Tag Archives: B12

Neuropathy can be a cause of extreme tiredness

An underlying problem affecting a main nerve or affecting many nerves can be a cause of tingling and numbness in the hands or arms and legs. An increased feeling of heaviness of the arms or legs or feeling tired from just holding the arms up in the air may be due to problems with the nerves rather than weakness of the muscles. Autoimmune disease or some nutrient deficiencies (vitamin B12 deficiency most common) can be causes of neuropathy, or nerve damage. Other common causes are mentioned later.

Autoimmune disease itself can be very tiring and a cause of muscle cramps and diffuse chronic pain and it could make it very hard to cope with a physically demanding job. Some types of nerve damage can become permanent but may be reversible if caught early enough and the underlying causes are corrected. Vitamin B12 may be poorly absorbed by elderly people or for others with digestive problems; a monthly injection of B12, bypassing the digestive system, is a common treatment.  Dissolve in the mouth supplements of B12, cobalamin, are also used sucessfully by some people. In Parkinson’s Disease neuropathy has been seen and “perhaps we should be measuring MMA levels in these patients and treating with cobalamin supplementation to reduce MMA levels and prevent neuropathy.” [4]

Recognizing when tiredness is tiredness and when it is due to underlying nerve damage may be a step that can help prevent the nerve damage from becoming more permanent paralysis or numbness. Neuropathy can also affect gland or organ function as well as affecting motion and sensation. Poor coordination can become a problem with walking or with picking up and not dropping things because they just slipped from your fingers. Symptoms may also include feeling moments of burning or stabbing pain and bowel and bladder problems may include constipation or feeling unable to urinate. [1]

Neuropathy may affect approximately 24 million people in the United States. [1]

Neuropathy is more of risk for people with diabetes, about 30% of the cases are associated with diabetes. Heavy alcohol use and traumatic injury can be causes in addition to autoimmune celiac disease, hypothyroidism and other immune system diseases and viral infections sometimes can be a cause. Some types of antibiotics, radiation and chemotherapy treatments may cause neuropathy. Some cases of neuropathy are present at birth. [1]

Since celiac disease may be a cause of neuropathy trying a gluten free diet may be worth trying, (and hypothyroidism can also be a cause of neuropathy and for some people may be due to gluten sensitivity problems). Not overeating sugars and simple starches may help by promoting more stable blood sugar which would be especially important for diabetics but elevated blood sugar may be part of the cause of nerve damage: [3]. Hot pepper – and it’s active ingredient capsaicin may be helpful and warm showers or a bath may also help circulation and muscle relaxation. Taking care with toenail health is important as numbness becomes more extreme minor injuries may become infected and go unnoticed until they are major infections. [1]

Of the 16 million Americans with diabetes, approximately, about 25% have foot problems due to peripheral neuropathy.  Peripheral nerves are those extending out from the brain or spinal cord to the muscles and organs and skin. Neuropathy can progress from feeling tingling sensations of ‘pins and needles’ in the fingertips to not being able to feel sensations of hot, cold or pain. [2]

Peripheral neuropathy has been known to occur with Parkinson’s disease, possibly due to treatment with L-dopa [4], or possibly as a side effect with another commonly used treatment, dopamine hydrochloride. [5] Dopamine producing cells become dysfunctional in Parkinson’s Disease. [6] Dopamine is a brain neurostransmitter involved in movement but it is also has roles in immune system function.

Adequate levels of dopamine are involved in preventing both autoimmune disease and cancer. Research that compared the lifestyles of family members with and without Parkinson’s Disease found that siblings without the disease were more likely to have been coffee drinkers (three or more cups per day) and were more likely to have smoked tobacco cigarettes. Smoking tobacco has negative health risks but it may help boost dopamine levels and may have some protective effects on the dopamine producing cells. [7]

Smoking tobacco my have protective effects for some people but not others. Coffee has also been associated with less risk of developing non-alcoholic fatty liver disease, [8] but again it may be helping those with a certain type of genetics and be a negative risk for people with other types of genes. Obesity and smoking cigarettes once a patient already has non-alcoholic fatty liver disease is associated with the disease progressively getting worse. [9] Fructose, sugar from fruit or refined in the form of high fructose corn syrup, intake has also been associated with worsening of NAFLD. [10]

Protecting liver function may be important for protecting against cancer. The herb milk thistle has been found to have some protective affects for the liver. [12] Cirrhosis of the liver is also associated with peripheral neuropathy so protecting the liver may also help protect the nervous system and brain. [11]

Summary of tips for protecting against neuropathy:

  1. Stable blood sugar and not developing diabetes may help protect the nerves.
  2. Regular exercise and stretching and warm baths or showers and massage and other methods for increasing circulation may help protect the nerves.
  3. Not eating excessively of fructose or simple sugars may help prevent damage caused by glycation of proteins; by helping prevent obesity or diabetes.
  4. Moderate use of coffee may help protect the liver from non-alcoholic fatty liver disease and some types of liver disease have been associated with peripheral neuropathy.
  5. Dopamine or L-dopa when used as a medication to treat Parkinson’s Disease may be involved in development of peripheral neuropathy. Parkinson’s Disease involves dysfunctional production of dopamine so some other issue may be involved that causes peripheral neuropathy or it may be important to have adequate but not excessive levels of dopamine for health of the nerves.
  6. A deficiency of vitamin B12, also called cobalamin, can be non-reversible cause of peripheral neuropathy. [13]
  7. Smoking tobacco may have some protective affects against Parkinson’s Disease for some people but it has also been associated with worsening of non-alcoholic fatty liver disease in patients who already have the disease. It is unclear at this time what genes may be involved in why some people seem less at risk from tobacco smoking than others – overall it has been found to be associated with lung cancer. Chemicals within smoke cause blood vessels to constrict and reduces circulation. It has been associated with worsening of diabetic peripheral neuropathy so quitting smoking may be more protective of nerves. While it may help boost dopamine levels there are many other healthy ways to boost dopamine naturally. [14]
  8. Following a gluten free diet may be helpful in preventing peripheral neuropathy for some people. If hypothyroidism is also a problem then trying a strict gluten free diet may be beneficial as it may be a cause of autoimmune sensitivities. Eating less gluten in that case would still be exposing the body to the autoimmune ‘allergen’ so a trial of a gluten free diet may have to be very strict and last several months to six months before significant health benefits occur (in research on autoimmune celiac disease it took six months on a very strict gluten free diet in order for the levels of autoimmune antibodies against gluten to be reduced — and (potentially) the thyroid hormone which the gluten molecule resembles.

Disclaimer: Opinions are my own and the information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes.

  1. http://thelightmedia.com/posts/28389-neuropathy-12-ways-to-identify-and-manage-this-painful-disease
  2. http://www.foot.com/site/foot-conditions/neuropathy
  3. https://en.wikipedia.org/wiki/Glycation
  4. http://www.medscape.com/viewarticle/725699
  5. http://www.ehealthme.com/ds/dopamine%20hydrochloride/neuropathy%20peripheral/
  6. http://justneurology.com/
  7. https://www.newscientist.com/article/dn11568-do-coffee-and-cigarettes-protect-against-parkinsons/
  8. http://www.medicalnewstoday.com/articles/264995.php
  9. http://onlinelibrary.wiley.com/doi/10.1002/hep.23516/full
  10. https://www.sciencedaily.com/releases/2010/04/100427081044.htm
  11. http://www.medscape.com/viewarticle/460036
  12. http://umm.edu/health/medical/altmed/herb/milk-thistle
  13. http://www.webmd.com/a-to-z-guides/supplement-guide-vitamin-b12#1
  14. http://mentalhealthdaily.com/2015/04/17/how-to-increase-dopamine-levels/

 

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:

/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./

Autism may be able to be prevented prenatally with individualized perinatal education and nutrition therapy

This got long and complicated and I need to buy a couple of the articles and work on this more but in the meantime, I’m sorry for suggesting the food supply might have something to do with the increased rate of autism or that the health insurance companies don’t want a clear diagnostic procedure etc. but without a lab test that says someone is sick they can save money on paying claims — however costs in the long run may end up being a lot more than they might have been with an earlier diagnosis and preventative treatment. I’m sure the health insurance companies and government and FDA love us all and that autism must be a complete mystery – but leaving something a complete mystery still leaves it a worry for expectant parents and grandparents throughout the pregnancy and even into the early childhood years. The symptoms aren’t usually diagnosed until age two or older. But earlier diagnosis might help prevent more severe loss of function. The condition can cause a sudden or more gradual loss of social skills and development progress.  

Autism can leave a child unable to take care of themselves independently for the rest of their lives. At a rate of 1 child in 45, [Nov. 2015, CDC, http://health.usnews.com/health-news/articles/2015/11/13/cdc-child-autism-rate-now-1-in-45-after-survey-method-changes], there were 3,932,181 births in the USA in 2013, so roughly that would suggest that 87,381 of those children will go on to develop some symptoms of autism or pre-primary developmental delay — and that possibly 87,381 parents will no longer be able to work at their normal jobs because they will be needed as full time caregivers for their child with autism, possibly for the rest of their lives. So if that rate held steady for the decade then in ten years there could be 1,747,620 children with autism and parents who may not be able to work at a normal job. When will it be enough children and parents to do something about?

I closed with the following paragraph but I’m going to paste it here at the beginning too, as the best of the good news: a lab test has been developed that consistently predicted which infants would later go on to develop autism. This helps clear up the mystery of whether autism is a condition that a toddler can suddenly “get” like an infection or have suddenly develop as an acute reaction to something or whether it develops prentally — it develops prenatally and can get worse — which suggests that it might not also have to get worse if appropriate interventions can be provided. Autoimmune disease frequently can flair up, go into remission, flair up again, and go back into remission. Autism appears to be related to autoimmune conditions of the brain so dietary and lifestyle changes might be able to help keep the overactive white blood cells more in ‘remission’ and less busy doing brain damaging things — that would be my hope at least.

A method has been developed using samples of umbilical cord blood to identify which infants are likely to develop autism later in childhood. The method checks fifteen “biomarkers,’ — (various lab values or other physical signs, I haven’t read the full article yet, need to buy it) — infants whose values were more elevated or reduced compared to normal in a certain pattern were found to be predictive of which infants went on to develop autism. [6 ] This is early research but it would help identify which infants were at risk for autistic changes in a year or two, but at birth instead of having to wait — and worry — for a year or two.

I have some good news and some bad news. It looks plausible that autism could be caused prenatally by a combination of low vitamin D (or possibly a vitamin D system that is blocked by pathogens), and low folate availability (possibly due to a genetic methylation defect, [4], defects that may make the supplemental form, folic acid, not as helpful prenatally and possibly even harmful because the folic acid may inhibit the activity of whatever folate is available, [29] ), and increased formaldehyde either from dietary sources like Nutrasweet or from smoking or living in small enclosed rooms with poor ventilation. Other toxins might also be involved that add to an increased risk for there to be production of autoimmune antibodies in the vitamin D deficient mother and fetus. Malfunction in the vitamin D receptor immune functions could lead to malfunctions in the dendritic cell’s ability to inhibit autoimmune overactivity in the immune system. Autoimmune antibodies might cause problems during fetal brain development or later in the child’s life.

Low vitamin D in infants has been associated with autism – but not for all siblings with low vitamin D — so other factors must be involved. And not taking a prenatal vitamin during the three months prior to pregnancy and the first month of pregnancy has been associated with more risk for having a child with autism and certain genetic defects in the methylation cycle that helps make the B vitamin folate more bioactive have been associated with autism risk [4] – but not every mother who doesn’t take prenatal vitamins during the months prior to becoming pregnant has a child with autism — so other factors must be involved.

Not much information is available about Nutrasweet but during digestion the methanol portion of the larger molecule is released which then is broken down into formaldehyde – which is a known cause of birth defects and a known neurotoxin.

Formaldehyde is produced when something is burned so it could be a concern for any people who are around cigarette smoke or inhale other types of smoke regularly. Formaldehyde can also collect in the air in small enclosed spaces, and increased warmth may also increase volatility of the gas so warmer areas or overheated apartments may allow for more accumulation of the gas in poorly ventilated rooms.

Formaldehyde is also found in prepackaged juice products, particularly in older packages, as formaldehyde is produced as the fruit or vegetable juice ages. Formaldehyde is also produced during digestion from the methanol portion of the alternative sweetener Nutrasweet. Studies on the potential risk of the formaldehyde content that might be available to adults from dietary Nutrasweet found that it was a less significant risk than the amount an adult might receive as a cigarette smoker or from environmental exposures. However an adult has a fully mature liver while a fetus does not. Babies and children also have less mature livers and may be more at risk of having chemicals accumulate to toxic levels because they are not being broken down and excreted quickly enough. (Folate, a B vitamin, is necessary to break down formaldehyde, more on that later.)

Formaldehyde can cross the placenta to the fetus where it accumulates to a larger concentration than within the mother’s bloodstream. The fetal liver tissue is less able to detoxify formaldehyde than the mother’s.

Industrial exposure to formaldehyde is associated with an increased risk of the presence of cancer causing human alpha fetoprotein antigens. Occupational exposure to formaldehyde has also been associated with increased levels of alpha fetoprotein in adult male and female subjects. The study subjects with occupational exposure to formaldehyde were also found to have significantly reduced levels of Total Protein, Albumin, and White blood cell count. Subjects with workplace exposure to formaldehyde reported allergic type symptoms including: “sneezing/airways-related symptoms, itching and watery eyes.” [3] Formaldehyde exposure may also be a cause of systemic allergic contact dermatitis, [15, 16] possibly even on the eyelids. [13] A diet designed to avoid formaldehyde intake may be helpful for alleviating the eczema like rash. [14]

Levels of alpha fetoprotein are normally only elevated in pregnant women and the expected infant.

Levels of maternal serum alpha fetoprotein are already being checked regularly as a prenatal screening test because low levels are associated with having a baby with the genetic condition Down’s Syndrome. Levels of maternal serum alpha fetoprotein have been found to be more elevated for the mothers of children with autism than in mothers whose child did not have autism. [1] Alpha fetoprotein (AFP) has immunomodulatory effects and a recombinant human alpha fetoprotein (rhAFP) version has been found to help alleviate autoimmune symptoms in clinical trials that used mice with “experimental autoimmune encephalomyelitis (EAE), the animal model used for the study of MS.” [2] Alpha fetoprotein is normally produced by the fetus and it does cross into the fetal brain where it seems to be involved with controlling estrogen and helping baby girls to be more feminine and less masculine.

/Speculation: So if alpha fetoprotein antigens are involved in causing autism maybe boys are more at risk for the condition because the estrogen connection somehow is protecting baby girls from developing the antigens. However if the basic problem is a malfunctioning dendritic cell system which is making it more difficult for the mother’s body and fetus’ body to accept the presence of each other’s foreign DNA then other proteins might also have antigen/autoimmune antibodies develop. Male infants may simply be more susceptible to autism because their Y chromosome is more foreign to the mother’s body than a female infant’s X chromosomes. / — Someone already figured this part out and explains it better than me, in a Medical Hypotheses journal – if you have the money for the journal article ($31.50, now added to my shopping list). An excerpt from the Abstract: “Prenatal/maternal factors linked to increased autism risk include valproic acid, thalidomide, alcohol, rubella, cytomegalovirus, depression, schizophrenia, obsessive-compulsive disorder, autoimmune disease, stress, allergic reaction, and hypothyroidism. It will be shown how each of these risk factors may initiate expression of genes which are sensitive to retinoic acid and/or estradiol – whether by direct promotion or by reducing production of alpha-fetoprotein. It is thus hypothesized here that autism is not a genetic disorder, but is rather an epigenetic disruption in brain development caused by gestational exposure to chemicals and/or conditions which either inhibit alpha-fetoprotein production or directly promote retinoic acid-sensitive or estradiol-sensitive gene expression. This causation model leads to potential chemical explanations for autistic brain morphology, the distinct symptomology of Asperger’s syndrome, and the differences between high-functioning and low-functioning autism with regard to mental retardation, physical malformation, and sex ratio.” – CR King [29]

So speculatively,

  • if formaldehyde can make it more likely for someone to make alpha fetoprotein antigens,
  • and maternal serum alpha fetoprotein levels are more elevated in the mother’s of children with autism,
  • and low vitamin D is more common in babies who have autism,
  • and vitamin D helps the dendritic cells of the mother and infant accept each other’s foreign DNA instead of making autoimmune antibodies against each other’s foreign proteins,
  • then low vitamin D might leave the dendritic cells unable to prevent autoimmune antibodies from developing
  • which then may cause changes in the developing fetal brain and may leave the child with autoimmune antibodies that may continue to cause changes in the child’s developing brain later in life.
  • The formaldehyde could be from Nutrasweet and bottled juice products and/or from cigarette smoke or other environmental sources or the combined total of all of the sources. The timing of the introduction of aspartame/Nutrasweet to the U.S. food supply in 1981 and the increase in rate of children with autism is very closely correlated. [5] Nutrasweet and Neotame were both inventions of the Monsanto Company and limited research about them is available. Neotame was invented as the patent for Nutrasweet was expiring and Monsanto was able to get FDA approval for it by 2002. The patent for Neotame was sold to a private equity firm, the J.W. Childs Equity Partners II. L.P.. [https://theredpillguide.wordpress.com/2012/02/23/the-red-pill-guide-neotame/]

So in summary the good news is autism may be preventable – but the bad news is that it will be difficult to prove and preventative education and treatment will likely need to be individualized as so many factors are involved.

A summary of the factors that may interact during the prenatal and/or perinatal  (three months prior to conception) time period in a way that may lead to the development of autism within the fetal brain.

Possible Vitamin D Issues – it might not just be a lack of vitamin D or sunshine:

  • Simple vitamin D deficiency
  • An underlying genetic defect in the Vitamin D Binding Protein causes a tendency to become vitamin D deficient more easily than normal. [10, 11, 12] (Might a simple protein deficiency then also add a risk to a simple deficiency of all important proteins?)
  • An underlying infection is present with a pathogen that is suppressing the vitamin D receptor system.

Possible Folate Issues:

  • Simple folate/folic acid deficiency/lack of prenatal vitamin during the perinatal time period. [4]
  • Genetic defect in mother affecting the methylation cycle makes her more susceptible for folate deficiency. [4]
  • Genetic defect in the fetus affecting the methylation cycle makes it more at risk for autism. [4]
  • A methylated form of the vitamin may be more effective for reducing risk of developing autism. The natural food form, folate, is more bioactive than the supplemental form, folic acid, that is used in prenatal vitamins. [29]

Formaldehyde might be accumulating from several sources [3, 5]:

  • Aseptically packaged juices
  • Nutrasweet
  • Neotame
  • Smoking
  • Badly ventilated air.
  • Workplace exposure

Other, other factors that may be involved in development of autism may include a variety of chemicals known to be toxic for brain development and which may be common in our modern environment.  From the Abstract of a review article by Dr. Philippe Grandjean, MD and Philip J. Landrigan, MD, Neurobehavioural effects of developmental toxicity., (The Lancet Neurology, 2014):  “In 2006, we did a systematic review and identified five industrial chemicals as developmental neurotoxicants: lead, methylmercury, polychlorinated biphenyls, arsenic, and toluene. Since 2006, epidemiological studies have documented six additional developmental neurotoxicants—manganese, fluoride, chlorpyrifos, dichlorodiphenyltrichloroethane, tetrachloroethylene, and the polybrominated diphenyl ethers. We postulate that even more neurotoxicants remain undiscovered. To control the pandemic of developmental neurotoxicity, we propose a global prevention strategy.” [30]

And other factors associated with autism that were mentioned in the other hypothesis about autism and folic acid included: “valproic acid, thalidomide, alcohol, rubella, cytomegalovirus, depression, schizophrenia, obsessive-compulsive disorder, autoimmune disease, stress, allergic reaction, and hypothyroidism.”  – CR King [29]

  1. valproic acid, a medication commonly used to prevent seizures in epilepsy, may also be prescribed for bipolar disorder or to prevent migraine headaches. (Valporate (VPA), sodium valproate, and divalproex sodium, Depakote). It has been known to cause serious abnormalities in babies when used by pregnant women and is no longer typically prescribed to women of childbearing years. [Wikipedia]
  2. thalidomide,a medication that was prescribed to pregnant women for preventing nausea in the 1960s but it was discovered to cause serious birth defects. It is still used for the treatment of leprosy and still has been known to cause birth defects in the babies of women with leprosy who become pregnant. [http://toxsci.oxfordjournals.org/content/122/1/1.full]
  3. alcohol, – alcohol use by the mother during pregnancy or by the father during the days prior to conception can be a cause of Fetal Alcohol Syndrome in the infant. A zinc deficiency in the pregnant woman may increase the risk of the expected infant developing FAS. [search term alcohol FAS zinc deficiency]
  4. rubella, – also known as German measles, it is the R part of the MMR vaccine. It is rare in the U.S. now with less than ten cases per year but can cause defects in an expected infant if a pregnant woman gets sick with the infection prior to 20 weeks gestation. [http://www.whattoexpect.com/pregnancy/pregnancy-health/complications/rubella.aspx]
  5. cytomegalovirus, a viral disease that may affect vitamin D levels: “However, when outliers were removed, the association was not apparent. The effect of outliers could not be assessed when vitamin D was dichotomized because no patients with CMV antibodies had sufficient vitamin D levels after outliers were dropped.” [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3134182/]
  6. depression, – can be a symptom of hypothyroidism and has been associated with vitamin D deficiency [webmd.com/depression/news/20120627/vitamin-d-deficiency-linked-to-depression] and with folate deficiency. And the methylated form was given as a supplemental treatment, L-Methylfolate, rather than the unmethylated form, folic acid, which is the form used in prenatal vitamins.   [psychologytoday.com/blog/the-integrationist/201310/depression-wont-go-away-folate-could-be-the-answer] Depressive disorders have been associated with impaired methylation: [http://www.ncbi.nlm.nih.gov/pubmed/16194269] And with zinc deficiency: [https://www.psychologytoday.com/blog/evolutionary-psychiatry/201309/zinc-antidepressant]
  7. schizophrenia, vitamin D deficiency is more common in people diagnosed with schizophrenia. [http://psychcentral.com/news/2014/07/23/vitamin-d-deficiency-common-in-schizophrenia/72813.html] And folate and B12 have both been found to help treat schizophrenia symptoms (or help treat those patient’s whose symptoms are actually due to an underlying deficiency of folate or B12 which may cause symptoms that resemble schizophrenia and providing the nutrients simply is helping the brain to function normally again.) [http://www.naturalnews.com/039453_vitamin_B12_folate_schizophrenia.html] And a zinc deficiency/copper excess is more common in schizophrenia: [http://www.academia.edu/1096257/The_Role_of_Zinc_Supplementation_in_the_Treatment_of_Schizophrenia] And a zinc deficiency prenatally may be involved in the causing schizophrenia later in life: [http://www.ncbi.nlm.nih.gov/pubmed/1491625] [http://www.bmj.com/rapid-response/2011/10/30/does-zinc-deficiency-early-foetal-life-cause-schizophrenia]
  8. obsessive-compulsive disorder, – can be early symptoms of a B12 deficiency. [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3271502/] Has been associated with folate deficiency, elevated homocysteine levels and impaired methylation function: [http://www.ncbi.nlm.nih.gov/pubmed/16194269]
  9. autoimmune disease, – associated with vitamin D deficiency and malfunction of the dendritic cells ability to promote self tolerance of the immune system. The dry cleaning chemical and degreaser tetrachloroethylene has been shown to cause autoimmune disease in lab animal studies on toxicity: [http://www.atsdr.cdc.gov/sites/lejeune/tce_pce.html]
  10. stress, – increases cortisol and inflammatory stress chemicals, a lack of antioxidant nutrients may make it more difficult for the body to recover from the stress response. [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1876613/] And may use up stores of folate and cause elevated levels of homocysteine. [http://www.nejm.org/doi/full/10.1056/NEJMc066569] Elevated levels of cortisol during pregnancy has been shown to cause reduced growth rate in the babies in animal studies. [https://en.wikipedia.org/wiki/Cortisol]
  11. allergic reaction, and the vitamin D receptor and the Dendritic cells are what control the immune system’s allergic reaction. Excerpt: “1α,25-dihydroxyvitamin D(3) (calcitriol), the biologically active form of vitamin D, is an immunomodulatory hormone, e.g. it inhibits IgE synthesis in B cells. As its clinical application is limited by hypercalcemia, synthetic vitamin D receptor (VDR) agonists that mediate immunomodulatory activities without adverse hypercalcemic effects are of great interest.“- [http://www.ncbi.nlm.nih.gov/pubmed/21121929]
  12. hypothyroidism. – may be associated with iodine deficiency which prenatally can cause mental retardation and thyroid defects in the expected infant. Hypothyroidism in female workers has been associated with the flame retardant, polybrominated diphenyl ethers,  [http://www.ncbi.nlm.nih.gov/pubmed/26606679], and the insecticide chlorpyrifos,  [http://www.iss.it/binary/inte/cont/CPF_ENG.pdf], and the pesticide known as DDT dichlorodiphenyltrichloroethane also  [https://preventdisease.com/news/10/022510_pesticide_exposure_underactive_thyroid.shtml], [http://www.ncbi.nlm.nih.gov/pubmed/24064777], and polychlorinated biphenyls [https://www.researchgate.net/publication/26873383_Hypothyroidism_Induced_by_Polychlorinated_Biphenyls_and_Up-Regulation_of_Transthyretinand fluoride are also associated with risk of hypothyroidism.

To help prevent autism from occurring prenatally we may need to work together to show that a combination of nutritional deficiencies or metabolic defects and environmental toxins may be causing autism to develop in infants prenatally. And we may need to work together as a group of concerned individuals rather than waiting for the government or a medical corporation to look further into a problem that might leave them at some risk of legal repercussions. Historically there have been several examples of government and corporate interests blocking the lawsuits of factory workers or townspeople whose health was damaged by industrial chemicals. The lawyers were able to show expert testimony demonstrating that the supposedly ‘harmful’ toxin really had some beneficial use and was really a safe and helpful ‘treatment.’ If we could make this about helping the babies stay healthier and more on track developmentally then insurance companies and governments would probably save a lot of money in the long run actually.

Pretending things are a mystery makes it harder to work on solving the underlying problems and preventing more cases from developing into future years or future decades. Thalidomide was a mystery that got solved. Only a few pregnant women with leprosy have to worry about whether their baby might be born with thalidomide birth defects. Before the cause was known every pregnant woman of that generation probably was scared. Now we do have a variety of information about autism and putting together the puzzle is a little complicated but the good news is that it is not a complete mystery and may be preventable with individualized health guidance that begins at least one to three months prior to conception – the prenatal vitamin research suggests that the pre-conception diet is important.

Fetal Alcohol Syndrome has been shown to be related to the father’s alcohol intake around the time of conception as well as the mother’s alcohol intake during the pregnancy so the father’s diet on the days before conception may also be involved in autism development — zinc is very important for male fertility. A longevity type study could include information about both the mother and the father’s health prior to conception and then follow the pregnancy and infancy and hopefully the preventative diet and lifestyle changes would have prevented autism from occurring. 

Part of the bad news that didn’t make it into the earlier discussion of the digestion of menthol and formaldehyde is that humans have a genetic defect that makes menthol extremely more toxic to us than to all other animals — so lab research would demonstrate that menthol isn’t really that bad after all –(to lab animals, that is, but let’s keep that part a secret between corporate research scientist’s and their consciences). So in a global corporate NAFTA/TPP type world where a corporation can sue nations over lost profits, feasibly corporate research scientists and lawyers could force nations to either accept the products made with aspartame and Neotame whether it is a risk to their citizen’s health or not, or else pay the corporation for their estimated lost profits.

Aspartame and Neotame are so much sweeter than sugar that they are simply cheaper to use in food products than sugar, and since its introduction in 2002 Neotame has never even had to be listed with the ingredients, so sweet, delicious, calorie free and guilt free, no alternative sweetener was used in that product according to the label. Aspartame is the number one food additive for consumer complaints to the FDA about adverse side effects. With Neotame not ever being listed on the food label consumers have no idea if they consumed it or not even if they do have an adverse effect and we have no idea if the FDA would have received consumer complaints about the food additive because it was never required to be added to the ingredient label. People who avoid aspartame due to it causing migraines can’t look for Neotame on the ingredient list.

Avoiding all processed foods and all restaurant meals seems like a lot to ask of pregnant women but that might be necessary in order to avoid Neotame. And with Neotame as a possible source of formaldehyde for the developing fetus then as a prenatal nutrition counselor that would be the most cautious advice given the research that is already known about menthol and formaldehyde’s risks to fetal development. Avoiding all toxins and reducing stress and risk of infection would be the ideal goal for all pregnant women.

Working towards removing aspartame/Nutrasweet and Neotame from the food supply may be an impossible goal given the deep pockets of corporations but trying to get Neotame added to the ingredient list seems like a necessary compromise or first step if we are really going to be able to help prenatal and perinatal women avoid all sources of formaldehyde in the hopes of helping prevent autism from developing in the child later in life.

*This got long and complicated and there’s more: The other, other factors would include undiagnosed cases of hypothyroidism and undiagnosed iodine deficiency and BPA/pthalate exposure. Each individual mother/child with autism probably have a slightly different combination of genetic and nutritional susceptibilities and negative load of various environmental toxins and maybe even a sensitivity to the supplemental folic acid (supposedly helping prevent spina bifida but may be adding to autism risk for the babies of moms who have certain genetic defects in the methylation cycle).

So this is a preliminary draft of a preventative health education strategy for trying to prevent autism. A longevity study that started with women at least three months prior to conception and followed them and their children for years would be able to try a multi-factored prevention plan and wait and see if fewer of the children developed autism than compared to the rate of children developing autism in the average population. [rate at 1 in 45 births, Nov. 2015, CDC, http://health.usnews.com/health-news/articles/2015/11/13/cdc-child-autism-rate-now-1-in-45-after-survey-method-changes] Imprecise diagnostic criteria makes it easier for insurance companies to deny coverage.

A method has been developed using samples of umbilical cord blood to identify which infants are likely to develop autism later in childhood. The method checks fifteen “biomarkers,’ — various lab values — infants whose values were more elevated or reduced compared to normal in a certain pattern were found to be predictive of which infants went on to develop autism. [6 ] This is early research but it would help identify which infants were at risk for autistic changes in a year or two, but at birth instead of having to wait — and worry — for a year or two.

/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./

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Elevated parathyroid hormone (PTH) and 1-25-D, calcium deficiency and calciphylaxis

I’m feeling so much better after only two days of calcium supplements that I feel like throwing a party. Fatigue is tiring. Replenishing supplies of a trace nutrient deficiency can help resolve symptoms so quickly that it feels like a miracle. I’ve experienced rapid resolution of symptoms in the past when I had a problem with low B1 intake [2] that was due to a low intake of everything – I had an anorexic appetite at the time which I later found may have been due to an underlying zinc deficiency.

The anorexic appetite symptom resolved when I added zinc and B6 supplements after reading about pyroluria. Pyroluria is not yet treated or accepted by most main stream health practitioners but it is believed to be due to a genetic defect affecting an enzyme that helps break down old hemoglobin for reuse and recycling. Molecules of B6 and zinc are involved in the process and in normal health would be recycled but if the person has the genetic modification than the B6 and zinc is released in urine rather than being retained for reuse. [1]

Calciphylaxis is a symptom that is not well understood but is associated with severe hyperparathyroidism. It is a rare symptom in the general population but is seen more frequently in people with end stage renal disease. When the kidneys are no longer able to make normal amounts of 1, 25 dihydroxy D the plasma calcium levels can drop. And to try to maintain normal calcium levels the body responds by having the parathyroid glands increase production of parathyroid hormone which in normal health would tell the kidneys to activate more 1, 25 dihydroxy D which would then tell the intestines to absorb more calcium and would tell the bones to release more calcium from storage. [3] But in end stage renal disease there aren’t functional kidneys and the elevated levels of parathyroid hormone can cause other symptoms like irregular or rapid heart rate or in severe cases calciphylaxis may occur.

Calciphylaxis “is a poorly understood and highly morbid syndrome of vascular calcification and skin necrosis.” [4] The word calciphylaxis may refer to the syndrome or to the patches of necrotic (decaying) tissue which may occur internally on the surface of bones or externally in patches on the surface of the skin. The decaying areas occur more commonly on the lower legs. The areas can first appear as reddish or purplish bruised areas that may feel like they have small hardened nodules under the skin. The skin surface may be itchy and eventually may break down to be an open wound that doesn’t heal easily. There is a risk of skin infections developing in the open wound which can become severe enough to cause sepsis and death as the patches of decaying skin or bone areas do not heal well.

Calciphylaxis is more of a risk with end stage renal disease but it has also been found in people who had normal vitamin D levels and normal kidney health. And “high dose vitamin D administration is capable of inducing STC (soft tissue calcification) and calciphylaxis in murine models. [56, 57] In an attempt to reestablish normal calcium-phosphate homeostasis, ESRD patients receive vitamin D analogs that could theoretically increase their risk of calciphylaxis if hyperphosphatemia and hypercalcemia ensued. [58, 59]” [3]

“Experimental sensitizing events and agents included nephrectomy and exposure to parathyroid hormone (PTH) and vitamin D. Substances used as challengers included egg albumin and metallic salts. Calciphylaxis was the end result.4  – from a 1962 study, abstract is free. [4.5]

Eczema is something I’ve had to cope with since infancy along with severe congestion problems. The images of calciphylaxis do not look quite like the itchy patches that I’ve been dealing with for a few months but they resemble the images of calciphylaxis more than they look like the patches of eczema that I’ve had off and on since infancy.

The fun thing about autoimmune disease is all the nifty weird symptoms that you get to experience – and which are so rare that many physicians don’t want to see you or the symptoms in their office –  because those unusual symptoms must be covered by some other specialist’s field. This quote said it well:  Calciphylaxis “is a poorly understood and highly morbid syndrome”. [4]  Maybe I wouldn’t want that syndrome to be my professional responsibility either, and maybe it is just too bad for me that it might be my personal responsibility whether I like it or not. However maybe I’m lucky that my professional and personal experiences have left me more informed about odd symptoms than other health professionals, and therefore I may possibly be better equipped to cope with the odd symptoms.

Thankfully just two days of calcium supplements (while continuing to avoid excess vitamin D and sunshine) have left me feeling less itchy and my open wound areas are beginning to form scabs instead of remaining open wounds with seeping plasma.

In normal physiology the activated hormone form, 1, 25 dihydroxy D, is typically found in elevated amounts only in areas of rapid growth or membrane breakdown, such as in scab formation by white blood cells, [6], and within the placenta during pregnancy. [5] – Maybe elevated 1, 25 dihydroxy D can also be an underlying problem causing calciphylaxis rather than it being due only to deficiency of the inactive vitamin 25-D or the active hormone 1, 25-D.

Yes, my vitamin 25-D level was low at 10.9 ng/mL and anything below 20-30 is considered deficient and I was recommended by my endocrinologist to take vitamin D and calcium. However my hormone 1, 25-D level was 55 pg/mL which is considered within the normal range by mainstream medicine (range: 18-72 pg/mL). Specialists in vitamin D/hormone D metabolism would consider levels of 1, 25-D above 42 pg/mL to be elevated enough to be an osteoporosis risk because above that level the bone cells start releasing calcium, phosphorus, and magnesium into the blood supply instead of absorbing the minerals from circulating plasma and storing them for increased bone strength or for later use. [7]

Calcium and magnesium are so important as electrically active ions that the body has a variety of ways to maintain the blood levels of the two minerals within a narrow range. Blood tests for calcium and magnesium levels may be normal even though there is inadequate dietary intake because the bones can act like a savings account at the bank. In normal health if the blood plasma dips a little low for calcium or magnesium, more minerals are released from the bone, and if levels are getting too elevated than more would be excreted by the kidneys, less would be absorbed by the intestines, and more would be absorbed into the bones for long term storage.

However if 1, 25-D levels are elevated above 42 pg/mL than even if calcium levels were elevated in the blood the abnormally elevated 1, 25-D level would still be telling the bones to release more calcium and for the intestines to absorb more calcium which would lead to way too much calcium for the kidneys to be able to excrete during good health let alone during renal disease (elevated blood calcium would normally signal the body to make more of the enzyme that de-activates 1, 25-D but some microbial pathogens seem to bypass our immune system by disabling our body’s ability to make that enzyme). Adequate magnesium is necessary for the kidneys to be able to excrete calcium and elevated 1, 25-D causes the intestines to preferentially absorb calcium rather than magnesium.

And it turns out that eczema is an autoimmune disease so I may have been trying to figure out how to feel healthier since I was a baby. [8]

My mother gave up trying to spoon feed me. She said I would spit food into my hand, look at it, then put it back into my mouth before swallowing. She put cookie sheets around my highchair to block the mess (and possibly the view) and left me to feed myself from a fairly early age. I still don’t like to be fed by others, whether it’s just a taste of something on a spoon, or whether it is a dietary supplement that might cause my underlying autoimmune condition to worsen.

I’m feeling less itchy and the open wound areas are beginning to heal. The tachycardia problem is better, (having a rapid heart rate with little exercise), and an internal jittery feeling is less. The problem with trying to medicate a nutrient deficiency with psychiatric drugs is that the psychiatric drug can’t take the place of a nutrient in metabolic pathways. For years now physicians, family members and friends have been encouraging me to just take the psychiatric medication as prescribed and stop complaining about psychosomatic symptoms and imaginary problems. But the psychiatric medications that were offered all had bad side effects and while some helped slow down whirling thoughts they didn’t make the thoughts less sad or negative and they didn’t take away the internal feeling of tension.

I felt like a coiled spring internally, very jittery all the time and unable to concentrate as well as normal. I knew something was wrong and I knew feeling like a coiled spring all the time wasn’t an imaginary delusion and the feeling didn’t go away with the three different anti-psychotic medications that physicians or psychiatrists had me try.

We can’t afford ineffective health care as individuals or as a global community. Harsh medications that cause side effects in humans are probably also causing side effects in the health of the environment once the chemicals become waste products. Expensive pharmaceuticals that cause side effects in patients without addressing the person’s underlying condition are primarily helping the pharmaceutical company and may be causing the person’s condition to worsen over the long term.

Low protein intake may be involved as hypoalbuminemia is a risk factor for calciphylaxis. [9 -includes images of calciphylaxis wounds.] I don’t know for sure that my weird skin patches are early stage calciphylaxis wounds but I hadn’t been eating much protein in the weeks before my bruise like symptoms became more like open painful sores and I have probably had a low calcium intake ever since I started limiting my use of dairy products. I did take calcium supplements in the past but my chronic muscle cramps became a problem and the calcium seemed to make it worse. More recently not eating much for a couple weeks would have further reduced my intake of calcium from the sources such as sesame seeds and tree nuts that I normally do eat. Just two days of calcium supplements have helped me feel calm internally instead of jittery (I’m using about 500 mg spread out through the day in low doses). I’m also eating a more adequate amount of protein and other foods and the odd skin patches have less of a burning itchy painful feeling and the areas are starting to heal rather than remain open seeping wounds.

Twenty three and a half to fifty million Americans may have one or more types of autoimmune diseases. [10] So I don’t think that I am the only one who has been regularly told that her symptoms must all be imaginary and to go see a talk therapist or to go get stronger and stronger psychiatric medications. We can’t afford ineffective health care because it doesn’t help the patient and the medications may be bad for the environment once they become waste products. Calcium is a natural mineral that is not harmful to the environment and it is inexpensive.

6/15/15 lab values:

  • Parathyroid hormone level – PTH Intact – 154.1 pg/mL — normal range: [15.0-75.0]
  • Calcium – 8.8 mg/dL — normal range: [8.4-10.2]
  • Phosphorus was not ordered but would probably be good to check.
  • Vitamin D, 25 – 10.9 ng/mL — normal is considered: [30.0-100.0]
  • Vitamin D 1, 25 – 55 pg/mL — normal is considered: [18-72]

I did schedule an appointment with a physician but it will be a few weeks and the tachycardia was not pleasant, the internal coiled spring feeling made it hard to concentrate and hard to not over react to outside events, and the open seeping sores were painful.

I don’t see why I should not try to take care of myself rather than having to follow the orders/recommendations of physicians or psychiatrists when they are working from the premise that “we don’t know what is causing your symptoms or how to cure them but we would really like you to take these harsh medications anyway because we guess that they might reduce some of your symptoms – and please just ignore the negative side effects that the medication is actually adding to your problems because we guess that the medication might help reduce some of the symptoms that you originally came to see us about.” That is an example of circular logic based on guesses and I’m not buying it anymore now than I did when I was sitting in a highchair covered with eczema, milk based formula, and baby food.

Medications can be life saving and certainly are a modern miracle but nutrients will always be our body’s building blocks. Providing medicines to reduce symptoms of nutrient deficiency will only prolong the time the body is left without adequate nutrients and some deficiencies can cause long term damage that is not reversible once the nutrient is added back to the diet. A long term deficiency of Vitamin B12 can cause irreversible nerve damage, [11], and it turns out that calcium or vitamin D deficiency can cause osteoporosis if the deficiency is chronic enough to lead to secondary hyperparathyroidism.

/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./

Bibliography:

  1. Pyroluria: anxiety and deficiency of B6 and zinc
  2. Thiamin: people with anorexia or alcoholism are more at risk for vitamin B1 deficiency
  3. Julia R Nunley, MD, “Calciphylaxis,” Medscape, July 21, 2014, [4-Overview,  4.5-Pathophysiology]
  4. Liu NQ et al., “Vitamin D and the regulation of placental inflammation.” J Immunol. 2011 May 15;186(10):5968-74. doi: 10.4049/jimmunol.1003332. Epub 2011 Apr 11, [5]
  5. Eleftheriadis T., et al., “Vitamin D receptor activators and response to injury in kidney disease.” JNephrol 2010: 23(05): 514-524 [6]
  6. Meg Mangin, Rebecca Sinha, and Kelly Fincher, “Elevated 1,25(OH)2D appears to be evidence of a disabled immune system’s attempt to activate the VDR to combat infection.” Inflamm Res. 2014; 63(10): 803–819., 2014 Jul 22. [7]
  7. by Charlotte LoBuono, “For the First Time, Study Proves Eczema Is an Autoimmune Disease.” Jan. 5, 2015, [8]
  8. Dermnet NZ, “Calciphylaxis,” [9]
  9. AARDA, “Autoimmune Statistics,” [10]
  10. Vitamin B12 deficiency can cause long term nerve degeneration.” August 21, 2013, [11]

Additional references about risk factors for calciphylaxis in dialysis patients:                   These articles are not mentioned in the text above and the research studies are not about secondary hyperparathyroidism but they do suggest that adequate protein intake may help reduce risk for calciphylaxis and that having elevated phosphorus or alkaline phosphatase levels may increase the risk.

  • Zacharias JM, Calcium use increases risk of calciphylaxis: a case-control study. Perit Dial Int. 1999 May-Jun;19(3):248-52.  [link] *This small research study is about calciphylaxis occurring in patients on kidney dialysis – calcium supplements were found to increase risk of calciphylaxis, while iron intake may have been protective, vitamin D intake made no difference between groups, (n=8 women). The study group’s parathyroid hormone and albumin levels were not found to be significantly different then the lab values of the control group of dialysis patients who did not have calciphylaxis. The conclusion includes the suggestion that “use of calcium salts as a phosphate binder” during dialysis might have something to do with the increased rate of calciphylaxis that was being seen at dialysis centers at the time.
  • A Rauf Mazhar, et. al., Risk factors and mortality associated with calciphylaxis in end-stage renal disease.  Kidney International (2001) 60, 324–332; doi:10.1046/j.1523-1755.2001.00803.x [link] *This study (n=19) found an increased risk for calciphylaxis in dialysis patients who were female, and when the patient had elevated phosphorus and/or alkaline phosphatase levels and/or low serum albumin levels. “Calciphylaxis independently increased the risk of death by eightfold.”
  • Doweiko JP, Nompleggi DJ. The role of albumin in human physiology and pathophysiology, Part III: Albumin and disease states. JPEN J Parenter Enteral Nutr. 1991 Jul-Aug;15(4):476-83. [link] *Albumin is the main protein found in blood plasma and having low albumin levels is also associated with poor wound healing and an increased risk of death.
  • Albumin levels can be low even when there is adequate protein intake in the presence of edema. Fluid imbalance can make the albumin values seem lower due to the change in concentration of the blood serum rather than due to changes in diet. However edema and low protein intake may both be problems. A low protein intake can increase the risk for edema.
  • Pickwell K, Predictors of lower-extremity amputation in patients with an infected diabetic foot ulcer. Diabetes Care. 2015 May;38(5):852-7. doi: 10.2337/dc14-1598. Epub 2015 Feb 9. [link] *Severe edema is also a sign of ill health. the presence of edema increased the risk of poor wound healing and the need for amputation for patients with a diabetic foot ulcer.

 

Elevated levels of BPA found in children with autism

Recently published research has found that children with autism had elevated levels of the plastic bisphenol A (BPA) compared to the children in the control group. [1] BPA is a contaminant in the food supply from its use in the plastic lining of cans and in other food packages such as plastic drink bottles. It may also be found on the slick surface coating of some types of register receipts.

This is a significant step compared to “we don’t know what causes it or how to stop it,” because BPA is something that could be avoided by prenatal women and people with autism. It is also good news because it may also be possible to reduce the risks of exposure to BPA by increasing intake of the plant phytoestrogen, soy genistein, or methyl donors such as vitamin B12 and folate and choline. [2]

/Disclosure: This information is provided for educational purposes and is not intended to provide individual health guidance. Please see a health professional for individual health care purposes./

Methyl Donors and BPA

Methyl donors are chemicals that can donate a methyl group which is made up of one carbon atom and three hydrogen atoms. Methyl groups on DNA signal the genes to remain unactivated, to stay in an off position. Removing the methyl groups can signal the gene to become active. A gene that has few methyl groups atttached may be more easily activated than normally.

This excerpt includes methyl donors and at least one methyl remove-er (BPA).

“Nutritional components that may influence the methylation of epigenetically susceptible loci include folic acid, vitamin B6 and 12, selenium, choline and betaine, methionine, soy genistein, bisphenol A, tocopherols, diallyl disulfide in garlic, and tea polyphenols [28]” [1]                                               *tocopherols are the vitamin E group.

Bisphenol A is not a natural component of food as I understand nutrition but BPA may be part of the plastic lining of cans and other food packages such as plastic drink bottles. It is also found on the slick coating of some types of register receipts. BPA may cause hypomethylation of DNA, fewer methyl groups on the DNA may cause activation of genes.

Bisphenyl A can act similarly to the hormone estrogen. Soy genistein is a phytoestrogen that may help block harmful effects of the estrogen mimetics. Other methyl donors that may help block the effects of BPA are the B vitamins folic acid, vitamin B6 and B12 and choline and betaine.

Avoiding the supplement forms and eating more food sources of Folate and methyl B12 may be more beneficial for people with defects in the methylation cycle.(MTHFR is one example). Taking the unmethylated supplement forms may interfere with the smaller quantities of bioactive folate and B12 that might be found in natural sources.

Adequate B vitamins prenatally may also help protect against DNA changes in the infant.

Folate or Folic Acid:

Folate is the form of the vitamin found in food and it is more bioactive than Folic acid. Folic acid is the form that is commonly available as a supplement and in fortified foods however it requires adequate supplies of vitamin B12 to be available in order to be converted into a more usable form. A genetic difference may exist in some individuals that prevent the body from being able to convert the inactive Folic acid form into Folate, the methylated bioactive form of the vitamin.

Food Sources of Folate, the bioactive natural form, include: most beans and peanuts, black eyed peas, green peas, grains, asparagus, most dark green vegetables, orange juice, citrus fruits. Fortified cereal and rice are good sources of folic acid, the supplemental form.

Vitamin B12:

Food Sources of Vitamin B12 include: shellfish, fish, meat, poultry, eggs, milk, cheese, dairy products, Nutritional or Brewer’s yeast. Vegetarians who don’t eat dairy, eggs, fish or other meat products may need a supplement or nutritional yeast, a vegan food source of vitamin B12.

Injections of B12 may be needed for better absorption of the nutrient for some individuals with stomach problems. Adequate stomach acid and a cofactor are required for normal absorption of vitamin B12. A genetic difference may be a problem for some people causing them to need the methylated active form of B12 rather than being able to benefit from the more commonly available unmethylated supplement.

Vitamin B6:

Food Sources of Vitamin B6 include: fortified cereal, barley, buckwheat, avocados, baked potato with the skin, beef, poultry, salmon, bananas, green leafy vegetables, beans, nuts, sunflower seeds.

Choline and Betaine:

Choline is also a water soluble essential nutrient that is frequently grouped with the rest of the B vitamins. Choline is found throughout the body but is particularly important within the brain. Betaine is a metabolite of choline. Spinach and beets are rich in betaine. Good sources of choline include egg yolks, soy beans, beef, poultry, seafood, green leafy vegetables and cauliflower.

/Disclosure: This information is provided for educational purposes and is not intended to provide individual health guidance. Please see a health professional for individual health care purposes./

  1. Kyung E. Rhee, et al., Early Determinants of Obesity: Genetic, Epigenetic, and In Utero Influences, International Journal of Pediatrics, Vol. 2012
  2. J. Higdon & V. Drake,  An Evidence-based Approach to Vitamins and Minerals:  Health Benefits and Intake Recommendations, 2nd Ed., (Thieme, Stuttgart / New York, 2012)
  3. “Choline” on whfoods.com: [whfoods.com]
  4. Betaine,” (Feb. 11, 2012) PubMed Health: [ncbi.nlm.nih.gov/]  *link not working, part of the information is available here: [med.nyu.edu]
  5. Rebecca J. Schmidt, et. al. , “Prenatal vitamins, one-carbon metabolism gene variants, and risk for autism,” Epidemiology. 2011 Jul; 22(4): 476–485. [ncbi.nlm.nih.gov]
  6. MTHFR C677T Mutation: Basic Protocol,”