ADHD may be simply a vitamin B6 deficiency symptom

Discussion in 'Scientific Studies' started by haidut, Oct 30, 2014.

  1. haidut

    haidut Member

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    The study claims that multi-year adminstration of vitamin B6 completely "normalized" ADHD symptoms. It was a human study, so it should have even more weight / relevance.

    http://www.ncbi.nlm.nih.gov/pubmed/24321736

    "...The disturbed activity of PLP dependent enzymes apparently forms those profound disturbances of neurotransmitter systems, which are inherent in ADHD: low concentrations of monoamines and disordered amino acid metabolism. If vitamin B6 disorders are the core biochemical disturbances inherent in ADHD, then the long-term pyridoxine treatment is pathogenetically based replacement therapy of the disease. According to our data, multi-year pyridoxine treatment normalizes completely the pattern of ADHD behavior, without causing any serious side effects."
     
  2. aguilaroja

    aguilaroja Member

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    Thumbs up for bringing this to attention.

    The data in the paper concern comparisons between Ritalin treated & untreated ADHD persons and control subjects. The experience with P5P (PLP) treatment is mentioned in the discussion, with much less description. Hopefully, full report of the PLP treatment success follows, perhaps in a higher profile journal.

    "We collected urine samples of 64 patients aged 6–11 years: healthy controls (n = 41); untreated ADHD patients (n = 13); and ADHD patients treated with Ritalin (n = 10). Urinary tryptophan and its metabolites were analyzed by HPLC with simultaneous ultraviolet and fluorimetric detection."

    "The consideration of vitamin B6 disorders as core biochemical disturbances inherent in ADHD let us – after Coleman and coauthors ...- to suggest multi-year pyridoxine treatment as pathogenetically based replacement therapy of the disease. The doses of pyridoxine hydrochloride we use are at least three times less than those proposed by Coleman: 8–10 mg/kg daily (up to 100 mg /day in children of 4–8 years; 200 mg/day in adolescents). Long-term pyridoxine treatment is both safe and effective. After several weeks of such treatment the pattern of behavior in ADHD patients is normalized. We did not observe any side effects during years. However, 1–2 months holding of treatment restores ADHD symptoms"
     
  3. tara

    tara Member

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    I thought there were concerns about neuropathy or other issues with prolonged highish dose B6? I'm sure there is a thread expressing these concerns, including people backing off because of other symptoms?
     
  4. OP
    haidut

    haidut Member

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    AFAIK, the reports of neuropathy are linked exclusively to pyridoxine hydrochloride and not P5P. In fact, there was a study saying that the neuropathy symptoms stemmed from low conversion of the Hcl salt into the active form P5P. Also, another study stated that B6 should lower prolactin effectively and if it does not then it is due to lack of conversion of Hcl salt into P5P. So, treatment with P5P may be preferable for most cases. Since the studies on B6 and prolactin on PubMed are mostly from the 1970s and 1980s the authors used the Hcl salt due to cost concerns since P5P was apparently very expensive at the time. Nowadays you can find P5P at much more reasonable prices and not much more expensive than the Hcl salt.
     
  5. aguilaroja

    aguilaroja Member

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    I have surveyed the pyridoxine safety issue research intermittently for years, in part due to such clear cautioning about dangers of a single nutrient, in comparison to pharmaceutical side effect reporting. I am not familiar with any published case reports of toxicity of the pyridoxal phosphate (P5P) form, though I some years back read one anecdote on the web. I have never encountered a person with any side effect from P5P.

    There is a recent review of the topic which uses many sources. I have not had the opportunity to go back to all cited sources to see if each study involved the HCl form (pyridoxine hydrochloride).

    http://www.ncbi.nlm.nih.gov/pubmed/25137514

    J Clin Neuromuscul Dis. 2014 Sep;16(1):25-31. doi: 10.1097/CND.0000000000000049.
    Revisiting the evidence for neuropathy caused by pyridoxine deficiency and excess.
    Ghavanini AA1, Kimpinski K.

    "PYRIDOXINE EXCESS AND NEUROPATHY Several individual cases of neuropathy attributed to excessive pyridoxine intake have been reported in the literature. These cases all involve high doses of pyridoxine ranging from 2 to 10 g. Various temporal evolutions (eg, gradual vs. subacute onset) and pathophysiologic patterns (sensory neuronopathy, sensory and autonomic neuropathy, axonal sensory-motor neuropathy, and demyelinating sensory-motor neuropathy) have been reported in association with pyridoxine excess. The patients had a wide age range (31–81 years). Although occasional improvements in motor symptoms were reported, the inherent selection bias of case reports does not allow generalization of the data. In a case series of 7 patients taking 2–6 g/d of vitamin B6, all patients showed severe sensory neuropathy. None of the patients showed motor involvement, and all patients improved upon discontinuation of this vitamin."

    There used to be dogma about B vitamin "balance" protecting against B6 neuropathy.. But there a recent case series notes pyridoxine toxicity in a B1/B6/B12 combination:

    http://www.ncbi.nlm.nih.gov/pubmed/25056196
    Neurol Sci. 2014 Jul 24.
    Pyridoxine-induced sensory ataxic neuronopathy and neuropathy: revisited. Kulkantrakorn K.

    "High dose pyridoxine is neurotoxic. Previous case reports were sparse and little is known about the clinical and electrodiagnostic findings. Three patients with pyridoxine-induced sensory ataxic neuropathy were studied and a review of the involved literature was performed. Three patients, aged 80, 83 and 83 years old, presented with sensory ataxia for 3-8 months. Examination showed signs of polyneuropathy and sensory ataxia. Six hundred milligrams of pyridoxine was consumed each day for 3-10 years, in the form of vitamin B1-6-12 combination tablet. Investigations for other causes of neuropathy were unremarkable. Blood levels of vitamin B6 were markedly elevated at 104.6, 81.4 and 66.9 times of upper normal limits. Electrodiagnostic tests showed symmetric axonal sensory polyneuropathy in two patients. Two years after vitamin discontinuation, all patients showed no significant improvement in the neuropathy and gait. In conclusion, consumption of high dose pyridoxine can cause sensory neuronopathy and axonal sensorimotor polyneuropathy, leading to sensory ataxia which may not be reversible."
     
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