Vitamin B6 Pyridoxine/P-5-P information:

mrsD · 10-24-2007, 11:28 AM

I've been meaning to start an informational thread here for Vitamin B6 Pyridoxine. So here it is.

Please feel free to post here anything you feel is helpful to the subject, or ask questions. I will be adding to this thread frequently as I consolidate data that I find.

Many years ago, over 10 actually, I started posting about P-5-P on various health boards. This is an activated form of pyridoxine which is the form the body actually uses. Pyridoxine in most vitamins has to be converted to this form. That process may be inhibited by liver damage, or use of certain drugs (theophylline). Those interested in chemistry can view Pyridoxine here:
http://web.indstate.edu/thcme/mwking/vitamins.html

Today we have a new RX vitamin that contain P-5-P. It is called Metanx (promoted for neuropathies and homocysteine defense).
When looking at labels, look for the words coenzymated B6 as an ingredient.
The best manufacturers enteric coat their P-5-P like NOW brand does.

For now I'd like to give some links to B6 information.
This one is very good, and run by NIH
http://ods.od.nih.gov/factsheets/vitaminb6.asp

Another great source is The Linus Pauling Institute:
http://lpi.oregonstate.edu/infocente...nB6/index.html
This link provides alot of medical information about B6. It gives RDA recommendations, Toxicity warnings, and examples of food sources.

The University of Maryland has a great Alternative website, that cross references to drug use also.
http://www.umm.edu/altmed/articles/v...-b6-000337.htm

Vitamin B6 is really critical today. The lowering of homocysteine by conversion to SAM in the body is crucial for hundreds of chemical methylation reactions.
B6 works with B12 and folic acid to accomplish this.
So because of this focus, we hear more about B6 than we used to.
B6 is also used to prevent nausea in pregnancy. (the FDA approved its use a couple of years ago).

And B6 does so much, it is really very important to us. Over 100 drugs interfere with B6 in the body or deplete it.
Estrogens, many antibiotics, diuretics, INH, theophylline, penicillamine, Evista,
hydralazine are the families studied so far.

There has been an increased interest in a condition Pyroluria recently. This is a genetic trait that has an error in heme synthesis that creates a by-product called kryptopyrrole. While this is relatively harmless to the body, and is excreted in the urine, it complexes B6 and zinc while doing so and removes those nutrients from the body as well. We have an experienced poster who has done the testing here and I have invited her to come on this thread. Until then, the link below provides some information. I know there are others here, I just can't recall at this moment...so please feel free to post on this thread.
This can be tested using a urine sample, and requires a specialized laboratory to do it accurately. You can read more about that here:
http://www.pyroluriatesting.com/ This is the Pfeiffer Treatment Center

Vitamin B6 is a huge subject, so I will be adding to this thread as I gather data on various medical and alternative uses for it.

glenntaj · 10-24-2007, 03:31 PM

--just a question about the post--did you mean to put in a url link after the line "We have a long thread on Pyroluria here:" ? If you did, it didn't come up (at least for me).

mrsD · 10-24-2007, 03:47 PM

I recalled that long thread by Ona...then after looking here, I realized it was
on "that other forum"...

This happens when you get old you know...thoughts fly right out of your
brain sometimes and land somewhere else!

I'll edit the wording to reflect that.
I have asked a Pyroluria experienced person to come on...hope she does.

mrsD · 10-29-2007, 08:15 AM

This thread will have information about this complex subject.

B6 is the most documented B vitamin in regards to toxicity. It is ironic that B6 deficiency causes a neuropathy. And that extreme excess of this vitamin also causes nerve damage.

I've gathered some links to illustrate both points.
I hope those interested here will read them carefully.

Here is a typical PubMed monograph about toxicity:

Quote:

Ned Tijdschr Geneeskd. 2005 Nov 12;149(46):2545-6.Links

Comment in:
Ned Tijdschr Geneeskd. 2005 Nov 12;149(46):2541-4.
Ned Tijdschr Geneeskd. 2006 Feb 4;150(5):277; author reply 277.
Ned Tijdschr Geneeskd. 2006 Feb 4;150(5):278; author reply 278.

[How much vitamin B6 is toxic?]
[Article in Dutch]

Katan MB.

Wageningen Centre for Food Sciences en Wageningen Universiteit, afd. Humane Voeding, Bomenweg 2, 6703 HD Wageningen. martijn.katan@wur.nl

Vitamin B6 (pyridoxine) causes neuropathy at intakes of 1000 mg per day or more, which is about 800 times the daily intake from foods. There have also been occasional reports of toxicity at intakes of 100-300 mg per day. The US authorities set the no-observed-adverse-effect-level at 200 mg per day and the safe upper limit at 100 mg per day. A report of neurotoxicity in 2 patients who had taken 24 mg and 40 mg of vitamin B6 per day respectively, may be coincidence rather than a true toxic effect of such relatively low doses. However, physicians need to remain alert to high intakes of vitamin B6 as a cause of unexplained neuropathy.

PMID: 16320662 [PubMed - indexed for MEDLINE]

Because some people cannot activate B6 because pyridoxal kinase is damaged or not working for some genetic reason, B6 doses in that very low range may be indicative of NO active pyridoxal reaching the tissues.

Here is a good link I found at a nutrition website:
http://drirene.healthandage.com/qa3/qa280132.htm

And this one explains P-5-P and states that P-5-P has yet to have reported toxicities:
http://www.encyclopedia.com/doc/1G1-71948217.html

There have been over the years posters here and at another similar site,
asking why their plasma values of B6 are elevated, even though they do not
take supplements. It appears to be a puzzle, and I have always answered that perhaps they are not converting to active pyridoxal normally, and hence the B6 is high in the serum. B6 is however excreted as a water soluble vitamin by the kidneys.
Then I found this paper, that illustrated autistic patients, have elevated B6 levels:

Quote:

J Altern Complement Med. 2006 Jan-Feb;12(1):59-63.Click here to read Links
Abnormally high plasma levels of vitamin B6 in children with autism not taking supplements compared to controls not taking supplements.
Adams JB, George F, Audhya T.

Arizona State University, Tempe, AZ 85287-6006, USA. jim.adams@asu.edu

BACKGROUND: There have been many studies of the effect of high-dose supplementation of vitamin B6 on children and adults with autism, with all but one reporting benefits. OBJECTIVE: The aim of this study was to investigate the biochemical basis for vitamin B6 therapy by measuring the level of total vitamin B6 in the plasma of unsupplemented children with autism spectrum disorder compared to unsupplemented control subjects. PARTICIPANTS: Children with autism spectrum disorders (n = 35, age 3-9 years) and unrelated typical children (n = 11, age 6-9 years), all from Arizona, were studied. (This includes the data from 24 children with autism from our previous study.) METHODOLOGY: A microbiologic assay was used to measure the level of total vitamin B6 (including phosphorylated and unphosphorylated forms), in a blinded fashion. RESULTS: Children with autism had a 75% higher level of total vitamin B6 than the controls (medians of 56 versus 32 ng/mL, respectively, p = 0.00002). Most of the autistic children (77%) had levels that were more than 2 standard deviations above the median value of the controls. The autistic girls (n = 5) also had elevated levels (mean of 54.6 ng/mL, median of 60 ng/mL). DISCUSSION: These results are consistent with previous studies that found that: (1) pyridoxal kinase had a very low activity in children with autism and (2) pyridoxal 5 phosphate (PLP) levels are unusually low in children with autism. Thus, it appears that the low conversion of pyridoxal and pyridoxine to PLP results in low levels of PLP, which is the active cofactor for 113 known enzymatic reactions, including the formation of many key neurotransmitters. CONCLUSIONS: Total vitamin B6 is abnormally high in autism, consistent with previous reports of an impaired pyridoxal kinase for the conversion of pyridoxine and pyridoxal to PLP. This may explain the many published studies of benefits of high-dose vitamin B6 supplementation in some children and adults with autism.

PMID: 16494569 [PubMed - indexed for MEDLINE]

Vitamin B6 is just very critical for our bodies to maintain health.
In the past there were experimental studies giving very high doses daily for PMS (500mg a day) and Carpal Tunnel Syndrome. The actual number of reported toxicities from these megadoses, was in the range of 15-20 patients, which is not really common. Given that people do not know their status of pyridoxal kinase, increasing doses past 100mg a day of regular pyridoxine, is not really going to increase one's response. So if you do not feel better, with B6 or if your homocysteine levels do not go down when you use it in conjunction with B12 and folic acid, then you need to consider taking the activated form called P-5-P. You may have to buy this online, but I have found it in stores, that carry, NOW brand aggressively. It is not as inexpensive as folic acid, but it is not really out of reach of most people, that is it is fair in price. A good quality P-5-P will be enteric coated to protect it from stomach acids.

There are a small number of people with a genetic disorder called pyridoxine dependency.
http://www.emedicine.com/ped/byname/...-syndromes.htm
This typically manifests in infancy as intractable seizures. And is reversed with very high doses of B6. This requires a doctor's supervision to find the dose of pyridoxine that works for each patient.

Also for pyroluria patients, B6 is critical. I suggest for these patients that P-5-P be used, since it is far more efficient biologically. 50mg/day is enough and any further increase in dose should be monitored by a doctor.

I had this link in my older B6 thread, and it is still active on the net:
http://www.nutrition4health.org/NOHAnews/NNSp99B6.html
and in this that link is this quote about P-5-P:

Quote:

I've heard criticisms that pyridoxal 5-phosphate is destroyed in the stomach or in the gut. These criticisms have come, without documentation,

Then next, the pyridoxine phosphate has to be oxidized by an oxidase enzyme that is assisted by vitamin B2, riboflavin, as flavin mononucleotide, "FMN." Here's one of the rubs in supplementing with pyridoxine. If vitamin B2 is low as FMN, then the rate of P 5-P production is typically decreased by 60%.

from pyridoxine fans. Actually, it's likely that some of the phosphate is knocked off. That's alkaline phosphatase's job--to rearrange the phosphate supply. But who cares? We've still got the pyridoxal--stomach won't make pyridoxine from pyridoxal. And once absorbed, the pyridoxal is more readily phosphorylated-according to the very authoritative enzymology reference cited earlier. And, the pyridoxal doesn't need FMN and another enzyme to reach the coenzyme form.

At the Klaire Laboratories International Symposium in Athens, Greece, in 1995, Dr. Emar Vogelaar reported on blood analyses of human subjects taking pyridoxal 5-phosphate. He found a better than 15% average increase in blood pyridoxal after two weeks of supplementation with 50 milligrams per day. So, there's no question about bioavailability-it gets in.

Finally, there's the problem of interfering vitamers in pyridoxine (substances that are similar to pyridoxine). At doses above 500 milligrams per day, peripheral or sensory neuropathy can occur in some individuals. This was widely reported over 10 years ago. Pyridoxine took the blame, but less publicized research later focussed the blame on vitamer impurities in the pyridoxine. Nothing is 100% pure, and pyridoxine is no exception: 4-deoxypyridoxine and methoxy-pyridoxine are known pyridoxine antagonists. However, when pyridoxine is carefully processed through several refinements to form pyridoxal 5-phosphate, the concentration of interfering vitamers drops substantially. Also, less P 5-P is needed than pyridoxine. No controlled studies have given exact comparisons, but I've found 50 milligrams per day of P 5-P to do the work of 200 to 500 milligrams of pyridoxine hydrochloride. Also, some case histories are worthwhile here. Several individuals presenting sensory neuropathy following high doses of pyridoxine had their conditions completely relieved by discontinuing the pyridoxine, taking no B6 in any form for 3 days, then taking 50 milligrams per day P 5-P for five days with no further symptoms.

To summarize, pyridoxal 5-phosphate has the advantages over pyrodoxine hydrochloride of:

* Being the actual coenzyme form,
* Avoiding the need of oxidation to pyridoxal, which requires FMN,___ which in turn has to be formed from vitamin B2 (riboflavin), which itself has to be phosphorylated-something that occurs in the intestinal mucosa and depends on proper mucosal function. And this phosphorylation of riboflavin is magnesium dependent.
* Pyridoxal phosphate may avoid phosphorylation, which may be zinc-dependent or magnesium-dependent in humans and could be a weak step if there is zinc or magnesium insufficiency.
* The P 5-P form is purer, and less is needed to achieve the same cofactor effects.
* To my knowledge no sensory neuropathy has ever been reported with use of P 5-P.

So, P 5-P has the edge over pyridoxine in magnesium deficiency, in zinc deficiency, in purity, and in potency.

Edit to add: Here is a paper from 1992...where 5 normal people were given massive doses of pyridoxine 1 to 3 grams/day (1000 to 3000mg)--all five reacted with nerve damage:

Quote:

Neurology. 1992 Jul;42(7):1367-70.Links
Dose response, coasting, and differential fiber vulnerability in human toxic neuropathy: a prospective study of pyridoxine neurotoxicity.
Berger AR, Schaumburg HH, Schroeder C, Apfel S, Reynolds R.

Department of Neurology, Albert Einstein College of Medicine, Bronx, NY.

We administered either 1 or 3 g/d of pyridoxine (vitamin B6) to five healthy volunteers and repeatedly followed serum pyridoxal phosphate levels, clinical symptoms and signs, quantitative sensory thresholds (QSTs), and sural nerve electrophysiology. Pyridoxine was discontinued at the first sign of either clinical or laboratory abnormality. In all subjects, sensory symptoms and QST abnormalities occurred concurrently. Subjects receiving higher doses became symptomatic earlier than low-dose subjects. Elevation of thermal QSTs preceded or exceeded that for vibration in the three low-dose subjects; vibration and thermal QST became abnormal simultaneously in the higher-dose subjects. A reduction in the amplitude of the sural sensory potential lagged behind QST changes in two of three subjects. Symptoms continued to progress ("coasting") for 2 to 3 weeks despite stopping pyridoxine administration and the return of serum pyridoxal phosphate levels to normal. This study suggests that (1) there is a clear dose-percent relationship for pyridoxine-induced neuropathy, (2) QST is a sensitive measurement for detecting early peripheral neuropathy; QST abnormalities may precede changes in nerve conduction studies, (3) coasting appears unrelated to persistently elevated blood levels of the toxin, and (4) a dose-dependent vulnerability may exist among nerve fibers of different caliber when exposed to an axonal toxin, such as pyridoxine.

PMID: 1620347 [PubMed - indexed for MEDLINE]

theresej · 11-03-2007, 02:31 PM

mrsd, thank yo for this information. My PCP and I have been trying to understand why my B6 has been elevated.

I have discovered that even though my B12 is well within normal (last was over 700) I am functionally deficient in methyl-B12 as evidenced by lowering of my homocystiene levels to below high normal for the first time a week after starting sublingual methyl-B12 mega doses - this was a few weeks ago. I have developed a number of neurological symptoms, especially over the last year and a half that appeared to mimic MS. Many of those symptoms are improving now.

I guess its not such a far stretch of the imagination that my ability to covert B6 into P5P might be impaired as well.

mrsD · 11-11-2007, 02:36 PM

Today I am searching for more pyridoxal kinase problems. When I was first on the net 10 yrs + ago the data on pyridoxal kinase was just being released in some nutrition journals. Today there is much more available.

Here is an interesting 2007 paper that found that certain things in Gingko
block the actions of pyridoxal kinase:

Quote:

FEBS J. 2007 Feb;274(4):1036-45. Epub 2007 Jan 19.Click here to read Links
The human pyridoxal kinase, a plausible target for ginkgotoxin from Ginkgo biloba.
Kästner U, Hallmen C, Wiese M, Leistner E, Drewke C.

Institut für Pharmazeutische Biologie, Universität Bonn, Germany.

Ginkgotoxin (4'-O-methylpyridoxine) occurring in the seeds and leaves of Ginkgo biloba, is an antivitamin structurally related to vitamin B(6). Ingestion of ginkgotoxin triggers epileptic convulsions and other neuronal symptoms. Here we report on studies on the impact of B(6) antivitamins including ginkgotoxin on recombinant homogeneous human pyridoxal kinase (EC 2.7.1.35). It is shown that ginkgotoxin serves as an alternate substrate for this enzyme with a lower K(m) value than pyridoxal, pyridoxamine or pyridoxine. Thus, the presence of ginkgotoxin leads to temporarily reduced pyridoxal phosphate formation in vitro and possibly also in vivo. Our observations are discussed in light of Ginkgo medications used as nootropics.

PMID: 17250738 [PubMed - indexed for MEDLINE]

And here is a paper on racial differences in red blood cells and pyridoxal kinase:

Quote:

Haematologica. 2006 Jun;91(6):801-4. Epub 2006 May 16.Click here to read Links
The genetic basis of human erythrocyte pyridoxal kinase activity variation.
Flanagan JM, Beutler E.

Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA.

Thirty years ago we reported that erythrocyte pyridoxal kinase activity of African-Americans was strikingly lower than that of persons with European ancestry in a tissue-specific manner. At the time, it was impossible to elucidate the mechanism by which evolution had selectively lowered the enzyme activity in one cell type but not in others. We have now identified a promoter mutation with potential erythroid-specific properties that could be the basis of a novel mechanism of controlling cell-specific decreased activity of an essential enzyme.

PMID: 16704963 [PubMed - indexed for MEDLINE]

I don't have access however to the whole paper, to understand the meaning of it.

This paper is from 1997...and mentions alcohol:

Quote:

Eur J Clin Nutr. 1997 Nov;51 Suppl 3:S39-45.Links
Dietary and other determinants of vitamin B6 parameters.
Brussaard JH, Löwik MR, van den Berg H, Brants HA, Bemelmans W.

TNO Nutrition and Food Research Institute, Zeist, The Netherlands.

OBJECTIVE: To assess the dietary, physical, biochemical and lifestyle determinants of vitamin B6 status parameters among healthy adults. DESIGN AND SUBJECTS: Dietary intake and status variables as well as other relevant characteristics were determined among 444 adults, aged 20-79 y and stratified for sex and 10-years age classes with a randomly selected control group (n = 300) and an over representation of persons with a low habitual vitamin B6 intake (n = 144). RESULTS AND CONCLUSIONS: The direct status parameters (plasma pyridoxal-5'-phosphate (PLP), plasma pyridoxal + PLP (PL + PLP), and 4-pyridoxic acid (4-PA) excretion) were clearly related to dietary variables and plasma concentrations of vitamin C (women only), vitamin B12 and folate. The total percentage of variance in p-PLP explained in multivariate regression analysis was 41 and 30% in men and women, respectively. The most important explaining variables besides vitamin B6 intakes were variables closely related to PLP-metabolism: albumin and alkaline phosphatase. Biochemical function related status parameters showed less statistically significant correlations with dietary variables. Four to 24% of the variance in the stimulation coefficients of erythrocyte aspartate aminotransferase (alpha-EAST) and erythrocyte alanine aminotransferase (alpha-EALT) and change in homocysteine excretion after a methionin load was explained by a combination of dietary, physiological and lifestyle related variables. The low percentages explained for some variables, notably alpha-EAST (women) and the change in homocysteine excretion after a methionin load (men), suggests that these parameters are not sensitive to the level of vitamin B6 intake as found in the present study. Alcohol contributed in many of the explaining models for vitamin B6 status parameters. Therefore, when assessing the vitamin B6 status of a population, it is important to estimate the level of alcohol intake as well. Furthermore, the results illustrate the importance of sex related differences in the metabolism of some parameters, especially homocysteine excretion. The variance in the clinical function related status parameter measured in the present study, handgripstrength, was explained for 50% by a combination of age, body weight and Quetelet Index (QI) with no important contribution of dietary variables.

PMID: 9598767 [PubMed - indexed for MEDLINE]

This is another version of that paper...

Quote:

1: Eur J Clin Nutr. 1997 Nov;51 Suppl 3:S32-8.Links
Micronutrient status, with special reference to vitamin B6.
Brussaard JH, Löwik MR, van den Berg H, Brants HA, Kistemaker C.

TNO Food and Nutrition Research Institute, Zeist, The Netherlands.

OBJECTIVE: To assess the adequacy of micronutrient status among the adult population, with special reference to vitamin B6 status. DESIGN AND SUBJECTS: Micronutrient status was assessed among a random sample of the adult Dutch population (reference group, n = 300), aged 20-79 y, stratified for age and gender, and among a group with a low vitamin B6 intake (n = 144). RESULTS: Low vitamin B6 groups had lower mean levels of erythrocyte and plasma pyridoxal (PL) and pyridoxal-5'-phosphate (PLP), urinary excretion of 4-pyridoxic acid, basal and stimulated erythrocyte aspartate aminotransferase (EAST) and erythrocyte alanine aminotransferase (EALT) activities and EAST stimulation coefficients but not of EALT stimulation coefficients, handgripstrength and 24 h homocysteine excretion before and after a methionin load test. Besides, plasma levels of vitamin C, B12 and folate were lower among low B6 than among reference groups indicating a combined low vitamin status. Direct biomarkers of vitamin B6 intake (plasma PLP and 4-pyridoxic acid excretion) were significantly related to more functional parameters (EAST, EALT and alpha-EAST). Among random reference groups the prevalence of plasma PLP values below 19 nmol/l was 3-7% for different age-gender groups, with the highest value of 16% among men aged 50-79 years. The prevalence of high values of erythrocyte glutathion reductase stimulation coefficient (alpha-EGR) and low levels of serum vitamin B12 and C was not more than 5% among different age-gender reference groups. CONCLUSIONS: Direct biomarkers of vitamin B6 intake confirmed the preselection of a group with a low vitamin B6 intake. The results suggest that the sensitivity of vitamin B6 status parameters for low vitamin B6 intake was highest for the direct vitamin B6 status parameters and lowest for handgripstrength and homocysteine excretion after a methionin load; results for enzyme stimulation coefficients were intermediate. The prevalence of below adequate status parameters for vitamin B2, B6, B12 and C was not more than 7% among the different age-gender groups, with the exception of a value of 16% for plasma PLP levels below 19 nmol/l among men aged 50-79.

PMID: 9598766 [PubMed - indexed for MEDLINE]

Zinc deficiency may impact B6 metabolism:

Quote:

Nutr Rev. 1990 Jun;48(6):255-8.Links
Zinc and the regulation of vitamin B6 metabolism.
[No authors listed]

Pyridoxal kinase, a key enzyme in the formation of vitamin B6 coenzymes, requires a zinc-ATP complex as a substrate. Recent findings show that zinc-metallothionein facilitates the formation of the zinc-ATP complex. Thus, the concentration of zinc-metallothionein in tissues may serve in the regulation of vitamin B6 metabolism.

PMID: 1365753 [PubMed - indexed for MEDLINE]

This is a huge article and note the date 1982:

Quote:

Q Rev Drug Metab Drug Interact. 1982;4(4):289-331.Links
Drug-pyridoxal phosphate interactions.
Ebadi M, Gessert CF, Al-Sayegh A.

In this review it has been pointed out that vitamin B6 and its vitamers can be involved in many interactions with a number of drugs, as well as with the actions of various endocrines and neurotransmitters. Nutritional deficiencies, especially of vitamins and proteins, can affect the manner in which drugs undergo biotransformation, and thereby may also modify the therapeutic efficacy of certain drugs. The differences between nutritional vitamin B6 deficiency and the hereditary disorder producing pyridoxine dependency are discussed. In addition to a pyridoxine deficiency being able to adversely affect drug actions, the improper supplementation with vitamin B6 can in some instances also adversely affect drug efficacy. A decrease by pyridoxine in the efficacy of levodopa used in the treatment of Parkinsonism is an example. The interrelationships and enzymatic interconversions among pyridoxine vitamers, both phosphorylated and non-phosphorylated, are briefly discussed, particularly regarding their pharmacokinetic properties. The ways in which the normal biochemical functions of vitamin B6 may be interfered with by various drugs are reviewed. (1) The chronic administration of isoniazid for the prevention or treatment of tuberculosis can produce peripheral neuropathy which can be prevented by the concurrent administration of pyridoxine. An acute toxic overdose of isoniazid causes generalized convulsions, and the intravenous administration of pyridoxine hydrochloride will prevent or stop these seizures. (2) The acute ingestion of excessive monosodium glutamate will, in some individuals, cause a group of symptoms including among others headache, weakness, stiffness, and heartburn, collectively known as the 'Chinese Restaurant Syndrome.' These symptoms can be prevented by prior supplementation with vitamin B6. The beneficial effect is ascribed to the correction of a deficiency in the activity of glutamic oxaloacetic transaminase, an enzyme that is dependent on pyridoxal phosphate. Some interesting relationships are pointed out between vitamin B6, picolinic acid, and zinc. It is postulated that the intestinal absorption of zinc is facilitated by picolinic acid, a metabolite of tryptophan. The derivation of picolinic acid from tryptophan depends on the action of the enzyme kynureninase, which is dependent on pyridoxal phosphate; therefore, the adequate absorption of zinc is indirectly dependent on an adequate supply of vitamin B6. The formation of pyridoxal phosphate, on the other hand, appears to be indirectly dependent on Zn2++ which activates pyridoxal kinase.(ABSTRACT TRUNCATED AT 400 WORDS)

PIP: This review examines the interaction of pyridoxal phosphate with select neuroendocrine and neuropharmacological systems and their health related therapeutic implications. Vitamin B6 and its vitamers can be involved in many interactions with a number of drugs as well as the actions of various endocrines and neurotransmitters. Nutritional deficiencies, particularly of vitamins and proteins, can affect the manner in which drugs undergo biotransformation and thus may modify the therapeutic efficacy of certain drugs. In addition to pyridoxine deficiency adversely affecting drug actions, improper supplementation with viatmin B6 can in some instances also adversely affect drug efficacy. A decrease by pyridocxine in the efficacy of levodopa used in the treatment of Parkinsonism is an example. The interrelationships and enzymatic interconversions amony pyridoxine vitamers, both phosphorylated and nonphosphorylated, are briefly discussed, particularly concerning their pharmacokinetic properties. The chronic administration of isoniazid for the prevention or treatment of tuberculosis can produce peripheral neuropathy which can be prevented by the concurrent administration of pyridoxine. An acute toxic overdose of isoniazid causes generalized convulsions, and the intravenous administration of pryidoxine hydrochloride prevents or stops these seizures. The acute ingestion of excessive monosodium glutamate will, in some persons, cause a group of symptoms, including headache, weakness, stiffness, and heartburn, collectively known as the "Chinese Restaurant Syndrome." These symptoms can be prevented by prior supplementation with vitamin B6. It is postulated that the intestinal absorption of zinc is facilitated by picolinic acid, a metabolite of tryptophan. The derivation of picolinic acid from tryptophan depends on the action of the enzyme kynureninase, which is dependent on pyridoxal phosphate. Therefore, the adequate absorption of zinc is indirectly dependent on an adequate supply of vitamin B6. The formation of pyridoxal phospate appears to be indirectly dependent on Zn2++ which activates pyridoxal kinase. Treatment with daily pyridoxine can reverse a state of depression induced in women who take oral contraceptives (OCs). 1 hypothesis to explain this effect is that the OC is somehow causing a deficiency of seroton serotonin in the brain and that the vitamin B6 helps to overcome this deficiency through the stimulation of 5-hydroxytryptophan decarboxylase by pyridoxal phosphate. In sum, the stimulation of 5-hydroxytryptophan decarboxylase by pyridoxal phosphate. In sum, pyridoxal phosphate in physiological concentrations seems to function as an endogenous "down regulator" of several receptor sites, including estrogen, progesterone, and androgen.

PMID: 6087425 [PubMed - indexed for MEDLINE]

lahgarden · 11-13-2007, 06:15 PM

Dear MrsD.

How would you feel about publishing a book entitled, "Vitamin b6 for dummies"?

I'm lost.

I suppose being six weeks into another neuro flare and loaded for bear with baclofen doesn't help my wee little brain.
But a gigantic THANK YOU to you for your helpful post and info.

b12 started @ 220 now up to 668! after nearly 2 years (big whup.)
b6- 92 ?!?!? what in the world- I don't even take vitamins but occassionally!

neuro is going to test zinc in this boat load of blood work.....he suspects my kidney issues to be partly the culprit..........I/he has no idea where to look for info, he's been asking around in his circles and no one knows anything about it.

This is a huge help, I can email my neuro with a the info you posted.

thanks so much!
lah

ps. Hi therese

rose · 11-13-2007, 07:06 PM

Lah,

Sorry if we've already done this, but what type of B12 and how much have you been taking these two years?

rose

mrsD · 02-18-2008, 06:06 PM

With all the questions on other forums here about antidepressants, I thought it would be helpful to bump up this post, since B6 is so important to serotonin synthesis...

watsonsh · 02-18-2008, 10:32 PM

Thanks Mrsd..I did not know about the connection to serotonin.

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