It is known from research that B6 is a neurotoxin. It is also known from research that B6 in large quantities does contribute to sensory, autonomic and motor neuropathies (known collectively as Small Fiber Polyneuropathy). The Dalton and Dalton 1987 article shows that B6 toxicity was possible in smaller amounts of the vitamin. The problem for the B6T Smart Understanding B6 Toxicity Facebook group is the medical community did not understand this.
Even though there is a diagnosis code for B6 toxicity (E67.2 – Megavitamin-B6 Syndrome), our members found very few doctors that believed that B6 toxicity existed. We found even fewer doctors that understood that B6 toxicity was possible with minimal supplementation. We know of one neurologist that is aware that toxicity is possible from food alone. We have yet to find a doctor that could answer why toxicity existed with smaller amounts of supplementation and/or food.
It was the B6T Smart Understanding B6 Toxicity Facebook group that put the pieces of the puzzle together. We combined group experiences with western research for a logical explanation of B6 toxicity with smaller amounts of the supplement and/or food. In the Defined section of this webpage, we mention that B6 toxicity is over-RDA incoming B6 combined with full muscle storage and a dehydrating event. Let’s dissect this.
RDA stands for Recommended Dietary Allowances. As per NCBI, “Recommended Dietary Allowances (RDAs) are the levels of essential nutrients that, on the basis of scientific knowledge, are judged by the Food and Nutrition Board to be adequate to meet the known nutrient needs of practically all healthy persons.” In most adults, RDA B6 is 1.3 mg. Men and women over 50 need 1.7 mg and 1.5 mg respectively. We also know from research that the United States daily dietary intake of B6 is 1.9 mg. Most Americans get more B6 in their diet than the RDA.
Diet alone is an adequate intake for vitamin B6. As a society, we have been convinced it is not enough. We’ve added in multivitamins that have a minimum 100% RDA of B6. An energy drink can contribute another 2,000% to your RDA. If you’re taking a B6 complex it could easily have 200 mg which is 10,000% RDA B6. Finally, there are B6 vitamins that offer 500 mg of B6. This is 25,000% RDA. B6 is a known neurotoxin; yet, there are vitamins that allow us to ingest 25,000% RDA. Sigh.
We’ve been told all our lives that all of the B vitamins are water-soluble. Well, that is partly true. What is not widely known is that vitamin B6 is stored extensively in our muscles. What is also not known is the effects of dehydration on B6 elimination. Lastly, the most important unknown is that B6 can be stored in nerve cells. Let me scream this: WE HAVE A KNOWN NEUROTOXIN BEING STORED IN OUR NERVE CELLS!!
We know from the research that B6 is stored in muscles. It is stored as pyridoxal phosphate (aka PLP/P5P) associated with glycogen phosphorylase. Black’s 1978 study in the Journal of Nutrition shows that muscles storage of B6 does not come out with B6 deficiency. Stephan P Coburn, et al, 1988 study reveals that 70% to 80% of B6 body pools is stored in muscles. Beynon, et al, 1996 study estimates the human muscle pool at 200 mg. Coburn, et al, 1991 study confirms that vitamin B6 in muscles is resistant to depletion. Also in this study, Coburn states, “that in humans with constant body weight, vitamin B6 supplementation is NOT associated with marked increases in vitamin B6 in muscle”. The research also shows us that the only healthy way B6 comes out of the muscle is with exercise.
We interpreted this information as 70% to 80% of all incoming B6 is programmed by our body to be put into the muscles. Muscle storage is not a reservoir to be used by the body during times of B6 deficiency. The muscle storage is used as a reservoir for the excess needed during exercise. Finally, once that muscle storage is full we are not adding more B6 to the muscles. Since human muscle storage is only about 200 mg, it doesn’t take much to fill it up.
Coburn, et al, again in their 2015 summary of the research points out that most studies of vitamin B6 metabolism involve growing rats. Growing rats that have growing muscles which have more room for incoming B6 to be stored. He questions the amounts of B6 needed for animals maintaining constant body weight. In his 1991 study, he states, “that for normal human adults maintaining constant weight and subject to minimal metabolic stress, the minimum daily vitamin B6 requirement maybe 0.02 – 0.04 nmol/g body weight” (which is about .23 to .43 mg for a 150-pound person). He also states, “further studies will be needed to confirm in greater detail whether such intakes can support normal metabolism, particularly of the nervous system, and can maintain long-term health”. Coburn is suggesting that even RDA B6 is too much for an adult that isn’t growing muscles through extensive exercise.
If 70% to 80% of incoming B6 is supposed to go to muscles and muscle storage is full then where does extra incoming B6 go? Conventional wisdom states that it goes into the bloodstream to be urinated out. What happens when you are dehydrated? When dehydrated we know the body conserves water and decreases urine output. At the beginning of the group, we found a case study about a yoga instructor that got toxic after a bout of diarrhea (a dehydrating event).
Over and over members gave us evidence of their onset of toxicity after a dehydrating event. This concept is stated in Seymour Levine’s 2004 research. His abstract states that urinary losses of the toxicant (B6) are reduced with decreased water consumption and decreased urinary output. If dehydrated, you are not urinating out excess B6.
If you are not putting B6 into muscles storage and you are not urinating it out, then where is it going? Our high B6 blood work shows that B6 is staying in the blood. We also know through the group that once you follow the B6T Protocol that the higher B6 blood numbers come down within two to four weeks. Once we have the blood work back to normal, we should be on our way to healing, right? This is the assumption that doctors are making. Their logic is that once the blood level goes down to normal, then the nerve irritant is removed from the body.
The B6T Smart Understanding B6 Toxicity Facebook group figured out that this is only part of the story.
The group knows that getting bloodwork back to normal is just the start of healing. On our healing journey, the original group members encountered different layers of symptoms that are not described in the literature. These newer symptoms have not been described because there are no long-term studies of people recovering from B6 toxicity. The B6T Smart Understanding B6 Toxicity Facebook group was the first source to understand the long-term healing process.
We realized the neurotoxin stays in the body after blood work has gone back to normal. It was Stephen Coburn’s 2015 publication that gave us some answers. Coburn states that B6 is stored extensively in cells other than muscle cells. His review of the research then shows B6 being stored in the nervous system of different animals. Based on research we realized we have a known neurotoxin being stored extensively in our nerve cells.
We get another glimpse of vitamin B6 being stored in the nerves from Berger, A.R. et al, 1992 paper entitled, “Dose Response, Coasting and Differential Fiber Vulnerability in Human Toxic Neuropathy: A prospective study of pyridoxine neurotoxicity”. As these authors are discussing their results they state, “Additionally, despite progressive symptomatology, the serum pyridoxal phosphate levels of subjects 1, 2 and 4 soon returned to normal. These features suggest that clinical progression was not due to a persistently elevated body burden (excess B6 in the blood), but either due to TOXIN REMAINING IN THE LOCAL NERVE ENVIRONMENT OR TO PERSISTENT NEURONAL METABOLIC CHANGES THAT SLOWLY REVERSED”.
These authors who subjected themselves to the excess B6 in this study have the best first-hand knowledge of B6 toxicity. They realize that it’s not the excess B6 in the blood that is creating the symptoms, but instead the B6 that has been stored in the nerves. In their continued discussion in this paper, they summarize that the lower dose (1 gram) subjects had predominately small fiber dysfunction. They suggest that in previous research on human subjects the small fiber dysfunction was ignored.
The nerve damage that B6 causes is within the peripheral nervous system. The best summary of the type of damage done to peripheral nerve cells is Bernard Jortner’s 2000 paper entitled, “Mechanisms of Toxic Injury in the Peripheral Nervous System: Neuropathologic Considerations”. Bernard summarizes the nerve damage research caused by vitamin B6 in animal experimental studies. The authors of this paper also became human guinea pigs. They ingested from 12 mg to 56.9 mg of vitamin B6. The authors found that the smaller amount of vitamin B6 eventually affected the peripheral nerves. The 56.9 mg of the vitamin took only 1.5 months of use to create the symptoms of B6 toxicity. The 12 mg required seven months to elicit the same symptoms of nerve damage. Although the study was limited to just the authors of the paper, it supports the Dalton & Dalton long-term study that toxicity can happen at lower doses of the vitamin.
On top of this, these authors described the increase of symptoms for weeks after stopping supplementation. In their words, “Interestingly, such sensory effects progressed for a period of weeks despite cessation of dosing and a return to normal of serum pyridoxal phosphate (B6) levels”. The authors of this paper called this period coasting. The B6T Smart Understanding B6 Toxicity Facebook group has relabeled the term Recoil. Coasting implies that the symptoms remain the same. They do not.
This study was significant for the B6T Smart Understanding B6 Toxicity group. It confirmed what we knew that toxicity was possible on smaller amounts of the vitamins. It also confirmed that smaller amounts over a longer period of time can also get us toxic. It states clearly that smaller amounts of the vitamin create peripheral nervous system damage. The peripheral nervous system controls our sensory, autonomic and motor nerves. Finally, it also discusses even after the B6 blood work becomes normal again, the symptoms STILL PROGRESS and PERSIST.
In summary, we get toxic on small amounts of vitamin B6 due to full B6 muscle storage combined with a dehydrating event. The dehydration does not allow a normal release of vitamin B6 in our urine. It instead gets pushed into nerve cells which causes nerve damage.
Any unlinked research can be found in our Index of Sources.