Tag: glutamate

Posted on

Snake venom toxin in the spike protein?

Unusual gene insertions within the SARS-CoV-2 viral gene sequence were found that resemble the protein structure and genetic code of a snake venom toxin. That is the bad news. The good news is that an anti-clotting snake venom anti-toxin medication was found helpful in the treatment of patients with severe COVID19. The anti-clotting medication is Tirofiban/Aggrastat, see image, and Dr. Fauci was emailed about the success of the treatment on April 27, 2020. It would have been nice of Dr. Fauci to let the rest of us know the good news last year.

*7-6-21 – addition – that was sarcasm and sarcasm is no longer adequate – it was Dr. Fauci’s job to let the US public know of effective remedies rather than obstruct investigations and use of early treatment. He and Ralph Baric and their team need to be investigated by an independent (non US corrupt) group and be charged with global homicide – seriously. We can’t just joke about bioweapons or gain of function ‘vaccine’ research that accidentally gets out, gets covered up, and early treatments suppressed for the apparent purpose of pushing emergency approval through for an inadequately tested experimental genetic manipulation treatment.

Image via Dr. Tau Braun, on Facebook.

The other good news is that nicotine is protective, by blocking access to the toxic spike protein to nicotinic Acetylcholine Receptors (nAChRs) which both nicotine and the neurotransmitter acetylcholine can activate (agonists of the receptor type, rather than antagonists).

“Based on the clinical observation of low prevalence of smoking among hospitalized COVID-19 patients, we examined and identified a “toxin-like” amino acid (aa) sequence in the Receptor Binding Domain of the Spike Glycoprotein of SARS-CoV-2 (aa 375–390), which is homologous to a sequence of the Neurotoxin homolog NL1, one of the many snake venom toxins that are known to interact with nicotinic acetylcholine receptors (nAChRs).” (1)

Anyone feeling a little tired? – a similar type of nerve toxin from a cone snail: Neurotoxin homolog NL1: “Antagonist [inhibitor] of muscle and neuronal nicotinic acetylcholine receptors (nAChR) with highest affinity for neuronal alpha-7/CHRNA7 nAChRs.” (9)

The Cholinergic System

The Cholinergic System effects health and cognition in many ways: “The cholinergic system is the network of acetylcholine receptors clustered within certain brain regions which the activation of, or inhibition of, in total effects most of our actions. More specifically effecting the cholinergic system might cause symptoms of “dry mouth, tachycardia or bradycardia [rapid or slow heart rate], drowsiness, sedation, and short-term memory loss,”…” Low levels of acetylcholine can cause difficulty forgetting traumatic memories, while higher levels help with the formation of new memories. (The Cholinergic & Dopaminergic Systems: previous post)

Formaldehyde – a neurotoxin that also inhibits acetylcholine receptors.

Formaldehyde has an inhibitory effect on acetylcholine receptors as it leads to increased break down of acetylcholine, so excess amounts of it may worsen symptoms of spike toxicity. Increased formaldehyde levels leads to an increase in levels of the enzyme that breaks down acetylcholine, resulting in less of the neurotransmitter being available for stimulating the acetylcholine receptors of nerve cells. (12)

Formaldehyde is found in smoke toxins whether you are the smoker, or there is fresh secondhand smoke, or a long term lingering thirdhand smoke on the walls & surfaces of everything in the home. Formaldehyde is also breathed in from smog or air pollution, and may off-gas (be released) from vinyl or other environmental sources. More bad news – we also make our own formaldehyde when our stress level is elevated. (References & more info, The Cholinergic & Dopaminergic Systems – also has dietary tips for Parkinson’s Disease: previous post)

Formaldehyde is a chemical used to embalm corpses. No need to make it for ourselves.

Peace – tranquility – focus on the now, not the worries of the future or the regrets of the past. By focusing on the present we can take decisive action steps towards a different future.

Jumping ahead to my own present time – I am using a half a nicotine patch per day (= 10.5 mg), for the last few days and it has helped my health, after a colitis like flair-up that was lingering longer than ever before. To me three weeks of colitis is three weeks too many – however some people suffer from it most days for years. It can end lives prematurely. I lost 30 pounds in three weeks during my initial problem – extreme stress was happening at that time. of the nicotinic Acetylcholine Receptors can be involved in Inflammatory Bowel Disease. (2)

Nicotine activates most types of nAChRs.

Nicotine activates most of the subtypes of nicotinic Acetylcholine Receptors, except for two subtypes, which it inhibits: “Nicotinic receptors are so named because they are activated by the tobacco plant alkaloid nicotine, but curiously, α9 and α9α10 nAChRs are not activated by nicotine and instead are inhibited by this ligand [8,13,25].” (2) Those two types have not been identified within the gastrointestinal tract, although many other subtypes are found there. (Table 1, 2)

Where are they found? It is the standout details that provide clues.

“Upon its release, acetylcholine activates a nicotinic acetylcholine receptor (nAChR) composed of α9 and α10 subunits14,15,16,17. In vertebrates the expression of these 2 subunits is limited mainly to the cochlear and vestibular end organs14,15,18,19. ” (3)

>>> “Neurons of the medial olivary complex inhibit cochlear hair cells through the activation of α9α10-containing nicotinic acetylcholine receptors (nAChRs).” (3)

Vertigo & Tinnitus can result from cochlear hair cell damage.

Vertigo and tinnitus might be related to something affecting the cochlear hair cells. They are very delicate and prone to irreversible damage. Dehydration, certain medications, and lack of magnesium may all be risk factors in addition to very loud noise, particularly if typically on one side more than the other – so one set of cochlear hair cells are damaged and the other is still okay – leaving the person off balance in perception and causing vertigo or tinnitus. The conditions have been reported as symptoms of COVID19 and as adverse reactions following CoV injection.

Magnesium is needed to protect cochlear hair cells.

“... intravenous administration of magnesium sulfate improved hearing recovery…” (4)

Epsom salt soaks provide a topical source of magnesium and sulfate which is absorbed through skin pores, bypassing any potential intestinal malabsorption.

Nicotine activates nAChRs, except for the type found in the inner ears.

Bath time over – back to the subtypes of nicotinic Acetylcholine Receptors – toxins can be very specific to subtype. Conus imperialis snails have a toxin that affects only the α7 subtype, making it useful in research of the brain’s cholinergic system. “It has no effect on nAChRs composed of α2/ß2, α3/ß2, α4/ß2, α2/ß4, α3/ß4, or α4/ß4 subunits.” (5)

That doesn’t rule out an effect on the α9 and α10 subunits, does it? Do the snake venom like toxin on the spike protein effect the α9 and α10 subunits? Based on reports of tinnitus and vertigo, it seems likely that they are effected by the spike protein.

Nicotine for better hearing and balance? Odd world today. Though, the nicotine doesn’t activate the α9 and α10 subunits so it might not protect them – bath time is fun according to Ernie from Sesame Street.

What other nutrients might help the inner ear cochlear hair cells?

Antioxidants and polyphenols and other NfKB inhibitor phytonutrients would also help protect the hair cells of the inner ear. Supplements of the antioxidant/metabolite CoQ10 and vitamin E have been found beneficial for tinnitus patients. (4) Nrf2 promoting foods have the double bonus of increasing our own antioxidant production and inhibiting the inflammatory NfKB. See: Nrf2 Promoting Foods for nutrient and foods that might be helpful.

“The levels of nitric oxide, peroxynitrite, oxidative stress, nuclear factor kappa-beta (NF-kappa), glutamate receptor (N-methyl-D-aspartate), and calcium are elevated in patients with tinnitus.12,13 About 21% to 42% of tinnitus cases are induced by exposure to noise.14 About 34% of tinnitus patients have post traumatic stress disorder (PTSD), suggesting there may be some linkage of neuronal mechanisms that cause both tinnitus and PTSD.15 Evidence for increased oxidative stress and chronic inflammation has also been found in patients with PTSD.” (4)

*Adequate levels of acetylcholine is needed to help forget things like trauma memories. (The Cholinergic & Dopaminergic Systems: previous post)

Reducing glutamate in the diet and use of glutamate inhibitors may be protective as excess glutamate is formed as a result of damage to hair cells.

“When hair cells become damaged, gluta-mate—an excitatory neurotransmitter responsible for converting vibrational sound into electrical signal—is produced in excessive amounts. Excessive amounts of gluta-mate are very toxic to neurons. Damage to peripheral auditory and somatosensory systems causes imbalance between excitatory and inhibitory neurotransmitters in the mid-brain auditory cortex and brainstem. This imbalance causes hyperactivity in the auditory cortex leading to the perception of phantom sounds (tinnitus).” (4)

Avoiding loud noise also protects the hair cells, which are motion sensitive and can be broken by physical pressure change. Loud noises do cause a change in the air pressure as the sound wave passes by – the vibration of a loud concert has the beat of the music.

From an old post:

  • A review of the negative side effects possible with an excess intake of the hormone calcitriol:  [drugs.com]

Ringing in the ears and inner ear pressure is not mentioned on the list but  – I am personally and professionally pretty sure that tinnitus can be part of the cluster of symptoms that might occur from a calcitriol overdose. The symptom list would be similar to a list of magnesium deficiency symptoms. The symptoms won’t go away simply by taking a magnesium supplement alone however. The intake of the vitamin D would continue to signal the bones to release calcium into the blood if it is being converted into hormone D. When excess of the calcitriol/hormone 1,25-D is present the intestines preferentially absorb calcium and magnesium is wasted in the kidneys and is poorly absorbed in the intestines.

An Epsom salt bath or foot soak can help relieve physical and mental symptoms and slightly reduce the ringing in the ears. Zinc, inositol and B vitamins seem to be involved in the tinnitus – magnesium alone doesn’t make it go away. B1 and zinc seem to be involved with the risk of cardiac arrhythmia as well as adequate supplies of taurine, an amino acid that can be converted from the more common cysteine but in the elderly that conversion can malfunction.

α9 and α7 are structurally similar, bad news doesn’t stop does it?

Back from the search engine – Structurally 7 and 9 are similar, (9 is curvier, haha): “Despite the recent upsurge in research interest in these subunits, there is much unknown about their functions and the underlying molecular mechanisms. They are most similar to the α7* nAChR; α-bungarotoxin and strychnine are antagonists of α7* and α9* receptors and α7* and α9* highly permeable to calcium. Recent evidence suggests a functional interaction of the subunits and potentially a structural association.” (6)

The alpha 9 and 10 subunits are not found within the brain’s cholinergic system, just in the inner ear, at the post-synapse area of the nerve connections – however the 9 and 10 subunit types are found throughout the rest of the body and immune system:

“There is an emerging literature that the distribution of the α9 and α10 subunits in peripheral tissues is widespread and non-synaptic, regulated in disease states, and may not always be assembled as heteromeric receptors. One or both subunits are expressed in most immune cells, dorsal root ganglion, keratinocytes, brain glioblastoma, colon, human breast cancer. Their expression levels may be prognostic in cancer and osteoporosis, and recent evidence suggests they may be involved in immune regulation. Importantly, they are potential targets for treatment of pain, cancer, and inflammatory diseases.” (6)

The alpha-7 type of receptors are found in the colon and are involved in glutamate release. They may be involved in pain relief. “Additionally, α7 nAChRs located on DRG neuron terminals in the dorsal horn of the spinal cord modulate the release of glutamate and have been proposed to be involved in nicotine mediated analgesia [34].” (2)

A computer modeling image shows the α7 receptor being blocked by a snake toxin, (7), the receptor is made of five similar subunits that form a channel through the cell membrane. Once activated the channel allows certain minerals to pass through, such as calcium. Excess can cause overactivity to the point of cell death.

Figure 4. Structural model of the α7 receptor–α-Cbtx complex. The five subunits of the receptor are depicted with their β-sheets colored blue and the apical helices colored red and yellow. One toxin molecule is shown at an arbitrary subunit interface with its β-sheet in yellow and its backbone in red. (A) Top view of the model. (B) The receptor is seen perpendicularly to the 5-fold axis with the toxin in an equatorial position.
(Fruchart-Gaillard et al, 2002) (7)

“How can this situation explain the antagonistic property of the snake toxin? Small ligands also bind at the interface of two α7 subunits (10–13) on loops A, B, C, D, and F for ACh, nicotine or DHβE and A, B, C, and E for conotoxin ImI (α-ImI). This and previous (13) pairwise analyses indicate that α-ImI and α-Cbtx clearly bind to overlapping sites. Even both toxins possess an arginine residue that seem to establish homologous cation π interactions with the α7 receptor. ” (7)

Nicotine is a strong agonist of the α7 subunits, and activating that type of receptor helps reduce inflammation. (10, 13)

“We examined the anti-inflammatory effect of nicotine, a potent α7 nicotinic acetylcholine receptor (α7nAChR) agonist, with regard to TLR expression and signaling during sepsis.” (10)

Nicotine for prevention of snake venom-like poisoning? Odd world today.

Lobeline sulfate is chemically similar to nicotine, but less potent of an activator of the nicotinic Acetylcholine Receptors. (8)

“Where there is a will, there is a way,”

– as my mother always said. And when the first attempt doesn’t work, you try something else until something works. That is the stick-with-method. Try, try again.

Feeling a little better, rather than worse, may be the goal – sorry. Autoimmune conditions may have occurred.

There are no guarantees in life and trying dietary solutions or any treatment may not restore full health. Infections or other traumatic damage can increase risk of autoimmune antibodies developing – and there is often ups and downs rather than any true cure like resolution. Once autoimmune antibodies are formed the memory immune cells remember. Avoiding any dietary chemicals that were similar to the one the body is reactive against can help reduce the level of antibodies that are currently being produced rather than a memory cell type waiting to be needed again. Wheat gluten is similar to the thyroid hormone for example.

Demyelination conditions such as the autoimmune like condition Multiple Sclerosis may involve misfolded proteins too.

Multiple sclerosis also has been found to likely involve misfolded proteins. “MS may be a transmissible protein misfolding disorder, study suggests. SAN DIEGO – Multiple sclerosis appears to be a transmissible protein misfolding disorder like Alzheimer’s and Parkinson’s diseases, results of a new study suggest. ” (11)

Strategies that support myelination and prevent demyelination may also be helpful for protecting against a prion like toxin that does other damage too. Malnutrition is a risk factor for demyelinating conditions of which MS is one, however excess calories and carbohydrates may also be a risk factor. Our body needs to get hungry in order for the cellular debris mechanisms to function. When we are eating a lot of food, the body is busy using or storing those nutrients and there is no time or need to scavenge for extra tangled piles of misfolded proteins. Niacin, B vitamins, C, magnesium, CoQ10, are all needed for energy production in our mitochondria and also may help with the cellular debris functin.

  • Other tips for promoting good myelin coating around the long axons of nerve cells are on this webpage: G12. Demyelination.

See previous posts for more about the potential prion like risks of the spike protein:

Excess free iron & iron chelators

And about other risks such as blood clotting: Spike protein is a toxin. Please stop trusting the experiment.

Excess free iron is a frequent problem. Vitamin C would help, quercetin, resveratrol, artemisinin, lactoferrin, and possibly turmeric might all help as an iron chelator to protect against some of the vascular risks and excessive level of inflammatory cytokines.

“Artemisinin is an iron chelator and helped me right away with post recovery fatigue. In 1-2 days had more energy. Took am & pm. Still using 1/day. It felt like anemia of chronic infection – standard body response to move iron out of pathogen risk.” (one of my Tweets) -> (artemisinin-arteannuin-b-and-covid-19/)

Anemia of chronic infection or inflammation (post) is a natural immune response of the body, which seems to be an over-response in the case of COVID19 and LongCovid. Iron is stored as ferritin instead of being made into new hemoglobin for immature red blood cells. Less oxygen carrying capacity is in the blood – but also less potential nutrients for a pathogen. This condition is readily reversible with vitamin C and iron chelators – and address the underlying chronic infection that is causing the immune response. – And in the meantime avoid high altitudes such as mountain drives or airplane flights as hypoxia and loss of consciousness may result. Airplane pilots have experienced some problems post CoV injections.

“(Reuters) – United Airlines and its pilots’ union have reached an agreement to prohibit the airline from mandating COVID-19 vaccinations to its pilots, the Air Line Pilots Association said. “Pilots who elect not to be vaccinated will not be subject to any discipline,” “ – @GillianMcKeith. (ref)

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.

Reference List

  1. Farsalinos K, Eliopoulos E, Leonidas DD, Papadopoulos GE, Tzartos S, Poulas K. Nicotinic Cholinergic System and COVID-19: In Silico Identification of an Interaction between SARS-CoV-2 and Nicotinic Receptors with Potential Therapeutic Targeting Implications. Int J Mol Sci. 2020;21(16):5807. Published 2020 Aug 13. doi:10.3390/ijms21165807 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7461543/
  2. Lola Rueda Ruzafa, José Luis Cedillo, and Arik J. Hone. Nicotinic Acetylcholine Receptor Involvement in Inflammatory Bowel Disease and Interactions with Gut Microbiota. Int. J. Environ. Res. Public Health 2021, 18(3), 1189; https://doi.org/10.3390/ijerph18031189 https://www.mdpi.com/1660-4601/18/3/1189/htm
  3. Characterization of HA-tagged α9 and α10 nAChRs in the mouse cochlea. https://www.nature.com/articles/s41598-020-78380-5
  4. The Case for Using Multiple Antioxidants in Hearing Disorders. hearingreview.com, https://www.hearingreview.com/hearing-loss/hearing-disorders/the-case-for-using-multiple-antioxidants-in-hearing-disorders
  5. α-conotoxin-IMI, α7 nAChR selective blocker. smartox-biotech.com, https://www.smartox-biotech.com/product/nicotinic-acetylcholine-receptor-blocker/conotoxin-imi
  6. Nicotinic Alpha9 and Alpha10 Subunits: Ancient Receptors in Modern Times and Modern Places, collection of 13 articles, Excerpt from: “About this Research Topic” frontiersin.org, https://www.frontiersin.org/research-topics/5176/nicotinic-alpha9-and-alpha10-subunits-ancient-receptors-in-modern-times-and-modern-places
  7. Fruchart-Gaillard C, Gilquin B, Antil-Delbeke S, et al. Experimentally based model of a complex between a snake toxin and the alpha 7 nicotinic receptor. Proc Natl Acad Sci U S A. 2002;99(5):3216-3221. doi:10.1073/pnas.042699899 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC122499/
  8. Lobeline sulfate, PubChem CID 120636, pubchem.ncbi.nlm.nih, https://pubchem.ncbi.nlm.nih.gov/compound/Lobeline-sulfate
  9. UniProtKB – Q9DEQ3 (3SO8_NAJAT), Protein: Neurotoxin homolog NL1, Naja atra (Chinese cobra) https://www.uniprot.org/uniprot/Q9DEQ3
  10. Tae-Hoon Kim, So-Jin Kim, Sun-Mee Lee, Stimulation of the α7 Nicotinic Acetylcholine Receptor Protects Against Sepsis by Inhibiting Toll-like Receptor via Phosphoinositide 3-Kinase Activation, The Journal of Infectious Diseases, Volume 209, Issue 10, 15 May 2014, Pages 1668–1677, https://doi.org/10.1093/infdis/jit669 https://academic.oup.com/jid/article/209/10/1668/855517
  11. Randy Dotinga, MS may be a transmissible protein misfolding disorder, study suggests. Feb 2, 2018, mdedge.com, https://www.mdedge.com/multiplesclerosishub/article/157658/multiple-sclerosis/ms-may-be-transmissible-protein-misfolding
  12. Zendehdel R, Fazli Z, Mazinani M. Neurotoxicity effect of formaldehyde on occupational exposure and influence of individual susceptibility to some metabolism., Environ Monit Assess. 2016 Nov;188(11):648. Epub 2016 Oct 31. parameters. https://www.ncbi.nlm.nih.gov/pubmed/27796833
  13. de Jonge WJ, Ulloa L. The alpha7 nicotinic acetylcholine receptor as a pharmacological target for inflammation. Br J Pharmacol. 2007;151(7):915-929. doi:10.1038/sj.bjp.0707264 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2042938/
Posted on

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 Disorders, Trends Neurosci. 2008 Jul; 31(7): 361–370.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2486416/ [45]
  4. Butler C, Zeman AZJ, Neurological syndromes which can be mistaken for psychiatric conditions. Journal of Neurology, Neurosurgery & Psychiatry 2005;76:i31-i38. https://jnnp.bmj.com/content/76/suppl_1/i31 (Neurological syndromes)
  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 JB, Blain PG, Neurotoxicology: what the neurologist needs to know.
    Journal of Neurology, Neurosurgery & Psychiatry 2004;75:iii29-iii34. https://jnnp.bmj.com/content/75/suppl_3/iii29

    (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 sclerosis. Purinergic 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 Excitotoxins, http://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)
Posted on

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 Media, Dec 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 sclerosis, Neuromolecular 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 Foods, http://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, 154-171, http://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 18, 2018, 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)
Posted on

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 ALS,  transcendingsquare.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 Macrophages. Nutrients 2013, 5, 2577-2589. http://www.mdpi.com/2072-6643/5/7/2577/htm (5)
  1. Dario Siniscalco, James J. Bradstreet, Alessandra 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)