Antimony, SIDS, autism and mattress covers

SIDS, Sudden Infant Death Syndrome, is the primary cause of death among infants and children under age one — in the United States. In New Zealand, however, SIDS rates have dramatically declined since 1994 when a specially designed mattress cover was developed to help protect infants in their cribs from toxic fumes released from the mattress due to chemical additives or molds. Antimony is one of the chemicals that may be a common risk to infants. Chemicals added to reduce risk of the mattress catching fire may be gradually released and absorbed through the infant’s skin or be breathed by the baby.

In the United States a “Back to Sleep” educational campaign was developed to try to reduce the rate of SIDS deaths because the problem was associated with infants sleeping on their stomachs. That position would place their nose and mouth more directly into the mattress where the toxic chemicals tend to be most prevalent. The “Back to Sleep” campaign and the tendency to leave infants sitting in their infant seats for long periods of time may also have led to more flat-headed babies. Specially shaped neck and head support pillows were developed and sold to worried parents to then prevent the flat-headed problem.

Antimony is a heavy metal which may also be associated with autism risk. Wrapping a mattress in a protective cover is a non-toxic, completely safe and low cost investment that might help protect against SIDS risk and possibly reduce the long term build up of toxins that might increase autism risk. However the United States health guidelines have not endorsed/accepted/supported the simple solution that has been saving the lives of infants in New Zealand since 1994. Research there has proven statistical significance of the method.

The U.S. may be dragging it’s collective heals because of fear of liability or fear of agreeing that fire retardant chemicals that were supposed to save lives may be costing lives — speculation doesn’t save many lives but wrapping an infant mattress in a specially designed cover might. Replacing infant mattresses between infants might also help. The mold risk may be an increased problem for second or third children — who tend to have an increased risk to die from unknown causes while asleep (SIDS) compared to the firstborn infant.

Tweets on the topic from my social media Twitter account; #1, 2 and 3 are to the same link, “Has the Cause of Crib Death, SIDS, been Found?; and #5 and 7 are to a link that sells the specially designed BabeSafe brand mattress covers; the link to which I found on #4, prevent-SIDS.org website’s article “BabeSafe Mattress Wrapping Success”; and #6 is to an Autism website that mentions antimony and fire retardants as a possible risk but which does not mention the New Zealand SIDS research or specially designed mattress covers; #7 is a Tweet where I combined a different autism prevention article with the BabeSafe mattress cover link (#5):

  1. Wrapping crib mattresses to reduce toxic off-gassing has reduced SIDS rate in New Zealand. .
  2. “no babies have died sleeping on a properly wrapped mattress.” 2,100 babies die/yr in U.S. via .
  3. Has The Cause of Crib Death (SIDS) Been Found? /statistics~1 billion x level generally required/ via
  4. BabeSafe Mattress Wrapping Success
  5. “Babe-safe mattress covers,” made to the New Zealand design to safely reduce off-gassing toxins,
  6. Aluminum, Antimony, Autism and Answers
  7. Minimizing Risks | Autism Research Institute /babesafe covers decrse antimony   .

Infants, at least some of them, some of the time, like to sleep on their stomachs. Do they have to move to New Zealand in order to have that freedom? Or in a free country couldn’t parents have the right to buy their infant a specially designed mattress cover that might help protect them from volatile chemicals and molds that might be off-gassing from the mattress and increasing risk of SIDS and autism?

Freedom was a core principle for our nation’s Founding Fathers. They might have voted for the right to wrap mattresses rather than enforcing an educational message designed to reduce health risks but may have led to increased risks of flat-headed-ness. Flat-headed babies sometimes have their skull shape round out again without intervention beyond encouraging the parent to hold their baby more and to use the specially designed neck and head supports and to make sure baby has ‘tummy time’ while awake, but sometimes the infants have to wear specially designed football like helmets for weeks or months in order to encourage the skull to grow into a more typical shape.

Encouraging baby in “Tummy time” can then sometimes become a challenge if the infant gets so used to the back position that they lose muscle strength and interest in spending time on their tummies. The position is important for increasing neck, back and arm strength necessary for learning how to roll over and press up to a hands and knee position for learning how to crawl. And learning how to crawl has been associated with improved skills in coordination between the right and left halves of the body and with more advanced skills later in life such as reading and writing. The “Back to Sleep” education campaign was started in the U.S. in 1994. [http://www.medcentral.org/main/Whatssoimportantaboutcrawling.aspx ] The mattress cover campaign that started around the same time in New Zealand had a much more significant reduction in infants dieing from SIDS and probably didn’t lead to as many babies developing flattened heads.

We don’t know what we don’t know until we learn it the hard way or listen to other people who have also experienced the problem and developed sensible solutions.

Guessing, but an educated guess — if the infant has any asthma or other respiratory issues the BabeSafe Mattress Covers might also help their health. Mold and volatile chemicals can add to asthma and breathing difficulties.

/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./

Methylation Cycle Defects – in me – genetic screening “for research purposes only”

I purchased an independent genetic analysis which clearly states that it is “For research purposes only. Not for use in diagnostic procedures.” The screening is for informational purposes as there isn’t a physician providing individual care. But that is okay since I enjoy research with an experimental group of N=1 (me).

The genetic screening panel, is self pay, not covered by insurance, and while the company provides free information it also sells nutritional supplements designed to support the special metabolic needs associated with defects in the methylation cycle, which can affect levels of B12 and folate in particular. The screening assessed my genes, (from a finger stick blood sample that I provided by mail), for thirty different gene mutations known to be involved in the methylation cycle, and found — drum roll — eleven mutations in my genes. Four of them are double mutations which I think means that the mutation is on both genes – no normal genes for that protein for me, means that my body has no recipe card to make four types of proteins.

And — drum roll — one of the single gene mutations is on my Vitamin D Receptor gene — specifically of the Fok1 type which has been associated with an increased risk for autoimmune disease.  With a single gene mutation I think roughly half of my Vitamin D Receptors might be normal and half might be three amino-acids longer than normal as described in the following excerpt from a research article about Type 1 Diabetes:

“Variants of the VDR gene have been associated with susceptibility to several autoimmune processes. The roles of the VDR gene polymorphisms depend on their locations (Slattery, 2007). FokI polymorphism is within the DNA binding domain, near the 5′ end, and the rest of the SNPs are in the 3′UTR region within the ligand binding domain. The FokI polymorphism creates an alternative ATG initiation codon in exon 2 leads to a 3 amino-acids longer VDR protein by directly introducing a start codon. A functional impact of this polymorphism on the immune response has been demonstrated (Colin et al., 2000; van Etten et al., 2007). However, VDR gene SNPs influence on VDR expression differ in different populations.” – Elham O. Hamed et. al., “Vitamin D Level and Fok-I Vitamin D Receptor Gene Polymorphism in Egyptian Patients with Type-1 Diabetes,” [http://app.egyptlearn.com/eji/pdf/june2013/1-Elham-Sohag.pdf]

I’m not sure if having an extra “start” codon on half of my Vitamin D Receptors makes them more “startable” / more over active, or whether it would make them less effective. The article suggests the mutation does leave patients more likely to become calcium and vitamin D deficient but it never mentions whether hormone D levels were ever measured or not.

Additional link 7/14/16, suggests that the Fokl polymorphism may have long and short versions and the long version may cause over activity of the vitamin D receptor and the short version may be under active. And it mentions that defects in the VDR gene may increase risk for hyperparathyroidism, osteoarthritis, cancer and infection risk. Increased intestinal absorption of calcium and increased bone turnover may be a factor in the increased risk for osteoarthritis. Excerpt:

“In a series of 20 fibroblast cell lines of different VDR genotype, the relative transcription efficiency was measured of the endogenous VDR protein which was differing by the genotype at the FokI RFLP (F and f alleles) and the poly(A) stretch with long (L) and short (S) alleles which is acting as a transcription factor for a 1,25-dihydroxyvitamin D3-responsive reporter gene. This study provided evidence for so-called high (of the “FL” genotype) and low (of the “fS” genotype) VDR activity.”

“Indeed, the VDR gene has been found associated with a number of different phenotypes of which, especially, the associations with osteoarthritis, hyperparathyroidism, cancer and infection-susceptibility, so far are supported by several independent and large studies reporting similar associations.” “For example, VDR gene variants can influence calcium metabolism through differential absorption in the intestine and, at the same time, influence bone turnover, while also the occurrence of osteophytosis (as a part of osteoarthritis) can be influenced, together resulting in a net effect on BMD measured at a certain site, at a certain age and in a subject with a certain diet.”

[Uitterlinden A., et. al., Vitamin D receptor gene polymorphisms in relation to Vitamin D related disease states. Journal of Steroid Biochemistry & Molecular Biology 89–90 (2004) 187–193http://web.udl.es/usuaris/e4650869/Morella06/BB/VDR%20related%20diseases.pdf] [via http://questioning-answers.blogspot.com/2015/07/vitamin-d-metabolic-gene-variants-and-risk-for-autism.html]

That is interesting as I’ve had osteoarthritis symptoms in two of my toes for years (there’s an increased risk for dancers and people in other sports to have osteoarthritis develop due to overuse or injury and I had broken two toes as a teen. The toes healed at the time but lost range of motion later in life. I’ve also experienced secondary hyperparathyroidism which was diagnosed more recently and the hormonal imbalance can cause significant mental health symptoms. Maintaining my calcium and magnesium intake in balance  while limiting intake of vitamin D and exposure to excessive sunlight seems to be adequate for helping me to be able to keep my parathyroid hormone level within normal limits without further medication or other treatment.

A different older post has a citation that clarified the roles of vitamin D and hormone D. Vitamin D is actually only associated with a carrier protein that seems to act as an “off” switch and prevents it from activating the Vitamin D Receptor. Any free D that is not carried by the special carrier protein, becomes activated to the hormone. And since there are typically many, many more open Vitamin D Receptors in the body than the supply of active hormone could ever fill, any free D, if there is a deficiency or lack of the carrier protein, is likely to become activated to hormone D and then proceed to activate a Vitamin D Receptor. My lab tests and symptoms have always been worse when I have excess D so I’ve been wondering if I might have a genetic mutation in my D carrier protein gene, but this methylation cycle panel didn’t check that gene.

The four double mutations are in the genes: MTHFRC677T (Call – T), MTRR/A66G (Call – G), BHMT/1 (Call – T), and MAO A/R297R (Call – T).

The seven single mutations are in the genes: SHMT/C1420T (Call – Hetero), MTR/A2756G (Call – Hetero), BHMT/8 (Call – Hetero), CBS/A360A (Call-Hetero), COMT/V158M (Call-Hetero), COMT/H62H (Call-Hetero), as well as the VDR/Fok1 (Call-Hetero) mutation.

Genetic defects in the methylation cycle of expectant mothers or in the expected infant have been associated with an increased risk for autism developing in the infant later in life. Children with a COMT mutation were at increased risk to develop autism, but I will have to dig through old posts, (1, 2), to find that citation: [4: Schmidt RJ1, Hansen RL, Hartiala J, Allayee H, Schmidt LC, Tancredi DJ, Tassone F, Hertz-Picciotto I., Prenatal vitamins, one-carbon metabolism gene variants, and risk for autism., Epidemiology. 2011 Jul;22(4):476-85, [http://www.ncbi.nlm.nih.gov/pubmed/21610500] I didn’t include the specific genetic mutations in the old posts; the article mentioned two for mothers and one for the child. The COMT 427 AA gene in the child turns out to be a slightly different mutation than the COMT mutations reported in my genetic panel, however I do have the double T mutation in my MTHFR 677 gene mentioned in this article as placing expectant mothers at increased risk for having a child with autism. But my CBS mutation is single and also different than the one mentioned in the following excerpt:

Excerpt from the Abstract:

“Significant interaction effects were observed for maternal MTHFR 677 TT, CBS rs234715 GT + TT, and child COMT 472 AA genotypes, with greater risk for autism when mothers did not report taking prenatal vitamins periconceptionally (4.5 [1.4-14.6]; 2.6 [1.2-5.4]; and 7.2 [2.3-22.4], respectively). Greater risk was also observed for children whose mothers had other one-carbon metabolism pathway gene variants and reported no prenatal vitamin intake.”

Excerpt from the article:

“However, children with the COMT 472 AA genotype were at increased risk for autism if their mothers reported having taken periconceptional prenatal supplements (OR = 1.8 [CI = 0.99–3.5]), and were at substantially higher risk if their mothers did not (7.2 [2.3–22.4];”              [4, full text article available]

The four double mutations are in the genes:

  1. MTHFRC677T (Call – T), Methylene tetrahydrofolate reductase, This version of the gene may have less activity than the more typical version of the gene (the T stands for Thymine, the more effective version has a C, cytosine). https://en.wikipedia.org/wiki/Methylenetetrahydrofolate_reductase  It may cause hyperhomocysteinemia especially if levels of folate, B6 and B12 are deficient. [http://www.mayomedicallaboratories.com/test-catalog/Clinical+and+Interpretive/81648] May make deficiency of methylated folate more of a risk and make folic acid supplements not useful.
  2. MTRR/A66G (Call – G), 5-methyltetrahydrofolate-homocysteine methyltransferase reductase or methionine synthase reductase, This mutation may increase risk for elevated levels of homocysteine and may affect folate and vitamin B12 methylation. Levels of B12 might be normal but not functional due to the lack of methylation. [http://mtrra66g.com/] * this site is commercial and recommends a methyl form of B12 however one of my other mutations might be affected negatively by excess methyl donors, see the selfhacked.com link in the #4 “warrior gene” within this list.  [https://ghr.nlm.nih.gov/gene/MTRR] [http://www.ncbi.nlm.nih.gov/gene/4552]
  3. BHMT/1 (Call – T), Betaine-homocysteine methyltransferase (BHMT),  This enzyme helps produce  the amino acids methionine and Dimethylglycine (DMG). DMG has been found helpful in ADHD, autism, allergies, alcoholism drug addiction, and chronic fatigue syndrome among other chronic issues. Methionine has been found helpful in treating depression, allergies, alcoholism and schizophrenia among other chronic issues. Hypothyroidism may be associated with over expression of this gene: [http://www.wikigenes.org/e/gene/e/635.html] Choline deficiency disease and hyperhomocysteinemia (a heart disease risk factor) may be associated with this gene — (not necessarily with this specific mutation though). The protein that the gene normally produces is necessary in metabolism and in the CDK-mediated phosphorylation and removal of Cdc6 SuperPath: [http://www.genecards.org/cgi-bin/carddisp.pl?gene=BHMT] And the CDK-mediated phosphorylation and removal of Cdc6 SuperPath involves 97 other pathways which include a Calcium2+ pathway and a Parkinsons Disease pathway and creatine metabolism (important for muscles) and synthesis of DNA and many other metabolic paths/chains of chemical events  (so a double mutation in this gene may make it difficult for me to make phospholipids endogenously, but this information is out of my depth, organic chemistry wise): [http://pathcards.genecards.org/card/cdk-mediated_phosphorylation_and_removal_of_cdc6] This double mutation in combination with the single mutation (+/-) in (#3 below) BHMT/8 and (#4 below)CBS/A360A may exacerbate each other’s negative effects on my body, causing an up-regulation of the CBS pathway and also may make it more difficult for me to remove toxic heavy metals from my body – see #4 in the next list for the link.
  4. MAO A/R297R (Call – T). “Monoamine oxidase A (MAO-A) is an enzyme in the brain,” Nick-named “The Warrior Gene” because levels need to be just right because it causes the breakdown of neurotransmitters and too little or too much can cause different symptoms from increased violence to increased anxiety and less aggression. “The G or GG allele indicates higher levels of the enzyme, while the T allele indicates lower levels (T is the ‘risk’ allele). (R)   In females, the G allele was associated with higher outward anger (p = 0.002) and it seems like G allele also causes aggression in males. (R)” The T version of R297R mutation is associated with generalized anxiety disorder (which was one of my earlier “diagnoses” but it was from talk therapy with a MSW so it never really “counted” with psychiatrists that I saw more recently.) “Females with TT reported higher levels of ‘‘angry temperament’’.  Female suicide attempters with TT reported higher ‘‘self-aggression’’” “Women are less likely to have these genes.” “People with the low activity MAO-A gene (2R, 3R) are overall more prone to violence. Specifically, when these people feel very provoked or socially isolated their aggression will come out. People with low MAO-A are more likely to be risk takers.  They are are also more likely to take revenge and use greater force if they get screwed over, but not for small screw overs. Mice with low MAO-A are also more aggressive in general and are more likely to start turf wars. People and mice with low MAO-A are more impulsive and aggressive. People with low MAO-A who are abused as kids show more aggressive behaviour as an adult.” The herbal supplement Gingko biloba, riboflavin (vitamin B2), bio-identical progesterone, and keeping to my circadian rhythm, (keeping a regular day/night wake/sleep cycle instead of pulling all-nighters and then sleeping in), may help me if I have low levels of the enzyme (and excess aggression/anxiety): [http://selfhacked.com/2014/12/07/about-mao-a-and-what-to-do-if-you-have-the-warrior-gene/] Reserpine, a drug based on an herb called Rauwolfia serpentina, or Indian snakeroot or sarpagandha may also help: [http://www.warriorgene.info/] * a commercial site.

The seven single mutations/polymorphisms are in the genes:

  1. SHMT/C1420T (Call – Hetero), Serine hydroxymethyltransferase, This polymorphism was not found to have an increased risk of Down’s Syndrome (DS) (thought possible because it affects folate) and levels of metabolites of the folate pathway seemed similar between the experimental groups of mothers (had children with DS) and control groups of mothers (did not have children with DS).  A protective role was actually found for this polymorphism (which sounds nicer than mutation, allele is another word for variations of the same gene.) [http://www.ncbi.nlm.nih.gov/pubmed/21687976]
  2. MTR/A2756G (Call – Hetero), methionine synthase gene, This mutation may cause up-regulation of the conversion of homocysteine to methionine which requires and might use up stores of methylated B12. [http://mtra2756g.com/] * a commercial site.
  3. BHMT/8 (Call – Hetero), see #3 above for general information about this gene’s protein.
  4. CBS/A360A (Call-Hetero), “CBS (cystathionine beta synthase) is a gene that converts homocysteine into cystathionine. 
The CBS pathway is the gateway into a number of essential biochemical processes. 
The biochemical pathways that follow and are linked to CBS are Transsulfuration and Glutathionine Synthesis.

 It is essential to address that Glutathione (GSH) is among the most important endogenously-produced antioxidants in every cell of the body. Glutathione activity in cells is critical for normal detoxification and defense mechanisms in every cell.” (I’m suggested to eliminate eggs from my diet — too late, they are already gone, but also cruciferous vegetables, onions and garlic – sad face. but I’m also suggested to avoid excess methyl donors like choline — and coffee is a methyl donor – sad face – it is already gone too, very sad face): “Restriction of supplemental methyl groups is important. We all need methyl groups, but those with active CBS up-regulations 
need to be cautious with how much sulfur and how many methyl groups they are taking in daily.
 This includes common supplements such as: L-methionine, L-cysteine, L-taurine, MSM, Glucosamine,  L-Glycine, DMSO, SAMe, NAC, methylcobalamin, methyl-folate, Betaine HCL, Choline. Restricting Vitamin B6 may also be warranted in CBS up-regulations. P5P (pyridoxal 5 phosphate), however, does not appear to increase CBS activity.” [http://metabolichealing.com/metabolic-gateways-cbs-gene-mutations-glutathione/] *That link is to a clinic. (So when my B6 runs out, I should special order the P5P version — which a pharmaceutical company is trying to patent as a prescription medication, if it can gain the FDA’s approval to make the more biologically active form of an essential nutrient unavailable without a prescription because it would interfere with their potential profits: “How does Medicure think it can get away with this? Its petition states rather candidly: “Pharmaceutical companies developing new drugs must be protected from companies that may seek to market the ingredients in those drugs as dietary supplements. The marketing of such products has the potential to undermine the incentive for the development of new drugs because many people may choose to purchase the supplements rather than the drugs.”” An essential nutrient is not a drug — companies have to tack on a fluoride or bromide or something else that makes the new chemical slightly different in order to be able to patent a chemical within the normal process. Bio-identical nutrients are not usually able to be patent protected – because they are essential, especially for people with metabolic defects in their ability to convert less active forms to the more active form. In my state, the Michigan Consumer Protection Act of 1976 is supposed to protect people from having their disability used against them in business transactions such as buying a supplement or prescription medication. 445.903x: “(x) Taking advantage of the consumer’s inability reasonably to protect his or her interests by reason of disability, illiteracy, or inability to understand the language of an agreement presented by the other party to the transaction who knows or reasonably should know of the consumer’s inability.“, And products aren’t supposed to misrepresented such as calling an essential nutrient a prescription medication: 445.903e: “(e) Representing that goods or services are of a particular standard, quality, or grade, or that goods are of a particular style or model, if they are of another.”  [http://www.legislature.mi.gov/(S(45hcye5dzt3luno152p33nku))/mileg.aspx?page=getobject&objectname=mcl-445-903])
  5. COMT/V158M (Call-Hetero), Catechol-O-Methyltransferase, Variations of this gene may lead to swings in dopamine levels that can cause mood swings. Red and purple foods may not be processed well and also may cause problems in mood swings for some people (like purple berries and red food dye (?) just reading, aghast that I’ve survived this long. Red food dye was one of my earliest migraine triggers.) [http://resqua.com/702188759/what-does-the-comt-gene-mutation-mean] Defects in this gene are associated with ADD/ADHD. [http://www.snpedia.com/index.php/Yasko_Methylation] And with panic disorder. [http://www.genecards.org/cgi-bin/carddisp.pl?gene=COMT]
  6. COMT/H62H (Call-Hetero), see #5 above.
  7. VDR/Fok1 (Call-Hetero). – the gene for the Vitamin D Receptor, see the excerpts within the earlier text of this post. And: “VDR Fok is involved with Blood sugar regulation. VDR mutations oppose COMT mutations in the regulation of dopamine levels. A VDR mutation means that a person is less sensitive to methyl group supplement levels. (Mood swings.) A VDR mutation can result in behaviors opposite to a COMT mutation. See Dr. Roberts comments at http://www.heartfixer.com/AMRI-Nutrigenomics.htm#VDR%20Taq:%20%20Vitamin%20D%20Receptor%20Taq%20Abnormality ” [http://www.snpedia.com/index.php/Yasko_Methylation] Dr. Roberts comments suggest that my normal VDR Taq gene helps balance the COMT +/- genes so that I have reasonable dopamine production but might have increased risk for mood swings. hmmmm

So I went and bought some more wild yam progesterone cream because I had run out a while ago and forgot to buy more and it has helped my mood and other peri-meopausal symptoms in the past. I also bought some Gingko biloba because I have also used that in the past with no problems and mood swings and self-aggression are no fun.

/Disclaimer: 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./

The voices that people with schizophrenia are hearing are probably their own inner thoughts

This is kind of breaking news — new news: A research scientist, with the aid of a powerful microphone, was able to record a patient with schizophrenia speaking to themselves in a sub-vocal voice. The patient was not aware that they were speaking at the time.

The research is very early, a first in its field perhaps, but the theory seems to suggest that the patient’s with schizophrenia symptoms may have some disconnect with the normal ability to identify internal thoughts and sub-vocal speech as being self generated and instead are interpreting the internal thoughts as coming from some external source of whatever type the person might think.

(Example of my interpretation of sub-vocal speech: the almost silent muttering under your breath that you don’t notice yourself doing, until suddenly you do notice that you’re talking to yourself, and then you stop because you don’t want anyone to notice. The brain of a someone with schizophrenia may no longer recognize the voices of self-talk, or those of voices in memories or in imagined conversations, as being internally self-generated and instead probably tend to make up some explanation for  whatever or whoever might be doing the talking that is being heard — hearing voices. Our internal chatter can get busy and sometimes pretty mean, it would be scary to not realize that it is just yourself. )

Read more, of the actual article:  [http://www.slate.com/articles/health_and_science/medical_examiner/2016/03/schizophrenia_and_subvocal_speech_why_schizophrenics_hear_the_voices_of.html]

This seems like very important news — patients with schizophrenia may be able to be gently reminded that those voices are just brain mumbles, and to try to ignore them.

People with schizophrenia are generally not associated with violence unless there is also a history of violent behavior, alcohol or drug abuse, or more persecutory fantasies. [citation missing, I don’t remember where I read that recently, but I posted it in a comment somewhere.]

Mental health symptoms sometimes may be due to underlying issues that could be easily fixed, rather than considering the patient as being ‘mentally ill’ for the rest of their life and likely being placed on medications that tend to have severe side effects. Effective health care would seek for any underlying causes that can be returned to a state of normal function with the simplest solutions possible, “Let food be thy medicine,” the first part of the quote by Hippocrates may be the most important part.

There are several different nutrient deficiencies that can cause symptoms similar to schizophrenia or may be involved in an underlying cause for the condition, this information was from an older post of mine but it was not grouped together:

Summary update written for something else, (clearly this post could use editing): The balance of cannabinoids is a problem in Schizophrenia. (2-AG ~ noneuphoric CBD is decreased in ratio to anandamide ~ euphoric THC compared to normal health, (66)) Use of CBD as a treatment has showed promise for schizophrenia, particularly during early stages of the condition. (67) The genetic difference that might make someone more susceptible to developing schizophrenia may involve a deficiency in Cannabinoid Receptor type 2. (68) (*Additional Note for anyone interested – several nutrient deficiencies can also cause symptoms similar to schizophrenia – and would need to be treated with diet or supplements – and all or some of them might be involved and need to be treated with diet or supplement changes in order for the underlying symptom causing deficiencies to be resolved.

The nutrient deficiencies may include zinc or an excess of copper in ratio to zinc level; the methyl donor B vitamins folate and vitamin B12 – so if a genetic problem existed in methylation than standard supplements of folic acid and unmethylated B12 might make it worse instead of better as the non-bioactive forms would be competing with whatever bioactive dietary folate and methylated B12 were being consumed (wrong puzzle piece blocking a spot for the right puzzle piece); hypothyroidism and elevated bromide is associated with schizophrenia so iodine may be low and goitrogens in excess; Vitamin D and/or an underlying infection with Toxoplasma gondii may be present, and a genetic difference in the Vitamin D Receptor or vitamin D metabolism may increase risk for infection with T gondii (catbox litter of a young cat is a risk factor for T gondii infection).

Soapbox moment for patient advocacy – the prognosis/quality of life for patients with schizophrenia was better a hundred years ago then it is now. Prescription medications are never going to be able to resolve one or several nutrient deficiencies or metabolic differences.

Regarding trends seen around the world in rate of schizophrenia, it has been dropping in South Korea and increasing in Japan. North Korea has the highest rate for the region: http://global-disease-burden.healthgrove.com/l/58241/Schizophrenia-in-South-Korea

Malnutrition in North Korea is more likely involved in the increased rate for the nation than cat ownership due to the many years of sanctions against the country. B12, folate, zinc and vitamin D deficiencies and excess copper may be involved in risk of developing schizophrenia like symptoms. Folate and calcium are considered to be potentially deficient for the typical Korean diet. Fortified milk products aren’t typically consumed so extra vitamin D from that source wouldn’t be available. Iodine is also a nutrient that may be deficient in the diet. http://adoptionnutrition.org/nutrition-by-country/korea/

And low iodine levels can increase risk for hypothyroidism which has been found to be more common as a comorbid condition with patients with schizophrenia. https://www.ncbi.nlm.nih.gov/pubmed/30350120

Bromine excess can compete with iodine and may increase risk of hypothyroid or schizophrenia symptoms. http://www.kumc.edu/school-of-medicine/integrative-medicine/health-topics/iodine-supplementation.html

Low thyroid levels have been associated with schizophrenia in early treatment of the disease and has been used in more recent care of patients by an alternative physician. The following link includes excerpts from many older research articles and one mentions kryptopyrroles being elevated in some patients so a genetic cause may be involved for some patients that would cause low zinc and low B6 levels (pyroluria). http://www.orthomolecular.org/library/jom/2001/articles/2001-v16n04-p205.shtml

Schizophrenia treatment and other psychiatric care in Russia does not seem to be an ideal to follow anywhere else – or there: http://www.sras.org/snezhnevsky_schizophrenia_soviet_psychiatry However Russians on average do own a lot of cats, especially in comparison to residents of South Korea: https://www.statista.com/chart/10267/which-countries-have-the-most-cat-owners/?utm_content=buffer35f5b&utm_medium=social&utm_source=twitter.com&utm_campaign=buffer 

/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./

Prenatal Vitamin D deficiency may be associated with the infant’s risk for developing Multiple sclerosis later in life

Vitamin D deficiency at levels equal to or below 12 ng/dL in prenatal women was associated with the baby’s later risk for developing Multiple sclerosis as an adult. No potential reasons for the association were discussed in the article. Read more: [http://neurosciencenews.com/vitamin-d-ms-3809/]

Two to three servings of dairy products fortified with vitamin D provide an adequate amount of vitamin D for the average person. A pregnant person may be recommended to have one additional serving per day for both the vitamin D content and the calcium. Mushrooms and egg yolk are natural sources of vitamin D. Canned salmon and sardines provide vitamin D and are a good source of calcium due to the tenderized bones that remain in the prepared fish. Sesame seeds, almonds and other nuts, beans, seeds, and deep green vegetables are also non-dairy sources of calcium.

/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./