Pantothenic Acid – vitamin B5

Vitamin B5 is typically referred to by its chemical name Pantothenic Acid. Why some of the B Vitamins are called a name and some by the number may have to do with the variety of the forms commonly found in the body or in the food supply. Vitamin B6 has several important chemical forms as do vitamin D and vitamin E. Getting a variety of foods within the diet on a regular, daily, weekly or even monthly basis can help to provide some of the various forms. Vitamin E in a supplement might only provide one of the bioactive forms of the group of nutrients while eating nuts and seeds would be providing some of all of the group in addition to B vitamins and other minerals.

Pantothenic Acid – vitamin B5. Food Sources and Symptoms of Deficiency.

Pantothenic Acid is a water soluble B vitamin that is essential in metabolic pathways in all forms of life, plants, animals and microbes. It is a precursor chemical for coenzyme A which is involved in many reactions that help sustain life and is needed for other proteins that are needed for making fatty acids – fats of different lengths and types. It does have other active chemical forms but is not typically referred to by their names, pantothenol – may help with healing skin wounds, research is in early stages; and pantethine – may help lower cholesterol and lipid (fat) levels in the blood. (1)

Dietary deficiency of Pantothenic Acid is very rare as the vitamin is found in most animal and plant food products. There have been no known cases of overdose/toxicity so no Upper Limit for safety has been set. Deficiency is so rare it has only been documented in prisoners of war (POWs) and the symptoms relieved by supplementation of Pantothenic Acid were reported by the POWs to be “numbness and painful burning and tingling in their feet.” (1)

Pantothenic Acid is involved in converting the B vitamin folate into an active form so a deficiency in Pantothenic Acid might result in folate deficiency symptoms, (1) (megaloblastic anemia with fatigue and normal levels of iron but with fewer red blood cells that are immature, too large (macrocytic) and nonfunctional (2). Vitamin B12 deficiency can also be a cause with similar lab values but supplements or injections of that B vitamin wouldn’t help if deficiency of the active form of folate was the cause. Supplements of folic acid, the inactive form most commonly used in multi-vitamins or fortified foods, wouldn’t help either. Beans, peas and asparagus are good food sources of folate, more information about that B vitamin is available here: (Folate is essential and Folic Acid is commonly available)

Genetic differences may affect some individual’s ability to phosphorylate (add atoms of the mineral Phosphorus) to the molecule of Pantothenic Acid for the transformation of the vitamin precursor into the bioactive coenzyme A. The enzyme is needed for transporting fatty acids (lipids/fats) into the mitochondria for use for energy production. Someone with a genetic difference might not be able to use fats for energy as well as someone with typical ability to phosphorylate the Pantothenic Acid molecules in the production of Coenzyme A. One known gene that could inhibit the production of Coenzyme A is Pantothenic acid kinase II (PANK2) . Symptoms of people with a double gene difference in PANK2 may include changes in movement control (dystonia), and impaired vision, intelligence, speech, and behavior, and personality disorders (15). (1)

Symptoms of deficiency of Coenzyme A might include gaining weight more easily than average and more readily getting tired when exercising for longer amounts of time. That is my interpretation though.

I have a different genetic difference that affects phosphorylation so I may also have trouble producing Coenzyme A. Betaine-homocysteine methyltransferase (BHMTis a gene involved in protein metabolism that could cause reduced Dimethylglycine and methionine.  Chronic Fatigue Syndrome has been associated with a lack of Dimethylglycine (the amino acid – glycine). The metabolic pathways are very complex chemistry and it looks like this gene is more involved in the chemistry of the B vitamins choline and betaine. The phosphorylation problem is more specifically with phospholipids and  glycerophospholipids – both essential parts of membranes and cannabinoids. (Glycerophospholipid biosynthesis) (Phospholipid metabolism)

I will discuss betaine and choline in additional posts. An overview about phospholipids and food sources is available in the post Macro & micro-nutrients, an overview & food sources.

Symptoms of Pantothenic Acid deficiency in lab animals or other groups of animals found to have deficiency of vitamin B5 in their food supply included skin irritations, graying of fur or feather abnormalities, anemia due to reduced heme production,  nerve problems involving reduced myelin sheath, low blood glucose, rapid breathing and heart rate, and damaged adrenal glands. (1)

So it is good that Pantothenic Acid is readily available in many foods because clearly it is very important to our health. However supplements of Pantothenic Acid or rubbing it directly on the scalp or gray hair did not restore hair color in humans with gray hair. (1)

Food Sources for Pantothenic Acid (vitamin B5):

Organ meats (liver and kidney), Meats, Fish and Shellfish, Salmon, Egg yolk, MIlk, Yogurt, Cheese, Avocado, Broccoli Sweet Potato, Carrot, Celery, Mushrooms, Pomegranate Seeds, Sesame Seeds/Tahini, Beans, Nuts, Seeds, Almonds, Walnuts, Whole Grains, Brown Rice, Enriched Flour Products depending on the source – Canadian guidelines require it while the U.S guidelines do not.  (4, 5) “Processing and refining grains may result in a 35 to 75% loss. Freezing and canning of foods result in similar losses (16).” (1)

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.

References:

  1. Pantothenic Acid, Linus Pauling Institute, Oregon State University, http://lpi.oregonstate.edu/mic/vitamins/pantothenic-acid
  2. Anemia of Folate Deficiency, https://www.hopkinsmedicine.org/healthlibrary/conditions/hematology_and_blood_disorders/anemia_of_folate_deficiency_85,P00089
  3. Foods used in the 30% Calories from Carbohydrates Menu Plans, https://effectiveselfcare.info/2018/05/19/healthy-hair-is-the-proof-of-a-healing-diet/
  4. Institute of Medicine (US) Committee on Use of Dietary Reference Intakes in Nutrition Labeling. Dietary Reference Intakes: Guiding Principles for Nutrition Labeling and Fortification. Washington (DC): National Academies Press (US); 2003. 3, Overview of Food Fortification in the United States and Canada. https://www.ncbi.nlm.nih.gov/books/NBK208880/
  5. Guidance Document Repository (GDR), Prohibition against the sale of unenriched white flour and products containing unenriched flour. Canadian Food Fortification Guidelines; Grain and Bakery Products,  Canadian Food Inspection Agency, http://www.inspection.gc.ca/food/labelling/food-labelling-for-industry/grain-and-bakery-products/unenriched-flour/eng/1415915977878/1415915979471

15. Kurian MA, Hayflick SJ. Pantothenate kinase-associated neurodegeneration (PKAN) and PLA2G6-associated neurodegeneration (PLAN): review of two major neurodegeneration with brain iron accumulation (NBIA) phenotypes. Int Rev Neurobiol. 2013;110:49-71.  (https://www.ncbi.nlm.nih.gov/pubmed/24209433)

16. Food and Nutrition Board, Institute of Medicine. Pantothenic acid. Dietary Reference Intakes: Thiamin, Riboflavin, Niacin, Vitamin B6, Vitamin B12, Pantothenic Acid, Biotin, and Choline. Washington, D.C.: National Academy Press; 1998:357-373. National Academy Press,  (https://www.nap.edu/read/6015/chapter/12)

Luck is about being grateful for what you have

I’m not superstitious, I believe good luck is in part simply being grateful for what you have or what you receive. Having a positive attitude in itself may be more physiologically healthy than a negative attitude, so being grateful for what you have may help health by promoting a more positive mood.

Respecting tradition, or participating in tradition, is also something I appreciate. Having black-eyed peas for New Year’s Day wasn’t a family tradition while I was growing up. I first tried black-eyed peas  and tried cooking them after learning of their significant nutritional benefits. The southern tradition may have started out of a negative situation – no other food to eat, but the people left hungry got lucky in the food that was available.

Black -eyed peas are a very good source of folate, a B vitamin that is important for the immune system and for a good energy level by promoting healthy fully mature red blood cells. Without adequate folate a type of anemia with immature, non-functional or poorly functioning red blood cells can occur even when adequate iron is available in the diet. Black-eyed peas can help prevent anemia risk with the folate content and their iron content is also quite good at 2.2 milligrams per 1/2 cup serving. (Black-eyed Peas Health Benefits Including Anemia Prevention, Health Tips)

Per 100 grams of the food (about 4 ounces or 1/2 cup), black-eyed peas have 208 micrograms of folate while sugar has 1 microgram of folate. Green peas have 65 micrograms of folate per 100 grams. (Google: black eyed peas and folate)

So was it lucky to be left with very little food during the Civil War – no. Was it lucky to be hungry enough to try the legumes that were meant to feed farm animals – no. Was it sensible to cook them and see how they tasted – yes. Sometimes we make our own luck by working hard and accepting what is available as a positive rather than having a negative attitude and giving up. Black- eyed peas do have a slightly stronger flavor than many other beans and peas but sometimes strong flavor is a sign of more nutrients. Trying things because you learn they are good for you may be an unfamiliar habit but if you try something a few times or more the taste can become familiar and may even become something you enjoy.

With young children it is recommended to not force foods to be tried or eaten in large quantities if they are new but to offer a taste or two regularly. It can take thirty tries of a new food for a toddler to become used to the new food as something familiar and enjoyable. If force and negativity is involved however they may instead develop an aversion, a negative feeling about the food. I use the word toddler because that is the best time to accustom children to a wide range of foods. If caregivers give in too regularly to “I don’t like it” attitudes then that habit may become more fixed for the child and trying to change it later may be more difficult. Children also copy what they see adults doing so having a wide variety of healthy foods on the table and sharing a few tastes of what you are having can also be a good way to start toddlers and children with a taste for variety of flavors and foods. (Getting Kids to Try New and Healthy Foods, pbs.org)

If allergies are a problem then that should be taken into account but there are still many nutritious foods that are not regularly used and are not common allergens that could be added to a menu plan. Avoid this list of eight foods that cause up to 90% of allergies and you’ll be avoiding the most common food allergens, (unfortunately some of the ingredients are in practically most commonly used mixed dishes – so that isn’t easy to do):

  • Milk (mostly in children)
  • Eggs.
  • Peanuts.
  • Tree nuts, like walnuts, almonds, pine nuts, brazil nuts, and pecans.
  • Soy.
  • Wheat and other grains with gluten, including barley, rye, and oats.
  • Fish (mostly in adults)
  • Shellfish (mostly in adults) (this group may include shrimp as well as crab and lobster) (WebMD)

I am avoiding everything on the list except tree nuts so most of the recipes on this website do not use those foods. The almond meal in the recently posted Chocolate Cookie recipe that was included in the post with the Black-eyed Pea Soup recipe (New Year, new recipes) could be substituted with more brown rice flour or buckwheat flour is used in the original Chocolate Chip Cookie Recipe. A discussion of modifying recipes is included with that recipe: (G8. Chocolate Chip Cookies)

Herbs and spices that aren’t too hot with hot pepper or horseradish are also a good way to add flavor and nutrients to simpler foods. A child’s tastebuds don’t need too much hot pepper but a small amount of spicy things may be enjoyed and tolerated well. A child’s tastebuds may be more sensitive than an adult’s so they may prefer simpler things because they simply need less flavor to activate their tastebuds. A child’s sense of smell may also be more acute than an adult’s and aroma adds significantly to the apparent “flavor” of food. The tastebuds don’t notice as much difference as our sense of smell can appreciate and differentiate. (Do children have more sensitive taste buds than adults? Ella, age 7: blastscience.co.uk)

Luck and superstition are two different topics and I believe luck is one part hard work and two parts good attitude, throw in a dash of common sense and who knows what might be possible. And superstition may include some common sense, someone may have had an accident occur when they walked under a ladder and the superstition that it is unlucky may have grown out of the common sense habit to not walk under things when you don’t know what is above – it may have grown out of an ancient instinctual knowledge that predators leap down from hiding places.

I try to do the best I can to be careful and simply clean up salt that is spilled, tossing more over my shoulder seems silly rather than respecting a holiday tradition such as having black-eyed peas on New Year’s Day. However in more ancient times when salt was difficult to find and was treated as a rare and expensive commodity it may have been a worse catastrophe – very bad luck – to spill some. Throwing a tiny pinch of what was spilled over shoulder to ward off more bad luck may have occurred at that time. During the Middle Ages there was a saying regarding table placement – to be seated above the salt meant you were important and would get served sooner from the shared dish of salt or other more expensive and sparse entrees. To be seated below the salt meant you were of less noble lineage in medieval times. (wisegeek.com) Salt is an important nutrient and more is needed in situations where it is hot and more sodium is lost in sweat from working or just from the hot environment.

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

 

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Excerpt from the Abstract:

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

Excerpt from the article:

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

The four double mutations are in the genes:

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

The seven single mutations/polymorphisms are in the genes:

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

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

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

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