Causes

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 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 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. Society has convinced us 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 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. Dehydration means that less B6 is being urinated out of the system. This concept is described 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. BUT!!! We also know from Coburn’s work that B6 is stored extensively in other cells of the body. 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 hypothesized that B6 is indeed staying in the nerves after the decrease of excess supplementation.

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.

Berger, et al., also described the increase in symptoms for weeks after stopping supplementation. In their words, “All subjects reported an increase in symptoms intensity over the subsequent 2 to 3 weeks”. 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.

The Understanding B6 Toxicity Facebook group realized that normalizing bloodwork was just the beginning of healing. The phase Recoil was confirmed by many members with various other physical and mental symptoms not described in the literature. We concluded that the research subjects in the Berger papers removed excess supplementation as soon as they were symptomatic. Many of the Facebook group’s members were toxic for years before discovering their toxicity. The Facebook group members had more system-wide damage because of the longer exposure to B6.

The Facebook members also discovered a different phase of B6 toxicity symptoms AFTER RECOIL. This new phase of undocumented symptoms has been labeled Rebound. It is not in the literature because there are no long-term studies that address the reemergence of symptoms after Recoil. The Facebook group is the first source defining, describing and collecting data on Rebound. Rebound is the start of healing.

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. We also know that B6 toxicity on lower doses of the vitamin causes Small Fiber Neuropathy. Finally, there are two phases towards the path of healing: Recoil and Rebound.

Any unlinked research can be found in our Index of Sources.

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