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Old 06-03-18, 11:00 AM
unomie unomie is offline
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ADHD and Methylation Analysis

Anyone got good info on this? Writing a letter to my GP but would appreciate any input

------
Hey, I was told I needed to write a letter to request my blood test

Was researching the link between EDS & ADHD and someone mentioned MTHFR. Ran my 23andme data through a gene genie and I have quite a few genes which could be exacerbating my symptoms. The science is still in it’s infancy but I’m pretty sure it isn’t pseudoscience. I believe I have 8 heterozygous mutations which are linked to EDS or ADHD in someway.

Checks I need : calcium, phosphate, vit D, B12, Serine, Threonine, Zinc, glycine, folate, homocysteine*levels.
Hoping most of these are fine just not sure which ones were tested for during my blood test - would you be able to email it over to me?


---research ive been doing---

You have 0 homozygous (+/+) mutations and 8 heterozygous (+/-) mutations.

There seems to be conflicting evidence over whether individuals with the mutation can supplement with folate or folic acid to the same effect.

Gene & Variation rsID Alleles Result
COMT V158M rs4680 AG +/-
COMT H62H rs4633 CT +/-
COMT P199P rs769224 GG -/-
VDR Bsm rs1544410 CT +/-
VDR Taq rs731236 AG +/-
MAO-A R297R rs6323 GG -/-
ACAT1-02 rs3741049 GG -/-
MTHFR C677T rs1801133 AG +/-
MTHFR 03 P39P rs2066470 GG -/-
MTHFR A1298C rs1801131 TT -/-
MTR A2756G rs1805087 AA -/-
MTRR A66G rs1801394 AA -/-
MTRR H595Y rs10380 __ no call
MTRR K350A rs162036 AG +/-
MTRR R415T rs2287780 __ no call
MTRR A664A rs1802059 AG +/-
BHMT-02 rs567754 CC -/-
BHMT-04 rs617219 __ no call
BHMT-08 rs651852 CT +/-
AHCY-01 rs819147 TT -/-
AHCY-02 rs819134 __ no call
AHCY-19 rs819171 TT -/-
CBS C699T rs234706 GG -/-
CBS A360A rs1801181 AG +/-
CBS N212N rs2298758 __ no call
SHMT1 C1420T rs1979277 __ no call



MTHFR: Another Piece of the ADHD-Genetics Puzzle from ADDitude Magazine

MTHFR Treatment: The Complete Guide

Reddit: "Finding Genetic Markers that can contribute to ADHD, and Can Help Treat A Slew of Issues"

Reddit: "IsItBull****: MTHFR gene mutation and it's consequences"


COMT V158M - As S-adenosylhomocysteine (SAH) accumulates, the COMT enzyme may become impaired. Inhibitiion of COMT can increase dopamine levels in COMT V158M (-/-)

combinations of variations COMT and VDR Taq can lead to a wide range of dopamine levels

VDR Mutations (+/-)
Checks : calcium and phosphate, vit D

VDR (Vitamin D Receptor) encodes the nuclear hormone receptor for vitamin D3. Low or low normal vitamin D values are often seen in those with chronic illness and even the general population. Low vitamin D is related to a lot of neurological and immunological conditions. Vitamin D stimulates enzymes that create dopamine.
VDR Tak and VDR Bsm are usually inverse from eachother. So if there is a (+/+) VDR Tak, there would be a (-/-) VDR Bsm. However, this is not always the case.
It has been clinically observed that the body may have trouble tolerating methyl donors with a COMT V158M + and a VDR Taq + status. VDR Taq (-/-) individuals may already have higher levels of dopamine, and combinations of variations COMT and VDR Taq can lead to a wide range of dopamine levels. Those that are VDR Taq (+/+) and COMT (-/-) may have lowest dopamine levels.
Note: Some have pointed out that VDR Taq is reported backwards since majority of medical journals report a different risk allele or use different notation. These arguments are well-founded, but Genetic Genie reports this way so results are compatible with existing methylation nutrigenomics literature. Many claims about VDR and methylation are clinical observations. There are no medical studies to support some of the observations.


MTR/MTRR Mutations - MTRR A664A(+/-) / MTRR K350A (+/-)
Checks : B12

MTRR (Methionine synthase reductase) helps recycle B12. The combination of MTR and MTRR mutations can deplete methyl B12. MTR A2756G, MTRR A66G, MTRR H595Y, MTRR K350A, MTRR R415T, MTRR S257T, and MTRR A664A all work together to convert homocysteine to methionine.
MTR (5-methyltetrahydrofolate-homocysteine methyltransferase) provides instructions for making the enzyme methionine synthase. Methionine synthase helps convert the amino acid homocysteine to methionine. To work properly, methionine synthase requires B12 (specifically in the form of methylcobalamin). An MTR A2756G mutation increases the activity of the MTR gene causing a greater need for B12 since the enzyme causes B12 to deplete since it is using it up at a faster rate. Mutations in MTR have been identified as the underlying cause of methylcobalamin deficiency. Megaloblastic anemia can occur as a consequence of reduce methionine synthase activity.
A homozygous mutation of MTR A2756G is not very common (<1% of CEU population). Some studies have demonstrated that people with a combination of MTHFR C677T and MTR A2756G have persistently high homocysteine levels unless they are treated with both B12 and folate.

BHMT mutations 08 - +/-
Checks : Serine, Threonine, Zinc, glycine?
Main : Autism: Pathways to Recovery, She also states that a BHMT 08 mutation may "increase MHPG levels relative to dopamine breakdown (HVA)". This can result in attention type symptoms. It is common to see elevated glycine in someone with a homozygous BHMT 08 mutation.

BHMT*problems / Symptoms
* Problem with gut function
* Neural tube defects
* Liver detoxification problems
* Homocysteine imbalances

Serine deficiency*– Brain function, nervous system, immune system,*chronic fatigue syndrome (CFS), depression,*insomnia, confusion, anxiety, fibromyalgia.
Threonine deficiency*– Cardiovascular problems, liver, central nervous system, immune system, liver failure (fatty liver), depression,*Amyotrophic Lateral Sclerosis (ALS).

BHMT (betaine homocysteine methyltransferase) acts as a shortcut through the methylation cycle helping convert homocysteine to methionine. The activity of the enzyme can be negatively influenced by stress. The Information on this enzyme related to methylation is mostly based on Dr. Amy Yasko's clinical experience and research.
According to Dr. Yasko, a homozygous mutation of BHMT 01, BHMT 02, BHMT 04, can produce results similar to one with a CBS upregulation even if you don't have a CBS upregulation. In her book, Autism: Pathways to Recovery, She also states that a BHMT 08 mutation may "increase MHPG levels relative to dopamine breakdown (HVA)". This can result in attention type symptoms. It is common to see elevated glycine in someone with a homozygous BHMT 08 mutation.


CBS Mutations - A360A +/-
CBS (cystathionine beta synthase) catalyzes the first step of the transsulfuration pathway, from homocysteine to cystathionine. CBS defects are actually an upregulation of the CBS enzyme. This means the enzyme works too fast. In these patients, it's common to see low levels of cystathionine and homocysteine since there is a rapid conversion to taurine. This leads to high levels of taurine and ammonia. The CBS upregulation has been clinically observed to result in sulfur intolerance in some patients. It has also been observed that BH4 can also become depleted with a CBS upregulation. BH4 helps regulate neurotransmitters and mood. Other mutations, such as MTHFR A1298C, Chronic bacterial infections, and aluminum can also lead to low BH4 levels. Lack of BH4 can lead to mast cell degranulation and possibly mast cell activation disorder (MCAD).
Note: While some physicians think the CBS mutation is one of the most important mutations to address, there is very little medical research to support these claims and some doctors in the field disagree. In normal populations, studies have shown CBS upregulations to be protective against high homocysteine. However, CBS upregulations have shown to be harmful in Down Syndrome. Medical research has not determined if CBS upregulations are harmful in those with syndromes or disorders leading to impaired methylation.

Last edited by namazu; 06-03-18 at 01:27 PM.. Reason: Removed links to commercial websites and other forums -- not allowed -- see ADDF guidelines
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Old 06-03-18, 01:03 PM
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Re: ADHD and Methylation Analysis

I have the MTHFR mutation, and I've already noticed benefit just from addressing the folic acid/natural folate portion. I definitely need to get a more comprehensive test though, I'm sure there's more to it than what I've already discovered.
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Old 06-18-18, 10:26 PM
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Re: ADHD and Methylation Analysis

I couldn't manage to read through all of this, but I'm interested because my psychiatrist just put me on Deplin a few months ago. She got my "genetic" testing done and said that it showed I don't have enough folic acid or folate or something like that. Does the Deplin actually help with ADHD? Because I'm paying a lot for the Deplin, and my insurance won't cover it. So if it's not actually doing anything I don't think I want to keep taking it.
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Old 06-19-18, 08:42 AM
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Re: ADHD and Methylation Analysis

https://clinicaltrials.gov/ct2/show/NCT01853280

What concerns me is how many hits it gets for naturopaths and homeopathic sites.
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Old 06-19-18, 12:39 PM
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Re: ADHD and Methylation Analysis

I was told Deplin is far too high of a dose of methylated folate and that is why a lot of people see no benefit from it and even some negative effects. I take 1200 mcg of methylated B-12, along with 400 mcg of methylated B-6, every morning, and I pay close attention to food labels and avoid folic acid whenever possible. I know there's more to address, my gene test only covered the MTHFR gene and not any of the others that are usually also affected, but I've noticed an improvement in my reaction to Dex, as well as a longer dose duration (taking less per dose, less often). I think there is something to be said for all of these gene mutations, and their ability to mimic, cause, or worsen, many different ailments and health problems. That Sarah said, the research is a little convoluted right now, but it's a new branch of science and from what I've read, they've been having huge successes in treating and even potentially preventing all sorts of different things. I'm very curious to see where this research leads, for those who think that treating the source rather than treating the symptoms is the way to go, this is an exciting time indeed.
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Old 06-19-18, 12:42 PM
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Re: ADHD and Methylation Analysis

Quote:
Originally Posted by USMC View Post
I couldn't manage to read through all of this, but I'm interested because my psychiatrist just put me on Deplin a few months ago. She got my "genetic" testing done and said that it showed I don't have enough folic acid or folate or something like that. Does the Deplin actually help with ADHD? Because I'm paying a lot for the Deplin, and my insurance won't cover it. So if it's not actually doing anything I don't think I want to keep taking it.
I take Jarrow brand supplements, available OTC at any number of places. I went through the same situation, my doctor said the deplin might help me, I tried to get it, and my insurance flat out said no. So I went my own route, and I'm having just as much if not better luck.

I don't necessarily notice any improvements to my ADD, so much as I notice more therapeutic benefit for my medication in treating my ADD.
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Old 06-21-18, 11:31 PM
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Re: ADHD and Methylation Analysis

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Originally Posted by Funky1 View Post
I take Jarrow brand supplements, available OTC at any number of places. I went through the same situation, my doctor said the deplin might help me, I tried to get it, and my insurance flat out said no. So I went my own route, and I'm having just as much if not better luck.

Thanks for taking the time to reply. I just had one more question. I typed "jarrow" into amazon and it resulted in a lot of different types of supplements. Which do I need to take? Or is that something I need to ask my psychiatrist?
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