B6 for mthfr
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Vitamin B6, belonging to the group of water-soluble B vitamins, manifests in three primary forms: pyridoxine, pyridoxal, and pyridoxamine, each with distinct chemical compositions. These compounds are essential coenzymes in various metabolic processes, with pyridoxal 5’ phosphate (PLP), pyridoxine 5’ phosphate, and pyridoxamine 5’ phosphate (PMP) serving as active forms. Engaged in over 100 metabolic reactions, particularly in protein synthesis, vitamin B6 notably contributes to haemoglobin synthesis.
Moreover, vitamin B6 plays a pivotal role in carbohydrate, fat, and protein metabolism. Its significance extends to neurotransmitter production, vital for intercellular signaling in the nervous system. By facilitating the synthesis of neurotransmitters like serotonin and norepinephrine, B6 contributes significantly to mood regulation and circadian rhythm maintenance. Additionally, it aids in the production of other neurotransmitters such as glycine, D-serine, glutamate, histamine, and γ-aminobutyric acid, collectively influencing various physiological processes. Individuals carrying an MTHFR genetic mutation typically recognize the importance of supplementing with folate and vitamin B12 to support healthy methylation. However, it's imperative to acknowledge that pyridoxine (vitamin B6) also plays a crucial role in the methylation process.
Pyridoxine collaborates with folate and vitamin B12 in one-carbon metabolism, facilitating the conversion of homocysteine to methionine. Additionally, folate, vitamin B12, and B6 are vital for neuronal function, and deficiencies in these nutrients have been associated with an elevated risk of neurodevelopmental disorders, psychiatric conditions, and dementia.
Follow the link of the selected polymorphism to read a brief description of how the selected polymorphism affects Vitamin B6 (pyridoxine) and see a list of existing studies.
SNP polymorphisms related to the topic Vitamin B6 (pyridoxine):
| rs2276528 | The gene encodes pyridoxal kinase, which converts inactive vitamin B6 into the active cofactor p-5-p. Breakage can cause polyneuropathy, and high doses of p-5-p are recommended. |
| rs8128639 | The gene encodes pyridoxal kinase, which converts inactive vitamin B6 into the active cofactor p-5-p. Breakage can cause polyneuropathy, and high doses of p-5-p are recommended. |
| rs1106797 | The gene encodes pyridoxal kinase, which converts inactive vitamin B6 into the active cofactor p-5-p. Breakage can cause polyneuropathy, and high doses of p-5-p are recommended. |
| rs13050307 | The gene encodes pyridoxal kinase, which converts inactive vitamin B6 into the active cofactor p-5-p. Breakage can cause polyneuropathy, and high doses of p-5-p are recommended. |
| rs2275370 | Risk of a 1.4-fold decrease in the active form of vitamin B6 in blood and cerebrospinal fluid. |
| rs3767150 | Risk of a 1.4-fold decrease in the active form of vitamin B6 in blood and cerebrospinal fluid. |
| rs3767155 | Risk of a 1.4-fold decrease in the active form of vitamin B6 in blood and cerebrospinal fluid. |
| rs1256348 | Risk of a 1.4-fold decrease in the active form of vitamin B6 in blood and cerebrospinal fluid. |
| rs2242420 | Risk of a 1.4-fold decrease in the active form of vitamin B6 in blood and cerebrospinal fluid. |
| rs885813 | Risk of a 1.4-fold decrease in the active form of vitamin B6 in blood and cerebrospinal fluid. |
| rs1772719 | Risk of a 1.4-fold decrease in the active form of vitamin B6 in blood and cerebrospinal fluid. |
| rs5742905 | Responsible for vitamin B6 susceptibility in homocystinuria. |
| rs17679445 | Responsible for reducing the activity of the enzyme pyridoxamine-5-phosphatoxidase, leads to a significant decrease in the level of the active form of vitamin B6. |
| rs2236225 | Possible increased risk of fetal birth defects. A 1.5-fold higher risk for Caucasian mothers to give birth to children with DNT (neural tube defect). The association in children with this mutation with an increased risk of heart defects is greater if their mother did not get enough folic acid during pregnancy. The risk is reduced with adequate levels of folic acid and vitamin B6. |
| rs121964972 | Breakage increases the likelihood of homocystinuria, which is insensitive to vitamin B6. |
| rs4654748 | Breakage causes a deficiency of the active form of vitamin B6, pyridoxal-5'-phosphate (p-5-p). Supplemental intake of p-5-p is recommended. |
| rs1256335 | Breakage causes a deficiency of the active form of vitamin B6, pyridoxal-5'-phosphate (p-5-p). Supplemental intake of p-5-p is recommended. |
| rs11079804 | |
About The Author
Li Dali
Li Dali, a National Foundation for Outstanding Youth Fund recipient, is a researcher at the School of Life Sciences in East China Normal University. He earned his PhD in genetics from Hunan Normal University in 2007 and conducted collaborative research at Texas A&M University during his doctoral studies. Li Dali and his team have optimized and innovated gene editing technology, leading to the establishment of a world-class system for constructing gene editing disease models. MTHFR is an enzyme crucial for converting folic acid into an active form known as L-methylfolate,... Many individuals carry MTHFR mutations without being aware of their MTHFR status, while only a... Magnesium stands out as one of the most vital nutrients for overall health, facilitating over 300...
