7 replies to this topic

[ajnast4r]

now i know that ortho-core has rather odd (in comparison to other multis) levels of B vitamins... what AOR claims to be ideal based on clinical research.
im not sure exactly why they chose the levels they did , other than thiamine which will not be absorbed above 12mg in a single dose.

ive also read that dosing more than 200mg of b6 will create a physical dependency.


so ide just like to open the discussion on B vitamins... is there any real benefit to taking doses that could NEVER be achieved through food alone? what levels are ideal, dangerous, and why.

[health_nutty]

Nice topic. I unfortunately don't have much to offer.
When you look at ortho-core ingredients the nutrients that are at doses that would be impossible (or difficult) to get through food are:

1) Most of the b-vitamins
2) mixed tocopherols and tocotrienols
3) Vitamin D.
4) Vitamin K2 (K1 form is abundant, but not K2)

[s123]

The composition of 9 tablets:

B1 (Thiamine) …………………………………... 9 mg 750%
B2 (Riboflavin) ………………………………….. 2.5 mg 192%
B3 (Niacin (as 144 mg Inositol Hexanicotinate))… 115 mg 718%
B5 (d-Ca Pantothenate)………………………….. 100 mg 2000%
B6 (Pyridoxine)…………………………………… 25 mg 1470%
B12 (Cyanocobalamin)…………………………… 24 mcg 1000%
Folic Acid…………………………………………. 800 mcg 400%
Biotin……………………………………………… 300 mcg 1000%
Pyrroloquinoline quinone (PQQ)………………… 30 mcg *
Choline (from Bitartrate 500 mg)………………… 200 mg 36%
Inositol (from Inositol, Inositol Hexanicotinate)…… 100 mg *

For lowering homocystein Kurzweil advises in his book to take:
- 25 to 100 mg B2
- 50 to 100mg B6
- 100 to 2000mcg B12
- 800 to 10000mcg folic acid

[krillin]

With B2, benefits saturate pretty early on. The MTHFR polymorphism is cured by 1.6 mg. If you don't have the polymorphism, extra B2 won't affect homocysteine at all.

Circulation. 2006 Jan 3;113(1):74-80.
Comment in:Circulation. 2006 Jul 25;114(4):e65; author reply e66.
Riboflavin lowers homocysteine in individuals homozygous for the MTHFR 677C->T polymorphism.
McNulty H, Dowey le RC, Strain JJ, Dunne A, Ward M, Molloy AM, McAnena LB, Hughes JP, Hannon-Fletcher M, Scott JM.
Northern Ireland Centre for Food and Health, School of Biomedical Sciences, University of Ulster, Coleraine, Northern Ireland. h.mcnulty@ulster.ac.uk

BACKGROUND: Meta-analyses predict that a 25% lowering of plasma homocysteine would reduce the risk of coronary heart disease by 11% to 16% and stroke by 19% to 24%. Individuals homozygous for the methylenetetrahydrofolate reductase (MTHFR) 677C-->T polymorphism have reduced MTHFR enzyme activity resulting from the inappropriate loss of the riboflavin cofactor, but it is unknown whether their typically high homocysteine levels are responsive to improved riboflavin status. METHODS AND RESULTS: From a register of 680 healthy adults 18 to 65 years of age of known MTHFR 677C-->T genotype, we identified 35 with the homozygous (TT) genotype and age-matched individuals with heterozygous (CT, n=26) or wild-type (CC, n=28) genotypes to participate in an intervention in which participants were randomized by genotype group to receive 1.6 mg/d riboflavin or placebo for a 12-week period. Supplementation increased riboflavin status to the same extent in all genotype groups (8% to 12% response in erythrocyte glutathione reductase activation coefficient; P<0.01 in each case). However, homocysteine responded only in the TT group, with levels decreasing by as much as 22% overall (from 16.1+/-1.5 to 12.5+/-0.8 micromol/L; P=0.003; n=32) and markedly so (by 40%) in those with lower riboflavin status at baseline (from 22.0+/-2.9 and 13.2+/-1.0 micromol/L; P=0.010; n=16). No homocysteine response was observed in the CC or CT groups despite being preselected for suboptimal riboflavin status. CONCLUSIONS: Although previously overlooked, homocysteine is highly responsive to riboflavin, specifically in individuals with the MTHFR 677 TT genotype. Our findings might explain why this common polymorphism carries an increased risk of coronary heart disease in Europe but not in North America, where riboflavin fortification has existed for >50 years.

PMID: 16380544

Look at this ludicrous study. The active group got 400 mg and the placebo group got 25 mg! You can't absorb more than 20 mg and they seemed surprised that the placebo worked as well as the megadose. Peer pressure is real: PubMed gives 6 hits for "riboflavin 400 migraine."

Headache. 2004 Oct;44(9):885-90.
Comment in:Headache. 2006 Mar;46(3):531.
A combination of riboflavin, magnesium, and feverfew for migraine prophylaxis: a randomized trial.
Maizels M, Blumenfeld A, Burchette R.
Kaiser Permanente, Family Practice, Woodland Hills, CA, USA.

OBJECTIVE: To determine the efficacy for migraine prophylaxis of a compound containing a combination of riboflavin, magnesium, and feverfew. BACKGROUND: Previous studies of magnesium and feverfew for migraine prophylaxis have found conflicting results, and there has been only a single placebo-controlled trial of riboflavin. DESIGN/METHODS: Randomized double-blind placebo-controlled trial of a compound providing a daily dose of riboflavin 400 mg, magnesium 300 mg, and feverfew 100 mg. The placebo contained 25 mg riboflavin. The study included a 1-month run-in phase and 3-month trial. The protocol allowed for 120 patients to be randomized, with a preplanned interim analysis of the data after 48 patients had completed the trial. RESULTS: Forty-nine patients completed the 3-month trial. For the primary outcome measure, a 50% or greater reduction in migraines, there was no difference between active and "placebo" groups, achieved by 10 (42%) and 11 (44%), respectively (P=.87). Similarly, there was no significant difference in secondary outcome measures, for active versus placebo groups, respectively: 50% or greater reduction in migraine days (33% and 40%, P=.63); or change in mean number of migraines, migraine days, migraine index, or triptan doses. Compared to baseline, however, both groups showed a significant reduction in number of migraines, migraine days, and migraine index. This effect exceeds that reported for placebo agents in previous migraine trials. CONCLUSION: Riboflavin 25 mg showed an effect comparable to a combination of riboflavin 400 mg, magnesium 300 mg, and feverfew 100 mg. The placebo response exceeds that reported for any other placebo in trials of migraine prophylaxis, and suggests that riboflavin 25 mg may be an active comparator. There is at present conflicting scientific evidence with regard to the efficacy of these compounds for migraine prophylaxis.

PMID: 15447697

[krillin]

For B6, you can't convert more than 50 mg of pyridoxine to pyridoxal. The rest acts as a B6 receptor blocker and causes B6 toxicity.

Most of B6's homocysteine lowering effect is from the first 2.7 mg or so.

At these high B6 intakes[2.7-4.6 mg], there is little effect of B6 intake on homocysteine levels, which are mainly affected by changes in intake at much lower intakes.

[krillin]

The only B12 doses that make sense are 5-6 mcg and 500+ mcg. 5-6 mcg is about as much as you can absorb with intrinsic factor. If you lack intrinsic factor or are taking methylcobalamin sublingually to bypass liver conversion, passive diffusion is 0.5 - 1%.

[ajnast4r]

interesting on the b6 toxicity.. any references for that?
i thought b6 didnt start to become toxic until you got up to the 500mg range

[krillin]

interesting on the b6 toxicity.. any references for that?
i thought b6 didnt start to become toxic until you got up to the 500mg range

My wording was ambiguous. I meant to say that you can convert up to 50 mg, and the rest is useless or toxic at higher doses. 500 mg is a reasonable estimate for the beginning of the toxic range, but why take chances?

The toxicity mechanism is also more complicated than my off the cuff statement.

link

Interestingly, the effects of pyridoxine toxicity resemble those of pyridoxine deficiency. Rudman et al. [Rudman, D., Williams, P.J., "Megadose vitamins", NEJM, 309(8): 488-489, 1983.], proposed three mechanisms to describe the mechanism of pyridoxine toxicity. They are as follows: (1) Pyridoxine is a member of the pyridine family which are neurotoxic. The sparing of the central nervous system in pyridoxine toxicity can be explained by the limited transport of pyridoxine across the blood-brain barrier, in contrast to an unlimited gastrointestinal transport. Many of the cell bodies of peripheral sensory fibers are located in the dorsal ganglia outside the blood-brain barrier, whereas the cell bodies of the motor fibers are located within the spinal cord. This may explain the selective toxicity of pyridoxine for the sensory fibers of peripheral nerves. (2) Although some water-soluble vitamins depend on carriers for gastrointestinal absorption and hence transport is saturable, pyridoxine moves via passive transport. Also, pyridoxine must be converted to its active form, pyridoxal phosphate, via two enzymes, pyridoxal kinase and pyridoxine phosphate oxidase. High circulating pyridoxine can saturate these enzymes and then act as a biologically inactive competitive inhibitor of pyridoxal phosphate. Therefore, a pyridoxal phosphate deficiency is mimicked. (3) Finally, an additional toxic factor may reside in the impurities of the pharmaceutical product. FDA regulations allow a 2% impurity which increases exponentially when an individual is ingesting megadose amounts.