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)

Average Autism and Alzheimer’s Rates Differ by Gender

Autism is more of a risk for boys than girls by a factor of four boys for every one girl or three boys for every one girl diagnosed with autism depending on the type of study and diagnostic criteria. There is some speculation that autism in girls presents with less obvious symptoms than in boys. Girls with autism may have less repetitive behavior and be able to fit in socially better than boys with autism and may have less obvious focus on one main topic of interest. (1)

At the other end of the age spectrum females have a greater rate of Alzheimer’s Disease than males. (13)

The difference has been shown to be significant, not just a difference in diagnostic criteria. Estrogen is a female hormone that may be protecting girls from the risk of developing autism but then in menopause is no longer protecting older females from the risk of developing Alzheimer’s Disease. Patients with Autism and Alzheimer’s have been shown to have a tendency to have increased amounts of protein clusters (amyloid beta) in the brain which in normal health would be cleared away. An animal based study found a genetic strain of mice with a clear gender and age difference. Young male mice developed autism like symptoms and older female mice developed Alzheimer’s like symptoms.

A different study found a gender difference in the amount of a protective protein (ADNP) in young male mice with autism like symptoms and older female mice with Alzheimer’s like symptoms. (6) Complete lack of the protective protein leads to very early death with neural tube defects in animal studies.  (7) The neuroprotective protein (ADNP) seems to promote autophagy (our body’s recycling method, it makes us more energy efficient and helps detoxify/remove old cells or material such as the beta-amyloid protein for reuse, read more:  14) and the deficit of it may also be involved in schizophrenia. (8) The protein is involved with control of the dendritic branching of brain cells which is typically found to be  different in children with autism. The protein also plays a role in regulating over 400 genes involved in embryo development including ApoE and the tau protein which is found to collect in the brains of patients with Alzheimer’s Disease in addition to beta-amyloid protein. (9)

The role of apoE involves membranes, cholesterol, cannabinoid receptors and lipid rafts – chemistry geeks have fun, three dimensional drawings and a discussion of cholesterol within the brain and its role in several neurodegenerative diseases is available online in full text, the brain includes 25% of the body’s cholesterol even though the brain only accounts for 2% of the total body weight, on average. (10).  A briefer description of the role apoE plays in the brain and with estrogen and Alzheimer’s risk is available with a discussion of the gene differences that are known to increase but not guarantee risk of developing Alzheimer’s Disease. (11)

Disclosure: a genetic screening suggests I do have one of the higher risk differences in the ApoE gene. (rs2254958)

Strategies to help increase autophagy may help reverse some of the risk factors associated with reduced ApoE/reduced ADNP levels –

  1. vigorous exercise,
  2. a ketosis promoting, low carbohydrate diet, regularly or occasionally,
  3. fasting for a day or a partial day occasionally. (14)

The activity of the apoE protein on other genes can be affected by cannabinoids, too little cannabinoids may be a problem or too much.

The take home point – magnesium and adequate cannabinoids seem to be involved in helping clear the protein clusters during normal health.

  • Nutritional strategies recommended to help prevent Alzheimer’s disease include increasing intake of magnesium. Research has found that low levels of magnesium promoted build up of  beta amyloid protein while high levels of magnesium promoted breakdown of the misshapen proteins.

“Lab studies show that magnesium modulates enzymes involved in amyloid beta production; at low levels, magnesium favors amyloid beta buildup, while at higher levels it favors amyloid beta breakdown.101,102″ [2]  (from a  2014 post)

Certain genetic conditions and chronic health conditions or older age can make the body less able to make cannabinoids endogenously/internally. External sources of cannabinoids have been shown to be helpful for clearing the protein clusters involved in Alzheimer’s Disease. (https://www.sciencedaily.com/releases/2016/06/160629095609.htm)

An underlying infection with bacteria or yeast may be involved in the buildup of the protein clusters as they have a protective effect against some types of infection, so addressing low grade chronic infection may be needed to help stop the over production of the amyloid beta protein clusters in addition to providing adequate magnesium and cannabinoids. Note that there are non-euphoric cannabinoids and legal food sources in addition to medical marijuana. Pumpkin seeds are a good source, $200 billion per year is estimated to be spent on Alzheimer’s care annually at our current rate of the disease prevalence – that would buy a lot of pumpkin seeds. (15 )

That article also mentions that 192 pharmaceutical chemicals have been anticipated and tested in hope of a cure or effective treatment for Alzheimer’s Disease but which have ultimately not been found to be successful. One hundred and ninety two chemicals tested, one hundred and ninety two chemicals found ineffective – magnesium and cannabinoids however have been found effective at helping the body to naturally break down the tau and  beta-amyloid protein clumps that lead to brain damage and later symptoms of dementia in Alzheimer’s Disease and a few other neurological conditions including traumatic brain injuries and autism. (15 ) (links re tau/amyloid in autism & Alzheimers) (links re tau/amyloid protein in traumatic brain injury)

Ibuprofen is a pharmaceutical that is no longer covered by a patent and it has been found to be beneficial in protecting against Alzheimer’s Disease (link: 16) and the underlying reason is likely that ibuprofen prevents the break down of cannabinoids (17)(Search term: “ibuprofen prevents break down of cannabinoids”) – but you need cannabinoids first and some people might no longer be able to make them after a certain age or state of health or may never have been able to make them as well due to genetic differences.

So celebrate protecting your brain today by eating pumpkin seeds, cardamom spice, the herb rosemary, chocolate, or leafy green vegetables. – and the brightly colored tiny inner part of a piece of corn that you can see when eating corn on the cob is also a good source.

  • The misshapen tau/amyloid-beta proteins have a protective effect against bacteria and the yeast Candida albicans so a chronic lowgrade infection may be an underlying cause of the accumulation of beta amyloid placques. [3] [4] (from a  2014 post)

There are many more legal food sources of cannabinoids or a precursor available, a longer list is included below. The progression of Alzheimer’s Disease can take twenty years before symptoms are obvious, so getting an early start on protecting against the tau/beta-amyloid protein build-up makes sense to me (Disclosure, I have a direct family history of the disease in older relatives and a genetic screening suggests that I am more at risk, so I am biased towards preventing the disease in my own brain or other family members.)

Phospholipids are part of cannabinoids and other phosphorus containing nutrients are important in energy production. The phospholipids and cannabinoids are important for the health and function of skin and other membranes lining cells and organs, and/or if you care more about having a good hair day than whether you might get Alzheimer’s Disease in several decades, then the phospholipids are also important for hair growth: *The phospholipid mixture in this animal-based study was applied on the skin surface for hair loss associated with inflammatory skin dermatitis: (18)

(Additional Discloure: I am also genetically at risk for Male Pattern Baldness which became visibly apparent when my autoimmune disease was more severe, however with my switch to phospholipid rich foods my hair has since grown back and my autoimmune condition is in remission as long as I continue with my new health habits).

Other nutrients including the B vitamins, vitamin E, and zinc are also important for healthy hair growth (read more) but many of the following list would also be good sources of B vitamins, vitamin E, zinc and other trace minerals and essential omega 3 and omega 6 fatty acids. Pumpkin seeds are a good vegetarian source of zinc, otherwise the mineral is more commonly available in meats.

  • Food Sources of Phospholipids and other phospho-nutrients: 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)

That topic took a walk around the block and picked some daisies along the way but the important message might be that eating well and exercising regularly may promote healthy hair, a fit body right now while helping maintain healthy brain function into the future. Genetic susceptibility may be involved in the rate of young males with autism and older females with autism and prevention might include more magnesium and phospholipid rich foods in the diet with a diet that is moderate in carbohydrates and regular vigorous exercise to promote autophagy to help promote the natural recycling of tau and beta-amyloid protein that tends to accumulate in the brains of people with autism and Alzheimer’s Disease. Lack of ADNP protein may lead to lack of ApoE or a genetic difference may cause reduced ApoE and the deficiency may lead to a reduced level of autophagy.

Fasting for a day or partial day occasionally or a low carbohydrate diet, even just a diet balance as low as 30% of calories, and vigorous exercise are three natural ways that may help promote autophagy – our body’s natural method for removing and reusing old cellular material. (14) Those strategies might help a woman with Alzheimer’s risk but for an infant or toddler may need to be adapted to simply allowing vigorous, safe play, and a diet that with a greater percentage of healthy fats than average. The list of phosphonutrient rich foods are generally healthy and safe for prenatal diets or other stages of life and would likely promote a fit body and healthy hair for a person of any age and gender – and what is good for the hair is good for other membranes throughout the body and is also good for the brain. The hair is a protein that is a modified form of skin tissue and so is fingernail protein – beauty is more than skin deep.

Some daisies.

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. Thanks.

  1. Sarah Deweerdt,  Estimate of autism’s sex ratio reaches new low, April 27, 2017,  spectrumnews.org https://www.spectrumnews.org/news/estimate-autisms-sex-ratio-reaches-new-low/ 
  2. Liam Hawkins, Nutritional Strategies and Alzheimers, March 2013 lifeextension.com, http://www.lifeextension.com/magazine/2013/3/Nutritional-Strategies-to-Combat-Alzheimers/Page-02
  3. Lisa Conrick, What is Causing Beta-Amyloid Production in Alzheimer’s and Autism?, Oct. 23, 2012, ageofautism.com, http://www.ageofautism.com/2012/10/what-is-causing-beta-amyloid-production-in-alzheimers-and-autism.html
  4. Molnar Mark, Alzheimer’s Disease Emerging Role of Infection,  http://miklossy.ch/
  5. Why women have more Alzheimer’s disease than men: gender and mitochondrial toxicity of amyloid-beta peptide. J Alzheimers Dis. 2010;20 Suppl 2:S527-33. https://www.ncbi.nlm.nih.gov/pubmed/20442496
  6. Activity-dependent neuroprotective protein (ADNP) exhibits striking sexual dichotomy impacting on autistic and Alzheimer’s pathologies. Transl Psychiatry. 2015 Feb 3;5:e501. https://www.ncbi.nlm.nih.gov/pubmed/25646590
  7. Shmuel Mandel, Gideon RechaviIllana Gozes, Activity-dependent neuroprotective protein (ADNP) differentially interacts with chromatin to regulate genes essential for embryogenesis. Developmental Biology, Volume 303, Issue 2, 15 March 2007, Pages 814-824. https://www.sciencedirect.com/science/article/pii/S0012160606013960

  8. Shlomo Sragovich, Avia Merenlender‐Wagner, Illana Gozes, ADNP Plays a Key Role in Autophagy: From Autism to Schizophrenia and Alzheimer’s Disease. BioassaysVolume39, Issue 11, November 2017, Pages 1700054 https://onlinelibrary.wiley.com/doi/pdf/10.1002/bies.201700054

  9. Gozes Illana, (2015) Activity-dependent neuroprotective protein (ADNP): from autism to Alzheimer’s disease. SpringerPlus. 4. L37. 10.1186/2193-1801-4-S1-L37.  https://www.researchgate.net/publication/282802744_Activity-dependent_neuroprotective_protein_ADNP_from_autism_to_Alzheimer’s_disease
  10. M Maccarrone, G Bernardi, A Finazzi Agrò, and D Centonze, Review: Cannabinoid receptor signalling in neurodegenerative diseases: a potential role for membrane fluidity disturbance. British Journal of
    Pharmacology, Themed Issue: Cannabinoids in Biology and Medicine, Part I, Nov. 16, 2010. http://files.iowamedicalmarijuana.org/petition/2012/bjp-aug-2011-1379-1390.pdf
  11. Hilary Lampers, ND, 5 Reasons to Know Your APOE:  Understanding Your Alzheimer’s Disease Risk. June 13, 2016 thenatpath.com
  12. http://thenatpath.com/body/5-reasons-to-know-your-apoe/
  13. Maxwell A. Ruby, Daniel K. Nomura, Carolyn S. S. Hudak, Lara M. Mangravite, Sally Chiu, John E. Casida, and Ronald M. Krauss, Overactive endocannabinoid signaling impairs apolipoprotein E-mediated clearance of triglyceride-rich lipoproteins. Proc Natl Acad Sci U S A. 2008 Sep 23; 105(38): 14561–14566. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2567196/

  14. Nick English, Autophagy: The Science-Backed Way to Cleanse Your Body, July 4, 2016, greatist.com, https://greatist.com/live/autophagy-fasting-exercise
  15. Stuart W Titus, PhD, Dr. Titus’ Insights: Alzheimer’s Research and the Work of Dr. Schubert, Aug. 5, 2016, medicalmarijuanainc.com,  https://www.medicalmarijuanainc.com/dr-titus-insights-alzheimers-research-work-dr-schubert/
  16.  Neuroscientists say daily ibuprofen can prevent Alzheimer’s disease., March 26, 2018, sciencedaily.com,   https://www.sciencedaily.com/releases/2018/03/180326140239.htm

  17. K. D. Rainsford, IbuprofenDiscovery, Development and Therapeutics. 
    John Wiley & Sons, June 25, 2015, page 134, https://books.google.com/books?id=CAcLCgAAQBAJ&pg=PA134&lpg=PA134&dq=ibuprofen+prevents+break+down+of+cannabinoids&source=bl&ots=oJ_cjSrWXr&sig=yQgwSrdZOkA1MNDkbf7EF7waItY&hl=en&sa=X&ved=0ahUKEwjf7ZKPrcnaAhVlneAKHeDyAuAQ6AEIlQEwCA#v=onepage&q=ibuprofen%20prevents%20break%20down%20of%20cannabinoids&f=false
  18. Seong-Hyun Choi, Jeong-Su Moon, Byung-Suk Jeon, Yeon-Jeong Jeon, Byung-Il Yoon, and Chang-Jin Lim, Hair Growth Promoting Potential of Phospholipids Purified from Porcine Lung Tissues. Biomol Ther (Seoul). 2015 Mar; 23(2): 174–179. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4354319/
  19. ADNP related syndrome FTNW, *lack of ADNP genetically leads to reduced muscle tone and can cause eating problems in children. https://www.rarechromo.org/media/information/Chromosome%2020/ADNP%20related%20syndrome%20FTNW.pdf