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Vitamin B6 And Neuropathy

This blog post will walk you through: vitamin b6 and neuropathy.

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Vitamins known for treating symptoms of peripheral neuropathy may be found in certain high-protein foods such as meat, poultry, fish, and eggs.

B Vitamins

However, not everyone can obtain enough vitamins in their diet, so supplements may be necessary. Again, discuss these matters with your doctor.
Omega-3

Omega-3 fatty acids are anti-inflammatory and might help patients repair damaged nerves and relieve muscle stiffness. Some foods that contain omega-3 fatty acids include sardines, salmon, walnuts, flaxseeds, and oysters. A 2017 study found that fish oil (which contains omega-3) may potentially slow the progression of peripheral neuropathy and possibly stimulate the growth of neurons.
B vitamins

B vitamins such as B1, B6, and B12 are known for supporting the healthy function of the central nervous system. Vitamin B12 deficiency may cause permanent nerve damage if left untreated. B vitamins may be found in foods such as meat, fish, poultry, eggs, vegetables, and certain cereals.
This amino acid is known for creating healthy nerve cells and reducing neuropathic pain. A 2013 study found that curcumin may be especially helpful when taken regularly during the early stages of peripheral neuropathy.

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Xine (PN) is commonly used by the general population.
Therefore, the present review is focused on investigating the mechanistic link between PN supplementation and sensory peripheral neuropathy. Recent reports on hereditary neuropathy due to pyridoxal kinase (PDXK) mutations may provide some insight into the mechanism, as genetic deficiencies in PDXK lead to the development of axonal sensory neuropathy. High circulating concentrations of PN may lead to a similar condition via the inhibition of PDXK.
Compounds that inhibit PDXK lead to convulsions and reductions in GABA biosynthesis. For several reasons, we conclude that PDXK inhibition and consequently disrupted GABA neurotransmission is the most plausible mechanism of toxicit.

Abstract

The use of PN-containing supplements has gained lots of attention over the past years as they have been related to the development of peripheral neuropathy.
Despite a long history of study, the pathogenic mechanisms associated with PN toxicity remain elusive. Therefore, the present review is focused on investigating the mechanistic link between PN supplementation and sensory peripheral neuropathy. Recent reports on hereditary neuropathy due to pyridoxal kinase (PDXK) mutations may provide some insight into the mechanism, as genetic deficiencies in PDXK lead to the development of axonal sensory neuropathy.
Compounds that inhibit PDXK lead to convulsions and reductions in GABA biosynthesis. The absence of central nervous system-related symptoms in PDXK deficiency could be due to differences in the regulation of PDXK, where PDXK activity is preserved in the brain but not in peripheral tissues. Perturbed GABA signaling within sensory neurons may lead to excitotoxicity, neurodegeneration, and ultimately, the development of peripheral neuropathy.
For several reasons, we conclude that PDXK inhibition and consequently disrupted GABA neurotransmission is the most plausible mechanism of toxicity.

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