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What can we learn from B6 toxicity recovery?
Quote from Sarabeth on February 19, 2020, 11:29 amThat's a very helpful find, thanks! I know that some people (myself included) can have terrible reactions to one or another of the Bs, but other people seem immune to ANY seeming effect, and so I feel that a complex might be okay in that scenario - maybe everything is too out of whack at the moment to have a problem with an individual supplement? It is starting to make sense to me that a person might need an initial "push" using supplements for some or all Bs until the gut is functioning enough to produce and monitor the levels of them.
That's a very helpful find, thanks! I know that some people (myself included) can have terrible reactions to one or another of the Bs, but other people seem immune to ANY seeming effect, and so I feel that a complex might be okay in that scenario - maybe everything is too out of whack at the moment to have a problem with an individual supplement? It is starting to make sense to me that a person might need an initial "push" using supplements for some or all Bs until the gut is functioning enough to produce and monitor the levels of them.
Quote from Jenny on February 19, 2020, 11:41 amSarabeth I’ve ordered this one:
https://www.desertharvest.com/b-complex-without-b6-90-capsules.html
Having followed the B6 toxicity Facebook group for a few weeks I’m not keen to supplement B6!Â
Sarabeth I’ve ordered this one:
https://www.desertharvest.com/b-complex-without-b6-90-capsules.html
Having followed the B6 toxicity Facebook group for a few weeks I’m not keen to supplement B6!Â
Quote from Sarabeth on February 20, 2020, 7:43 pmPerfect! Thank you for doing the digging. Sometimes I forget and give up when there's actually a product out there that someone is already making... 🙂
Perfect! Thank you for doing the digging. Sometimes I forget and give up when there's actually a product out there that someone is already making... 🙂
Quote from Jiřà on March 24, 2020, 10:00 amThis is interesting. As a "bodybuilder" I was eating with chicken breasts and other foods like 8mg a day + taking B complex nonstop maybe like 10 years. Heh I think it is time to lower my B6 intake. Maybe it will have some benefits..
This is interesting. As a "bodybuilder" I was eating with chicken breasts and other foods like 8mg a day + taking B complex nonstop maybe like 10 years. Heh I think it is time to lower my B6 intake. Maybe it will have some benefits..
Quote from Даниил on August 7, 2021, 8:53 pmOh! Yeah!!
I already avoid vitamin A (and all carotenoids), vitamin F, vitamin E ( tocotrienols), oxalates, gluten. I know what else I can run away from! So, what do we have for breakfast today? Egg whites? Sugar? Are apples without peel definitely without oxalates?
Oh! Yeah!!
I already avoid vitamin A (and all carotenoids), vitamin F, vitamin E ( tocotrienols), oxalates, gluten. I know what else I can run away from! So, what do we have for breakfast today? Egg whites? Sugar? Are apples without peel definitely without oxalates?
Quote from Даниил on August 7, 2021, 9:11 pmQuote from tim on December 29, 2019, 10:33 pmThe symptoms of VAD are completely different from those of Hypervitaminosis A, some myths refuse to die. The only proven symptom of VAD is xerophthalmia.
The reason B6 toxicity symptoms are the same as deficiency symptoms is because toxicity is deficiency. Pyridoxine competitively inhibits P5P so a large amount of pyridoxine creates a deficiency. Some people have problems converting pyridoxine to P5P in the first place, these people are the likely ones that react negatively to small amounts of pyridoxine. These people have low pyridoxal kinase activity. Holistically restoring health to improve enzyme function is the correct approach, not life long supplementation with P5P.
Never take anything that contains a lot of pyridoxine. As an example Berocca contains 10 mg of pyridoxine, I doubt this is problematic for most people. I wouldn't go much higher than that though. If you take P5P you shouldn't have a problem however I would caution against taking any supplement over an extended period that provides any nutrient far in excess of what we would normally get in food.
The vitamin B6 paradox: Supplementation with high concentrations of pyridoxine leads to decreased vitamin B6 function.
Abstract
Vitamin B6 is a water-soluble vitamin that functions as a coenzyme in many reactions involved in amino acid, carbohydrates and lipid metabolism. Since 2014, >50 cases of sensory neuronal pain due to vitamin B6 supplementation were reported. Up to now, the mechanism of this toxicity is enigmatic and the contribution of the various B6 vitamers to this toxicity is largely unknown. In the present study, the neurotoxicity of the different forms of vitamin B6 is tested on SHSY5Y and CaCo-2 cells. Cells were exposed to pyridoxine, pyridoxamine, pyridoxal, pyridoxal-5-phosphate or pyridoxamine-5-phosphate for 24h, after which cell viability was measured using the MTT assay. The expression of Bax and caspase-8 was tested after the 24h exposure. The effect of the vitamers on two pyridoxal-5-phosphate dependent enzymes was also tested. Pyridoxine induced cell death in a concentration-dependent way in SHSY5Y cells. The other vitamers did not affect cell viability. Pyridoxine significantly increased the expression of Bax and caspase-8. Moreover, both pyridoxal-5-phosphate dependent enzymes were inhibited by pyridoxine. In conclusion, the present study indicates that the neuropathy observed after taking a relatively high dose of vitamin B6 supplements is due to pyridoxine. The inactive form pyridoxine competitively inhibits the active pyridoxal-5'-phosphate. Consequently, symptoms of vitamin B6 supplementation are similar to those of vitamin B6 deficiency.VA "deficiency" has many symptoms. I do not know what symptoms they confirmed or not, I do not want to understand all the details of this fraud. And these are just detoxification symptoms superimposed on deficiencies of other vitamins and minerals.
I would look at it differently, that it is the inhibition of the formation of a more teratogenic pyridoxAL that allows pyridoxine to show positive results in studies. So it is logical that pyridoxal always causes much more problems.
Quote from tim on December 29, 2019, 10:33 pmThe symptoms of VAD are completely different from those of Hypervitaminosis A, some myths refuse to die. The only proven symptom of VAD is xerophthalmia.
The reason B6 toxicity symptoms are the same as deficiency symptoms is because toxicity is deficiency. Pyridoxine competitively inhibits P5P so a large amount of pyridoxine creates a deficiency. Some people have problems converting pyridoxine to P5P in the first place, these people are the likely ones that react negatively to small amounts of pyridoxine. These people have low pyridoxal kinase activity. Holistically restoring health to improve enzyme function is the correct approach, not life long supplementation with P5P.
Never take anything that contains a lot of pyridoxine. As an example Berocca contains 10 mg of pyridoxine, I doubt this is problematic for most people. I wouldn't go much higher than that though. If you take P5P you shouldn't have a problem however I would caution against taking any supplement over an extended period that provides any nutrient far in excess of what we would normally get in food.
The vitamin B6 paradox: Supplementation with high concentrations of pyridoxine leads to decreased vitamin B6 function.
Abstract
Vitamin B6 is a water-soluble vitamin that functions as a coenzyme in many reactions involved in amino acid, carbohydrates and lipid metabolism. Since 2014, >50 cases of sensory neuronal pain due to vitamin B6 supplementation were reported. Up to now, the mechanism of this toxicity is enigmatic and the contribution of the various B6 vitamers to this toxicity is largely unknown. In the present study, the neurotoxicity of the different forms of vitamin B6 is tested on SHSY5Y and CaCo-2 cells. Cells were exposed to pyridoxine, pyridoxamine, pyridoxal, pyridoxal-5-phosphate or pyridoxamine-5-phosphate for 24h, after which cell viability was measured using the MTT assay. The expression of Bax and caspase-8 was tested after the 24h exposure. The effect of the vitamers on two pyridoxal-5-phosphate dependent enzymes was also tested. Pyridoxine induced cell death in a concentration-dependent way in SHSY5Y cells. The other vitamers did not affect cell viability. Pyridoxine significantly increased the expression of Bax and caspase-8. Moreover, both pyridoxal-5-phosphate dependent enzymes were inhibited by pyridoxine. In conclusion, the present study indicates that the neuropathy observed after taking a relatively high dose of vitamin B6 supplements is due to pyridoxine. The inactive form pyridoxine competitively inhibits the active pyridoxal-5'-phosphate. Consequently, symptoms of vitamin B6 supplementation are similar to those of vitamin B6 deficiency.
VA "deficiency" has many symptoms. I do not know what symptoms they confirmed or not, I do not want to understand all the details of this fraud. And these are just detoxification symptoms superimposed on deficiencies of other vitamins and minerals.
I would look at it differently, that it is the inhibition of the formation of a more teratogenic pyridoxAL that allows pyridoxine to show positive results in studies. So it is logical that pyridoxal always causes much more problems.
Quote from Jenny on August 8, 2021, 2:08 amJust seen my old comment. I don’t think that anymore. I’m actually back to having small doses of B6 when under stress (pyroluria related). I would love to understand the whole B6 toxicity thing. Something strange is going on for some people as symptoms are really acute. I’ve read various theories. I have no idea which, if any, are true. However, it makes sense to me that B6 toxicity is an abnormal reaction due to some other imbalance in the body.
Just seen my old comment. I don’t think that anymore. I’m actually back to having small doses of B6 when under stress (pyroluria related). I would love to understand the whole B6 toxicity thing. Something strange is going on for some people as symptoms are really acute. I’ve read various theories. I have no idea which, if any, are true. However, it makes sense to me that B6 toxicity is an abnormal reaction due to some other imbalance in the body.
Quote from Даниил on August 9, 2021, 7:55 amNow I started to climb the databases to eat with low B6 and found that muscle meat, as a rule, contains a lot of B6. Unlike gelatin. Maybe the reason for the positive effects of those studies of gelatin, which Ray Peat quotes, is in low B6, and not in amino acids?
I wrote down this thought here so as not to forget.
Now I started to climb the databases to eat with low B6 and found that muscle meat, as a rule, contains a lot of B6. Unlike gelatin. Maybe the reason for the positive effects of those studies of gelatin, which Ray Peat quotes, is in low B6, and not in amino acids?
I wrote down this thought here so as not to forget.
Quote from Даниил on August 10, 2021, 12:19 pmhttps://n.neurology.org/content/90/15_Supplement/P4.021
Case: 87-year-old right-handed Caucasian female with a four-year history of supplementing with B-Complex vitamins for chronic gastrointestinal illness, presents with five months of progressively worsening fatigue, left lower extremity weakness, numbness, and ataxia. Neurologic examination was notable for pronounced atrophy of foot intrinsics (right >left) and hand interossei. Sensory examination was notable for length dependent multimodal sensory loss in a stocking-glove pattern, and diminished joint position sense. She had absent deep tendon reflexes in both upper and lower extremities, and a steppage gait on the left. Work-up: Serum pyridoxine were markedly elevated at 398.4 nmol/L (ref: 20.0 – 125.0). Additional work-up, including serum B12, hemoglobin A1c, thyroid panel, SPEP/UPEP were unremarkable. MRI of cervical-lumbar spine showed degenerative changes, and was otherwise unremarkable. Nerve conduction studies of the left lower extremity were notable for evidence of chronic, length-dependent, sensorimotor, axonal, peripheral polyneuropathy with extensive active denervation in distal muscles. No evidence of radiculopathy was appreciated on paraspinal testing.
Intervention:Â Pyridoxine supplementation was discontinued and the patient underwent intensive physiotherapy. In a two-month follow up visit, her balance was markedly improved on the Berg Balance Test and Timed Up and Go tests. Repeat serum pyridoxine level was 23.9 nmol/L.
Conclusions:Â In conclusion, sensorimotor neuropathy secondary to pyridoxine toxicity can be debilitating, but is potentially reversible with timely cessation of vitamin B6 supplementation and intensive physiotherapy.
Â
https://n.neurology.org/content/90/15_Supplement/P4.021
Case: 87-year-old right-handed Caucasian female with a four-year history of supplementing with B-Complex vitamins for chronic gastrointestinal illness, presents with five months of progressively worsening fatigue, left lower extremity weakness, numbness, and ataxia. Neurologic examination was notable for pronounced atrophy of foot intrinsics (right >left) and hand interossei. Sensory examination was notable for length dependent multimodal sensory loss in a stocking-glove pattern, and diminished joint position sense. She had absent deep tendon reflexes in both upper and lower extremities, and a steppage gait on the left. Work-up: Serum pyridoxine were markedly elevated at 398.4 nmol/L (ref: 20.0 – 125.0). Additional work-up, including serum B12, hemoglobin A1c, thyroid panel, SPEP/UPEP were unremarkable. MRI of cervical-lumbar spine showed degenerative changes, and was otherwise unremarkable. Nerve conduction studies of the left lower extremity were notable for evidence of chronic, length-dependent, sensorimotor, axonal, peripheral polyneuropathy with extensive active denervation in distal muscles. No evidence of radiculopathy was appreciated on paraspinal testing.
Intervention:Â Pyridoxine supplementation was discontinued and the patient underwent intensive physiotherapy. In a two-month follow up visit, her balance was markedly improved on the Berg Balance Test and Timed Up and Go tests. Repeat serum pyridoxine level was 23.9 nmol/L.
Conclusions:Â In conclusion, sensorimotor neuropathy secondary to pyridoxine toxicity can be debilitating, but is potentially reversible with timely cessation of vitamin B6 supplementation and intensive physiotherapy.
Â
Quote from Даниил on August 10, 2021, 12:33 pmhttps://pubmed.ncbi.nlm.nih.gov/3178170/
Abstract
The model of human malignant tumors, heterotransplanted and passaged into athymic nude mice, proved to be a valuable tool for nutritional oncology. It showed that several human tumors proliferate in distinct dependence on the available vitamin B6. A surplus of the vitamin causes enhancement of growth. Proliferation is retarded in cases of reduced availability. The amount of vitamin B6 available does not only depend on the dietary supply. The contribution of the intestinal flora may be considerable. Therefore the adverse effect of a diet free of vitamin B6 is distinctly increased by additional application of a vitamin antagonist such as D-penicillamine for instance. It should be emphasized that this happens even in situations in which no clinical symptoms of vitamin deficiency could be observed at all. Our experimental findings may have consequences for those human patients who are stricken with vitamin B6 responsive tumors. A shifting supply of vitamin B6 should at least be avoided. Dietary guidance and a careful use of vitamin antagonists, such as D-penicillamine for instance, may be helpful.
https://pubmed.ncbi.nlm.nih.gov/3178170/
Abstract
The model of human malignant tumors, heterotransplanted and passaged into athymic nude mice, proved to be a valuable tool for nutritional oncology. It showed that several human tumors proliferate in distinct dependence on the available vitamin B6. A surplus of the vitamin causes enhancement of growth. Proliferation is retarded in cases of reduced availability. The amount of vitamin B6 available does not only depend on the dietary supply. The contribution of the intestinal flora may be considerable. Therefore the adverse effect of a diet free of vitamin B6 is distinctly increased by additional application of a vitamin antagonist such as D-penicillamine for instance. It should be emphasized that this happens even in situations in which no clinical symptoms of vitamin deficiency could be observed at all. Our experimental findings may have consequences for those human patients who are stricken with vitamin B6 responsive tumors. A shifting supply of vitamin B6 should at least be avoided. Dietary guidance and a careful use of vitamin antagonists, such as D-penicillamine for instance, may be helpful.