🧠 The Versatile Cofactor: Mastering Vitamin B6 (Pyridoxine)! 🧠
#USMLEStep1 #MedEd #MedicalStudent #Biochemistry #VitaminB6 #Pyridoxine #Step1Prep #HighYield #MedSchool #Hematology #Neurology #Isoniazid #USMLE #FutureDoctor #StudyGram #MedTwitter
Vitamin B6 (as PLP) is perhaps the most versatile co
#REVIVE #ADSERVER
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#PYRIDOXINE
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well yes, they've studied and known that since 2020
but also, there's no cure for it like everything else #LongCovid
btw everyone needs to make sure they are not
consuming any of the inactive form of B6 #PYRIDOXINE
as it contributes to neuropathy
so that's a small vaguely helpful step some can do
Key point: Dogs with IE show a distinct plasma metabolome compared to healthy dogs.
doi.org/10.1111/epi....
#epilepsy #ILAE #metabolomics #pyridoxine #seizure
Muscle stem cells in regeneration and aging
#Medsky🧪#publichealth #Musclebiology Could #Nicotinamide and #pyridoxine stimulate muscle #stemcell expansion and enhance regenerative capacity during aging ?
@jci-insight.bsky.social
www.jci.org/articles/vie...
www.jci.org/articles/vie...
many #LongCovid develop #Raynauds permanently (like me)
I suspect combo of bad #vagus CNS response and #VenousInsufficiency as I have small purple spider-veins all over now, never had before covid and nothing cures: not aspirin, Natto, Iron for RBC, etc
Be sure to read my alert about B6 #Pyridoxine
![https://ncbi.nlm.nih.gov/books/NBK554500/
Paradoxically the most common symptoms associated with vitamin B6 toxicity are similar to those with vitamin B6 deficiency. A patient will experience peripheral sensory neuropathy. Most commonly, this causes numbness in a stocking-glove distribution over the extremities. In addition to peripheral neuropathy, patients can experience ataxia and disequilibrium as well. One large study found that patients also could experience hyperesthesia, bone pains, muscle weakness, numbness, and fasciculations.
One study examined the role of pyridoxine toxicity on human cells to examine the neurotoxic effects further. They found that pyridoxine induced cell death in a concentration-dependent fashion and inhibited pyridoxal-5-phosphate-dependent enzymes.[12] Thus it appears that the inactive form of B6, pyridoxine, competitively inhibits the active vitamin B6 form, pyridoxal-5’-phosphate causing the symptoms of vitamin B6 toxicity to mimic the symptoms of vitamin B6 deficiency.](https://cdn.bsky.app/img/feed_thumbnail/plain/did:plc:zdgme4l2jb5umtd43mcp46td/bafkreibvuitudvrrqscpqoj7mesjffwwqd6yebskedqocdfcyziuoainoq)
https://ncbi.nlm.nih.gov/books/NBK554500/ Paradoxically the most common symptoms associated with vitamin B6 toxicity are similar to those with vitamin B6 deficiency. A patient will experience peripheral sensory neuropathy. Most commonly, this causes numbness in a stocking-glove distribution over the extremities. In addition to peripheral neuropathy, patients can experience ataxia and disequilibrium as well. One large study found that patients also could experience hyperesthesia, bone pains, muscle weakness, numbness, and fasciculations. One study examined the role of pyridoxine toxicity on human cells to examine the neurotoxic effects further. They found that pyridoxine induced cell death in a concentration-dependent fashion and inhibited pyridoxal-5-phosphate-dependent enzymes.[12] Thus it appears that the inactive form of B6, pyridoxine, competitively inhibits the active vitamin B6 form, pyridoxal-5’-phosphate causing the symptoms of vitamin B6 toxicity to mimic the symptoms of vitamin B6 deficiency.
![https://doi.org/10.26481/dis.20170614mv
The vitamin B6 paradox
In the last decades, various cases of vitamin B6 induced polyneuropathy have been reported [15,17,18]. People chronically taking vitamin B6 supplements reported complaints such as pain in the extremities and muscle weakness. These complaints were reversible as they faded away after stopping the supplementation. Most often, these complaints were seen when taking mega doses (>50 mg/day) of vitamin B6 for a longer period of time.
However, recently, Lareb reported cases in which lower doses (2mg/day) of vitamin B6 gave the same complaints [16].
Up to now, the mechanism of vitamin B6 induced polyneuropathy is still unknown, making it difficult to give well substantiated advices.
Six different vitamers of vitamin B6 exist, namely PN, PL, PM and their phosphorylated derivatives PNP, PLP and PMP. PLP is the biological active form of vitamin B6, being a well-known coenzyme in a wide variety of enzymatic reactions. Of the vitamers, PN is most
commonly taken as a food supplement. Since vitamin B6 is considered to be safe, supplements with high doses of PN are on the market. Once taken up, PN is converted into PLP in several steps, of which phosphorylation by pyridoxal kinase to PLP is the most critical
one. All the supplements that caused adverse effects contained PN. Therefore, the focus was on PN. We hypothesized that PN is the vitamer responsible for the neurotoxic effects, by competing with the active form PLP.
Our study indeed showed that PN significantly increases cell death in the neuronal cell line SHSY5Y after a 24 hours exposure. The concentrations were selected based on plasma levels that were found in several studies [19-21]. In contrast, the other vitamers did not
affect cell viability. Additionally, PLP was able to prevent PN induced cell death, indicating that PN toxicity is caused by competition with PLP, which is in line with our hypothesis.](https://cdn.bsky.app/img/feed_thumbnail/plain/did:plc:zdgme4l2jb5umtd43mcp46td/bafkreigqh2oofhusihyvhe7yntgryugu3wxlo6ktwujeufh7uye6mgehxu)
https://doi.org/10.26481/dis.20170614mv The vitamin B6 paradox In the last decades, various cases of vitamin B6 induced polyneuropathy have been reported [15,17,18]. People chronically taking vitamin B6 supplements reported complaints such as pain in the extremities and muscle weakness. These complaints were reversible as they faded away after stopping the supplementation. Most often, these complaints were seen when taking mega doses (>50 mg/day) of vitamin B6 for a longer period of time. However, recently, Lareb reported cases in which lower doses (2mg/day) of vitamin B6 gave the same complaints [16]. Up to now, the mechanism of vitamin B6 induced polyneuropathy is still unknown, making it difficult to give well substantiated advices. Six different vitamers of vitamin B6 exist, namely PN, PL, PM and their phosphorylated derivatives PNP, PLP and PMP. PLP is the biological active form of vitamin B6, being a well-known coenzyme in a wide variety of enzymatic reactions. Of the vitamers, PN is most commonly taken as a food supplement. Since vitamin B6 is considered to be safe, supplements with high doses of PN are on the market. Once taken up, PN is converted into PLP in several steps, of which phosphorylation by pyridoxal kinase to PLP is the most critical one. All the supplements that caused adverse effects contained PN. Therefore, the focus was on PN. We hypothesized that PN is the vitamer responsible for the neurotoxic effects, by competing with the active form PLP. Our study indeed showed that PN significantly increases cell death in the neuronal cell line SHSY5Y after a 24 hours exposure. The concentrations were selected based on plasma levels that were found in several studies [19-21]. In contrast, the other vitamers did not affect cell viability. Additionally, PLP was able to prevent PN induced cell death, indicating that PN toxicity is caused by competition with PLP, which is in line with our hypothesis.
yesterday warned #LongCovid & #meCFS NEVER use #nicotine
BUT now a supplement MANY are taking without realizing, HARMFUL yet FDA refuses to regulate!
Check food/vitamin labels:
#Pyridoxine INACTIVE form of B6
TOXIC in studies, for some just 2mg/day!
Causes #neuropathy like #Raynauds & #Fibromyalgia!
