumped by 9-fold to 107-fold among the various types of statin drugs.  The relative risk for ALS was apparent in all statin drugs.

    It appears there are cases of ALS that are totally statin drug induced.  In a small survey of ALS patients, 10 of 10 subjects reported reduction of symptoms when they reduced statin drug dose or withdrew from statin drug use altogether.  In one study statin drug use resulted in a 63% increase in functional decline among ALS patients.

    In weighing the benefits against risks of statin drugs among ALS patients, it may help to know that ALS is a mortal disease while statin drugs only confer an extra 3-4 days of life in the prevention of cardiovascular disease.

    Physicians are used to hearing about muscle pain, not nerve degeneration, among statin drug users.  Physicians may not be alert enough to distinguish one from the other.

    A review of circulating cholesterol levels among subjects with ALS or Alzheimer’s disease found a higher (not lower) cholesterol level correlated with 3.25 times improved survival.  Lower triglycerides and HDL cholesterol were apparent in all subjects studied and correlated with fat and calorie intake.

    Given that cholesterol reduction has been the paradigm of modern medicine over the past 4+ decades, a giant misdirection is evident.

    Diet and ALS

    Antioxidant and omega-3 oil supplementation may be beneficial for those individuals with familial (inherited) ALS (mutant SOD1). But these nutritional therapies may be of little value to the vast majority of ALS patients whose disease is not inherited. Ketogenic (90% fat) diets have also shown to be beneficial in animal experiments with ALS.  But again, the animals were genetically altered.

    A new direction

    Writing in the World Journal of Stem Cells, Greg Maguire of BioRegenerative Sciences in La Jolla, California points modern medicine in a different direction in its pursuit of a cure for ALS.  It is just like the recent revelation why oncologists can’t find a cure for cancer.  Because it is not cancer cells but the gooey connective tissue that surrounds living cells that determines whether cells become malignant or not.

    Likewise, ALS patients have motor neurons where proteins are misfolded and where cells lack energy and are vulnerable to attack by toxins or bacteria.  But therapies that directly address these issues have failed.

    Maguire suggests a new way of thinking about ALS – extracellular factors that disrupt and motor neurons.  Utilizing epigenetics, the dynamic protein-making properties of cells, he proposes utilization of stem-cell derived proteins to produce regenerated nerve cells.

    The very mention of stem cell technology may cause biologists to roll their eyes in disbelief as stem cell therapy has a long history of disappointment and failure.  The primary drawback is that injected stem cells often don’t survive very long.

    Says Maguire: “I believe the predominant cause of ALS is a breakdown of the microenvironment surrounding motor neurons.”  Then, as he explains, since 80% or more of the therapeutic properties of stem cell therapy are derived from the release of molecules (proteins) it would be advantageous to employ these proteins rather than the stem cells.  This type stem cell/protein therapy is more economical and far less problematic.  The use of stem cell-derived proteins encased in small vesicles called exosomes also averts immune rejection.

    Whether stem cell-derived protein therapy becomes a reality that is widely available to ALS patients is to be seen.  But given Maguire’s focus on the extracellular factors (connective tissue) rather than motor neurons themselves, it is worth learning more about the role of connective tissue in ALS.

    ALS starts in connective tissue

    A bacterium may be breaking down connective tissue to facilitate entry of a toxic bacterium into the blood circulation.  Clostridium difficile infection breaks down tight junctions in the gut via erosion of extracellular tissue to result in undigested proteins as well as the bacterium itself entering the blood circulation to stir up chronic inflammation and autoimmune reactions.

    The extracellular tissue (outside cells) or so-called connective tissue that connects cells exhibits abnormalities among ALS patients.  ALS patients exhibit higher levels of a water-holding gel called hyaluronic acid (HA).

    There is also increased HA in arteries of ALS sufferers.  And there is more HA in urine of ALS patients.  This could mean that more hyaluronic acid is being degraded and disposed of via arterial and urine flow.

    Hyaluronidase inhibitors

    Hyaluronic acid is broken down by an enzyme – hyaluronidase.  There are natural hyaluronidase inhibitors, in particular, quercetin, found naturally in red apple peel and red onions, as observed in ALS lab studies.  Quercetin bested 4400 other drugs and natural molecules.  Other studies confirm quercetin is a very strong inhibitor of hyaluronidase.

    It is not surprising to learn that coffee and tea consumption significantly reduce the relative risk for ALS whereas red meat increases the risk by almost 3-fold (2.96).  Coffee (chlorogenic acid) and tea (catechin) contain hyaluronidase inhibitors.

    In a promising study, ALS patients were given a polyphenol (curcumin) for 12 months and only 3.7% of ALS subjects given curcumin succumbed to their disease versus 22.2% among ALS patients given an inactive placebo pill.  Researchers concluded: “curcumin is safe and might improve the probability of survival as an add-on treatment in patients with ALS.”

    It is not surprising to learn that curcumin along with other polyphenolic molecules (resveratrol, quercetin, catechin) inhibit hyaluronidase and therefore the degradation of hyaluronic acid, the molecule that hydrates and gives substance to connective tissue and insulation for nerves.

    Inhibition of hyaluronidase has also been demonstrated to allow stem cells to mature and re-insulate (remyelinate) nerves.  (Myelin is an insulator of nerve sheaths.)

    Cells called oligodendrocytes produce myelin that insulate nerve cells.  Damage to these oligodendrocytes precedes death of motor neuron cells.  Likewise, disruption of cells that line the gut precede ALS symptoms.

    Pain and ALS

    Pain is frequently reported among ALS sufferers.  Pain may precede motor nerve dysfunction by up to 2 years.  In a large study of 424 patients, 318 (75%) reported pain of various types, including low back pain, arthritis, headache, surgical pain, pain from injury, or cancer pain, that started before their diagnosis of ALS. The majority of these complaints (82%) were attributed directly to ALS, and in 34% of cases, it was the triggering factor leading to diagnosis.  These bouts of pain throughout the body may indicate a lack of hyaluronic acid to cushion nerves.

    It is of interest to learn that the most common condition that can mimic ALS is arthritis of the spine, either within the neck or low back.  Pinching of nerve or spinal cord may produce signs and symptoms that can be confused with ALS.  MRI evaluation is necessary to rule out arthritis of the spine.  Oral hyaluronic acid often relieves low back pain that is an early sign of ALS.

    Vitamin B1

    Thiamin (vitamin B1) deficiency is associated with nervous system issues.  The recent finding of nerve pathology among ALS patients who were thiamin-deficient heightens the importance of thiamin sufficiency for ALS patients.  Thiamin deficiency produces symptoms that closely resemble ALS.

    Plan of action

    Given what has been learned herein, ALS sufferers may tentatively begin to employ certain health practices on a daily basis:

    1. Avoid over-consumption of iron-rich red meat that provides a form of iron (heme iron), which is absorbed whether the body needs it or not.  Iron limitation is more appropriate for full-grown males and post-menopausal females who accumulate iron.  Young adult females control iron via their monthly blood flow.
    2. Recognize the cholesterol theory of heart disease has been a misdirection.  Current cholesterol guidelines do not pertain to ALS sufferers.  Avoid statin cholesterol-lowering drugs and consider them to be the liver toxins that they are.
    3. Be aware of the role of gut bacteria in all disease, particularly ALS, and consume fermented foods (unsweetened pickles, sauerkraut, miso soup) and probiotics (Acidophilus, Bifidus) and prebiotics (resveratrol, beta glucan, apple pectin).  Avoid antibiotics unless absolutely necessary and be aware of the symptoms of post-antibiotic Clostridium difficile infection (bloating, watery diarrhea, blood in stool, loss of appetite, rapid heart rate, nausea, dehydration, fever).  Carvacrol derived from oil of oregano and cinnamaldehyde from cinnamon as well as allicin from fresh-crushed garlic cloves and menthol are natural C-diff. eradicators.
    4. Quercetin extracted from apple peel or onions along with other polyphenols (catechin from green tea, resveratrol from grapes or giant knotweed, curcumin from turmeric spice) inhibit hyaluronidase, the enzyme that breaks down connective tissue.  Supplementation may be beneficial.
    5. Oral hyaluronic acid (HA) stimulates fibroblast cells in the body to produce more HA and HA supplements may be employed. Oral HA is absorbed, something many physicians are unaware of.
    6. Contact with nerve toxins in herbicides and pesticides should be avoided at all cost.
    7. Vaccination against any pathogenic virus or bacterium should be avoided as a weakened immune system often plagues ALS sufferers and they will not adequately produce antibodies.  Tetanus and polio vaccination should be avoided at all cost.
    8. Avoid foods sweetened with high fructose corn syrup as fructose serves to facilitate the growth of C-diff.
    9. A commercially available yeast (Saccharomyces boulardii) inhibits the growth of C-diff.
    10. Thiamin (vitamin B1) supplements should be utilized in cases of ALS.  The fat-soluble benfotiamine form of B1 is preferred because of superior absorption.  Allithiamine is a form of vitamin B1 that crosses the blood brain barrier and should also be explored by ALS sufferers.  Magnesium is a co-factor in thiamin metabolism and should be added to a daily vitamin B1 regimen.

    ©2018 Bill Sardi, Knowledge of Health, Inc.  Not for posting on other websites.


    The Steenblock Theory of ALS

    David Steenblock MS, DO, based upon his observation that more than 9 of 10 ALS patients, when carefully questioned, report a history of neck injury or tenderness, theorizes an inflammatory breach in the blood-spinal fluid barrier permits toxic misfolded proteins to enter the central nervous system and selectively destroy motor neurons.  A special type of MRI scan can reveal this breach says Dr. Steenblock.  Given that modern medicine has few theories as to what causes ALS, Dr. Steenblock’s theory deserves consideration.  His theory is published at The Townsend Letter For Doctors & Patients.

Comments are closed.