Neurotransmitter
Serotonin
B12
GABA
Dopamine
Folate
Methylation
Biosynthesis
Bioactivation
DNA Synthesis
B Vitamins
Thiamine
Niacin
Heterocyclic
Heterocycle
Heteroatom
Gene Mutation
Serine Metabolism
Serine Synthesis Pathway (SSP)
PHGDH (gene)
MTHFR (gene)
Methyl / Folate
SAM Cycling
Lipid Metabolism
Triglyceride
Polymorphism
Plasmid Plastid Protist Phage
P53 C677T
B Vitamins and the Brain: Mechanisms, Dose and Efficacy
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4772032/
B Vitamins in the nervous system:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6930825/
Folate and DNA Methylation:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3262611/
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PHGDH and its inhibitors for regulating cancer metabolism
Emerging evidence suggests that cancer metabolism is closely associated to the serine biosynthesis pathway (SSP), in which glycolytic intermediate 3-phosphoglycerate is converted to serine through a three-step enzymatic transformation. As the rate-limiting enzyme in the first step of SSP, phosphoglycerate dehydrogenase (PHGDH) is overexpressed in various diseases, especially in cancer.
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MTHFR (gene)
Methylenetetrahydrofolate reductase deficiency
Methylenetetrahydrofolate reductase (MTHFR) is the rate-limiting enzyme in the methyl cycle, and it is encoded by the MTHFR gene.
Methylenetetrahydrofolate reductase deficiency is the most common genetic cause of elevated serum levels of homocysteine (hyperhomocysteinemia). It is caused by genetic defects in MTHFR, which is an important enzyme in the methyl cycle.
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Methylenetetrahydrofolate (MTHFR), the One-Carbon Cycle, and Cardiovascular Risks
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8703276/
Allosteric inhibition of MTHFR prevents futile SAM cycling and maintains nucleotide pools in one-carbon metabolism
https://www.jbc.org/article/S0021-9258(17)50430-5/fulltext
Methylenetetrahydrofolate reductase and psychiatric diseases
https://www.nature.com/articles/s41398-018-0276-6
One-Carbon and Polyamine Metabolism as Cancer Therapy Targets
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9775183/
Is the MTHFR C677T variant a genetic risk factor in the etiology of autism spectrum disorder? Is it alone or by combined with rare variants of the PHGDH gene? Running Title: Is the MTHFR C677T a genetic risk factor for autism?
https://www.bibliomed.org/?mno=85003
Nutrigenomics and Nutrigenetics
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3481686/
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Pyrethroid
Developmentally exposed mice had disruptions in 116 metabolites which clustered into pathways for folate biosynthesis, retinol metabolism, and tryptophan metabolism.
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What The Science Says About B3 Vitamins And Methylation
https://www.aboutnad.com/scientific-analysis/what-the-science-says-about-b3-vitamins-and-methylation
Emerging Role of Nicotinamide Riboside in Health and Diseases
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9571518/
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Nicotinamide Riboside
Inositol Nicotinate
Simple Sugar:
Ribose
Inositol
Mannitol
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Sirtuin
Sirtuin activators and inhibitors: Promises, achievements, and challenges
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6342514/
The SIRT6 activators bind, independent from substrate, to the acyl channel and might induce an enzyme conformation with increased substrate peptide affinity as suggested by such kinetic effects of free fatty acids, which are assumed to also bind to the acyl channel
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Role of Sirtuins in Retinal Function Under Basal Conditions
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6276360/
NAD+ and sirtuins in retinal degenerative diseases: a look at future therapies
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6235699/
Implications of NAD+ Metabolism in the Aging Retina and Retinal Degeneration
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7238357/
SIRT1, a histone deacetylase, regulates prion protein-induced neuronal cell death
https://www.sciencedirect.com/science/article/abs/pii/S0197458010003994?via%3Dihub
Sirtuins and Their Roles in Brain Aging and Neurodegenerative Disorders
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5357501/
A neuroprotective role of SIRT1 has been also observed in prion diseases.
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i think one of the key goals is to get the Vitamin A flipped in the right direction, then the enzymes start working.
seems everything depends upon enzyme unlocking, specially with Vitamin A.
i dont think we need much A, but its the main malfunction that stops everything else.
found papers explaining..
B-Vitamins & NAC-Acetyl flip Retinol into Sirtuin.
NAD is required to manufacture SIRT, but Niacin inhibits this process by stealing the Methylation OH from the liver, and requires a simple sugar to neutralize.
Retinol toxicity is likely the dark pigments of Phosphorus, locked into toxic acids.
Resveratrol from grapes have only Phenol, while grapes naturally have Nitrogen & Sulfur.
Castor oil is allowing the simple B3 & B1 vitamins to morph into tue ither more complex B vitamins & Heterocycle compounds, drawing out the locked acid Phosphorus plaque from organs.
Phosphorus
Phosphate
Polyphosphate
Glyphosate
Hypervitaminosis A
Retinoid
Retinol
Retinal
Retinyl
Retinaldehyde
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Efficacy and Safety of Inositol Hexa Nicotinate (IHN) in Improving Serum Lipid Profile in Patients with Low HDL Levels
RE: o