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./

What do we have in common with pine trees and ticks?

Cannabinoids is the short answer.

Excerpts from p59 and p62, Editors, Emmanuel S. Onaivi, Takayuki Sugiura, Vincenzo Di Marzo, Endocannabinoids: The Brain and Body’s Marijuana and Beyond, (Taylor & Francis Group, 2006, Florida), pages 59 and 62 are from Chapter 3, by: E.S. Onaivi, H. Ishiguro, P. W. Zhang, Z. Lin, B. E. Akinshola, C. M. Leanoard, S. S. Chirwa, J. Gong, and G. R. Uhl, Chapter 3, Endocannabinoid Receptor Genetics and Marijuana Use,

“This chapter discusses the current state of description of the genes encoding the CBRs, [cannabinoid receptors], from their serendipitous identification to the existence of an EPCS, [Endogenous P_?__ Cannabinoid System – I can’t find the acronym spelled out within the text]. This previously unknown but ubiquitous EPCS consists of the membrane cannabinoid receptors, their ligands, endocannabinoids that are known to act as retrograde messengers, and the associated proteins for their biosynthesis, e.g., phospholipase D, and for their inactivation, e.g., fatty acid amide hydrolase (FAAH) and monoacylglycerols.” (p59)

Cannabinoids are essential throughout the body and in most forms of life, including plants, animals and some insects:

“The occurrence of a novel cannabimimetic molecule 2-scia-donoylglycerol (2-SG) in the plant seeds of umbrella pine (Sciadopitys verticillata) has also been reported (Nakane et al., 2000). 2-SG was found to have effects on the CB1R similar to, but with lower activity than, 2-AG, demonstrating the occurrence of these interesting molecules, not only in plants and animals but also in disparate organisms such as ticks. This widespread occurrence of endocannabinoids and related fatty acid amides and their receptors appears to be highly conserved in nature, indicating a fundamental role in biological systems. For example, the salivary glands of ticks, which are ectoparasitic and obligate blood-feeding arthropods, can make endocannabinoids and their congeners with analgesic and anti-inflammatory activity, which possibly participate in the inhibition of the host defense reactions (Fezza et al., 2003).” (p 62)

Ticks know that cannabinoids have medical properties – are U.S. politicians dumber than ticks? – or are they just under the control of corporate profit influence? The Eli Lilly company made $4.8 billion off of the cannabinoid system in 2007 alone with the sale of olanzapine/Zyprexa.

The paragraph continues:

“Apparently, the EPCS plays a critical role in the survival and mechanisms of cell death.”

In other words the endogenous cannabinoid system is essential for controlling apoptosis – the enzymatic blast of death that white blood cells can deliver to infected, cancerous, or otherwise damaged cells. The cure for cancer has always been within us – when we are well nourished and functioning correctly.

The paragraph continues (it’s a long paragraph, which actually started half way up the previous page, but this does include the rest of the paragraph.):

“Previously, the existence of anandamide analogs in chocolate had been demonstrated (di Tomaso et al., 1996). It is thought that chocolate and cocoa contain N-acylethanolamines, which are chemically and pharmacologically related to anandamide. These lipids could mimic cannabinoid ligands either directly by activating CBRs or indirectly by increasing anandamide levels (Bruinsma and Taren, 1999). These observations demonstrate that endocannabinoid analogs exist in plants and animals and further illustrate that evolutionary conservation of the cannabinoid system in nature. In this section, we will briefly review the properties and functions of these endocannabinoids. Thus, the EPCS represented by CBRs, endocannabinoids, and enzymes for the biosynthesis and degradation of these ligands is conserved throughout evolution. Endocannabinoids are present in peripheral as well as in brain tissues and have recently been demonstrated to be in breast milk. In addition, the recent demonstration of the expression of functional CB1R in the preimplantation embryo and synthesis of anandamide in the pregnant uterus of mice suggested that cannabinoid ligand-receptor signaling is operative in the regulation of preimplantation embryo development and implantation (Paria and Dey, 2000). 2-AG has been characterized as a unique molecular species of the monoacylglycerol isolated from rat brain and canine gut as an endogenous CBR ligand (Sugiura and Waku, 2000). 2-/ag also exhibits a variety of cannabimimetic activities in vitro and in vivo, and clearly further studies are necessary to determine the relative importance of 2-AG and anandamide in the human body and brain. This is because the levels of anandamide (800 times lower than the levels of 2-AG) found by some investigators in several mammalian tissues, and its production mainly in the postmortem period in the brain, have led to questions about the physiological significance of anandamide, especially in the brain, despite its high-affinity binding to CBRs (Sugiura and Waku, 2000). These research findings undoubtedly have advanced cannabis research and have allowed us to hypothesize that the EPCS consists of a previously unrecognized but elaborate network of endocannabinoid neuromodulators complete with their accompanying biosynthetic, uptake, and degradation pathways just like the monoaminergic and opiodergic systems.” (p62)

So olanzapine/Zyprexa prevents the breakdown of anandamide – which normally becomes more elevated in the postmortem (dead) brain while a different endocannabinoid – 2-AG – is normally more elevated in the live brain. Personally I like my brain to function more like a live brain than a dead brain, as I’m not partial to zombies or negative side effects such as diabetes, suicide, or homicide. So the Eli Lilly company may be similar to blood sucking parasitic ticks in that they are pleasuring some patients to the point of sickness or death with the prescription medication olanzapine/Zyprexa.

There was a warning from the FDA about Zyprexa in 2005, but regarding a problem with it being given in error to people who actually had been prescribed the allergy medication Zyrtec. Zyprexa causes many negative side effects and Zyrtec doesn’t cause any — at least for me, I’ve used it for allergies in the past. Zyprexa is described within the FDA warning as being an anti-psychotic that is only for the short term or maintenance management of schizophrenia or for the short term use for manic episodes associated with bipolar disorder. So be sure to check your Zyrtec bottle every time you refill it, just in case the pharmacist makes a mistake and grabs Zyprexa instead or couldn’t read a hand written prescription accurately and thought that it did say Zyprexa.[http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm152869.htm]

The medication, in an injectable form, was also under FDA review due to two patient deaths — autopsy found higher than expected levels in the blood of the two patients a few days following a standard injection (a one month sustained release dose is given as a intramuscular injection). The FDA required animal studies which showed that some animals did have increased amounts of the drug in their blood following death. No changes were required for the medication’s patient care or label requirements. The article includes the information that since 2011 that total sales of olanzapine had dropped for the year 2014, due to an increase in the use of generics. “Zyprexa’s 2014 sales have fallen to $1.04 billion from $4.62 billion in 2011, primarily due to competition from generic medications, Reuters reported. ” [http://www.biospace.com/News/deaths-review-of-eli-lillys-antipsychotic-zyprexa/369798?type=twitter_zyprexalilly032415]

The two patients are still dead though. Maybe enough patients complained to their doctors in 2012 and 2013 about the negative side effects of the medication to cause the large increase in use of different generics. — No that isn’t what happened, the FDA approved a generic form of olanzapine in 2014, so now Eli Lilly isn’t the only parasitic tick pleasuring patients to sickness or death. [http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm277022.htm]

Obviously Eli Lilly and the generic drug company is making billions off of our cannabinoid system — so clearly cannabinoids have medical uses within the body.

Cannabinoids are essential throughout the body and not all people can make them from other molecules. They may have a deficiency of the nutrient since birth, due to genetic defects, or some people may have been able to make adequate cannabinoids when they were young but then they may have lost the ability later in life due to malnutrition, disease, or aging. So for some individuals from birth and for others later in life cannabinoids are an essential nutrient that has to be obtained from external sources. The nutrient guidelines need to be changed to reflect the fact that some people and some babies may need an external source of cannabinoids in their diet or with an alternate external source, (such as medical marijuana or the prescription Sativex which contains a balanced amount of THC and CBD extracted from medical marijuana), and all infant formula should be required to have cannabinoid content equivalent to what would be provided naturally within breastmilk.

The herb rosemary, from the pine family, is a natural source of cannabinoids, so is nutmeg, cardamom, chocolate and cocoa, buckwheat, the inner germ of corn, and some seeds such as cucumber seeds and pomegranate seeds.

Sources: 1. Weihrauch et al, 1983 The Phospholipid Content of Foods (JAOCS, vol 60, no. 12 (December 1983) and 2. James Duke – Greenpharmacy.com for the herbal plants, Ethnobotanical and Phytochemical Database of medicinal plants and chemical activities, (This website still exists, however the Database is no longer available.)

See a couple of my older posts for more information and excerpts about the phospholipid content of many foods:

/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:

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./