Epigenetic changes may also be involved in Covid19 or LongCovid

Epigenetic changes may be involved in Covid19 and LongCovid, which might be able to be changed back with the addition of plenty of methyl donor vitamins. People with methylation genetic alleles would be more at risk for epigenetic changes to DNA or actin protein filaments. Actin are semi flexible proteins in a double helix shape which support the fluid and organelles inside of cells and around cells and organs of our bodies. Actin also is involved in guiding the work of DNA replication and growth and development of cells or infants.

Methylation is the addition of a methyl group – one carbon atom and three hydrogen atoms, to genes, or actin filaments. A methylated gene is not active for encoding proteins while a demethylated gene is available to be transcribed into a messenger mRNA to be made into a matching protein. Actin filaments are a double helix shape like DNA but do other functions throughout our body. Some have methyl groups also that seem to be essential for proper function of the actin protein whether in muscle contraction or in guiding chemicals within cells to make DNA or do other work. Actin filaments add structure to the jelly like fluid around and in cells and may tether chemicals in place for chemical reactions or guide cellular organization during growth and development.

Actin may be involved with energy fields of our body along with microtubules also, but that is not discussed in greater detail in this post (more information about quantum energy fields and actin is included in Cracking Nature’s Code (2019) (1), and in several posts on another site of mine first in the series, 2nd, 3rd, 4th).

Viral infection and epigenetic changes with a focus on Postural Orthostatic Tachycardia Syndrome and possible dietary and lifestyle changes that may help reverse epigenetic changes is the focus of this post – which got long. It is also available as a section of this document that includes the series on Mast Cells and Histamine. Current standard of treatment for patients with POTS symptoms may leave them unwell for years – a few get better more rapidly. I got better on my own within a few months – twice. More about possible strategies for improvement of epigenetic changes will be included later in the post. More about the epigenetics involved in POTS is included in the Genetics/Epigenetics chapter of my book draft which is available on a platform where you can get an e-copy early (minimum price Free, Leanpub/Tipping The Clock Toward Health) and then be informed of updates with an email subscription.

Viral infection can cause Epigenetic changes.

Bacterial (Pacis et al., 2015, 2) and viral infection (Lichinchi et al., 2016, 3) directly impact methylation patterns, most likely orchestrated by actin since it is universally hi-jacked in viral infectivity (Cudmore et al. 1997, 4; Ohkawa and Volkman, 1999, 5; Lu et al., 2004, 6; Marek et al., 2011, 7).

page 34, JB Head, PhD, Cracking Nature’s Code (2019) (1)

I found I have methylation gene alleles in a genetic screening (post: Methylation Cycle Defects – in me – genetic screening “for research purposes only”). Since finding out I stopped taking standard supplements of B12 and folic acid because they are not methylated, not bioactive. I take methyl B12 & methyl folate supplements now. Postural Orthostatic Tachycardia Syndrome (POTS) (9) has been a problem for me in past years a couple times and I got better. Symptoms include a rapid heart rate, tachycardia, and feeling faint or blacking out, especially when getting up quickly from a seated or laying down position to standing. (9) I have heard anecdotal reports of it being a symptom for some LongCovid survivors who had never had the problem before.

To slow the rapid heart rate during an episode I found it helpful to stop and sit or lay down with my feet above my heart if possible and just wait a couple minutes for the rapid heart rate to slow again. Continuing to exercise would make the rapid heart rate worse. Preventing the faintness upon rapidly getting up required trying to remember to slow down and have a support ready to hold if I felt wobbly. I did faint once, odd to find yourself on the floor unexpectedly.

POTS has been found to potentially involve a genetic difference in the norepinephrine transporter gene (SLC6A2) sequence and it can also be an epigenetic problem with links to excess formaldehyde. (9) Formaldehyde can donate methyl groups to DNA that normally would be unmethylated – active. (10) Methylation of DNA is a little like a on/off switch for genes, or the cap on bottle – add the methyl groups and the DNA gene is inactive.

Formaldehyde as a methyl donor for the methylation of DNA, RNA, and histone acts as an epigenetic factor participating in the reversible and dynamic methylation. DNA demethylation elicits formaldehyde generation in the dividing cells and post-mitotic neurons.” (10) Memory formation involves methylation of DNA and cognitive impairment in older adults is associated with increased internal formaldehyde levels (self-made) and demethylation of DNA. Use of nutrients to remove formaldehyde helped improve memory in an animal based study. (10)

Formaldehyde can be prevalent in secondhand or thirdhand smoke in enclosed rooms, or smog, or we make our own during normal metabolism, and physical or emotional stress conditions may cause an increase, as well as the level potentially increasing in older adults. (11) Elevated levels of formaldehyde within cells causes more breakdown of sugar for energy and increased removal of an antioxidant out of the brain cells, which may increase risk for cognitive damage. “As excess formaldehyde accelerates glycolysis and glutathione export in neural cells, formaldehyde‐induced alterations in brain metabolism and oxidative stress may contribute to the pathological progression of neurodegenerative disorders.” (11)

Formaldehyde is very reactive and can use the methyl group to form links between protein groups or parts that wouldn’t normally be linked – like bungee cords holding parts together in places that would be separate in normal function. (11) Formaldehyde is used with tissue samples to preserve material for viewing under a microscope. Studies of the effect of formaldehyde on the actin protein of live cells that were low on blood sugar found that modifications to the protein did occur – the authors suggest any prior research on the actin protein in formaldehyde treated samples may be inaccurate. (12) Take home point – formaldehyde is not good for our brain cells and may effect the protein of our brain cytoskeleton structure. (12) Protein tangles in brain cells are associated with dementia and autism.

What is a cytoskeleton? We are mostly water, so how do we walk around? With a balance in tension between string like ligaments and muscles and rod like bones of our skeleton. Within the cellular environment, inside and outside the cell membrane – the tent wall, there are rod like microtubules and string like actin protein that is more flexible, it can change shape but isn’t stretchy as much as structurally able to modify in shape. Actin is a double helix, two spirals like DNA except without the ladder like steps joining the two lengths of protein. When force is applied the double helix can get a little longer or shorter as the coils compress or lengthen slightly – tensile strength – and the protein gets stiffer from a side to side direction – torsion – and is less flexible along the length, less able to bend sideways. (13)

The actin protein may act as torsion sensors – is the environment changing in pressure around that section of the protein length – from increased fluid or gas? How full is the balloon like membrane? (14) Channels in a membrane will open and start to leak rather than letting the membrane burst like an overfull balloon. This may seem like a silly discussion – however it is your brain and organs – leaking is better than bursting. Leaking membranes will release fluid and some types of chemicals while a bursting open, as when viral replication is complete and the virus exit a cell, the membrane bursts and all the remaining chemicals in the cell flood into the surrounding cytoskeleton and can cause inflammatory damage to surrounding cells.

These flexible yet firm cytoskeleton actin filaments also may act like guidelines for directing traffic or tethering organelles in place for activity such as replication of DNA during cell division (one cell doubles its DNA and then divides into two cells). Too much of the proteins within a cell nucleus will prevent DNA replication rather than guiding it. (15) Actin is also involved in muscle fiber motion. The double helix structure can also be methylated with methyl groups doing an unknown but critical function. Loss of methylation of actin in one location is associated with cancer and autism spectrum disorders, (16), loss of it in another location along the protein chain is associated with muscle changes that cause female animals to have delivery problems and fewer babies. (17, 18)

So actin is important stringy protein that effects muscle power, cell division, and the brain – and formaldehyde can cause demethylation of DNA, likely it can cause demethylation of actin also which may lead to autism spectrum disorders, cancer, and muscle problems that can affect a healthy delivery of infants (in an animal study). The visual – we want our jelly like insides to have a strong yet flexible tent membrane, tent poles (microtubules), and tie downs (actin) – without having so many tie downs it starts looking like a haunted house full of cobwebs. The amyloid beta protein associated with Alzheimer’s dementia and autism may be protective against a low level infection (post: Magnesium might help protect against beta amyloid placques) but also may increase changes in actin stress fibers (24) and an excess seems to add to chronic inflammatory damage over time.

How do we achieve this? Healthy actin?

It may help promote appropriate methylation of DNA and actin to have adequate antioxidants and methyl donor nutrients in our diet, to reduce oxidative stress chemicals and provide adequate methylation to DNA and actin. Avoiding excessive physical and emotional stress may also be an important strategy, so we aren’t embalming ourselves with self produced formaldehyde (the mummy in the haunted house being our own brain).

We also want to avoid formaldehyde in our environment, which would include improving air quality, especially during sleep hours when our body is focused on detoxification of the brain. Parkinson’s Disease is another chronic condition that may involve epigenetic changes and reducing formaldehyde exposure may be protective. More information is in this post with a link to a longer post about formaldehyde sources: The Cholinergic System

Increasing methyl donor vitamin rich foods and/or supplements should focus on the methylated form if unsure whether there is a genetic allele problem causing lack of methylation.

Methyl groups are important for numerous cellular functions such as DNA methylation, phosphatidylcholine synthesis, and protein synthesis. The methyl group can directly be delivered by dietary methyl donors, including methionine, folate, betaine, and choline.” … “Studies that simulated methyl-deficient diets reported disturbances in energy metabolism and protein synthesis in the liver, fatty liver, or muscle disorders.” … “Hypomethylation has a wide spectrum of effects that include genetic, epigenetic, and metabolic alterations.” (8)

Gastrointestinal problems have been found to be common among patients with Postural Orthostatic Tachycardia Syndrome (POTS) with malfunction or slowing, dysmotility, of the smooth muscle lining of the intestinal tract. “Case study 1: A 20-year-old woman presented to clinic for further evaluation of a several year history of fullness and epigastric discomfort associated with eating and irregular bowel habits. Her weight was stable. She also described frequent migraine headaches, episodic palpitations and lightheadedness with progressively increasing episodes of syncope. A systems review was notable for profound fatigue, dry eyes and mouth and intermittent flushing and pruritus.” (19) The patient’s symptoms include many in common with Mast Cell Activation Syndrome, however testing for mast cell activation was normal. Patients whose symptoms followed a viral infection tend to get better more often than patients with a family history of POTS. (19)  

A number of chronic conditions are frequently seen in patients with POTS and contribute to symptom burden and reduced quality of life. Common comorbidities include chronic fatigue syndrome, fibromyalgia, interstitial cystitis, and migraine headaches. Other unique conditions that seem to occur with increased frequency in POTS are autoimmunity, the hypermobile form of Ehlers-Danlos syndrome (HM-EDS), and mast cell activation disorder (MCAD).” (19)  

“Unlike mastocytosis, idiopathic mast cell activation [MCAD] occurs in the absence of mast cell proliferation and with episodic accumulation of mast cell mediators in the plasma or urine, usually present when symptomatic. Patients with MCAD typically present with episodic “attacks” of flushing, urticaria and pruritus accompanied by lightheadedness, dizziness, dyspnea, nausea, headache, diarrhea, and/or syncope; symptoms representative of the hyperadrenergic type of POTS with biochemical evidence of MCAD (20).” (19)

The patient in case study 2 had ongoing nausea, vomiting, abdominal pain, and weight loss continuing for years following a viral infection. She was found to have deficiency in iron, zinc, and vitamin B12 and gastroparesis (slow or little intestinal muscle action). Intravenous iron and B12 were provided and an oral zinc supplement. Nutrient levels improved however the GI symptoms and weight loss continued and the patient was given tube feedings which improved weight, however some intolerance to the tube feedings continued and abdominal pain persisted. (19)  

If demethylation of actin protein in the muscle tissue of the intestinal wall was a problem for the patient in case study 2, then it may have been a factor in the gastroparesis. Genetic screening for methylation defects is not mentioned. Supplements of B12 are often an unmethylated form, cyanocobalamin, and which include cyanide. (21) In a study of 12 patients by Huang et al, (22): “Disturbances in GI motility were found to involve not only the stomach, but also multiple segments of the gut spanning the esophagus to the anus.” (19) The commonly used treatments for GI symptoms associated with POTS (see Table 5) do not include nutrients and do include proton pump inhibitors, (19),  a medication that takes the place of magnesium as a calcium channel blocker, and which may lead to worse magnesium deficiency for some people, a genetic difference may be involved. See post: Original Prilosec Warning, edited.

Small intestinal bacterial overgrowth (SIBO) may occur along with GI problems and lead to fat and carbohydrate digestion and absorption problems and bloating from excessive bacterial growth. Changes in diet due to the discomfort are common in patients with POTS and these more severe GI symptoms and which may lead to deficiencies in fat soluble vitamins A, D, E and K. Megaloblastic anemia may result from deficiencies in iron, folate and vitamin B12. (19) Sulfate deficiency may be an underlying factor (23) and providing Epsom salt soaks of the lower legs and feet, or in a bath one to two times a week might help by providing a topically absorbed form of magnesium and sulfate. See post: To have optimal Magnesium needs Protein and Phospholipids too.

Zinc is also involved in DNA methylation and deficiency of the trace mineral can lead to epigenetic changes and gene transcription problems. Zinc is needed along with actin and other proteins to tell the cell nucleus and cell which genes to make into mRNA to be encoded into a protein. “Accumulating evidence has demonstrated that several key enzymes and zinc finger proteins with zinc atom(s) in the reactive center and binding site play important roles in DNA methylation and histone modifications. Therefore, zinc deficiency may disrupt the functions of these enzymes and proteins and result in epigenetic dysregulation. Furthermore, zinc deficiency may enhance inflammatory response and subsequently alter DNA methylation status of the genes involved in inflammation.” (20) Also see posts: Zinc – big news, CoV and other illness related, and Zinc, cancer, and bitter taste receptors.

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. JB Head, PhD, Cracking Nature’s Code: The Potential Answer to Everything. (Balboa Press, Bloomington, IN, 2019) https://www.balboapress.com/en/bookstore/bookdetails/792280-cracking-natures-code
  2. Pacis A, Tailleux L, Morin AM, et al., Bacterial infection remodels the DNA methylation landscape of human dendritic cells. Genome Res 2015. 25: 1801-1811 https://doi.org/10.1101/gr.192005.115 https://genome.cshlp.org/content/25/12/1801
  3. Lichinchi G, Zhao BS, Wu Y, et al. Dynamics of Human and Viral RNA Methylation during Zika Virus Infection. Cell Host Microbe. 2016;20(5):666-673. doi:10.1016/j.chom.2016.10.002 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5155635/
  4. Cudmore S, Reckmann I, Way M. (1997). Viral manipulations of the actin cytoskeleton. Trends in microbiology. 5. 142-8. 10.1016/S0966-842X(97)01011-1. https://www.researchgate.net/publication/14077627_Viral_manipulations_of_the_actin_cytoskeleton
  5. Ohkawa T, Volkman LE, Nuclear F-Actin Is Required for AcMNPV Nucleocapsid Morphogenesis, Virology, Vol 264, Issue 1, 1999, Pages 1-4, ISSN 0042-6822, https://doi.org/10.1006/viro.1999.0008. https://www.sciencedirect.com/science/article/pii/S0042682299900089
  6. Lu, S., Ge, G. & Qi, Y. Ha-VP39 binding to actin and the influence of F-actin on assembly of progeny virions. Arch Virol149, 2187–2198 (2004). https://doi.org/10.1007/s00705-004-0361-4 https://link.springer.com/article/10.1007/s00705-004-0361-4
  7. Marek M, Merten OW, Galibert L, Vlak JM, van Oers MM. Baculovirus VP80 protein and the F-actin cytoskeleton interact and connect the viral replication factory with the nuclear periphery. J Virol. 2011;85(11):5350-5362. doi:10.1128/JVI.00035-11 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3094977/
  8. Obeid R. The metabolic burden of methyl donor deficiency with focus on the betaine homocysteine methyltransferase pathway. Nutrients. 2013;5(9):3481-3495. Published 2013 Sep 9. doi:10.3390/nu5093481 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3798916/
  9. Richard Bayles, Harikrishnan KN, Elisabeth Lambert, et al., Epigenetic Modification of the Norepinephrine Transporter Gene in Postural Tachycardia Syndrome. Arteriosclerosis, Thrombosis, and Vascular Biology. 2012;32:1910–1916 https://doi.org/10.1161/ATVBAHA.111.244343 https://www.ahajournals.org/doi/full/10.1161/atvbaha.111.244343
  10. Su, Tao & He, Rong-Qiao. (2017). Formaldehyde Playing a Role in (De)methylation for Memory. 10.1007/978-94-024-1177-5_3. https://www.researchgate.net/publication/320523716_Formaldehyde_Playing_a_Role_in_Demethylation_for_Memory
  11. Ketki Tulpule Ralf Dringen, Formaldehyde in brain: an overlooked player in neurodegeneration?, J. Neurochem. (2013) 127, 7– 21 https://onlinelibrary.wiley.com/doi/10.1111/jnc.12356
  12. Vasicova P, Rinnerthaler M, Haskova D, et al. Formaldehyde fixation is detrimental to actin cables in glucose-depleted S. cerevisiae cells. Microb Cell. 2016;3(5):206-214. Published 2016 Apr 12. doi:10.15698/mic2016.05.499 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5349148/
  13. Effect of tensile force on the mechanical behavior of actin filaments. J Biomechanics (2011), 44(9): 1776-1781, 2011-06-03 , https://repository.kulib.kyoto-u.ac.jp/dspace/handle/2433/152437 https://core.ac.uk/download/pdf/39280196.pdf
  14. Hayakawa K, Tatsumi H, Sokabe M. Actin filaments function as a tension sensor by tension-dependent binding of cofilin to the filament. J Cell Biol. 2011;195(5):721-727. doi:10.1083/jcb.201102039 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3257564/
  15. Hu, X., Liu, Z.Z., Chen, X. et al. MKL1-actin pathway restricts chromatin accessibility and prevents mature pluripotency activation. Nat Commun10, 1695 (2019). https://doi.org/10.1038/s41467-019-09636-6 https://www.nature.com/articles/s41467-019-09636-6
  16. Seervai RNH, Jangid RK, Karki M, et al., The Huntingtin-interacting protein SETD2/HYPB is an actin lysine methyltransferase. Science Advances, 02 OCT 2020 : EABB7854 SETD2 regulates actin dynamics and cell migration via methylation of actin at Lys68 in a cellular complex containing Huntingtin. https://advances.sciencemag.org/content/6/40/eabb7854?Disruption of the SETD2-HTT-HIP1R axis inhibits actin methylation, causes defects in actin polymerization, and impairs cell migration. Together, these data identify SETD2 as a previously unknown HTT effector regulating methylation and polymerization of actin filaments and provide new avenues for understanding how defects in SETD2 and HTT drive disease via aberrant cytoskeletal methylation.“… “Loss of SETD2 and the H3K36me3 chromatin mark is embryonic lethal in Drosophila (7) and mice (8), and SETD2 defects have been linked to several diseases, including cancer (911) and autism spectrum disorder (1214).”
  17. Wilkinson, A.W., Diep, J., Dai, S. et al. SETD3 is an actin histidine methyltransferase that prevents primary dystocia. Nature 565, 372–376 (2019). https://doi.org/10.1038/s41586-018-0821-8, https://www.nature.com/articles/s41586-018-0821-8 lack of the methylation at histidine 73 seems to interfere with muscles and causes the genetically different animals to have fewer babies due to maternal delivery problems. Graphic from the article shows a CH3 methyl group being added to an actin filament at Histidine 73: https://twitter.com/anandb4/status/1073255833813671937?s=20
  18. Kwiatkowski S, Seliga AK, Veiga-da-Cunha M, et al., SETD3 protein is the actin-specific histidine N-methyltransferase. bioRxiv 266882; doi: https://doi.org/10.1101/266882Now published in eLife doi: 10.7554/elife.37921 https://www.biorxiv.org/content/10.1101/266882v1?platform=hootsuiteFinally, Setd3-deficient HAP1 cells were devoid of methylated H73 in β-actin and exhibited phenotypic changes, including a decrease in F-actin content and an increased glycolytic activity.
  19. DiBaise JK, Lunsford TN, Harris LA, Nutrition Issues in Gastroenterology, Series #187: The POTS (Postural Tachycardia Syndrome) Epidemic: Hydration and Nutrition Issues. June 2019, Practical Gastro, Vol XLIII, Issue 6 https://practicalgastro.com/2019/10/14/the-pots-postural-tachycardia-syndrome-epidemic-hydration-and-nutrition-issues/
  20. Gu H.F., Zhang X. (2017) Zinc Deficiency and Epigenetics. In: Preedy V., Patel V. (eds) Handbook of Famine, Starvation, and Nutrient Deprivation. Springer, Cham. https://doi.org/10.1007/978-3-319-40007-5_80-1 https://link.springer.com/referenceworkentry/10.1007%2F978-3-319-40007-5_80-1
  21. Dody Chiropractic, Why Do Vitamin B12 Supplements Contain Cyanide?, dodychiro.com,  https://www.dodychiro.com/why-do-vitamin-b12-supplements-contain-cyanide/
  22. Huang RJ, Chun CL, Friday K, et al. Manometric abnormalities in the postural orthostatic tachycardia syndrome: a case series. Dig Dis Sci 2013;58:3207-3211 https://pubmed.ncbi.nlm.nih.gov/24068608/
  23. Elliot Overton, Sulfate IV: Chronic SIBO/Gut Dysbiosis As A Protective Adaptation To Supply Sulfate. July 21, 2018, Eonutrition.co.uk, https://www.eonutrition.co.uk/post/sulfate-iv-chronic-sibo-gut-dysbiosis-as-a-protective-adaptation-to-supply-sulfate 
  24. Song C, Perides G, Wang D, Liu YF. beta-Amyloid peptide induces formation of actin stress fibers through p38 mitogen-activated protein kinase. J Neurochem. 2002 Nov;83(4):828-36. doi: 10.1046/j.1471-4159.2002.01182.x. PMID: 12421354. https://pubmed.ncbi.nlm.nih.gov/12421354/
  25. Frederic Dorandeu, Guilhem Calas, Gregory Dal Bo, Raafat Fares, Chapter 36 – Models of Chemically-Induced Acute Seizures and Epilepsy: Toxic Compounds and Drugs of Addiction, Editor(s): Asla Pitkänen, Paul S. Buckmaster, Aristea S. Galanopoulou, Solomon L. Moshé, Models of Seizures and Epilepsy (Second Edition),Academic Press, 2017, Pages 529-551, ISBN 9780128040669, https://doi.org/10.1016/B978-0-12-804066-9.00037-7. https://www.sciencedirect.com/science/article/pii/B9780128040669000377Alterations of the neuronal cytoskeleton, and more precisely disruption of actin dynamics, seem then to contribute to changes in brain excitability, but the mechanisms leading to these changes remain still unresolved (Spence and Soderling, 2015).” Excerpt viewable in F-actin, ScienceDirect, https://www.sciencedirect.com/topics/neuroscience/f-actin

Cytokine Storm, SIDS, autism and Vitamin C

The over-reaction of the immune system to any infectious stimulant whether an infection or vaccines, may be a cause of Sudden Infant Death Syndrome (SIDS) (1) and the encephalopathy (2) that is a frequent factor in later development of autism. (3)

Sudden Infant Death Syndrome may be a toxin overload as success was achieved with mattress covers in Australia that prevented volatile chemicals or mold spores from reaching the baby. Crib mattresses often contain vinyl or fire retardants and a used mattress likely has mold even if not obvious. It can be healthy for infants to sleep on their belly as helps with even muscle development and skull shape. Babies that are held or left in the same position all the time can development flattened areas on the skull and limit muscle development. See previous post1, post2, post3.

Giving infants and children vitamin C prior to vaccines orally with juice may be protective against the harmful excess production of inflammatory cytokines. Giving a larger amount intravenously for adverse reactions may also be protective against the cytokine overreaction from worsening as the larger amount of vitamin C has an inhibitory effect on the production of them as well as helping as an antioxidant to detoxify the ones already made in excess. Giving extra vitamin C before vaccines was found to be protective even in lab animals that genetically can make vitamin C. (4)

Cytokine Storm over-reactions may be more of a risk due to genetic differences in as many as 10-15% of the population. (5) Symptoms of a Cytokine Storm reaction can include: “high fever, enlarged spleen, excessive bleeding, low counts of all types of blood cells (red, white and platelets) and, potentially, multiple organ failures.” (5) Diarrhea is unpleasant and can kill if it continues for long however multiple organ failures is more deadly.

Providing vitamin C as a protection against the risk of an overreaction of the immune system would be low cost and has had a low risk of side effects. Diarrhea occurs if excess is taken by mouth so there is little risk of too much being absorbed in the GI tract, and adverse reactions to higher doses of vitamin C given as intravenous therapy have not been prevalent (1%) in studies using the treatment as an addition to chemotherapy treatments. (6)

Phase I studies of IV C alone & in combination with chemotherapy have reported excellent safety profiles 1–8,33. A survey of providers who used IVC for 9328 patients reported an adverse event rate of 1.0% 68..side effects of IVC…nausea, dizziness, dry mouth, perspiration, & weakness. 6,7” (6)

Giving vitamin C to infants and children would be providing them with a nutrient than most animals can produce for themselves. Humans had a genetic change that caused a loss of the ability. Giving vitamin C to infants and children might also help protect against a potentially fatal or brain damaging over-reaction of the immune system. If 10-15% of the population are genetically more at risk for the excess production of cytokines, (5) , then a government policy that mandates vaccinations would be genetically targeting those individuals for increased risk of an adverse reaction or death – a genocide.

Learning more about the gene differences involved in the increased risk for a Cytokine Storm reaction, and screening the population for the genes would also be helpful so those individuals would know that they have increased risk of death if they have an infection or strong immune reaction to something.

The Committee  to Review Adverse Effects of Vaccines that was asked to assess the research on autism and vaccines did not say there was no risk of autism from vaccines – they said there was a lack of evidence – more research was needed.

The committee particularly counsels readers not to interpret a conclusion of inadequate data to accept or reject causation as evidence either that causation is either present or absent. Inadequate data to accept or reject causation means just that—inadequate. It is also important to recognize what our task was not. We were not charged with assessing the benefits of vaccines, with weighing benefits and costs, or with deciding how, when, and to whom vaccines should be administered.

Committee to Review Adverse Effects of Vaccines
Board on Population Health and Public Health Practice, Institute of Medicine (7)

Disclaimer: This information is provided for educational purposes within the guidelines of Fair Use. It is not intended to provide individual guidance. Please seek a health care provider for individualized health care guidance.

Reference List

  1. Siri Hauge Opdal, PhD., Chapter 30: Cytokines, Infection, and Immunity, from the book SIDS Sudden Infant and Early Childhood Death: The Past, the Present and the Future. Duncan JR, Byard RW, editors., Adelaide (AU): University of Adelaide Press; 2018 May. https://www.ncbi.nlm.nih.gov/books/NBK513388/
  2. Cytokine Storm, ScienceDirect.com, https://www.sciencedirect.com/topics/medicine-and-dentistry/cytokine-storm
  3. Kern JK, Geier DA, Homme KG, Geier MR. A ten year longitudinal examination of the incidence rate and age of childhood encephalopathy diagnoses in an autism spectrum disorder diagnosed cohort. Acta Neurobiol Exp (Wars). 2020;80(1):66–75. https://pubmed.ncbi.nlm.nih.gov/32214276/
  4. C. Alan B. Clemetson, M.D., Rapid Response: The prevention of vaccine reactions. BMJ 2004;328:51 https://www.bmj.com/rapid-response/2011/10/30/prevention-vaccine-reactions
  5. University of Alabama at Birmingham, Here’s a playbook for stopping deadly cytokine storm syndrome. Nov 11, 2019, theivcenter.net, https://theivcenter.net/wp-content/uploads/2018/05/Vit-C-and-Cancer-Support.pdf
  6. E. Klimant, H. Wright, D. Rubin, et al, Intravenous vitamin C in the supportive care of cancer patients: a review and rational approach. Curr Oncol. 2018 April;25(2):139-148, https://theivcenter.net/wp-content/uploads/2018/05/Vit-C-and-Cancer-Support.pdf
  7. Institute of Medicine (U.S.). Committee to Review Adverse Effects of Vaccines.  Adverse effects of vaccines : evidence and causality / Committee to Review Adverse Effects of Vaccines, Board on Population Health & Public Health Practice ; Kathleen Stratton … [et al.], eds.  ISBN 978-0-309-21436-0 (PDF)  https://www.nap.edu/read/13164/chapter/1

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

Autism rate is increasing at a rate faster than evolution can explain

The rate of autism in the 1970s was around 1 child in 10000. Prior to  the 1930s the disease was barely heard of and only a few children, fewer than ten, had even been documented in psychiatric medical records as having any symptoms similar to the autism spectrum symptoms. (Denial/Blaxill, Olmsted)

Around 1999 to 2000 there was a sharp increase in the rate of autism diagnosed. Changes in awareness and/or diagnosis criteria may have some impact on short term changes but the increase in rate from the 1970s is significant. Extrapolating into the future following the recent rate of change in the rate of children diagnosed with autism takes us to an estimated rate of 1 in 34 children in the year 2042. We all need to ask ourselves if now is a better time to try to prevent autism from occurring in our nation’s children or if we should wait until 2042. There are multiple risk factors including specific timing during the infant’s prenatal development, exposure to certain toxins, and nutrient deficiency and/or genetic susceptibility – complex, yes, but complex just takes a little more work to handle.

Autism Rate, U.S., Actual : 1970s-2018, Extrapolated from 2018 to 2042

U.S. Autism Rate Soars to 1 in 59 Children, SafeMinds.org

Improved screening for risk factors of mothers during perinatal and prenatal care and screening of infants and toddlers before symptoms occur could help provide individualized guidance to help reduce known risk factors associated with increased risk of developing autism.

This series of pages titled as Step 1, Step 2, etc. is a draft of steps for how to prevent autism or other chronic illnesses:

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.