Demyelination, continued.

The last post got a little long and it included a link to another health writer who was summarizing a large amount of material on the topic of demyelination – it is amazing what you can learn by reading. I only mentioned the article, (22), briefly because it was already a long post and I hadn’t checked the other writer’s references, (it is primarily all medical research from peer reviewed journals (22.1)); and some of his recommendations are not typical, however I had read of them elsewhere so it seemed thorough and well written. The truly intriguing part for me was just how many other conditions there are that may be susceptible to demyelination and increased negative symptoms due to nerve degeneration.

I have a few of the problems that were mentioned and I have had early symptoms of nerve numbness and pain in my extremities – fingertips particularly. Health is easier to maintain then to restore once chronic conditions develop. I have managed to reverse the nerve numbness and occasional pain that I was having in my fingertips but it is with several daily or weekly health habits, not just a simple take-this-medication-once-a-day solution.

The list of psychiatric conditions that may also have demyelination summarized in an article about possible ways to regenerate myelin, (22):

  • Attention deficit hyperactivity disorder
  • Depression 
  • Bipolar disorder 
  • Dyslexia 
  • Language disorders 
  • Stuttering 
  • Autism 
  • Obsessive-compulsive disorder 
  • Cognitive decline 
  • Alzheimer’s disease
  • Tourette’s syndrome 
  • Schizophrenia 
  • Tone deafness
  • Pathological lying
  • (22)

That is quite a list – protect your oligodendrocytes, because they protect your ability to think and communicate, to control your ability to control your movements and to have stable moods, reduce anxiety, and control your ability to be able to read and speak and to be able to control your impulses and ability to prevent yourself from lying or saying things you don’t intend to say, and to be able to understand that your thoughts are your own thoughts, and to be able to hear accurately. The reference given for the information is this article: [45].

Neurology is the study of the nervous system, Psychiatry or Psychology is the study of mental health and neuropsychiatry is the study of mental symptoms caused by neurological conditions.

This topic of psychiatric conditions and other conditions that may also have demyelination is also reviewed in a summary of Neurotoxicology for neurologists: (6.Neurotoxicology). Neurology is the study of the nerves and nervous system. The nervous system includes the brain and spinal cord and all of the nerves throughout the body. It is subdivided into two main categories: the Central Nervous System (CNS) refers to the brain, the spinal cord and nerves of the brain and spinal cord; and the Peripheral Nervous System (PNS) refers to the nerves throughout the rest of the body. Neurologists are medical doctors who specialize in conditions affecting the nervous system. They may focus on a subspeciality within the field of neurology (What is a neurologist?, HealthLine) Interestingly dementia, chronic headaches, and Multiple sclerosis are mentioned as possible conditions they treat but all the other psychiatric conditions mentioned in the list that may involve demyelination are not mentioned.

The overview article on Neurotoxicology does mention that psychiatric symptoms may occur in patients with neurological conditions but that the symptoms tend to be dismissed by neurologists, and are not studied in depth, so more reliable information is needed about psychiatric symptoms presenting with neurological disorders  – see “Psychiatric and behavioural disorders.” (6.Neurotoxicology) An article for neurologists goes into more detail about psychiatric symptoms that might deserve consultation with a neurologist rather than having the patient only see a psychiatrist: Neurological syndromes which can be mistaken for psychiatric conditions. Early symptoms of Multiple sclerosis for example sometimes may be mistaken for a psychiatric condition. (Neurological syndromes) Talk therapy or psychiatric medications are not going to help a patient regenerate their myelin after all. Neuropyschiatrists are neurologists that also have a degree in psychology and specialize in treating patients with mental health and behavioral symptoms related to neurological disorders. (neuropsychiatrists)

PTSD was also mentioned as a psychiatric condition that may have demyelination.[45]

Reading the article that was referenced for the list of psychiatric conditions that may also have demyelination [45] provided an additional condition that was not added to the list in the summary article about potential ways to help regenerate myelin (22) – PTSD also may involve demyelination, and confirmed the rest of the list were mentioned [45] . The article also includes more background information about the function and development of the myelin sheath in learning and behavior.

Nerves with myelin provide a much faster signal and oligodendrocytes myelinate several different nerves so there is additional benefit in signals that work in a coordinated manner to also improve speed of function. The myelination occurs over time so the phrase practice, practice, practice applies. Peak time of life to learn skills is in our youth because that is when the majority of myelination occurs -starting in early childhood and continuing until the early twenties even up to age thirty. Healing after injury or learning a new skill later in life would still require the practice, practice, practice so the speedy pathways between groups of nerve cells develop their myelin sheaths in coordinated connections. [45]

This information may help show the difficulties faced by people with PTSD or other psychiatric conditions – the brain connections are coordinated in patterns learned from traumatic memories or are stuck in Obsessive Compulsive patterns. The problem with impulse control might also make more sense if there is simply “leaky” wiring in the brain. Signals that were intended to do one thing might end up activating other behaviors because the myelin sheath is no longer functioning as expected.

A cognitive therapy technique, involving frequent practice/repetition of new ways to talk to yourself – it might help strengthen more positive neural networks with new myelin sheath connections.

Learning new patterns of thinking, replacing traumatic or anxious thoughts that were learned as a child or during a traumatic phase of life can take time and a lot of repetition but it is possible, just like it can be possible to relearn how to walk or do other basic life skills after a stroke or traumatic physical injury. A book by Shad Helmstetter, PhD discusses how to rephrase your own internal self talk to be more positive and gives examples for a number of different types of concerns. I found the technique helpful for emotional overeating and share phrases that I wrote regarding healthy eating and lifestyle and a link to the book in a previous post: “What to Say When You’re Talking to Yourself.” The recommendation that I followed was to read the statements several times every day – for a while, months even. I don’t remember how long I read them daily but it was for quite a while and I still have the little ring binder of statements that I wrote.

Often changing behavior patterns is easier when the new pattern is created first, rather then trying to stop the old first. Build the new and then the old is no longer needed.  Addition, I found the source of that idea:

“The secret of change is to focus all of your energy not on fighting the old, but on building the new.” – Socrates

A new way to think about demyelination – what is the underlying problem? Possibly excess cell death, at rates above the ability to breakdown and remove nucleotides (ATP, ADP, UTP, UDP).

The article on demyelination and cognitive disorders, [45] , also mentioned that adenosine plays a role in signaling oligodendrocytes to make myelin and an article with more information on the topic mentions that increased amounts of ATP, ADP, UTP, UDP can signal breakdown of myelin. Increased presence of those chemicals was suggested to possibly be due to increased cell death without normal clearing away of the old cellular material. And some types of Multiple sclerosis seems to involve increased levels of the enzyme that breaks down adenosine so there would be less available to signal the production of myelin. (8.adenosine in MS)

Take home point – protect against excessive cell death and/or mitochondria damage by not having excessive glutamate (11.link) or aspartate – excitatory amino acids that may be overly available in the modern processed food diet – and by having adequate magnesium to protect the cells from their interior by providing the needed energy to block ion channels in the cell membrane and prevent excessive amounts of calcium, glutamate or aspartate from being able to cross the cell membrane and enter the cell’s interior.

As usual however, it is not that simple, (not that avoiding glutamate and aspartate in the diet is easy, they are in many processed foods), other things can also cause excessive cell death.

  • Exposure to toxins in the environment or due to drug use, illicit or legal, can cause excessive cell death and lead to demyelination disorders. An overview:(6.Neurotoxicology)
  • Lack of oxygen can also be a cause. Lack of nutrients in general can increase the breakdown of cellular parts to provide enough nutrients however if malnutrition is severe and ongoing the breakdown (autophagy) can become excessive. (7.Metabolic Stress, Autophagy & Cell Death)
  • Traumatic injury and infection can increase the  rate of cell death above the level that the body’s detoxification systems can cope with clearing away the cellular material. Traumatic injury is associated with increased risk for infection for reasons that are not well understood, the immune system is considered functionally suppressed: (10.Immunobiology of Trauma) Also mentioned briefly in the Skeletal Muscle section of this overview: (6.Neurotoxicology).
  • Anything that causes excess oxidative stress may cause increased rates of mitochondria breakdown so protecting against stress is protecting the mitochondria which is protecting the cells. (7.Metabolic Stress, Autophagy & Cell Death) Mitochondria are the main energy producers within cells and make up about thirty percent of the volume of cardiac/heart cells. Other type of mitochondrial problems can also increase risk of their switching from promoting health through energy production into a mode that promotes cell death. One of the roles mitochondria play in normal health is storage of excess intracellular calcium. If the mitochondria become dysfunctional then the extra calcium is released into the cell where it can signal increased activity such as release of cannabinoids from the membranes. (9.mitochondria in CVD)

This is approaching really long again, so I am stopping here for now.

/Disclosure: This information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes./ 

  1. Jordan Fallis, 27 Proven Ways to Promote the Regeneration of Myelin. Feb. 18, 2017, Optimal Living Dynamics,   https://www.optimallivingdynamics.com/blog/25-proven-ways-to-promote-the-regeneration-of-myelin (22)
  2. Reference list: https://www.optimallivingdynamics.com/myelin-references (22.1)
  3. R. Douglas Fields, White Matter in Learning, Cognition, and Psychiatric DisordersTrends Neurosci. 2008 Jul; 31(7): 361–370.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2486416/ [45]
  4. Butler CZeman AZJ, Neurological syndromes which can be mistaken for psychiatric conditions
  5. Anne Masi, Marilena M. DeMayo, Nicholas Glozier, Adam J. Guastella, An Overview of Autism Spectrum Disorder, Heterogeneity and Treatment Options. Neuroscience Bulletin, Vol 33, Iss 2, pp 183–193, https://link.springer.com/article/10.1007%2Fs12264-017-0100-y (autism link)
  6. Harris JBBlain PG, Neurotoxicology: what the neurologist needs to know.

    (6.Neurotoxicology)

  7. Brian J. Altman, Jeffrey C. Rathmell, Metabolic Stress in Autophagy and Cell Death Pathways. Cold Spring Harb Perspect Biol. 2012 Sep 1;4(9):a008763 http://cshperspectives.cshlp.org/content/4/9/a008763.full (7.Metabolic Stress & Cell Death)
  8. Marek Cieślak, Filip Kukulski, Michał Komoszyński, Emerging Role of Extracellular Nucleotides and Adenosine in Multiple sclerosisPurinergic Signal. 2011 Dec; 7(4): 393–402.   https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3224637/ (8.adenosine in MS)
  9. Sang-Bing Ong, Asa B. Gustafsson, New roles for mitochondria in cell death in the reperfused myocardium. Cardiovascular Research, Vol. 94, Issue 2, 1 May 2012, pp 190–196, https://academic.oup.com/cardiovascres/article/94/2/190/268169 (9.mitochondria in CVD)
  10. Dr. Daniel Remick, pre-ARC Director, Immunobiology of Trauma, pre-Affinity Research Collaborative (ARC), Boston University Medical Center, http://www.bumc.bu.edu/evanscenteribr/files/2009/07/pre-arcimmunologytrauma.pdf  (10.Immunobiology of Trauma)
  11. Howard Prentice, Jigar Pravinchandra Modi, Jang-Yen Wu, Mechanisms of Neuronal Protection against Excitotoxicity, Endoplasmic Reticulum Stress, and Mitochondrial Dysfunction in Stroke and Neurodegenerative Diseases. Oxidative Medicine and Cellular Longevity, Vol. 2015, Article ID 964518, 7 pages,Hindawi.com https://www.hindawi.com/journals/omcl/2015/964518/ (11.link
  12. Blaylock, R.L. (1996). Excitotoxins: The Taste That Kills. Health Press. ISBN 0-929173-25-2
  13. Blaylock, R.L. (a neurosurgeon) podcast Excitotoxinshttp://www.blaylockhealthchannel.com/bhc-ep-18-excitotoxins (Excitotoxins podcast)
  14. Excitotoxicity, Wikipedia, https://en.wikipedia.org/wiki/Excitotoxicity (Excitotoxicity)
  15. Aspartic Acid, Wikipedia, https://en.wikipedia.org/wiki/Aspartic_acid (Aspartic Acid/Aspartate)

Good news/Bad news about Multiple sclerosis research

The good news about Multiple sclerosis (MS) research is that there seems to have been a major breakthrough in treatment, the bad news is that research regarding demyelinating disorders which includes MS seems to have slowed down (1) – finding a solution, a medical answer, that isn’t politically approved of or one that is able to be easily patent protected may be the reason for the bad news. Finding an answer that you don’t like shouldn’t mean we stop asking the question. Work is progressing on genetic modification of mitochondrial DNA differences that can cause demyelination disorders and success has been seen in animal models for disease. Aging increases the risk for different types of mitochondrial DNA changes that can cause a variety of symptoms and diseases. (mitoTALENS/session by Moraes/28)

(Ubiquitin (a protein, not the same as CoQ10/ubiquinone, an electron carrying quinone involved in energy metabolism, 29) is needed for identifying which mitochondria are damaged and need to be recycled in the normal way, by autophagy/mitophagy, which involves the debris being taken into a container particle called lysosomes – imagine a cellular vacuum cleaner that can then recycle any useful material and discard any non-useful, potentially toxic material. See the session on Mitochondria in Parkinson’s Disease/Youle: 28)

Cannabinoids seem to be the good news treatment for MS in humans, whether as purified extracts of medical marijuana or as the whole product which can contain many cannabinoids and medically active terpenes.  An overview published in 2016 regarding the role of cannabinoids in neurology in various types of autoimmune disease: (2). An overview of the role of cannabinoids in neuroinflammatory conditions published in 2008: (3). An opinion article published in 2018 regarding the potential role of cannabidiol ( a non-euphoric cannabinoid) to improve mobility for patients with Multiple sclerosis: (4).

What is Multiple sclerosis?

Multiple sclerosis is a chronic condition that seems to be autoimmune in nature where the body is breaking down the protective coating around the branching segments between nerves. The coating is called the myelin sheath and it acts a little like the plastic coating around an extension cord. Myelin on a nerve fiber or plastic on an extension cord keeps the electrical signals on the inside and out of danger of creating sparks elsewhere along the path of the cord or nerve fiber.

What are cannabinoids?

Cannabinoids are directly involved in making strong and flexible cell membranes as they are building blocks that make up portions of the membrane, like bricks in a wall. They can also be signaling chemicals that can be activated when released from the membrane. Excess calcium inside of a cell can be a signal that causes the release of cannabinoids. Once they are released they break down into their two basic components, phospholipids and a free fatty acid, often arachidonic acid. The problem is two part – 1) both of the components of cannabinoids once they are released from the membrane can become signaling chemicals that can lead to increased inflammation, NSAID pain killers (aspirin, naproxen, ibuprofen helped reduce level of fatigue experienced by MS patients) may help block the negative effects of excess free arachidonic acid (21); 2) if too many bricks are released from the wall, then the wall may no longer function – the plastic coating on the extension cord may allow sparks through that can be a risk for an electrical fire. In the case of Multiple sclerosis the nerve damage and lack of myelin sheathing around nerve fibers causes difficulties with muscle control and the patient may have increasing difficulty walking and doing other normal daily tasks.

Preventing the increased release of cannabinoids from the membrane walls would likely to the best plan for preventing the resulting increase in inflammatory signaling chemicals they form and the reduction in membrane function. The amount of cannabinoids present can cause opposite effects, small or medium amounts can have beneficial effects while large amounts may have significantly different effects. Mitochondria are the main energy production center of the cell, where sugar is turned into a usable form of energy with the chemical shorthand name ATP or ADP. Both are phosphochemicals differing in the number of phosphate groups, adenosine tri-phosphate and adenosine di-phosphate. The amount of calcium within the cell and within the mitochondria may be different and cannabinoid can affect the movement across the mitochondrial membrane and cause differenct effects depending on the amount of calcium in each area and the amount of cannabinoids that are present. It’s complicated is the short story. This article goes into a longer  but still simplified description of the chemistry. (23)

And part of the point is that having adequate cannabinoids and adequate phosphonutrients and adequate but not excessive calcium are all important for cellular health and the ability to produce energy – and to not be fatigued – excessively tired all of the time. And in order to have adequate calcium but not excessive the cells need adequate magnesium and adequate protein and phosphonutrients in order to hold it ready for use – like taxicabs circling the block ready to discharge magnesium as a free ion when and where it is needed. The topic of magnesium, and the need for protein and phosphonutrients was introduced in a recent post. Magnesium blocks entry of excess calcium from being able to enter the interior of the cell, where it can cause increased release of cannabinoids from their storage positions within the cell membranes. Ibuprofen, but not other NSAIDs such as naproxen, also help reduce the amount of breakdown of cannabinoids. (pp 82-83, 24)

What are oligodendrocytes?

A type of specialized brain cell called oligodendrocytes are responsible for building or repairing the myelin sheath. Multiple sclerosis involves increased loss of oligodendrocytes. The specialized cells have calcium permeable glutamate receptors and are more susceptible to oxidative stress than average cells so they are particularly at risk for being damaged by ongoing emotional or physical stress or a traumatic brain injury. (6) Sphingomyelin is one of the building blocks of the myelin sheath, (7),  and is formed by oligodendrocytes. (8)

The body is complicated and needs many/all of the nutrients for optimal health. More nutrients and other lifestyle issues that may benefit myelin production or increase risk are discussed in a list of tips for regenerating myelin, phosphatidylserine, a phospholipid, is one of the recommendations; other conditions that may include myelin breakdown besides Multiple sclerosis are also mentioned: (22). 

Problems with vitamin D availability may also be involved in the body being more prone to autoimmune reactions by the immune system (attack on our own healthy cells instead of only attacking foreign or damaged cells); and on the natural building or repair of the myelin sheath. (5) And just to keep things interesting – iron is important but too much within the oligodendrocytes may increase risk for MS; polyunsaturated fats are also important but their reactivity may increase risk to the oligodendrocytes from oxidative stress; lack of Nrf2 may be involved in the susceptibility to oxidative stress in the development of MS due to damage to the oligodendrocytes; and the oligodendrocytes have an abundance of calcium permeable glutamate receptors so excess glutamate may increase risk of excess calcium entry into the cells which can lead to cell death. (8)

Summary points for protecting oligodendrocytes –

  • all nutrients are important, (22), but balance is also important.
  • Avoid excess emotional and physical stress if possible.
  • Adequate iron is important because the oligodendrocytes need more than average in order to be able to make the myelin sheath. Some patients may have an underlying genetic difference that leads to their needing supplementation of a well absorbed form of iron throughout their life. Genetic screening and individualized metabolic guidance may be needed for optimal treatment of patients with MS as it may have differing causes. A true autoimmune antibody/antigen has not been identified. (10)
  • In general however, avoid excess iron (fortified breakfast cereals and meats for example; men and menopausal women who eat large servings of very iron-fortified foods or large servings of iron rich meats can be more at risk for iron overload. Donating blood occasionally can benefit society and may help protect against the risk of iron overload for people who do not menstruate. Food sources of iron and more information about donating blood: (9) Iron overload can be a cancer risk and tends to be more common than iron deficiency in the non-menstruating population.(11))
  • and avoid excess free glutamate (frequently used in seasonings and naturally found in fermented products such as soy sauce. It is in many processed foods, (12)).
  • Eat a balance of omega 3, (22), and omega 6 polyunsaturated fatty acids.
  • Eat plenty of antioxidant rich foods regularly that also include Nrf2 promoting phytonutrients and other phospholipid containing nutrients. Here is some Nrf2 promoting foods and menu ideas: G10: Nrf2 Promoting Foods.
  • And cannabinoids or other phospholipid/phosphonutrient containing foods include these, many of which are also Nrf2 promoting foods:

Food Sources of Phospholipids and other phospho-nutrients, a partial list:

Hemp seed kernels and oil; Artemisia turanica/wormwood leaf; amaranth seed; asparagus; avocado fruit or the inner kernel, dried and powdered; beans/legumes; cardamom seeds and powder; carrots; celery stalks and leaves; cocoa beans and cocoa powder, baker’s chocolate, dark chocolate and to a lesser amount milk chocolate and chocolate syrup; coconut; cumin seed/powder; fennel seed, flax seed, pine nuts; sesame seeds, pumpkin seed kernels, squash seeds; butternut squash and pumpkin; gingko leaf; grapefruit and orange juice with the pulp; Jerusalem artichoke (this is a root vegetable rather than a green artichoke); lettuce, spinach and mustard leaves and other leafy green vegetables and herbs; nuts/peanuts, cashews, walnuts; oats; okra seeds; onion root, leek leaves, garlic;  parsnip root; pomegranate seeds and pomegranate peel extract;rice, white or brown but the bran is the best source; rosemary; sorghum;  sweet potato or yam; buckwheat (a seed botanically that is not wheat and is gluten free); wheat. (G.26)

The current treatments for Multiple sclerosis are very costly, and may not help all patients while also tending to cause negative side effects.

Returning to the original question – why has the ratio of research being published about demyelinating disorders declined since 2013? It is possible that the answer might be that medical marijuana or a recommendation to eat more dark cocoa and beans, nuts, and seeds is not as profitable as the older MS treatments may average $60,000 per year and newer treatments cost 25-60% more than that, (13), which would be an average prescription cost of $75,000-96,000 per year per patient with Multiple sclerosis. Good quality cocoa is expensive but can fit within most grocery budgets. Being a medical marijuana patient might cost around $12,000 per year for a patient using it several times each day. Use of ibuprofen daily might cost a few hundred dollars per year depending on the amount used and whether it was a name brand or off brand. (21(24) (Note – long term use of ibuprofen may cause intestinal problems, ginger (about 1/2 teaspoon) can be healing for the intestines and help with pain relief as well as ibuprofen and provided better pain relief when used in combination with ibuprofen in a study with arthritis patients. Ginger may be reducing inflammation by reducing the amount of cannabinoid breakdown to free arachidonic acids and preventing transformation into inflammatory eicosanoids. (27))

Efficacy and negative side effects are also worth considering – for that $60,000-96,000/year price tag only half of the patients may gain health benefits while many will experience negative side effects in addition to needing time and copays for office visits to receive some types of treatments. Fewer than half of patients receiving interferon-β treatment were found to benefit medically and many experienced side effects. (13)

The pharmaceutical industry frequently does medical research involving new drug treatments. The use of medical marijuana for the treatment of Multiple sclerosis or other demyelinating disorders is not legal at the Federal level as the herb is still scheduled as a substance with no medical benefit. Private research in states that have legalized medical use could possibly be performed however. Enrolling patients would likely need to be by self selection though, and for comparison purposes an experimental group of patients could be given a phospholipid rich diet plan to follow and a control group of patients receiving standard pharmaceutical treatments could also be followed to compare health outcomes with the current standard of care.

How many patients have Multiple sclerosis?

More math – there are about 400,000 people in the U.S. with Multiple sclerosis and about 10,000 newly diagnosed patients each year. (14) Averaging the cost of standard treatments to $78,000 per year would mean the 400,000 patients require $31,200,000,000 per year in pharmaceutical care. Thirty one billion dollars would buy a lot of cocoa. The number of patients living with the condition globally is estimated to be around 2.3 million people. (15) If they all received treatment at the average U.S. cost it would require $179.4 billion in care.

People living farther from the equator tend to have a greater risk for developing Multiple sclerosis so vitamin D deficiency may be involved.

Looking at the global distribution map on the link does visually suggest that vitamin D deficiency may be involved – it is not as much of a risk for nations around the equator where more sunshine would consistently be available.  Genetic differences may also be involved as it is more of a risk for Caucasians and people of central and northern European descent. It is rare for Inuits, Aborigines and Maoris. (14) (The Inuit native diet is rich in vitamin D from seafood sources.) A map of distribution risk across the U.S. also suggests a sunshine factor – rates below the 37th parallel are reduced compared to farther north. (15)

Sphingomyelin is found in the diet but needs to be made by the oligodendrocytes.

Why discuss eating cocoa or sources of phospholipids or vitamin D? Why not just eat sphingomyelin? We do eat some but our digestive systems break it down into smaller types of fats, (16), and then our oligodendrocytes have to rebuild it. Sphingomyelin tends to be found with cholesterol within the body, and both can affect the digestion of the other. (16)

Genetic differences may be involved in risk for MS. Variations in genes involved in Vitamin D metabolism may be a risk factor. There also may be differences in the cannabinoid metabolism involved or in other metabolic pathways.

Vitamin D can be made out of cholesterol when our skin is exposed to adequate sunshine. Genetic differences in vitamin D metabolism may be why some people are more prone to developing multiple sclerosis than others – speculatively. Genetic differences in vitamin D metabolism have been studied in relation with multiple sclerosis risk and a correlation was found however studies with supplementation have been inconclusive. (17) One nutrient solutions can not solve multiple nutrient problems – adequate iron but not too much, adequate balance of polyunsaturated fats to promote health without increasing inflammation, avoiding excess free dietary glutamate, and having adequate phospholipids and Nrf2 promoting foods in the diet may also all be important – in addition to having adequate vitamin D in the diet or from sunshine or tanning lights.

Vegetarian based diets include many foods that help reduce inflammation & protect against oxidative stress, & may save money.

Some more good news – a vegetarian based diet can provide many of those dietary factors and save money (about $750/year, (18)) compared to a meat based diet (which tends to be more inflammatory – i.e. oxidative stress promoting). More math – the economical vegetarian diet (2015 U.S. prices) was estimated to cost about $2,762/year which would add up to $6,353 million per year for the 2.3 million global population of people with MS instead of the $179.4 billion that would be needed for current pharmaceutical treatments for Multiple sclerosis. Phosholipid rich, Nrf2 promoting foods can also provide a good balance of omega 3 fatty acids and include sources of vitamin D and iron and tend to include many high quality vegetarian sources of protein such as nuts, beans, and seeds.

Cocoa has been found to reduce fatigue for MS patients and is a good source of phospholipids and Nrf2 promoting flavonoids.

Better news – cocoa, which is made from a bean that is rich in flavonoids, which are Nrf2 promoting phytonutrients, G10: Nrf2 Promoting Foods, and is a good source of phospholipids, (G.26), has been found to help reduce fatigue levels in patients with Multiple sclerosis while not increasing high blood sugar risk factors. (19)

Skip the sugar if possible, Insulin resistance may increase breakdown of the myelin sheath.

I add a spoonful of dark cocoa powder (unsweetened Baking cocoa) to my coffee – like mocha coffee without the syrup. Once you stop using sugar your taste buds adjust to not needing as much sweet taste – or add a little sugar or honey but artificial sweeteners may not be that helpful because the sweet taste is still signaling the body to increase insulin levels which then increases appetite and studies have found snacking calories are then increased -resulting in no overall reduction in calorie intake. Avoiding insulin resistance, frequently a problem with Type 2 Diabetes and Metabolic Syndrome, may also help protect against Multiple sclerosis risk as it may have something to do with the breakdown of the myelin sheath. (20)

/Disclosure: This information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes. Thanks./ 

  1. James Lyons-Weiler, *A graph of all research studies regarding demylinating disorders such as Multiple sclerosis as a ratio of all medical research studies over time – there has been a significant decrease in the ratio since 2013. The graph begins with approximately 4/100,000 studies in 1944, peaks at approximately 46/100,000 in 1998/1999 and drops to approximately 7/100,000 in 2017/2018.   https://twitter.com/lifebiomedguru/status/1021794538682236929 (1)
  2. Katz D, Katz I, Shoenfeld Y,  Mini Review, Open Access, Cannabis and Autoimmunity – The Neurologic Perspective: A Brief Review. June 2, 2016, J Neurology, Neuromedicine. http://www.jneurology.com/articles/cannabis-and-autoimmunity–the-neurologic-perspective-a-brief-review.html (2)
  3. G. A. Cabral, L. Griffin-Thomas, Cannabinoids as Therapeutic Agents for Ablating Neuroinflammatory Disease. Endocr Metab Immune Disord Drug Targets. 2008 Sep; 8(3): 159–172.   https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2750822/ (3)
  4. Thorston Rudroff, Jacob Sosnoff,Cannabidiol to Improve Mobility in People with Multiple Sclerosis. Opinion Article, Front. Neurol., 22 March 2018.   https://www.frontiersin.org/articles/10.3389/fneur.2018.00183/full (4)
  5. Cell-based study reveals that vitamin D can drive the activity of neural stem cells that promote myelin repair, MS Society of Canada, March 30, 2015, https://mssociety.ca/research-news/article/cell-based-study-reveals-that-vitamin-d-can-drive-the-activity-of-neural-stem-cells-that-promote-myelin-repair (5)
  6. Attila Köfalvi, Cannabinoids and the Brain, Springer Science & Business MediaDec 22, 2007, pp 342 and 344, https://books.google.com/books?id=ZNIorLciZCoC&pg=PA342&lpg=PA342&dq=myelin+sheath+cannabinoid+metabolite&source=bl&ots=t0vcsRm2HK&sig=oDbCl2JBArCt9s5KT8xawwBrv5M&hl=en&sa=X&ved=0ahUKEwjf2MS3xbrcAhUBI6wKHdIEDbUQ6AEISDAE#v=onepage&q=myelin%20sheath%20cannabinoid%20metabolite&f=false (6)
  7. ElenaPosse de Chaves, Simonetta Sipione, Sphingolipids and gangliosides of the nervous system in membrane function and dysfunction. Frontiers in Membrane Biochemistry, FEBS Letters, Vol 584, Issue 9, 3 May 2010, Pages 1748-1759, ScienceDirect,   https://www.sciencedirect.com/science/article/pii/S0014579309010564
    (7)
  8. Arundhati Jana, Kalipada Pahan, Sphingolipids in Multiple sclerosisNeuromolecular Med. 2010 Dec; 12(4): 351–361.   https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2987401/ (8)
  9. Iron-Rich Food-List of Meats, Vegetables and Meals, American Red Cross, https://www.redcrossblood.org/donate-blood/blood-donation-process/before-during-after/iron-blood-donation/iron-rich-foods.html (9)
  10. Susan J. van Rensburg,Maritha J. Kotze, Ronald van Toorn, The conundrum of iron in multiple sclerosis – time for an individualised approach. Metab Brain Dis. 2012 Sep; 27(3): 239–253.   https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3402663/ (10)

  11. Iron: The Double-Edged Sword, The Physician’s Committee for Responsible Medicine, https://www.pcrm.org/health/cancer-resources/diet-cancer/nutrition/iron-the-double-edged-sword (11)
  12. Dr. Amy Yasko, Detecting Neuro-Provoking Foodshttp://www.dramyyasko.com/wp-content/files_flutter/1279663001Neuroprovokers8.pdf (12)
  13. Daniel M. Hartung, PharmD, MPH, Dennis N. Bourdette, MD, Sharia M. Ahmed, MPH, Ruth H. Whitham, MD, The cost of multiple sclerosis drugs in the US and the pharmaceutical industry: Too big to fail?,  Neurology. 2015 May 26; 84(21): 2185–2192. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4451044/ (13)

  14. MS Statistics, multiplesclerosis.net, https://multiplesclerosis.net/what-is-ms/statistics/ (14)
  15. Multiple sclerosis: Facts, Statistics, and You, healthline.com, https://www.healthline.com/health/multiple-sclerosis/facts-statistics-infographic#2 (15)
  16. Åke Nilsson, Rui-Dong Duan, Absorption and Lipoprotein Transport of Sphingomyelin, January 2006, The Journal of Lipid Research, 47, 154-171http://www.jlr.org/content/47/1/154.full (16)
  17. Shoemaker TJ, Mowry EM, A review of vitamin D supplementation as disease-modifying therapy. Multiple Sclerosis Journal, Volume: 24 issue: 1, page(s): 6-11 Jan 182018, http://journals.sagepub.com/doi/full/10.1177/1352458517738131 (17)
  18. Justin Caba, A Vegetarian Diet Can Save You Around $750 Each Year When Compared To A Meat-Eating Diet. Oct. 9, 2015, MedicalDaily.com, https://www.medicaldaily.com/vegetarian-diet-can-save-you-around-750-each-year-when-compared-meat-eating-diet-356670 (18)
  19. S. Coe, E. Axelsson, V. Murphy, M. Santos, J. Collett, M. Clegg, H. Izadi, J.M. Harrison, E. Buckingham, H. Dawes, Flavonoid rich dark cocoa may improve fatigue in people with multiple sclerosis, yet has no effect on glycaemic response: An exploratory trial. Clinical Nutrition ESPEN, Oct. 2017, Volume 21, Pages 20–25   https://clinicalnutritionespen.com/article/S2405-4577(17)30280-2/abstract (19)
  20. Kristina Fiore, Does Insulin Resistance Degrade Myelin? – Imaging study suggests insulin resistance is linked to loss of myelin., Oct. 23, 2015, MedPageToday.com, https://www.medpagetoday.com/meetingcoverage/sfn/54260 (20)
  21. Sara Palumbo, Chapter 7 Pathogenesis and Progression of Multiple Sclerosis: The Role of Arachidonic Acid–Mediated Neuroinflammation. from the book edited by Zagon IS, McLaughlin PJ, editors. Multiple Sclerosis: Perspectives in Treatment and Pathogenesis [Internet]. Brisbane (AU): Codon Publications; 2017 Nov 27. https://www.ncbi.nlm.nih.gov/books/NBK470143/ (21)
  22. Jordan Fallis, 27 Proven Ways to Promote the Regeneration of Myelin. Feb. 18, 2017, Optimal Living Dynamics,  https://www.optimallivingdynamics.com/blog/25-proven-ways-to-promote-the-regeneration-of-myelin (22
  23. Adrian Devitt-Lee, CBD Science: How Cannabinoids Work at the Cellular Level to Keep You Healthy, Project CBD,  Dec. 15, 2016, alternet.org, https://www.alternet.org/drugs/cbd-science-mitochondria-mysteries-homeostasis-renewal-endocannabinoid-system (23)
  24. Editors, Emmanuel S. Onaivi, Takayuki Sugiura, Vincenzo Di Marzo, Endocannabinoids: The Brain and Body’s Marijuana and Beyond, (Taylor & Francis Group, 2006, Florida), pages 82 and 83 are from Chapter 3, by: E.S. Onaivi, H. Ishiguro, P. W. Zhang, Z. Lin, B. E. Akinshola, C. M. Leanoard, S. S. Chirwa, J. Gong, and G. R. Uhl, Chapter 3, Endocannabinoid Receptor Genetics and Marijuana Use. https://www.crcpress.com/Endocannabinoids-The-Brain-and-Bodys-Marijuana-and-Beyond/Onaivi-Sugiura-Di-Marzo/9780415300087 (24)
  25. J. Depew, RD, G10: Nrf2 Promoting Foods, 2018, effectivecare.info, G10: Nrf2 Promoting Foods. Particularly helpful for an overview of plant phytonutrients groups: Maria de Lourdes Reis Giada, Chapter 4: Food Phenolic Compounds: Main Classes, Sources and Their Antioxidant Power, Biochemistry, Genetics and Molecular Biology » “Oxidative Stress and Chronic Degenerative Diseases – A Role for Antioxidants”, book edited by José A. Morales-González, ISBN 978-953-51-1123-8, Published: May 22, 2013    https://www.intechopen.com/books/oxidative-stress-and-chronic-degenerative-diseases-a-role-for-antioxidants/food-phenolic-compounds-main-classes-sources-and-their-antioxidant-power (G10.11)
  26. Arlen Frank, Chemistry of Plant Phosphorus Compounds, Elsevier, Jun 3, 2013, https://books.google.com/books/about/Chemistry_of_Plant_Phosphorus_Compounds.html?id=6btpFSV1T2YC (G.26)
  27. Ginger Decreases Colon Inflammation, Prime Endoscopy Bristol, Oct. 12, 2011,  http://www.primeendoscopybristol.co.uk/ginger-decreases-colon-inflammation/ (27) 
  28. From Pediatric Encephalopathy to Alzheimer’s: Linking Mitochondria to Neurological Diseases. 2016 Neurobiology of Disease Workshops, Neuronline.sfn.org, http://neuronline.sfn.org/Articles/Scientific-Research/2017/From-Pediatric-Encephalopathy-to-Alzheimers (28)

Amyotrophic Lateral Sclerosis (ALS) and CBD receptors

Addition, 7/30/2018 – ALS is a demyelination disorder. There is a 19% comordbidity rate with hyperthyroidism and ALS – so disclosure, not becoming paralyzed due to ALS is a personal goal of mine.  Legal sources of cannabinoids or some of the precursor building blocks – phospholipids or other phosphonutrients – include:

Hemp seed kernels and oil; Artemisia turanica/wormwood leaf; amaranth seed; asparagus; avocado fruit or the inner kernel, dried and powdered; beans/legumes; cardamom seeds and powder; carrots; celery stalks and leaves; cocoa beans and cocoa powder, baker’s chocolate, dark chocolate and to a lesser amount milk chocolate and chocolate syrup; coconut; cumin seed/powder; fennel seed, flax seed, pine nuts; sesame seeds, pumpkin seed kernels, squash seeds; butternut squash and pumpkin; gingko leaf; grapefruit and orange juice with the pulp; Jerusalem artichoke (this is a root vegetable rather than a green artichoke); lettuce, spinach and mustard leaves and other leafy green vegetables and herbs; nuts/peanuts, cashews, walnuts; oats; okra seeds; onion root, leek leaves, garlic;  parsnip root; pomegranate seeds and pomegranate peel extract;rice, white or brown but the bran is the best source; rosemary; sorghum;  sweet potato or yam; buckwheat (a seed botanically that is not wheat and is gluten free); wheat. (G.26)

Health – “the pursuit of life” is a right for United States citizens, and is included in the Preamble of the U.S. Constitution. (link)

~~~~

The cannabinoid receptor system is involved in the control of calcium movement across the cell membrane. Calcium has an electrically active ionic form which can initiate changes within the cell fluid. During normal health a similarly electrically active ionic form of magnesium is found in greater concentration within the cell fluid and greater concentrations of the calcium ion are found within the blood plasma. The energy available from the magnesium ions is used within the cell membrane protein channels. The protein transport channels act as gates that can be opened or closed to allow calcium or other types of chemicals to flow through the channel.

The US federal listing of the cannabis herb as a schedule one drug has limited research into the role of the cannabinoid receptor system to studies about the toxic or addictive properties of cannabinoids. A schedule one drug is considered as having no medicinal value so no research would be necessary. When the cannabis plant was classified as a schedule one substance less was known about the extensive role of cannabinoids in the health of humans and many other species. Suppressing research about the cannabinoid group of chemicals and the cannabinoid receptors may have left us in the dark about the cause and cure of many mystery diseases and conditions.

Amyotrophic Lateral Sclerosis (ALS) is a neurodegenerative disease that affects a small percentage of the population yet it has no known cause or cure — except —  cannabinoids may help:

However, there is increasing evidence that cannabinoids and manipulation of the endocannabinoid system may have therapeutic value in ALS, in addition to other neurodegenerative conditions. Cannabinoids exert anti-glutamatergic and anti-inflammatory actions through activation of the CB(1) and CB(2) receptors, respectively. Activation of CB(1) receptors may therefore inhibit glutamate release from presynaptic nerve terminals and reduce the postsynaptic calcium influx in response to glutamate receptor stimulation. [1]

Other information:

Oxidative stress and Vitamin D deficiency or oxidation of the Vitamin D Binding Protein (DBP) may be involved in the development of ALS, (2), and Multiple sclerosis. Levels may continue to be low or oxidized during remission and worsen during relapse. (G12.33) There is a slightly modified form of the Vitamin D Binding Protein (GcMAF) that can promote  macrophages, immune system white blood cells, to remove cancer cells by apoptosis (killing and engulfing the cell debris to remove it from the body without causing toxic chemicals to be released into the extracellular fluid). (5)

The cannabinoid system may have some control over the system and it may have effects on other chronic conditions. I’m reading more on the topic.  – More health tips and conditions that may have an increased risk for ALS developing as a comorbid/additional condition are included in a follow up post: Actually we do know quite a bit about ALStranscendingsquare.com/2014/09/02/.

Disclaimer: Opinions are my own and the information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes.

    1. http://www.ncbi.nlm.nih.gov/pubmed/18781981
    2. Greilberger J, Greilberger M, Herwig R, (2017) Measurement of oxidative stress parameters, vitamin D and vitamin D binding protein during vitamin D treatment in a patient with amyotrophic lateral sclerosis. Integr Mol Med, 4: DOI: 10.15761/IMM.1000311
      http://www.oatext.com/measurement-of-oxidative-stress-parameters-vitamin-d-and-vitamin-d-binding-protein-during-vitamin-d-treatment-in-a-patient-with-amyotrophic-lateral-sclerosis.php
    3. Rajda C, Pukoli D, Bende Z, Majláth Z, Vécsei L. Excitotoxins, Mitochondrial and Redox Disturbances in Multiple Sclerosis. Kleinschnitz C, Meuth S, eds. International Journal of Molecular Sciences. 2017;18(2):353. doi:10.3390/ijms18020353. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5343888/ (G12.33)
    4. Bíró T, Tóth BI, Haskó G, Paus R, Pacher P. The endocannabinoid system of the skin in health and disease: novel perspectives and therapeutic opportunities. Trends in pharmacological sciences. 2009;30(8):411-420. doi:10.1016/j.tips.2009.05.004. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2757311/ (4)
    5. Thyer, L.; Ward, E.; Smith, R.; Fiore, M.G.; Magherini, S.; Branca, J.J.V.; Morucci, G.; Gulisano, M.; Ruggiero, M.; Pacini, S. A Novel Role for a Major Component of the Vitamin D Axis: Vitamin D Binding Protein-Derived Macrophage Activating Factor Induces Human Breast Cancer Cell Apoptosis through Stimulation of MacrophagesNutrients 20135, 2577-2589. http://www.mdpi.com/2072-6643/5/7/2577/htm (5)
  1. Dario SiniscalcoJames J. BradstreetAlessandra Cirillo, Nicola Antonucci, 

    The in vitro GcMAF effects on endocannabinoid system transcriptionomics, receptor formation, and cell activity of autism-derived macrophages. Journal of Neuroinflammation 2014 11:78   https://jneuroinflammation.biomedcentral.com/articles/10.1186/1742-2094-11-78 (6)

  2. Bíró T, Tóth BI, Haskó G, Paus R, Pacher P. The endocannabinoid system of the skin in health and disease: novel perspectives and therapeutic opportunities. Trends in pharmacological sciences. 2009;30(8):411-420. doi:10.1016/j.tips.2009.05.004. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2757311/ (7)