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Vitamin B6 Pyridoxine Uses and Abuses by Jeffrey Dach MD

Posted Jan 26 2011 7:17am

Vitamin B6, Pyridoxine Uses and Abuses
by Jeffrey Dach MD

More on Vitamin B6 Pyridoxine  ( link to this article

From Carolyn Rutter

Dear Dr. Dach,

I was reviewing your book so kindly made available online - for our online reference library but have declined to link it due to the first chapter not mentioning the extreme potential for irreversible nerve damage caused by vitamin B6 toxicity especially as most supplements do not provide any of the B vitamins in the active form. Pyridoxine requires riboflavin for conversion  and it is increasingly clear that unbalanced supplementation in susceptible individuals causes neuropathy of the classic kind but probably symptoms confused with other problems early on at so called 'safe' doses. Other B vitamins can also cause distressing or life threatening symptoms when taken in excess. The idea that water soluble = safe is a myth.

Carolyn Rutter


Dr Dach's Reply to Carolyn Rutter on Vitamin B6 Toxicity

Dear Carolyn,

Unlike other water soluble B vitamin which are safe at high doses, vitamin B6 (pyridoxine) can be toxic, causing sensory neuropathy at dosages above 300 mg per day.  The biologically active form of pyridoxine P-5-P (pyridoxal-5-phosphate) has no reported toxicity.  Therefore, P-5-P is the preferred form of vitamin B6.   Make sure your B Vitamin Complex uses the P-5-P version rather than plain old pyridoxine.

Articles with Related interest

Vitamin B6, Pyridoxine for Trigger Finger and Carpal Tunnel by Jeffrey Dach, MD

regards from
Jeffrey Dach MD

Links and References
J Inherit Metab Dis. 2006 Apr-Jun;29(2-3):317-26.
B6-responsive disorders: a model of vitamin dependency.
Clayton PT. Pyridoxal phosphate is the cofactor for over 100 enzyme-catalysed reactions in the body, including many involved in the synthesis or catabolism of neurotransmitters. Inadequate levels of pyridoxal phosphate in the brain cause neurological dysfunction, particularly epilepsy. There are several different mechanisms that lead to an increased requirement for pyridoxine and/or pyridoxal phosphate. These include:
(i) inborn errors affecting the pathways of B(6) vitamer metabolism;
(ii) inborn errors that lead to accumulation of small molecules that react with pyridoxal phosphate and inactivate it;
(iii) drugs that react with pyridoxal phosphate;
(iv) coeliac disease, which is thought to lead to malabsorption of B(6) vitamers;
(v) renal dialysis, which leads to increased losses of B(6) vitamers from the circulation; (vi) drugs that affect the metabolism of B(6) vitamers; and
(vii) inborn errors affecting specific pyridoxal phosphate-dependent enzymes. The last show a very variable degree of pyridoxine responsiveness, from 90% in X-linked sideroblastic anaemia (delta-aminolevulinate synthase deficiency) through 50% in homocystinuria (cystathionine beta-synthase deficiency) to 5% in ornithinaemia with gyrate atrophy (ornithine delta-aminotransferase deficiency). The possible role of pyridoxal phosphate as a chaperone during folding of nascent enzymes is discussed. High-dose pyridoxine or pyridoxal phosphate may have deleterious side-effects (particularly peripheral neuropathy with pyridoxine) and this must be considered in treatment regimes. None the less, in some patients, particularly infants with intractable epilepsy, treatment with pyridoxine or pyridoxal phosphate can be life-saving, and in other infants with inborn errors of metabolism B(6) treatment can be extremely beneficial


Peripheral Neuropathy
J UOEH. 1985 Jun 1;7(2):201-5.
[Peripheral sensory neuropathy produced by a megadose of vitamin B6]
[Article in Japanese]
Ohnishi A, Ishibashi H, Ohtani K, Matsunaga K, Yamamoto T.
Clinical cases of sensory neuropathy produced by a megadose of vitamin B6 have been reported in English literatures. We investigated the ordinary daily dosage and maximal dose of vitamin B6 widely adopted in Japan, and the amount of vitamin B6 per unit (per tablet, capsule or ampule) available in our medical practice. We concluded that in Japan it is very rare to administer such a large dose of vitamin B6 that produced sensory neuropathy described in the literatures.

In our experimental study, Sprague-Dawley rats were intraperitoneally given a total amount of 14,000 mg/kg of body weight of pyridoxine hydrochloride in ten separate doses. They developed an ataxic gait. The occurrence of the degeneration of nerve cell bodies and peripheral axons of lumbar primary sensory neurons were histologically demonstrated. Although in Japan no clinical cases of neuropathy produced by a megadose of vitamin B6 have been reported to our knowledge, it is necessary to be aware of the possible occurrence of such neuropathy among patients with polyneuropathy of unknown etiology or who have been receiving vitamin B6 for a long time.
Ann Rheum Dis. 2006 December; 65(12): 1666–1667.
Pyridoxine toxicity courtesy of your local health food store C D Silva and D P D'Cruz
Med J Aust. 1987 Jun 15;146(12):640-2.
Pyridoxine neuropathy.  Waterston JA, Gilligan BS.
Abstract A case of sensory neuropathy in a young woman due to long-term ingestion of pyridoxine, with subsequent recovery, is described. Pyridoxine neuropathy may occur after the long-term ingestion of doses as low as 200 mg a day. Because of its widespread use in the community, both the general public and the medical community need to be aware of this recently described complication of megavitamin therapy.
Neurology. 1985 Oct;35(10):1466-8. Sensory neuropathy with low-dose pyridoxine.Parry GJ, Bredesen DE.  We describe 16 patients with neuropathy associated with pyridoxine abuse. The clinical picture of a pure sensory central-peripheral distal axonopathy was consistent. Pyridoxine dose was 0.2 to 5 g/d, and duration of consumption before symptoms was inversely proportional to the daily intake. In all patients with adequate follow-up, improvement followed discontinuation of pyridoxine. The ready availability of up to 1-gram tablets makes it likely that this neuropathy will continue to be seen.
N Engl J Med. 1983 Aug 25;309(8):445-8.
Sensory neuropathy from pyridoxine abuse. A new megavitamin syndrome.
Schaumburg H, Kaplan J, Windebank A, Vick N, Rasmus S, Pleasure D, Brown MJ.
We describe seven adults who had ataxia and severe sensory-nervous-system dysfunction after daily high-level pyridoxine (vitamin B6) consumption. Four were severely disabled; all improved after withdrawal. Weakness was not a feature of this condition, and the central nervous system was clinically spared.
Indices of Pyridoxine Levels on Symptoms Associated with Toxicity: A Retrospective Study Aliya N. Chaudary;1 Adam Porter-Blake;2 Patrick Holford2
Conclusions: There appeared to be no association between symptoms associated with vitamin B6 toxicity and vitamin B6 dose (between 30mg and 230mg) during a period of 3–27 months. A suitable vitamin B6 NOAEL of 100 mg / day and a suitable LOAEL of 150 mg / day is suggested.
Neuromuscul Disord. 2008 Feb;18(2):156-8. Epub 2007 Dec 3.
Severe sensorimotor neuropathy after intake of highest dosages of vitamin B6.
Gdynia HJ, Müller T, Sperfeld AD, Kühnlein P, Otto M, Kassubek J, Ludolph AC.
We illustrate a white caucasian patient with a severe sensorimotor neuropathy due to vitamin B6 hypervitaminosis. The patient used the pendulum to calculate his daily metabolic demands and ingested 9.6g pyridoxine/day. To our knowledge, this is the highest dosage of vitamin B6 administered to humans over prolonged periods of time ever reported in the medical literature. The unique aspect of this case is the muscle weakness and motor findings on electrophysiological testing in what is suggested by the literature to be a pure sensory neuronopathy.
Funct Neurol. 1993 Nov-Dec;8(6):429-32. Sensory and motor neuropathy caused by excessive ingestion of vitamin B6: a case report.
Morra M, Philipszoon HD, D'Andrea G, Cananzi AR, L'Erario R, Milone FF.
Department of Neurology, San Bortolo Hospital U.L.SS. n. 8, Vicenza, Italy.
We describe a patient who developed a severe sensory and a mild motor neuropathy. This syndrome was due to massive and prolonged ingestion of vitamin B6 (10 g daily for 5 years). To our knowledge this is the first published case of motor neuropathy caused by chronic abuse of vitamin B6.
J Vet Sci. 2008 Jun;9(2):127-31.
Pyridoxine induced neuropathy by subcutaneous administration in dogs.
Chung JY, Choi JH, Hwang CY, Youn HY.
Department of Veterinary Internal Medicine, College of Veterinary Medicine, Seoul National University, Seoul 151-742, Korea.
To construct a sensory neuropathy model, excess pyridoxine (150 mg/kg s.i.d.) was injected subcutaneously in dogs over a period of 7 days. During the administrations period, the dogs experienced body weight reduction and proprioceptive loss involving the hindquarters. After pyridoxine administration was completed, electrophysiological recordings showed that the M wave remained at a normal state, but the H-reflex of the treated dogs disappeared at 7 days. The dorsal funiculus of L(4) was disrupted irregularly in the axons and myelin with vacuolation. The dorsal root ganglia of L(4), and sciatic and tibial nerves showed degenerative changes and vacuolation. However, the lateral and ventral funiculi of L(4) showed a normal histopathologic pattern. Although this subcutaneous administration method did not cause systemic toxicity and effectively induced sensory neuropathy, this study confirmed the possibility of producing a pyridoxine-induced sensory neuropathy model in dogs with short-term administration.

B6 Treatment for INH
Pediatr Emerg Care. 2010 May;26(5):380-1.
Isoniazid-induced status epilepticus in a pediatric patient after inadequate pyridoxine therapy.  Minns AB, Ghafouri N, Clark RF.  Division of Medical Toxicology, Department of Emergency Medicine, University of California, Rady Children's Hospital, San Diego, CA, USA.

BACKGROUND: Isoniazid (INH) is an effective treatment for tuberculosis and among the most common causes of drug-induced seizures in the United States. Isoniazid intoxication produces a characteristic clinical syndrome including seizures, metabolic acidosis, and, in severe cases, respiratory depression and coma.
CASE: A 10-month-old male infant was presented after being found with his father's INH. The patient was brought to a local hospital where he had a witnessed generalized seizure and was given 650 mg pyridoxine intravenously, which was based on a 70 mg/kg recommendation. Five hours after the time of ingestion, the patient developed recurrent generalized seizures. He was given diazepam and then loaded with phenobarbital 20 mg/kg, while awaiting more pyridoxine from the pharmacy. He received an additional 2 g pyridoxine for a suspected ingestion of approximately 2.7 g INH (290 mg/kg total dose), and his seizures subsequently resolved.
DISCUSSION: Treatment of INH toxicity must address correction of gamma-aminobutyric acid deficiency with pyridoxine replacement and management of life-threatening events. For poisonings in which the amount of INH ingested is known, pyridoxine is dosed on a gram-for-gram basis. Several reference textbooks recommend pyridoxine dosing in children to be 70 mg/kg. This was the justification for the initial pyridoxine dose administered in our case. However, after review of the referenced literature, the rationale supporting this recommendation remains unclear. Benzodiazepines should also be given with pyridoxine as they have been shown to have a synergistic effect in terminating seizures in animal models.
CONCLUSIONS: As soon as possible after INH overdose is suspected or diagnosed, pyridoxine should be administered in a dose approximately equal to the estimated amount of INH ingested regardless of the age of the patient.

pyridoxine-dependent epilepsy
Dev Med Child Neurol. 2010 Jul;52(7):e133-42. Epub 2010 Mar 29.
Seizures and paroxysmal events: symptoms pointing to the diagnosis of pyridoxine-dependent epilepsy and pyridoxine phosphate oxidase deficiency.
Schmitt B, Baumgartner M, Mills PB, Clayton PT, Jakobs C, Keller E, Wohlrab G.
Department of Neurology, University Children's Hospital, Steinwiesstrasse 75, Zurich, Switzerland.

AIM: We report on seizures, paroxysmal events, and electroencephalogram (EEG) findings in four female infants with pyridoxine-dependent epilepsy (PDE) and in one female with pyridoxine phosphate oxidase deficiency (PNPO).
METHOD: Videos and EEGs were analysed and compared with videos of seizures and paroxysmal events archived from 140 neonates. PDE and PNPO were proven by complete control of seizures once pyridoxine or pyridoxal 5'-phosphate was administered and by recurrence when withdrawn. Mutations in the antiquitin gene were found in three patients and in the PNPO gene in one child.
RESULTS: Seizures began within 48 hours after birth in four newborns and at age 3 weeks in one. Frequent multifocal and generalized myoclonic jerks, often intermixed with tonic symptoms, abnormal eye movement, grimacing, or irritability, were observed in all infants with PDE and PNPO, but rarely in the other archived videos of neonates. EEGs were inconstant and frequently no discernable ictal changes were recorded during the seizures and the paroxysmal events. In addition, interictal EEGs were inconclusive, with normal and abnormal recordings. In older children tonic-clonic seizures, abnormal behaviour, inconsolable crying, frightened facial expression, sleep disturbance, loss of consciousness, paraesthesia, or intermittent visual symptoms were described during controlled and uncontrolled withdrawal or insufficient dosage.
INTERPRETATION: PDE or PNPO should be considered in infants with prolonged episodes of mixed multifocal myoclonic tonic symptoms, notably when associated with grimacing and abnormal eye movements.
Chang Gung Med J. 2010 Jan-Feb;33(1):1-12.
Neonatal vitamin-responsive epileptic encephalopathies.Gospe SM Jr.
Departments of Neurology and Pediatrics, the Center on Human Development and Disability, University of Washington, Seattle, WA, USA.

The treatment of neonatal seizures generally relies on the use of one or more anticonvulsant medications along with evaluation and management of any underlying etiology. In some circumstances, neonatal seizures are refractory to therapy and result in poor outcomes, including death. Certain rare vitamin- responsive inborn errors of metabolism may present as neonatal encephalopathy with anticonvulsant-resistant seizures. Therefore, it is vital for the clinicians of caring for seizing encephalopathic newborns to consider these particular disorders early in the hospital course. Pyridoxine-dependent seizures are due to deficiency of alpha-aminoadipic semialdehyde dehydrogenase (antiquitin) which is encoded by ALDH7A1. Seizures in infants who are pyridoxine-dependent must be treated using pharmacologic doses of pyridoxine (vitamin B(6)), and life-long therapy is required. Despite medical therapy, developmental handicaps, particularly in expressive language, are common. Folinic acidresponsive seizures are treated withe supplements of folinic acid (5-formyltetrahydrofolate). Recently, patients with this condition were also demonstrated to be antiquitin deficient. Pyridoxal phosphate-dependent seizures result from a deficiency of pyridox(am)ine 5'-phosphate oxidase which is encoded by PNPO. Patients with this cause of seizures respond to pyridoxal phosphate but not to pyridoxine. This review discusses our current understanding of these three neonatal vitamin-responsive epileptic encephalopathies and a diagnostic and treatment protocol is proposed.
J Inherit Metab Dis. 2007 Feb;30(1):96-9. Epub 2006 Dec 23.
Pyridoxal 5'-phosphate may be curative in early-onset epileptic encephalopathy. Hoffmann GF, Schmitt B, Windfuhr M, Wagner N, Strehl H, Bagci S, Franz AR, Mills PB, Clayton PT, Baumgartner MR, Steinmann B, Bast T, Wolf NI, Zschocke J.Department of General Pediatrics, Ruprecht-Karls-University Heidelberg, Heidelberg, Germany.

Neonatal epileptic encephalopathy can be caused by inborn errors of metabolism. These conditions are often unresponsive to treatment with conventional antiepileptic drugs. Six children with pyridox(am)ine-5'-phosphate oxidase (PNPO) deficiency presented with neonatal epileptic encephalopathy. Two were treated with pyridoxal 5'-phosphate (PLP) within the first month of life and showed normal development or moderate psychomotor retardation thereafter. Four children with late or no treatment died or showed severe mental handicap. All of the children showed atypical biochemical findings. Prompt treatment with PLP in all neonates and infants with epileptic encephalopathy should become mandatory, permitting normal development in at least some of those affected with PNPO deficiency.
Cancer Epidemiol Biomarkers Prev. 2009 April; 18(4): 1197–1202.
Prospective Study of Plasma Vitamin B6 and Risk of Colorectal Cancer in Men
Jung Eun Lee,1 Haojie Li,3 Edward Giovannucci,1,4,5 I-Min Lee,2,4 Jacob Selhub,6 Meir Stampfer,1,4,5 and Jing Ma1

lower risk of colorectal cancer

Vitamin B6 may lower risk of colorectal cancer by preventing aberrations in one-carbon metabolism or by anti-inflammatory effects. We prospectively evaluated the association between plasma levels of pyridoxal 5′-phosphate (PLP; the active form of vitamin B6) and risk of colorectal cancer in a nested case-control study within the Physicians’ Health Study. Among 14,916 men who provided blood specimens in 1982–1984, we identified 197 incident colorectal cancer cases through 2000 and individually matched them to 371 controls by age and smoking status. Plasma PLP levels were positively correlated with cold cereal intake and with plasma levels of folate and vitamin B12 (age- and smoking-adjusted partial correction r=0.28–0.48) and slightly inversely correlated with body mass index (BMI, r=−0.11) and plasma levels of homocysteine, C-reactive protein (CRP), tumor necrosis factor-α receptor (TNF-αR)2, and interleukin (IL)-6 (r ranged from −0.23 to −0.14). With control for these factors and known risk factors for colorectal cancer, plasma PLP levels were significantly inversely associated with risk of colorectal cancer; compared with men in the lowest quartile, those with PLP in quartiles 2–4 had relative risks (RR, 95% confidence interval, CI) of 0.92 (0.55–1.56), 0.42 (0.23–0.75), and 0.49 (0.26–0.92; P-trend = 0.01), respectively. In conclusion, vitamin B6 may protect against colorectal cancer independent of other one-carbon metabolites and inflammatory biomarkers.
JAMA. 2010 Mar 17;303(11):1077-83.
Vitamin B6 and risk of colorectal cancer: a meta-analysis of prospective studies.Larsson SC, Orsini N, Wolk A.
CONTEXT: Mounting evidence indicates that vitamin B(6), a coenzyme involved in nearly 100 enzymatic reactions, may reduce the risk of colorectal cancer.
OBJECTIVE: To conduct a systematic review with meta-analysis of prospective studies assessing the association of vitamin B(6) intake or blood levels of pyridoxal 5'-phosphate (PLP; the active form of vitamin B(6)) with risk of colorectal cancer.
DATA SOURCES: Relevant studies were identified by a search of MEDLINE and EMBASE databases to February 2010, with no restrictions. We also reviewed reference lists from retrieved articles.
STUDY SELECTION: We included prospective studies that reported relative risk (RR) estimates with 95% confidence intervals (CIs) for the association between vitamin B(6) intake or blood PLP levels and the risk of colorectal, colon, or rectal cancer.
DATA EXTRACTION: Two authors independently extracted data and assessed study quality. Study-specific RRs were pooled using a random-effects model.
DATA SYNTHESIS: Nine studies on vitamin B(6) intake and 4 studies on blood PLP levels were included in the meta-analysis. The pooled RRs of colorectal cancer for the highest vs lowest category of vitamin B(6) intake and blood PLP levels were 0.90 (95% CI, 0.75-1.07) and 0.52 (95% CI, 0.38-0.71), respectively. There was heterogeneity among studies of vitamin B(6) intake (P = .01) but not among studies of blood PLP levels (P = .95). Omitting 1 study that contributed substantially to the heterogeneity among studies of vitamin B(6) intake yielded a pooled RR of 0.80 (95% CI, 0.69-0.92). The risk of colorectal cancer decreased by 49% for every 100-pmol/mL increase (approximately 2 SDs) in blood PLP levels (RR, 0.51; 95% CI, 0.38-0.69).
CONCLUSION: Vitamin B(6) intake and blood PLP levels were inversely associated with the risk of colorectal cancer in this meta-analysis.

Myocardial Infarction in Women
Circulation. 2009 August 25; 120(8): 649–655.
Plasma Vitamin B6 and Risk of Myocardial Infarction in Women
John H Page, MBBS, MSc, ScD,1 Jing Ma, MD, PhD,2 Stephanie E Chiuve, ScD,3 Meir J Stampfer, MD, DrPH,1,2,3,4 Jacob Selhub, PhD,5 JoAnn E Manson, MD, DrPH,1,2,4 and Eric B Rimm, ScD1,2,3   Vitamin B6 is widely involved in amino acid metabolism and is a modulator of several reactions important to cardiovascular health. We prospectively evaluated relationships between fasting plasma levels of vitamin B6, as pyridoxal phosphate (PLP), to subsequent myocardial infarction risk in women. We also evaluated the predictors of fasting plasma concentration of pyridoxal phosphate.
Participants were adult nurses who completed questionnaires, and updated exposures every 2 years since 1976. Subjects for this analysis were selected by a nested case control design. Blood samples were collected between 1989 and 1990. We restricted our analysis to those women who had provided fasting blood samples (≥10 hours since last meal). During follow-up through June 1998, 144 were diagnosed with myocardial infarction (fatal and non-fatal). Cases were matched 1:2 by age, cigarette smoking status, and month and fasting status at the time of blood collection. Conditional logistic regression was used to adjust for potential confounders, including anthropometric factors, dietary intake, and selected biomarkers. Linear regression was used to determine which variables predict fasting total PLP concentration among control women.Results
Median age at blood collection was 63. Among controls, lower estimated creatinine clearance, plasma total homocysteine and body mass index were statistically significant predictors of higher plasma PLP, as were higher dietary vitamin B6, and folate intake (all P <0.05).
Plasma levels of pyridoxal phosphate were inversely associated with risk of MI, the multivariable adjusted rate ratio (RR) between extreme quarters was 0.22 (95% CI 0.09,0.55; Ptrend=0.05). The effect of plasma PLP varied by age. Among women who were aged less than 60 at blood sampling, the RR (95%CI) comparing top vs. bottom quarter was 0.03 (0.002,0.48), whereas among older women the corresponding RR (95%CI) was 0.43 (0.15,1.25).

Fasting plasma concentration of pyridoxal phosphate was inversely associated with MI risk. Plasma PLP is positively correlated with dietary vitamin B6, and is inversely correlated with renal function and body mass index.
Am J Clin Nutr 89: 204-209, 2009.
Pyridoxal-5'-phosphate deficiency after intestinal and multivisceral transplantation1,2,3 Laura E Matarese, Igor Dvorchik, Guilherme Costa, Geoffrey J Bond, Darlene A Koritsky, Ronaldo P Ferraris, Riva Touger-Decker, Julie K O'Sullivan-Maillet and Kareem M Abu-Elmagd
Conclusions: Serial monitoring of serum PLP concentrations is recommended for PN-dependent patients with short-bowel syndrome before and after transplantation for early detection and prompt initiation of preemptive therapy. Long-term measurement at frequent intervals is also recommended, particularly for transplant recipients, to diagnose late deficiency despite achievement of CNA and to prevent toxicity from overdose.
most of the patients required oral maintenance replacement with 25–50 mg daily or every other day.
TABLE 1. Proposed protocol for treating pyridoxal-5'-phosphate (PLP) deficiency according to serum concentrations
Serum concentration1 Treatment
GREATER THAN 3.3 ng/mL No treatment
2.5–3.2 ng/mL Oral supplementation with 50 mg pyridoxine HCl/d
LESS THAN 2.5 ng/mL Initial single intravenous dose of 50 mg pyridoxine HCl followed by daily oral dose of 50 mg2

1 Normal reference range: 3.3–26 ng/mL.
2 Dose reduction or discontinuation of maintenance therapy was based on serum concentrations 25 and 50 ng/mL, respectively.

Depressive Symptomatology

J Am Coll Nutr. 2008 June; 27(3): 421–427. Vitamin B6 Is Associated with Depressive Symptomatology in Massachusetts Elders   Cristina Merete, MS, Luis M. Falcon, PhD, and Katherine L. Tucker, PhD Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University (C.M., K.L.T.), Northeastern University, Department of Sociology (L.M.F.), Boston, Massachusetts

PLP was significantly associated with CES-D score and depressive caseness in the total sample and in non-supplement users. Deficient levels of plasma PLP (plasma PLP < 20 nmol/L) approximately doubled the likelihood of depressive caseness. dietary vitamin B6 was significantly associated with CES-D score and depressive caseness.
Plasma PLP below 30 nmol/L has been used as an indicator of inadequate status [17,37-39] while a cutoff of 20 nmol/L indicates deficient concentrations [37,40,41]. Both cutoffs have been widely used in the literature and demonstrate utility in assessing adequacy of vitamin B6 intake.

Plasma pyridoxal 5'-phosphate in the US population
American Journal of Clinical Nutrition, Vol. 87, No. 5, 1446-1454, May 2008
Plasma pyridoxal 5'-phosphate in the US population: the National Health and Nutrition Examination Survey, 2003–20041,2,3,4
Martha Savaria Morris, Mary Frances Picciano, Paul F Jacques and Jacob Selhub
1 From the Jean Mayer US Department of Agriculture Human Nutrition Research Center on Aging at Tufts University (MSM, PFJ, JS) and the National Institutes of Health Office of Dietary Supplements (MFP)
Background: No large-scale, population-based study has considered the descriptive epidemiology of vitamin B-6 status with use of plasma pyridoxal 5'-phosphate (PLP), the indicator of vitamin B-6 adequacy used to set the current Recommended Dietary Allowance, which is 2 mg/d for all subgroups.
Objectives: We sought to examine the epidemiology of vitamin B-6 status in the US population.
Methods: In >6000 participants aged 1 y in the National Health and Nutrition Examination Survey (2003–2004), we considered relations between plasma PLP and various subject characteristics and examined trends in plasma PLP and homocysteine with vitamin B-6 intake, both overall and in selected subgroups.
Results: In males, plasma PLP decreased with age after adolescence only in nonusers of supplemental vitamin B-6. Regardless of supplement use, plasma PLP concentrations of women of childbearing age were significantly lower than those of comparably aged men, and most oral contraceptive users had plasma PLP <20 nmol/L. The prevalence of low plasma PLP was significantly >3% at vitamin B-6 intakes from 2 to 2.9 mg/d in all subgroups and at intakes from 3 to 4.9 mg/d in smokers, the elderly, non-Hispanic blacks, and current and former oral contraceptive users. Intakes from 3 to 4.9 mg/d compared with <2 mg/d were associated with significant protection from low plasma PLP in most subgroups and from hyperhomocysteinemia in the elderly.
Conclusions: Vitamin B-6 intakes of 3 to 4.9 mg/d appear consistent with the definition of a Recommended Dietary Allowance for most Americans. However, at that intake level, substantial proportions of some population subgroups may not meet accepted criteria for adequate vitamin B-6 status.

Relation between pyridoxal and pyridoxal phosphate concentrations in plasma, red cells, and white cells in patients with critical illness.
Vasilaki AT, McMillan DC, Kinsella J, Duncan A, O'Reilly DS, Talwar D.

It has long been recognized that the physiologic active coenzyme form of vitamin B-6, PLP, is required for normal nucleic acid and protein synthesis and for cellular multiplication. Vitamin B-6 deficiencies cause a more profound effect on humoral and cell-mediated immune function than do deficiencies of any other B-group vitamins (1). Indeed, low vitamin B-6 status appears to impair lymphocyte proliferation in normal subjects and patients with critical illness (11, 15). Therefore, it is of considerable importance to identify critically ill patients with true deficiency of vitamin B-6 and to avoid inappropriate supplementation of vitamins that brings the risk of tissue accumulation and toxicity.

Jeffrey Dach MD

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