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ADHD caused by pyridoxine deficiency?

adhd pyridoxine

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#1 jack black

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Posted 09 July 2016 - 01:07 AM


When you search the web, you find all kinds of weird results: http://www.medical-h...0545-8/abstract

 

 

Almost identical parameters of TRP degradation in untreated ADHD and epileptic patients allow to assume that inborn disorders of vitamin B6 metabolism are the common biochemical background of both diseases. The disturbed activity of PLP dependent enzymes apparently forms those profound disturbances of neurotransmitter systems, which are inherent in ADHD: low concentrations of monoamines and disordered amino acid metabolism. If vitamin B6 disorders are the core biochemical disturbances inherent in ADHD, then the long-term pyridoxine treatment is pathogenetically based replacement therapy of the disease. According to our data, multi-year pyridoxine treatment normalizes completely the pattern of ADHD behavior, without causing any serious side effects.

 

Can it be possibly right?

I did notice that daily B-50 complex helped me some and has 50mg piridoxine (upper safe limit). But it was not curative of course and hence I'm still searching.


Edited by jack black, 09 July 2016 - 01:10 AM.

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#2 farware

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Posted 10 July 2016 - 01:16 AM

As a neurotransmitter, glutamate is actually one of the most abundant molecules in the brain. Under normal circumstances, glutamate gets converted into the inhibitory neurotransmitter GABA. The gene/enzyme most responsible for this reaction appears to be GAD1 (glutamate decarboxylase). GAD1 uses the B-vitamin, P5P (Vitamin B-6) as the cofactor for this conversion. Deficiency of GAD1 enzyme activity is known to lead to a condition known as "Pyridoxine-dependent epilepsy" (9, 10). It seems plausible that this type of epilepsy strongly features glutamate overload and GABA deficiency.

 

https://metabolichea...onal-solutions/

 

 

There are gene defects that cause folate and or B6 deficiency. Various defects can also cause B12 deficiency. In general, gut issues can contribute to malnutrition and worsen possible deficits. 


Edited by farware, 10 July 2016 - 01:31 AM.


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#3 farware

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Posted 10 July 2016 - 01:20 AM

1.45 ng/mL lower Vitamin B6 blood concentration
This is one of the SNPs reported by NutraHacker. Genetics and genomics of human aging. [PharmGKB:Non-Curated The C allele of this SNP is associated with lower blood concentration of vitamin B6 (Combined studies of Tuscan Italians ( inCHIANTI:N =1175 and Progetto Nutrizione study:N = 687) found 1.45 ng/mL lower vitamin B6 per copy of C (p = 8.3 x 10 (-18)))] [OMIM:?] [GWAS:Folate pathway vitamins] 
 more info

 

 

 

 

 

 


Make sure you dont take B6 but use P5P instead. If you are deficient in B6 its most likely a conversion issue .. also P5P is less toxic in high doses. 



#4 jack black

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Posted 10 July 2016 - 02:15 AM

 

1.45 ng/mL lower Vitamin B6 blood concentration
This is one of the SNPs reported by NutraHacker. Genetics and genomics of human aging. [PharmGKB:Non-Curated The C allele of this SNP is associated with lower blood concentration of vitamin B6 (Combined studies of Tuscan Italians ( inCHIANTI:N =1175 and Progetto Nutrizione study:N = 687) found 1.45 ng/mL lower vitamin B6 per copy of C (p = 8.3 x 10 (-18)))] [OMIM:?] [GWAS:Folate pathway vitamins] 
 more info

 

 

 

 

 

 


Make sure you dont take B6 but use P5P instead. If you are deficient in B6 its most likely a conversion issue .. also P5P is less toxic in high doses. 

 

 

I'm TT for that SNP. Have you tried P5P yourself? There seem to be only one study on this. Sounds a bit a stretch.

 

Edit: I found a patent for that P5P treatment: https://www.google.c...s/US20100104621

 

 


Edited by jack black, 10 July 2016 - 02:28 AM.

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#5 farware

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Posted 10 July 2016 - 01:38 PM

 

 

1.45 ng/mL lower Vitamin B6 blood concentration
This is one of the SNPs reported by NutraHacker. Genetics and genomics of human aging. [PharmGKB:Non-Curated The C allele of this SNP is associated with lower blood concentration of vitamin B6 (Combined studies of Tuscan Italians ( inCHIANTI:N =1175 and Progetto Nutrizione study:N = 687) found 1.45 ng/mL lower vitamin B6 per copy of C (p = 8.3 x 10 (-18)))] [OMIM:?] [GWAS:Folate pathway vitamins] 
 more info

 

 

 

 

 

 


Make sure you dont take B6 but use P5P instead. If you are deficient in B6 its most likely a conversion issue .. also P5P is less toxic in high doses. 

 

 

I'm TT for that SNP. Have you tried P5P yourself? There seem to be only one study on this. Sounds a bit a stretch.

 

Edit: I found a patent for that P5P treatment: https://www.google.c...s/US20100104621

 

 

Since you lack the C allele it shouldnt concern you. Myself I am taking P5P at least once per week. It is helping me with dream recall and neuroplasticity and is needed for the methylation cycle in particular the conversion of homocysteine. The process is also dependent on sufficient Glycine but you should be fine without it. You can of course try to see if it makes a difference but I would first try that Memantine you ordered. 



#6 PeaceAndProsperity

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Posted 17 July 2016 - 07:17 PM

also P5P is less toxic in high doses. 

 

Shouldn't it be the opposite, that p5p is more toxic? Where did you read that it's less toxic?

I get a weird smell (olfactory hallucination?) of almost turpentine, whenever I take p5p.



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#7 Mind_Paralysis

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Posted 17 July 2016 - 09:59 PM

RatherbeUnknown: you have distinctly different symptoms from farware though - it may be that you have very differing neuroanatomy and metabolism. What's your genetic data regarding the genes controlling B6-metabolism?

Can't recall anything about the toxicity at the moment... If no-one else finds the data, I'll try to look at it in a few weeks, when I'm hopefully less burnt out.

 

As I recall it, Pyritinol is far more bio-available than any of them - it crosses the blood-brain barrier, and can be cleaved into B6 inside the brain - good stuff. Wasn't it you, Jack Black btw, who showed that region of the brain that triggers norepinephrine and dopamine-release - in the brain-stem? Which apparently was heavily affected by Pyridoxine.

I think you even had anatomic charts, broddman areas and everything... it was in the SCT and Stress - thead, regarding the way glucocorticoids control dopamine-release in the PFC.

 

Farware:

I've got it too... we related or something??

 


Edited by Stinkorninjor, 17 July 2016 - 10:00 PM.






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