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Dopamine ,methylation , and genetics?

methylation genes promethese dopamine

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#1 Nocturno

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Posted 17 April 2017 - 02:21 AM


Following a DNA test , some analysis , and this dudes post :
http://www.longecity...hol-hangovers/ 

where he basically attenuated his dopamine issue after looking deeper into methylation and his genes . 

with my very much , unsophisticated/uneducated research :  

I found an interesting set of Polymorphisms COMBINATION  in my DNA , APPARENTLY(or wrongfully)  causing a clusterfuck of low dopamine effect . 

I'd like to share , give a brief explanation , and then hear some opinions/more educated take on it , and perhaps a smart course of action , not expecting magic bullet ofcourse . (but still interesting)
 

COMT V158M rs4680 
GG -/- 

29.2% Frequency 

COMT : Catechol-O-methyltransferase - this fucker degrades catecholamines (dopamine , serotonin etc) . 


This polymorphism means more activety of the enzyme , which means less dopamine . 
" The COMT gene codes for the COMT enzyme, which breaks down dopamine in the brain's prefrontal cortex. The wild-type allele is a (G), coding for a valine amino acid; the (A) substitution polymorphism changes the amino acid to a methionine. This alters the structure of the resultant enzyme such that its activity is only 25% of the wild type. As a result, A allele carriers have more dopamine in their prefrontal cortex"


NEXT 
 

VDR Taq rs731236 

AA +/+
34.5% Frequency
 

VDR (Vitamin D Receptor) encodes the nuclear hormone receptor for vitamin D3. 
(Taken with a grain of salt from genegenie) 

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.

UP NEXT TO MAO A : 

 

MAO A R297R rs6323
T +/+
65.5% Frequency

Lol this one is actually positive..

MAO-A (Monoamine oxidase A) is a critical enzyme involved in breaking down important neurotransmitters such as serotonin, norepinephrine, and dopamine.
When a (+/+) MAO-A mutation is combined with a (+/+) or (+/-) COMT V158M mutation, imbalances in neurotransmitters may be more severe. (With a grain of salt ) .

"Note: Genetic Genie reports the wild type as the defective variant as doctors have clinically observed that patients with methylation problems (especially those of Autism) often have trouble breaking down neurotransmitters. The high activity version of MAO-A (which is represented as -/-) can contribute to major depressive disorder. The significance of this SNP should be interpreted with caution." 
(idk...) 



Next 

MTRR A664A rs1802059 
AA +/+
9.1% Frequency

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.
This form = less recycling of b12 ...  

next 
 

CBS (C699T) rs234706 
AA +/+
7.62040% (fuck yea)
 

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.

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. 


More methyl stuff... 


Folate One-Carbon Metabolism / Methylation (FOCM)
Snp rs651852 C\C
frequency: 35.7726%

Does : Methylates homocysteine to methionine

This gene polyphormism causes :  Downregulation
"The activity of this gene product can be affected by stress, by cortisol levels and may play a role in ADD/ADHD by affecting norepinephrine levels."

and these two bums
 

AHCY-01 rs819147
CT +/-
 AHCY-19 rs819171
CT +/-

AHCY (S-adenosylhomocysteine hydrolase) is involved in breaking down the amino acid methionine. It controls the step that converts S-adenosylhomocysteine hydrolase to adenosine and homocysteine. Adenosine plays an important role in energy transfer as ATP and ADP. It helps promote sleep and suppress arousal. Dysfunction of this enzyme can affect levels of homocysteine

"
AdoHcy hydrolysis serves not only to sustain the flux of methionine sulfur toward cysteine, but is believed also to play a critical role in the regulation of biologic methylations." (from nutra hacker , with a big grain ) 



To throw in the mix (none dopa related , but possibly has to do with methylation and add some fire :D ) 

significantly higher plasma total homocysteine concentration
[PharmGKB:Curated Homozygotes for this variant allele in the CTH gene had significantly higher plasma homocysteine levels than other genotypes in a cohort of 496 Caucasian individuals.] [OMIM:?] 

 
Thats pretty much what I could find , and that is somewhat inline with the post  - I would like to get some help in regards to a course of action and better understanding . 

I got some cool snp's in regards to hippocampal volume ,
all the obesity and type 2 diabetes risks (although on the almost underweight bmi) 10+fold increase
GAD1 - 90 of the snps are in the 0-5% frequency . 

Major hearing loss risks(probably a typo , but 15 fold risk) has to do with acetyletransferase snp's 
9.7 times more risk of hypertension
5 times for thyroid cancer 

But: 
React well to amphetamine (lol) 
Rare and least likely for marijuana addiction (lol ) (but  there is another gene that actually says the opposite) 
More likely to smoke less due to niconic receptors polymorphisms (same as above) 
and a cluster of reduced heart disease rates Snps

(oh yea , and a shitload of schizophrenia risks/factors , guess I won't be trying any psychedelics in the future :0 ) 

"Cewl" 

Following a DNA test , some analysis , and this dudes post :
http://www.longecity...hol-hangovers/ 

where he basically attenuated his dopamine issue after looking deeper into methylation and his genes . 

with my very much , unsophisticated/uneducated research :  

I found an interesting set of Polymorphisms COMBINATION  in my DNA , APPARENTLY(or wrongfully)  causing a clusterfuck of low dopamine effect . 

I'd like to share , give a brief explanation , and then hear some opinions/more educated take on it , and perhaps a smart course of action , not expecting magic bullet ofcourse . (but still interesting)
 

COMT V158M rs4680 
GG -/- 

29.2% Frequency 

COMT : Catechol-O-methyltransferase - this fucker degrades catecholamines (dopamine , serotonin etc) . 


This polymorphism means more activety of the enzyme , which means less dopamine . 
" The COMT gene codes for the COMT enzyme, which breaks down dopamine in the brain's prefrontal cortex. The wild-type allele is a (G), coding for a valine amino acid; the (A) substitution polymorphism changes the amino acid to a methionine. This alters the structure of the resultant enzyme such that its activity is only 25% of the wild type. As a result, A allele carriers have more dopamine in their prefrontal cortex"


NEXT 
 

VDR Taq rs731236 

AA +/+
34.5% Frequency
 

VDR (Vitamin D Receptor) encodes the nuclear hormone receptor for vitamin D3. 
(Taken with a grain of salt from genegenie) 

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.

UP NEXT TO MAO A : 

 

MAO A R297R rs6323
T +/+
65.5% Frequency

Lol this one is actually positive..

MAO-A (Monoamine oxidase A) is a critical enzyme involved in breaking down important neurotransmitters such as serotonin, norepinephrine, and dopamine.
When a (+/+) MAO-A mutation is combined with a (+/+) or (+/-) COMT V158M mutation, imbalances in neurotransmitters may be more severe. (With a grain of salt ) .

"Note: Genetic Genie reports the wild type as the defective variant as doctors have clinically observed that patients with methylation problems (especially those of Autism) often have trouble breaking down neurotransmitters. The high activity version of MAO-A (which is represented as -/-) can contribute to major depressive disorder. The significance of this SNP should be interpreted with caution." 
(idk...) 



Next 

MTRR A664A rs1802059 
AA +/+
9.1% Frequency

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.
This form = less recycling of b12 ...  

next 
 

CBS (C699T) rs234706 
AA +/+
7.62040% (fuck yea)
 

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.

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. 


More methyl stuff... 


Folate One-Carbon Metabolism / Methylation (FOCM)
Snp rs651852 C\C
frequency: 35.7726%

Does : Methylates homocysteine to methionine

This gene polyphormism causes :  Downregulation
"The activity of this gene product can be affected by stress, by cortisol levels and may play a role in ADD/ADHD by affecting norepinephrine levels."

and these two bums
 

AHCY-01 rs819147
CT +/-
 AHCY-19 rs819171
CT +/-

AHCY (S-adenosylhomocysteine hydrolase) is involved in breaking down the amino acid methionine. It controls the step that converts S-adenosylhomocysteine hydrolase to adenosine and homocysteine. Adenosine plays an important role in energy transfer as ATP and ADP. It helps promote sleep and suppress arousal. Dysfunction of this enzyme can affect levels of homocysteine

"
AdoHcy hydrolysis serves not only to sustain the flux of methionine sulfur toward cysteine, but is believed also to play a critical role in the regulation of biologic methylations." (from nutra hacker , with a big grain ) 



To throw in the mix (none dopa related , but possibly has to do with methylation and add some fire :D ) 

significantly higher plasma total homocysteine concentration
[PharmGKB:Curated Homozygotes for this variant allele in the CTH gene had significantly higher plasma homocysteine levels than other genotypes in a cohort of 496 Caucasian individuals.] [OMIM:?] 

 
Thats pretty much what I could find , and that is somewhat inline with the post  - I would like to get some help in regards to a course of action and better understanding . 

I got some cool snp's in regards to hippocampal volume ,
all the obesity and type 2 diabetes risks (although on the almost underweight bmi) 10+fold increase
GAD1 - 90 of the snps are in the 0-5% frequency . 

Major hearing loss risks(probably a typo , but 15 fold risk) has to do with acetyletransferase snp's 
9.7 times more risk of hypertension
5 times for thyroid cancer 

But: 
React well to amphetamine (lol) 
Rare and least likely for marijuana addiction (lol ) (but  there is another gene that actually says the opposite) 
More likely to smoke less due to niconic receptors polymorphisms (same as above) 
and a cluster of reduced heart disease rates Snps

(oh yea , and a shitload of schizophrenia risks/factors , guess I won't be trying any psychedelics in the future :0 ) 

"Cewl" 

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Also tagged with one or more of these keywords: methylation, genes, promethese, dopamine

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