Glycine is an amino acid with neurotransmitter roles

Subtitle: Rebranding and the power of a name: “Essence of Meat-ade” or “Cheerful Juice.”

Sub-subtitle:  Genetic defects in metabolism can affect the entire body due to lack of essential nutrients.

Background: I was found to have eleven of thirty defects in the methylation cycle that were known to be more common in patients with autism spectrum disorder. The screening is not for diagnostic purposes at this stage but is available to consumers interested in the information for their own research purposes (which might include what to feed their child or themselves for better management of autism symptoms – but it is use at your own risk information rather than ‘evidence based’ medical treatment approved for a certain diagnosis).

One of my genetic defects affects my ability to break down betaine into the free amino acids glycine and methionine (roughly, I would have to review the chemistry for the specifics). So armed with this new information I ordered tablets of each amino acid and started taking them each day as supplements. They seemed to help but it wasn’t a dramatic change in how I felt.

A month or two later before reordering more bottles I considered the question of just how much glycine or methionine I might need each day if I had a defect that prevented me from digesting protein and releasing the essential amino acids. When I looked into how much glycine might be needed by the body each day, I didn’t find much research but there was some and the amount suggested was far greater than the amount I was taking in the form of a tablet — 200 milligram tablet compared to two grams of the essential amino acid as a minimum recommendation with up to ten grams being proposed as possibly beneficial. And no toxicity risks were mentioned. Two grams is equivalent to 2000 milligrams or ten of the tablets each day, which would be expensive and a lot of tablets.

Many things that are available as supplements are also available in bulk as a powder that companies might use to make capsules or tablets for the individual consumer to purchase. The amino acids glycine and methionine were available online in a package size that was designed for individual use, possibly being marketed to people interested in body building or weight lifting.

A teaspoon of a powder substance is roughly five grams, depending on the density of the powder. I decided to try one teaspoon of glycine and one teaspoon of methionine per day as that would easily provide two grams and might provide up to five grams per day.

Results: Free essential amino acids are acidic — like lemonade — but taste a little like protein aka meat, so two teaspoons of free amino acids in water tasted VERY BAD. My nickname for the concoction became “Essence of Meat-ade” for the first day or two, however almost immediately after drinking the vile drink my mood became incredibly cheerful and I was suddenly filled with energy. I was amazed — how could a horrible tasting glass of water change my mood? I started looking forward to the drink and while I had started taking it in the evening I gradually switched to taking it earlier in the day and even twice a day occasionally, which would provide about ten grams of the powder.

My mental nickname changed from “Essence of Meat-ade” to “Cheerful Juice,” it helped my mood so much that I loved the stuff no matter how silly my face looked while trying to gulp it down too quickly to taste. I was amazed, and a little sad to consider that I had been without “Cheerful Juice” for my first fifty years of life — but better late than never is a motto of mine. With a double genetic defect I wouldn’t have been able to release glycine or methionine from larger proteins for my entire life — and therefore wouldn’t have had the cheerful effects or boost in energy due to the incomplete digestion of my food.

Why would a bad tasting drink give me a good mood?

I knew the amino acids glutamine and aspartic acid can act as messenger chemicals within the brain so I looked up glycine and methionine and sure enough they both also can act as brain signaling chemicals.

The rest of this information is about glycine’s role as a brain neurotransmitter. It doesn’t cover methionine but it also has roles in brain chemistry.

Glycine is a Neurotransmitter: 

Glycine has inhibitory and excitatory roles in the brain as a neurotransmitter – a type of chemical that can serve as a messenger between brain cells which are called neurons.

“Interestingly, glycine receptors comprised of a1 subunits are efficiently gated by taurine and b-alanine, whereas a2-containing receptors are not (8). The a1 and a2 genes are expressed in the adult and neonatal brain, respectively.”

ie-the type of glycine receptor found within the baby brain is not as well protected as the type found within the adult brain, later in the next paragraph:

“Recently, the expression of a1 and a2 subunits has been shown to be developmentally regulated with a switch from the neonatal a2 subunit (strychnine-insensitive) to the adult a1 form (strychnine-sensitive) at about 2 weeks postnatally in the mouse (8). The timing of this “switch” corresponds with the development of spasticity in the mutant spastic mouse (5), prompting speculation that insufficient expression of the adult isoform may underlie some forms of spasticity.” [1]

Background: Glyphosate is chemically very similar to glycine in that it may be incorporated into proteins but is not functionally the same. A protein containing glyphosate instead of glycine would be dysfunctional. Glycine provides methyl groups which are important for turning strands of DNA on and off, (DNA is the genetic material that acts as recipe cards for making proteins).

If glyphosate is being physically incorporated within body tissues in place of the amino acid glycine, then the role of glycine within early fetal development discussed in the above excerpt might be part of the mechanism for how autism risk may be occurring during the prenatal stage of life.

From a Marketing Perspective: How to sell something that tastes horrible but makes certain people feel great?

From my experience working with special need infants and children I learned that sick children when given a formula they can tolerate will cheerfully start drinking the formula if it  isn’t making them feel sicker — no matter how bad the formula tastes — and some of them are like “Essence of Meat” because they are based on free amino acids that would be easy to digest and wouldn’t have the same allergy risk as the larger and more complex proteins.

So how to market a specialty product? Target the special needs market, and pitch having the genetic screening done first in order to find out who needs the special product — and put the bulk powder in capsules  😉 , I tried to add lemon flavoring to make it more like lemonade but that didn’t change the flavor enough — I’m working on acquiring a taste for it instead.

The genetic screening I had done is “For Research Purposes Only” but it was assembled by a specialist with a PhD and experience in genetics. She is not a medical doctor and no diagnoses are provided however some health information is provided I haven’t reviewed it yet and therefore can not provide any feedback regarding it.

  • The Methylation Cycle genetic screening test: http://www.holisticheal.com/dna-methylation.html
  • My results and my notes regarding the 11 defects, this is a list of notes rather than being in article format, see number three of the double defects for details about the gene BHMT/1 (Call – T), which is for the enzyme Betaine-homocysteine methyltransferase (BHMT): https://effectiveselfcare.info/2016/03/30/methylation-cycle-defects-in-me-genetic-screening-for-research-purposes-only/
  • An excerpt from that post regarding diagnoses that may be helped by use of dimethylglycine (DMG) and methionine as supplements : 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.

/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./

  1. Steven M. Paul, GABA and Glycine, https://www.acnp.org/g4/GN401000008/Default.htm

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.

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./

Folate is essential and Folic Acid is commonly available

Folate (L-methylfolate or vitamin B9) and Folic Acid:

Food Sources of Folate, the bioactive natural form, include:
  • beans, black eyed peas, green peas,
  • peanuts and other nuts and seeds,
  • whole grains,
  • asparagus, most dark green vegetables,
  • orange juice, citrus fruits.
  • Fortified cereal and rice are sources of folic acid, the supplemental form.
Folate is the natural form; Folic Acid is in supplements & fortified foods.

Folate is the form of the vitamin found in food and is more bioactive.  Folic acid is the form that is commonly available as a supplement and in fortified foods, however it is less bioactive, less able to function until methyl groups are added which requires adequate supplies of vitamin B12. 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. [More about methylation.]

Symptoms of Folate deficiency include:
  • Deficiency of folate can cause megaloblastic / macrocytic anemia which is characterized by red blood cells that are over-sized and ineffective.  Anemia symptoms include being short of breath and feeling tired and weak.  The symptoms are due to a shortage of normal red blood cells and reduced ability to transport oxygen with each breath.
  • Folate is needed for DNA synthesis and for DNA methylation which may be important for preventing cancerous changes from occurring in the DNA.
  • Lack of folate may increase heart disease risks due to less breakdown of homocysteine. Vitamin B6 and B12 are also necessary, a deficiency of any one of the three might cause an accumulation of homocysteine.
  • Folate is important during pregnancy for fetal development.  Spina bifida and cleft palate are birth defects that may be caused by folate deficiency.
  • Deficiency of several of the B vitamin group can cause changes in the appearance and surface texture of the tongue. B vitamins that can cause changes in the tongue are mentioned in the following excerpt and include “niacin (B3), riboflavin (B2), pyridoxine (B6), folic acid (folate/B9), and vitamin B12”:
  • “Deficiencies of niacin, riboflavin, pyridoxine, folic acid, or vitamin B12,  resulting from poor diet or from the administration of antagonists, may cause a sore, beefy-red tongue without a coat. In the chronic vitamin deficiency state, the tongue may become atrophic and smooth.”                   – “The Tongue – Clinical Methods – NCBI bookshelf  https://www.ncbi.nlm.nih.gov/books/NBK236/

  • See the post on Vitamin B6 for more information about how the group of B vitamins work together in energy metabolism and cell growth.
Reference used for food sources & symptoms of Folate deficiency:
Other References used for the food sources of Folate and Folic Acid:

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.