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.
  2. 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.
  4. C. Alan B. Clemetson, M.D., Rapid Response: The prevention of vaccine reactions. BMJ 2004;328:51
  5. University of Alabama at Birmingham, Here’s a playbook for stopping deadly cytokine storm syndrome. Nov 11, 2019,,
  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,
  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)

L-Serine, hope for Alzheimers and ALS

Misshapen proteins that collect in the brains of patients who eventually are diagnosed with Alzheimer’s dementia or in patients with ALS may be due to a substitution being made by BMAA a toxin in some types of cyanobacteria (a blue-green algae) in place of the amino acid L-serine.

Trials have begun with dietary intake of L-serine amino acid powder. The powder is readily available for purchase and is non toxic, (available online from bulk supplement companies that may market to weight lifters). Varying doses have been tried and 30 grams per day, slightly more than an ounce, have been found helpful. See: Alzheimer’s Disease – Could New Approach Lead to Breakthrough? (

The main researcher, Dr. Paul Cox, has a team or researchers involved now and has been focused on Alzheimer’s or ALS, however this is a breakthrough that might also help patients with autism as similar misshapen proteins are often found to be involved in that condition too. A review of research on levels of certain amino acid that have brain neurotransmitter roles in patients with autism diagnoses had some mixed results as there is a D-serine and L-serine form and levels of each can vary and whether a research study measured them separately of together was inconsistent, but several did find lower levels for patients with autism compared to the control group without an autism diagnosis.

See: Zheng HF, Wang WQ, Li XM, Rauw G, Baker GB. Body fluid levels of neuroactive amino acids in autism spectrum disorders: a review of the literature. Amino Acids. 2016;49(1):57-65.

More recent research has not replicated or reinforced the theory that BMAA is involved in development of Alzheimer’s disease.

The role of the non-essential amino acid BMAA as a causal agent of Alzheimer’s or ALS may involve other factors in addition to chronic buildup of BMAA over time as a review of research about the topic did not conclude a causal relationship of the amino acid with neurodegenerative disorders.

  • See: A critical review of the postulated role of the non-essential amino acid, β-N-methylamino-L-alanine, in neurodegenerative disease in humans. Chernoff, et al, 2017, (
  • Reanalysis of samples of the suspected source of BMAA from the initial research did not find significant amounts, see: The analysis of underivatized β-Methylamino-L-alanine (BMAA), BAMA, AEG & 2,4-DAB in Pteropus mariannus mariannus specimens using HILIC-LC-MS/MS. Foss et al, 2018, (
  • β- N-Methylamino-l-alanine (BMAA) Not Involved in Alzheimer’s Disease. Rauk, 2018, (

The prevailing theory that Beta amyloid protein is a causal agent in Alzheimer’s disease is now being questioned as almost 200 experimental drugs designed to decrease levels of the protein have been found ineffective as treatments for the disease. The protein is involved but likely isn’t the initial problem — regarding Beta amyloid in Alzheimer’s disease: “Brain amyloid is therefore generally accepted as being essential for disease progression but not sufficient on its own to drive disease. The next observable change in brain is impaired glucose metabolism within AD brain,” … “Based on these imaging and biomarker studies it is emerging that brain glucose
(reduced glucose metabolism) and tau toxicity (increased phosphorylation of the Tau protein making it malfunction) likely reflect central events in the progression of AD (1,2,8).”  – Zhu et al, 2014, The emerging link between O-GlcNAc and Alzheimer’s disease, (

So if BMAA is not a causal agent and Beta amyloid itself also isn’t the primary factor in development of Alzheimer’s disease – that leaves us asking what is involved? The answer is likely multifactorial – multiple issues that may vary somewhat for different patients.

Causal Agent versus Multifactorial Disorder.

Causal roles of a toxin traditionally look at toxins individually and as a toxin that would have the same risk for all people or animals if an animal study. Multifactorial disorders however may involve increased risk for some people based on genetic differences from average, or also require nutrient deficiencies to be present or other infectious or inflammatory conditions to also be present chronically.

Cyanotoxins including BMAA and a metabolite, DAB, have been analyzed for risk of cell death or inflammation in murine (aquatic rather than land based species) brain cells. Low doses of some of the cyanobacteria toxins were found to be a concern but not the BMAA or DAB.

  • See: Cyanotoxins at low doses induce apoptosis and inflammatory effects in murine brain cells: Potential implications for neurodegenerative diseases. Takser, et al, 2016 (

The research by Dr. Paul Cox with BMAA in Alzheimer’s found that the risk association was with concentrated doses over decades,
(, so lower doses may not be a significant risk or possibly risk may also require other factors to be present such as a chronically low intake of L-serine.

Many factors have been associated with increased risk for autism spectrum disorder some involving the early prenatal time of conception and implantation of the fetus and later stages of fetal development. Infants may seem to be developing typically and develop symptoms later as a toddler when rapid changes generally occur in the number of connections between brain cells. Genetic and environmental and nutrient deficiencies may also increase risk for the child later developing symptoms of autism or other cognitive conditions such as Attention Deficit/Hyperactive Disorder (ADHD).

  • For more information see: Causal Agent versus Multifactorial Disorder, which I am modifying into an easier to use format from a long series of posts on another of my sites, Believing is the First Step Towards Change.
  • An excerpt from that earlier document – Mice bred to be genetically defective in their ability to produce L-serine, a component of sphingolipids, all died as embryos – they never made it to birth. And: “As expected, all brain L-serine-derived lipids such as phosphatidylserine, phosphatidylethanolamine, sphingomyelin, and GD3 ganglioside are greatly reduced in Phgdh knockout mice.” – See: Hirabayashi Y. A world of sphingolipids and glycolipids in the brain–novel functions of simple lipids modified with glucose. Proc Jpn Acad Ser B Phys Biol Sci. 2012;88(4):129-43.
  • Sphingolipid and serine synthesis are somewhat dependent on each other – inhibiting or increasing one or the other can inhibit or increase production of the other. This may help in treatment of cancer and help with better understanding of intellectual disability conditions as sphingolipid is important for a type of cell common to both. “Sphingolipid levels are tightly linked to serine synthesis, and inhibiting either serine or sphingolipid synthesis can specifically impair the fitness of aneuploid cells “– “Deciphering these mechanisms is important because aneuploidy is associated with diseases including intellectual disability and cancer.” — Hwang S, Gustafsson HT, O’Sullivan C, et al. Serine-Dependent Sphingolipid Synthesis Is a Metabolic Liability of Aneuploid CellsCell Rep. 2017;21(13):3807-3818.

So is metabolic problems in serine metabolism or lack of protein in the diet an initial problem? or O-GlcNAc?

Serine is considered a non-essential amino acid because it can be made out of the amino acid glycine in normal health, or it can be converted back into glycine. (ScienceDirect/serine) Both glycine and serine are used in large amounts within myelin, the protein used to form the white fatty coating around the connecting channels between nerve cells. There are 18 molecules of serine within a molecule of myelin protein (172 amino acids long per an older source). See: Amino Acid Sequence of the Basic Protein of the Myelin Membrane, Eylar, 1970, ( – an old source but the graphic is viewable.

O-GlcNAc is a type of sugar/amino acid linkage that may have protective effects against Tau protein, another type of protein that seems to collect in the brain tissue of patients with Alzheimer’s disease. “O-GlcNAcylation is a dynamic form of protein glycosylation which involves the addition of β-d-N-acetylglucosamine (GlcNAc) via an O-linkage to serine or threonine residues of nuclear, cytoplasmic, mitochondrial and transmembrane proteins.” – Wani, et al, 2017, O-GlcNAcylation and neurodegeneration, (

(*N-Acetylglucosamine is a type of monosaccharide that can be formed from a molecule of glucose in times of normal health. It is available as a supplement marketed for arthritis pain as glucosamine, generally derived from chitin found in shellfish. It is not typically found in common foods in the human diet.)(Health is a miracle of complex chemistry, in my opinion.)

Food Sources of L-Serine.

The research on BMAA and trials providing extra L-serine as a possible treatment for ALS (Amyotrophic lateral sclerosis, also known as Lou Gehrig’s Disease, a degenerative nerve condition which causes muscle paralysis) is discussed on another site in an article that includes a list of food sources of L-serine. Animal products such as dairy foods and a variety of meats are good sources but sesame, sunflower, and pumpkin and squash seeds are also sources along with hemp kernels, soy products and other beans, and peanuts and pistachio nuts. See: What is L-Serine and What is Research Telling Us? (

This very exciting as there is no shortage of L-serine, it is non-toxic commonly available in foods or as a bulk powder supplement, there would be no wait for a drug approval process. The clinical trials help prove efficacy, safety, and dosage recommendations.

Pumpkin seed kernels, raw, unsalted, with a standard size teaspoon.

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.

Additional notes 2/19/2018:

  1. Suspected Link between ALS and Head Trauma (focus on sports trauma like soccer and football)
  2. Links on brain injury and increased free glutamate
  3. L-Serine deficiency elicits intracellular accumulation of cytotoxic deoxy-sphingolipids and lipid body formation, when L-alanine and L-serine levels are out of balance, when an external source of L-serine is limited, sphingolipid production changes and
    1-deoxy-sphingolipids (doxSLs) are created
  4. Localization of 1-deoxysphingolipids to mitochondria induces mitochondrial dysfunction, “1-Deoxysphingolipids (deoxySLs) are atypical sphingolipids that are elevated in the plasma of patients with type 2 diabetes and hereditary sensory and autonomic neuropathy type 1 (HSAN1). Clinically, diabetic neuropathy and HSAN1 are very similar, suggesting the involvement of deoxySLs in the pathology of both diseases ” suspected mechanism of deoxySLs: “localized to mitochondria, causing mitochondrial fragmentation and dysfunction” which then may lead to neuropathy

Glutathione, Nrf2, Autism and glyphosate

Glyphosate use has escalated (1) at a similar rate and overlapping time frame to the increase in autism in children. The rate of autism in Japanese children is even greater than in U.S. children. The Japanese children may be consuming a larger percent of GMO soy from the U.S. as the country is a significant importer of the crop. (4)Testing has shown that basically all GMO soy, Roundup Ready, has residue of glyphosate. (1) Glyphosate residue has been found in all foods tested by the FDA except for broccoli. (6)

The herbicide Roundup has been shown to induce oxidative stress in animal studies (5), and children with autism have been shown to have an increase in oxidative stress and reduced levels of an antioxidant, glutathione, (2), that is made within our bodies during normal health.

Use of Nrf2 promoting foods might help increase our own production of glutathione. (3) Broccoli is one food that may help promote our own supply of Nrf2 which then helps us make the antioxidant glutathione.

Glyphosate may be metabolized into other chemicals within the body and it or the metabolites may inhibit enzymes important for a variety of functions throughout the body. (7) Radioactive labeling of glyphosate in animal studies by the company Monsanto showed that bioaccumulation of the chemical does occur, particularly in blood cells found in bone and bone marrow, also in the testes and ovaries, see slide 11 for a copy of the table of data: (8).

A thorough overview of the theoretical and known health risks of glyphosate is available by a personal fitness coach from Australia, Alex Fergus, (9), in part two of a three part series on his website. Part one covers the history of the synthetic chemical’s discovery and patent history and increased agricultural use in the U.S. and globally, (10), and his list of tips on how to protect yourself and try to reduce exposures through diet and supplements, (11). The list is comprehensive however doesn’t include Epsom salt/magnesium sulfate as an additional source of bioactive sulfate. Baths or footsoaks provide a topical absorption route that would bypass any problems with malabsorption in the digestive system or problems with sun exposure to bioactivate other forms of sulfur into the bioactive sulfate form.

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. John Peterson Myers, Michael N. Antoniou, Bruce Blumberg, Lynn Carroll, Theo Colborn, Lorne G. Everett,Michael Hansen, Philip J. Landrigan, Bruce P. Lanphear, Robin Mesnage, Laura N. Vandenberg, Frederick S. vom Saal,Wade V. Welshons, and Charles M. Benbrook,

    Concerns over use of glyphosate-based herbicides and risks associated with exposures: a consensus statement.  Environ Health. 2016; 15: 19. Pub. online 2016 Feb 17,

  2. S. Rose, S MelnykO PavlivS BaiT G NickR E Frye,  S J James, Evidence of oxidative damage and inflammation associated with low glutathione redox status in the autism brain, Translational Psychiatry Vol. 2, page 134 (2012),,
  3. Megan L. Steele, Stacey Fuller, Mili Patel, Cindy Kersaitis, Lezanne Ooi, and Gerald Münch, Effect of Nrf2 activators on release of glutathione, cysteinylglycine and homocysteine by human U373 astroglial cellsRedox Biol. 2013; 1(1): 441–445. Published online 2013 Sep 12,

  4. Zen Honeycutt, Shockingly Higher Rates of Autism and Developmental Delays in Asia, Report from Japan speaking tour, March 1-10, March 21, 2017,,
  5.  Low toxic herbicide Roundup induces mild oxidative stress in goldfish tissuesChemosphere, Vol. 76, Issue 7, Aug 2009, pp 932-937
  6. Toxic Weed Killer Glyphosate Found in Most Foods Sold in the U.S.,,
  7. Ford et al., Mapping Proteome-wide Targets of Glyphosate in Mice, Cell Chemical Biology (2016),
  8. Anthony Samsel, Glyphosate Herbicide Pathways To Modern Diseases Synthetic Amino Acid And Analogue of Glycine Mis-incorporation Into Diverse Proteins , Slides 2016,, (8)
  9. Alex Fergus, Glyphosate: Why You Need to Eat Organic, (9)
  10. Alex Fergus, Glyphosate: The Weed Killer Found in Our Food & Water, (10)
  11. Alex Fergus, How to Protect Yourself from Glyphosate, (11)